The Science of Drinking

The Science of Drinking
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The Science of Drinking
How Alcohol Affects
Your Body and Mind
Amitava Dasgupta
ROWMAN & LITTLEFIELD PUBLISHERS, INC.

Lanham • Boulder • New York • Toronto • Plymouth, UK
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Published by Rowman & Littlefield Publishers, Inc.
A wholly owned subsidiary of The Rowman & Littlefield Publishing Group, Inc.
4501 Forbes Boulevard, Suite 200, Lanham, Maryland 20706
http://www.rowmanlittlefield.com
Estover Road, Plymouth PL6 7PY, United Kingdom
Copyright © 2011 by Amitava Dasgupta
All rights reserved. No part of this book may be reproduced in any form or by
any electronic or mechanical means, including information storage and retrieval
systems, without written permission from the publisher, except by a reviewer
who may quote passages in a review.
British Library Cataloguing in Publication Information Available
Library of Congress Cataloging-in-Publication Data

Dasgupta, Amitava, 1958–
The science of drinking : how alcohol affects your body and mind /
Amitava Dasgupta.
p. cm.
Includes bibliographical references and index.
ISBN 978-1-4422-0409-6 (cloth : alk. paper) — ISBN 978-1-4422-0411-9
(electronic)
1. Alcohol—Physiological effect. 2. Drinking of alcoholic beverages—
Psychological aspects. I. Title.
QP801.A3D37 2011
615'.7828—dc22
2010051613
™ The paper used in this publication meets the minimum requirements of
American National Standard for Information Sciences—Permanence of Paper
for Printed Library Materials, ANSI/NISO Z39.48-1992.
Printed in the United States of America
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To all responsible, law-abiding citizens
who drink sensibly in moderation
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Contents
Preface ix
1 Alcohol Use and Abuse: Past and Present 1
2 How the Human Body Handles Alcohol: A Guide
to Drinking Sensibly and Avoiding a DWI 15
3 How Alcohol Affects the Human Mind 37
4 Health Benefits of Moderate Alcohol Consumption 55
5 Harmful Effects of Chronic Alcohol Consumption 77
6 DWI and Alcohol Testing: Breath Analyzer versus
Blood Alcohol 101
7 Biomarkers of Alcohol Abuse 129
8 Pharmaceuticals, Drugs of Abuse, and Alcohol:
A Potentially Deadly Mix 153
9 Workplace Alcohol and Drug Testing: When Not
to Drink at All 173
10 Why Not to Drink at All When You’re Pregnant 191
11 Dangers of Moonshine Whiskey and Related Illegally
Produced Liquors 207
12 More Dangerous than Alcohol: Methanol and Ethylene Glycol 221
Index 249
About the Author 265
vii
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Preface
W hat happens when you drink your favorite cocktail? How does it
go from beverage to buzz? Or from buzz to blotto? As a practicing
toxicologist and researcher in the field of alcohol and drugs, I will present
answers for everything you ever wanted to know about drinking—from
what creates the high to how you reach a blood alcohol level that gets you
into trouble. Did you know that the smell we commonly perceive as alco-
hol is not alcohol but is from other volatile substances present in a drink?
Did you know that alcoholism is an illness and that proper treatment can
restore an alcoholic to a normal life? Overwhelming scientific research
and evidence points toward the beneficial effects of drinking in modera-
tion, including a lower risk of cardiovascular disease and stroke, a lower
risk of developing dementia with advancing age, and some increase in
longevity. Many people do not know that drinking red wine protects the
heart more than white wine, while beer, margaritas, and hard liquor are
less effective in providing such protection.
I want to share the latest scientific facts on the effect of alcohol on one’s
body and mind. Drinking in moderation is a good way to loosen inhibi-
tion in a relationship and let your creativity flow. The key is to distinguish
between drinking sensibly and drinking insensibly. Scientific research has
provided some guidance on how much and how often we should drink
to get the benefits of alcohol and at what point drinking hurts our bod-
ies. In addition, there are clear guidelines about how much alcohol is safe
to drink in an evening before driving home to avoid being charged with
a DWI. While those with advanced science backgrounds can decipher
the technical medical literature written about this subject, my goal is to
ix
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x Preface
present these scientific facts in a more accessible fashion that everyone

will be able to understand. I want to provide you with clear guidance on
what constitutes a healthy drinking habit based on scientific information.
In order to understand the effect of alcohol on the human body, I will
discuss the pharmacology and toxicology of alcohol so that readers will
understand the body’s response to alcohol. I also provide guidelines for
what amount of alcohol is safe before driving, explain why you should al-
ways consume alcohol with food, and why you should sip alcohol rather
than drinking it like soda or water. I also discuss the loopholes of alcohol
testing so that you’ll know if you have been wrongly charged with a DWI.
This book will also be useful for lawyers who need to understand the sci-
entific basis of alcohol testing and how the human body handles alcohol.
Most auto accidents are due to a deadly combination of drugs and alco-
hol. This book will focus on which particular combinations of drugs and
alcohol cause the most harm. Alcohol and recreational drugs are deadly
combinations and must be avoided at all times. Other than alcohol, meth-
anol and ethylene glycol (antifreeze) abuse is also common, especially in
winter, and such overdoses may be more life threatening than an alcohol
overdose. Most consumer health books don’t even address this issue. I
have provided many of the sources of the information covered in this
book in the notes at the end of each chapter so that advanced readers,
especially health care professionals, can go and read the source material
for more in-depth information. I hope readers enjoy this book and get all
the information they need on alcohol.
Amitava Dasgupta
Houston, Texas
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1

Alcohol Use and Abuse
Past and Present
A lcohol is a drug (pharmaceutical) with medicinal value. One of the

first drugs known to mankind, alcohol use can be traced back to
10,000 years ago. In pharmacology class we learn that another name for a
drug is “poison.” A drug is beneficial if consumed in recommended doses
but harmful if taken in excess. Most of the drugs used in medicine do not
have any abuse potential except for a few classes of drugs, such as benzo-
diazepines, which are used for anxiety and insomnia, and opioids, which
are used for treating severe pain. Commonly prescribed benzodiazepines
include alprazolam, lorazepam, temazepam, and diazepam, while opioids
include hydrocodone, hydromorphone, and oxycodone, among others.
Alcohol is the most widely used legal drug available without a prescrip-
tion. Another legal drug with high abuse potential available without a pre-
scription is tobacco. However, it is important to mention that tobacco has
no known health benefits, while drinking alcohol in moderation has many
health benefits, including prolonging life. Many studies have concluded
that moderate drinkers live longer than nondrinkers and enjoy a better
quality of health (see chapter 4). In addition, abuse potential of opioids
(both synthetic and natural opiates) is much higher than alcohol. Drinking
one drink or less a day may actually keep the doctor away, but consump-
tion of five or more drinks per day for a prolonged period makes a person
alcohol dependent. However, women, underage drinkers, the elderly, and
people with a genetic predisposition for addiction to alcohol may become
alcohol dependent with fewer drinks per day over a long period of time.
Another proof that alcohol is a drug is that it is known to interact with
many other drugs. For example, alcohol can be toxic to a person taking
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2 Chapter 1
Tylenol (acetaminophen) regularly for pain control, even if that individual

consumes alcohol in moderation (see chapter 8). A majority of Americans
consume alcohol, but only a small percentage of the population becomes
alcohol dependent. However, this small percentage of people (approxi-
mately 8 percent of Americans are alcohol dependent) makes a huge
impact on society, costing the U.S. economy about $185 billion a year (see
chapter 5). In this chapter, alcohol use in both historic and modern times
will be discussed, but the emphasis of the chapter is to convince you that
alcohol should be treated as a drug. As a practicing toxicologist, I treat
drugs with respect. If you treat alcohol with respect, you will reap the
benefits of drinking in moderation and enjoy a long, healthy life.
FRUIT RIPENING AND HISTORICAL ORIGINS

OF DRINKING: DRUNKEN MONKEY HYPOTHESIS
Originally proposed by Professor Robert Dudley of the University of

California, Berkeley, the “drunken monkey hypothesis” proposes that
the human attraction to alcohol may have a genetic basis due to the high
dependence of early primates on fruit as a food source. For 40 million
years, primate diets were rich in fruits, and in the humid tropical climate
where the early evolution of humans took place, yeasts on fruit skin and
within fruit converted fruit sugars into ethanol (alcohol). Since it is small
in size, when the alcohol molecule diffused out of the fruit, an alcoholic
smell identified the food as ripe and ready to consume. In tropical forests
where early primates (referred to simply as “monkeys” in the hypothesis
name) lived, competition for ripe fruits was intense, and those capable of
following the smell of alcohol to identify ripe foods and consuming them
rapidly survived better than others. Eventually natural selection favored
primates who had a keen appreciation for the smell and taste of alcohol.
Fossilized teeth show that fruit was a major component in the primate
diet between 45 million and 34 million years ago, and some of the closest
ancestors of human species—gorillas, chimpanzees, and orangutans—ate
diets based on fruit. Primates are known to have a higher olfactory sen-
sitivity to alcohol than other mammals. As human evolution continued,
fruits were mostly replaced by roots, tubers, and meat. Although our
ancestors stopped relying heavily on fruit, it is possible that the taste for
alcohol arose during our long-shared ancestry with primates.1
The yeasts that occur on fruits consume sugar molecules as a source of
energy and in the absence of oxygen (anaerobic fermentation) produce
alcohol. For example, unripe palm contains no alcohol, but ripened palm
has about 0.6 percent alcohol content, and overripe palm falling on the
ground has approximately 4 percent alcohol. Monkeys usually prefer
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Alcohol Use and Abuse 3
ripe fruits with approximately 1 percent alcohol content but avoid over-
ripe fruits with 4 percent alcohol and lower sugar content. Anecdotally,
humans often consume alcohol with food, suggesting that drinking with
food is a natural combination. For millions of years, the amount of alco-
hol consumed by our ancestors was strictly limited, and the situation did
not change even 10,000 years ago when humans became agriculturists
and could produce plenty of barley and malt, the raw material for fer-
mentation. Yeasts stop producing alcohol when the alcohol level reaches
between 10 and 15 percent because yeasts start dying at this alcohol con-
centration. Ancient beers and wines probably contained only 5 percent
alcohol until alcohol distillation was invented in Central Asia around AD
700. Then drinks with a higher alcohol content became available and the
history of alcohol abuse by humans began.2
ALCOHOL FROM A HISTORICAL PERSPECTIVE
The first historical evidence of alcoholic beverages came from an ar-

chaeological discovery of Stone Age beer jugs from approximately
10,000 years ago. The first palm date wine was probably brewed in
Mesopotamia. Evidence of wine appeared in Egypt about 5,000 years
ago—Osiris was worshipped as a wine god throughout the nation. The
first beer was probably brewed in ancient Egypt and both wine and
beer were offered to the gods. Egyptians used alcoholic beverages for
pleasure and rituals, and for medical and nutritional purposes. How-
ever, even in ancient times the Egyptians were aware of the harmful
effect of excess consumption of alcohol and emphasis was on moderate
use. The earliest evidence of alcohol use in China dates back to 5000
BC when alcohol was mainly produced from rice, honey, and fruits. A
Chinese imperial edict ca. 1116 BC made it clear that the use of alcohol
in moderation was the key and was prescribed from the heavens. In an-
cient India, alcoholic beverages were known as “sura,” a favorite drink
of Indra, the king of all gods and goddesses. Use of such drinks was
known in 3000–2000 BC, and ancient Ayurvedic texts concluded that
alcohol was a medicine if consumed in moderation but a poison if con-
sumed in excess. Beer was known to Babylonians as early as 2700 BC.
In ancient Greece winemaking was common in 1700 BC. Hippocrates
(ca. 460–370 BC) identified numerous medicinal properties of wine but
was critical of drunkenness.3
In ancient civilizations, alcohol was used to quench thirst because wa-
ter was often contaminated with bacteria. Hippocrates specifically cited
that only water from springs, deep wells, and rainfall was safe for drink-
ing. In the event that water was contaminated, alcohol was preferred for
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4 Chapter 1
drinking because alcoholic beverages were free from bacteria and other
pathogens (alcohol is an antiseptic agent). When alcoholic beverages were
added to contaminated water, the alcohol killed most pathogens and made
water safer for drinking. In ancient Western civilization, people consumed
beer and wine more than water for quenching thirst. Beer was a drink for
common people, while wine was reserved for elites. Around 30 BC, wine
became available to common Romans due to the expansion of vineyards.
During ancient times, beer and wine produced from fermentation of cere-
als, grapes, or fruits had much lower alcohol content than today’s beer or
wine and were safer for human consumption in larger quantities. Neverthe-
less, some folks drank too much alcohol, and drunkenness was greatly con-
demned in ancient Western cultures. In the New Testament Jesus approved
alcohol consumption by miraculously transforming water into wine. His fol-
lowers extended the balance between use and abuse of wine and practiced
moderation. In ancient Eastern civilization, drinking alcoholic beverages to
quench thirst was less common than in Western civilization because drink-
ing tea was very popular in Eastern countries. During boiling to prepare tea,
all pathogens died, thus making tea drinking very safe.4
Yeast can produce alcoholic beverages with up to 15 percent alcohol
content. In order to produce a higher alcohol content, a process known
as distillation is needed. Distilled spirits originated in China and India
ca. 800 BC, but the distillation process became common in Europe only
during the eleventh century and later. Alcohol consumption was common
during the Middle Ages, and monasteries produced alcoholic beverages
to nourish their monks and to sell to the public. Before the Renaissance
most Europeans had mastered the art of brewing, and distillation pro-
duced not only beers and wines but also hard liquor.
During early American history, colonials showed little concern over
drunkenness, and production of alcoholic beverages was a major source
of commerce. In 1791, however, a tax, popularly known as the “whis-
key tax,” was imposed on both privately and publicly brewed distilled
whiskey. The whiskey tax was repealed by President Thomas Jefferson
in 1802, but a new alcohol tax was imposed between 1814 and 1817 to
help pay for the War of 1812. In 1862 President Abraham Lincoln intro-
duced a new tax (which included taxing whiskey) to help defray Civil
War costs. The same act also created the office of the commissioner of
Internal Revenue. In 1906 the Pure Food and Drug Act was passed,
which regulated the labeling of products containing alcohol, opiates,
cocaine, and cannabis (marijuana), among others. The law became effec-
tive in January 1907. In 1920 alcohol was prohibited in the United States,
but Congress repealed the law in 1933. In 1978 President Jimmy Carter
signed a bill to legalize home brewing of beer for personal use for the
first time since prohibition.5
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SCIENCE OF FERMENTATION AND DISTILLATION
Fermentation is a process by which yeasts convert sugar into alcohol in

the absence of oxygen, a process first scientifically understood by Louis
Pasteur. There are different types of sugar, such as glucose, fructose
(fruit sugar), galactose (milk sugar), and sucrose (cane sugar, which
contains two sugar molecules: glucose and fructose joined together).
Glucose and fructose are monosaccharides or simple sugar, while su-
crose (table sugar) is a disaccharide and is more structurally complex
than monosaccharides. Yeast is capable of converting simple sugars like
glucose and fructose into alcohol. Yeast converts glucose into pyruvate
and finally ethanol (alcohol) is produced from acetaldehyde. Yeast
converts simple sugars to alcohol through a complex biochemical enzy-
matic pathway involving yeast enzymes (fig. 1.1). The overall reaction
is, however, quite simple.
Figure 1.1. Fermentation of glucose by yeast-producing alcohol

Key: ADP: Adenosine diphosphate; ATP: Adenosine triphosphate; NAD: Nicotinamide adenine dinucleo-
tide, a cofactor for reduction (loss of hydrogen from the molecule) of acetaldehyde to alcohol; NADH:
Reduced form of NAD
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6 Chapter 1
Overall reaction:
C6H12O6 —————➝ 2 CH3CH2OH + 2 CO2
Fermentation is a natural process where various species of wild yeasts
and bacteria convert fruit sugars to alcohol. Overripe fruits and rotten
fruits contain a much higher alcohol content than ripe fruits. Yeasts are
classified as fungus, and there are more than 1,500 different species found
in nature. The yeast species Saccharomyces cerevisiae has been used for
thousands of years for baking and fermenting alcoholic beverages. Other
species of yeast, for example, Candida albicans, are pathogenic and cause
yeast infections in humans. For preparing bread, the amylase present in
flour breaks down starch into maltose. During baking maltase enzymes
present in baking yeast split maltose into two glucose molecules, which
are then fermented into alcohol and carbon dioxide. The released carbon
dioxide causes dough to rise, while the little alcohol produced adds to
bread’s flavor, although most alcohol is evaporated during the baking
process. The yeast species used for baking, although classified broadly as
“brewer’s yeast,” is a different type from that used for beer manufacturing.
Brewing Beer
Beer is the most popular alcoholic beverage in the world. In the first step of
beer brewing (malting), malted barley is soaked in hot water, allowing malt
to germinate, thus releasing amylases, the enzymes needed for converting
the starch that is present in grains into sugars. Different roasting times and
temperatures produce different colors of malt from the same grain; the
darker the malt, the darker the beer. Although barley is the main grain used
for brewing beer, other sources of starch, such as rye, wheat, and even rice,
may also be used. The malting process can be broken down into three parts:
steeping, where barley (or other grains) are added to the vat and water is
added for soaking; then a five-day period for germination, where grains
may be spread on the floor; and finally kilning, where germinating malt is
dried under higher temperature to produce the final product, “malt.” The
malt is then cracked in a process called “milling,” followed by “mashing,”
where supplementary grains such as corn, rye, or sorghum may be added
to the malt. The next step is “lautering,” where liquid containing sugar is
separated from grains. Then the malt extract is boiled to ensure sterility.
During this step hops are added as a flavoring agent, which gives the beer
its characteristic bitter taste. This step may last for one to two hours, and
this produces the “wort.” The wort is cooled to bring it back to fermenting
temperature and yeast is added, which produces alcohol from the sugars
present in the wort (which is produced by a complex process starting from
the starch present in barley).
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Brewers classify yeasts for beer manufacturing into “top-fermenting”

and “bottom-fermenting” yeasts. Top-fermenting yeasts form foam at the
top of the fermenting vessel; these yeasts can produce a higher alcoholic
content, and the fermentation process is carried out at relatively higher
temperatures (61°F–75°F). Beers produced by these yeasts are commonly
called “ale-type” beers, which are fruitier, sweeter beers. An example
of a top-fermenting yeast is Saccharomyces cerevisiae. Bottom-fermenting
yeasts, which are used for the production of the majority of beers, ferment
sugars at lower temperatures (50°F–64°F). Bottom-fermenting yeasts are
larger yeast strains that tend to settle at the bottom as the fermentation
process is progressing to completion. Beer-fermenting yeasts can tolerate
up to 5 or 6 percent alcohol concentration before they start to die.
The fermentation process is carried out anaerobically (in the absence
of air containing oxygen) in a fermentor that is sealed off during the pro-
cess, except for a vent pipe through which liberated carbon dioxide gas
can escape from the vessel. The fermentation process may take a week
or longer. When fermentation is nearly complete, most yeasts will settle
at the bottom (if the beer is brewed using bottom-fermenting yeast),
and the carbon dioxide vent is sealed off so that residual carbon dioxide
may stay within the beer, making it carbonated. Alternatively, carbon
dioxide may be added to the beer. Then beer is pumped off, cooled, and
bottled for shipment.6 For commercial production of beer, strict quality
control procedures are adopted in each step of production to ensure
quality, such as measuring specific gravity and other parameters to
ensure that the final product meets all classifications determined by the
manufacturer.
Producing Wine
Wine is brewed using a different strain of yeast capable of tolerating more
alcohol than brewer’s yeast. Wine-producing yeasts can tolerate up to 12
to 15 percent of alcohol content.
Wines are primarily made from grapes, although other fruits such as
plums, peaches, and apples may also be used for winemaking. Usually
wines are made from harvesting ripe grapes in a vineyard. Wild yeasts
are present in ripe grapes. Although wild yeast can produce wine, the
fermentation process may be unpredictable. Usually, cultured yeasts
are added to the crushed grapes and expressed juice, which is called the
“must.” For producing red wine, grape skins are added to the must and
contribute to the reddish color of the wine. For making white wine, grape
skins are removed prior to the fermentation process. Red wine is fermented
at a higher temperature (up to 85°F) than white wine (64°F–68°F). After
fermentation, solid residues are allowed to settle and wine is pumped
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8 Chapter 1
off to a new container for storage, sometimes in wooden oak barrels. Then
wine is allowed to age for a year or more while a complex chemical reac-
tion takes place, producing small molecular weight compounds that add
to the distinct taste and flavor of a particular wine. Sake, Japanese wine,
is fermented from rice, while mead is made from honey, and hard cider is
made from apples. Again, strict quality control procedures are adopted by
commercial breweries in each step of wine manufacturing to ensure high
quality of the end product. Acidity and specific gravity of wine is carefully
controlled by the manufacturers to meet their specifications.
The formation of flavor in wine is from original compounds present in
grapes, some of which may be transformed biochemically during fermen-
tation. In addition, during the aging process, if the wine is stored in oak
barrels, trace chemicals present in the wood may leach into the wine and
participate in a complex chemical process that produces other molecules.
Phenolic compounds present in grapes are responsible for wine color
and its distinct taste. These compounds include anthocyanins, gallic acid,
catechin, and so on.7
The aroma of wine consists of 600 to 800 volatile compounds mostly
characteristic of grapes used for wine production. Various monoterpene
compounds and sulfur-containing thiol compounds are responsible for
the characteristic aroma of various wines. During wine production com-
pounds such as esters (ethyl acetate, amyl acetate, phenyl ethyl acetate,
etc.), higher alcohols (higher molecular weight than alcohol or ethyl alco-
hol), volatile fatty acids (acetic acid, isovaleric acid), and other complex
compounds such as mercaptans and ketones are generated, contributing
to the aroma of wine. During aging, a complex chemical process may take
place that modifies the structures of certain compounds already present
in the wine.8 Usually, residual carbon dioxide is not allowed to stay in
wine. However, champagne is supplemented with carbon dioxide in
order to achieve its bubbly appearance. Carbon dioxide is also added to
produce sparkling wine. In port wine alcohol is added after production in
order to increase its alcoholic content.
Preparation of Distilled Spirits

Beverages produced by fermentation followed by distillation are known
as spirits. After fermentation alcohol content is usually 14–16 percent, but
in order to make alcoholic beverages with 45–75 percent alcohol content,
vaporizing the alcohol from the original preparation (which contains
approximately 85 percent water) and then condensing alcohol vapor in
specialized equipment is needed. This is possible because the boiling
point of alcohol is 78°C (172.4°F), while the boiling point of water is 100°C
(212.0°F). When water is boiled, the temperature rises until it reaches
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Table 1.1. Fermenting Materials Used for Preparing Some Popular Spirits
Alcoholic Beverage Fermenting Material Alcohol Content
Brandy /cognac Grapes (distilled wine) 40–50%
Bourbon Corn 40–55%
Gin Malt, other grains and juniper berry 38–45%
Rum Sugarcane or molasses 40–57%
Schnapps Fermented grains or fruits 30–40%
Tequila Tequila agave (blue agave) stem 40–45%
Vodka Malt, molasses or potatoes 40–50%
Whiskey* Barley 40–55%
*There are different types of whiskeys, such as Scotch whiskey, Irish whiskey, Canadian whiskey, American
whiskey, and so on. Scotch whiskeys are usually distilled twice or three times, distilled in Scotland, and
aged for a minimum three years in oak cases.
100°C, and then water starts evaporating and temperature no longer in-
creases. Similarly, when an alcohol and water mixture is boiled, alcohol
starts evaporating at 78°C, and the vapor is mostly composed of alcohol.
Then the vapor is allowed to pass through a tube called a condenser,
which is cooled, and alcohol vapor is converted into liquid alcohol again.
The instrument in which alcohol distillation is carried out is called a still.
The still can be a pot, which is usually used for home distillation (in the
United States a license is required for distilling alcohol), while the column
still is used for industrial production of various spirits. Bourbon, gin,
vodka, whiskey, and rum are all made through the distillation process
using various fermenting materials (table 1.1).
NUTRITIONAL VALUE OF ALCOHOLIC BEVERAGES
Alcoholic drinks consist primarily of water, alcohol, and variable

amounts of sugars and carbohydrates (residual sugar and starch left af-
ter fermentation). Sometimes sugars are also added before fermentation
to enhance the alcohol content of the beverage. Alcoholic drinks con-
tain negligible amounts of other nutrients, such as proteins, vitamins,
or minerals. Therefore, any calories derived from drinking alcoholic
beverages come mostly from alcohol content and some from the carbo-
hydrate and sugar, which are present in the drink. However, distilled
liquors, such as cognac, vodka, whiskey, and rum, contain no sugars.
Red wine and dry white wines contain 2 to 10 gm of sugar per liter,
while sweet wines and port wines may contain up to 120 gm of sugar
per liter of wine. Beer and dry sherry contain 30 gm of sugar per liter.
Usually a standard drink contains approximately 14 gm of pure alcohol
(see chapter 2). Burning 1 gm of alcohol produces more calories than
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10 Chapter 1
burning carbohydrate. Therefore, drinking one can of beer provides ap-

proximately 100 calories.9
CURRENT USE AND ABUSE OF ALCOHOL
According to a survey by the U.S. government of adults ages eighteen

and older, approximately 50 percent of adults are currently drinkers (at
least twelve drinks in the past year) and 14 percent are infrequent drink-
ers (one to eleven drinks in the past year). In addition, 6 percent are for-
mer regular drinkers, 9 percent are former infrequent drinkers, while 21
percent are lifetime abstainers. Among current drinkers 61 percent are
men and 42 percent are women. Women and Asian Americans are more
likely to be lifetime abstainers than are men. In general, older adults
drink less frequently than young adults.10 Only a small percentage of
Americans who drink on a regular basis are heavy drinkers.
Unfortunately, underage drinking in the United States is a serious
problem because the adolescent brain is more susceptible to alcohol-
related damage than the adult brain. According to a 2006 report by the
National Institute of Alcohol Abuse and Alcoholism, each year approxi-
mately 5,000 young people under the age of twenty-one die as a result
of underage drinking (approximately 1,900 deaths from motor vehicle
accidents, 1,600 as a result of homicide, 300 from suicide, and others from
injuries such as falls, burns, and drowning).11 According to the National
Survey on Drug Use and Health Report published in November 2008,
more than one-quarter of people ages twelve to twenty (28.1 percent)
used alcohol in the past month, 51.1 percent of ages eighteen to twenty,
25.9 percent of ages fifteen to seventeen, and 6.1 percent of ages twelve
to fourteen. This is a shocking statistic because alcohol has a devastating
effect on the developing brain of a twelve-year-old person. Nearly one-
third of the current underage alcohol drinkers (30.6 percent) paid for the
last alcoholic drink they consumed, 14.6 percent got it free from another
underage person, 8.5 percent received it from another relative, and an
alarming 5.9 percent received their last drink from a parent or guardian.
Current alcohol users ages twelve to twenty consumed more drinks on
average (six drinks) if they paid for the drink than those who received
their drinks free (an average of nearly four drinks). Underage women
more often received their last drink free compared to men and more men
consumed alcohol than did women.12
Binge drinking is also very problematic for adolescents, and statistics
for binge drinking among underage drinkers, as well as adverse effects
of drinking on adolescents’ brains, are discussed in chapter 3. Underage
drinking is a major public health and safety issue, because young people
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who start drinking at an early age have a much greater risk of becoming
alcohol dependent later in life than individuals who start drinking at age
twenty-one or older.
WHY ALCOHOL IS A DRUG
According to the American Council for Drug Education, alcohol is the

oldest and most widely used drug in the world. Nearly half of all Ameri-
cans consume alcohol. Although most drink only occasionally and sensi-
bly, there are 10 to 16 million alcoholics and problem drinkers (this num-
ber is lower than the estimated 18 million given as a recent estimate by a
U.S. government study; see more on this in chapter 5), which includes 4.5
million adolescents with drinking problems. Alcohol intoxication results
in crime, violence, and disturbances that consume more resources than
other aspects of police operations, and the health consequences of alcohol
abuse are a huge economic burden on the nation. Although illegal drugs
cause addiction more rapidly than alcohol, and in much smaller doses, ac-
cording to the American Council for Drug Education, alcohol is America’s
most serious drug problem.13
Alcohol can be considered a psychoactive drug because it has com-
plex interactions with various neurotransmitters and receptors in the
brain, producing pleasurable effects when consumed in moderation.
However, with excess consumption, the positive effects of drinking are
replaced by negative effects, such as anxiety and depression. If con-
sumed in moderation, alcohol can protect against age-related dementia
and Alzheimer’s disease, but if consumed in excess it can cause severe
brain damage. In addition, alcohol shares many pathways of various
psychoactive drugs for its pharmacological actions (see chapter 3).
Therefore, alcohol can be considered a drug. The Substance Abuse and
Mental Health Services Administration (SAMHSA) has published many
reports on substance abuse where alcohol and drugs are placed in the
same category.
Alcohol, like any drug, has prophylactic effects in preventing many
diseases, including coronary heart disease (the number one killer in
America), stroke, various cancers, diabetes, arthritis, and other dis-
eases, as well as increasing longevity (see chapter 4). However, if con-
sumed in excess, it is detrimental to health (see chapter 5). Therefore,
like a drug, alcohol is effective in low doses and toxic in higher doses.
Like a drug, alcohol is metabolized by liver enzymes, and a toxic me-
tabolite of alcohol known as “acetaldehyde” is generated. If acetalde-
hyde is accumulated in the body due to excess alcohol intake, it can
cause liver damage.
10-649_Dasgupta.indb 11 1/17/11 6:40 AM

12 Chapter 1
Many individuals with a genetic makeup susceptible to alcohol abuse are

also susceptible to drug abuse, indicating that alcohol can be compared to
an illicit drug, but with lower abuse potential. According to a current survey
(Dick and Agarwal 2008), 8.5 percent of American adults met the criteria for
an alcohol use disorder, 2 percent met the criteria for a drug abuse disorder,
while 1.1 percent met the criteria for both, indicating that many abusers of
illicit drugs are also dependent on alcohol. People ages eighteen to twenty-
four had the highest rates of co-occurring alcohol and illicit drug abuse
disorders. Researchers have established that some of the risk of addiction
to both drugs and alcohol are inherited. Children of alcoholics are 50 to 60
percent more likely to abuse alcohol, while children of parents abusing illicit
drugs are 45 to 79 percent more likely to abuse illicit drugs. This suggests
that risk factors for alcohol and illicit drug dependence are rooted in the
genes.14 In their study Dick and Agarwal concluded that some of the same
genes that increase a person’s risk for problems with alcohol might also put
him or her at greater risk for illicit drug dependence. Moreover, the same
genes might increase the risk of other psychiatric problems, such as conduct
disorders, adult antisocial behavior, borderline personality disorder, and
so on (fig. 1.2). Studies with twins suggest that the overlap between depen-
dence on alcohol and other drugs largely results from shared genetic factors.
There are various genes that make a person susceptible to alcohol and drug
abuse. Certain genes control metabolism of alcohol, while other genes rein-
force the effect of alcohol in the brain.15
CONCLUSION
Alcohol is the oldest drug known to mankind. Human fondness for alco-
hol may have originated from the genetic makeup of early primates 30 to
40 million years ago who lived on a diet of ripe fruits (drunken monkey
hypothesis). Ancient alcoholic beverages were low in alcohol content, but
with the discovery of distillation, alcohol content surged. Modern beers
and wines have a higher alcohol content than ancient beer and wine. Al-
cohol was recognized as a drug by physicians of ancient Greece and other
ancient civilizations as well as by Muslim doctors and Indian Ayurvedic
doctors. Alcohol has many health benefits if consumed in moderation, but
it is toxic if consumed in excess.
NOTES
1. R. Dudley, “Ethanol, Fruit Ripening, and the Historical Origins of Human

Alcoholism in Primate Frugivory,” Integrative and Comparative Biology 44, no. 4
(August 2004): 315–23.
10-649_Dasgupta.indb 12 1/17/11 6:40 AM

Figure 1.2. A schematic representation illustrating common influences of genetic

factors on alcohol and drug dependence, personality, and conduct disorders. Some of
the proposed genetic factors are considered to have a general influence on all types of
externalizing personality, whereas others are thought to have disorder-specific influ-
ence. Externalizing psychopathy is defined as psychiatric disorders characterized by
disinhibition behavior, antisocial personality disorder, attention deficit/hyperactivity
disorder, and conduct disorder.
Source: Reference 14, a U.S. government publication; information in public domain.
2. D. Stephens and R. Dudley, “The Drunken Monkey Hypothesis: The Study

of Fruit-Eating Animals Could Lead to an Evolutionary Understanding of Human
Alcohol Abuse,” Natural History magazine, December 2004.
3. David Hanson, Preventing Alcohol Abuse: Alcohol Culture and Control (West-
port, CT: Greenwood, 1995).
4. B. L. Vallee, “Alcohol in the Western World,” Scientific American, June 1998.
5. “History of Alcohol Use,” Heads Up! Loyola Marymount University, Los
Angeles, http://www.lmu.edu/pages25071.aspx.
6. Barrie Pepper, The International Book of Beer: A Guide to the World’s Most Popu-
lar Drink (New York: New Line Books, 2006).
7. J. S. Jensen, S. Demiray, M. Egebo, and A. S. Myers, “Prediction of Wine
Color Attributes from Phenolic Profiles of Red Grapes (Vitis vinifera),” Journal of
Agriculture and Food Chemistry 56, no. 3 (February 2008): 1105–15.
8. P. Polásková, J. Herszage, and S. E. Ebeler, “Wine Flavor: Chemistry in a
Glass,” Chemical Society Review 37, no. 11 (November 2008): 2478–89.
10-649_Dasgupta.indb 13 1/17/11 6:40 AM

14 Chapter 1
9. C. S. Liber, “Relationships Between Nutrition, Alcohol Use and Liver Dis-

ease,” Alcohol Research and Health 27, no. 3 (2003): 220–31.
10. Summary of Health Statistics for U.S. Adults: National Interview Survey
2008, National Center for Health Statistics, United States, Hyattsville, ND.
11. Alcohol Alert #67, “Underage Drinking,” National Institute on Alcohol
Abuse and Alcoholism, January 2006, http://pubs.niaaa.nih.gov/publications/
aa67/aa67.htm.
12. “Underage Alcohol Use: Where Do Young People Get Alcohol?” National
Survey on Drug Use and Health Report, November 20, 2008, Office of Applied
Studies, Substance Abuse and Mental Health Services Administration (SAMHSA).
13. “Basic Facts about Drugs,” American Council for Drug Education, http://
www.acde.org/common/Alcohol.htm.
14. Alcohol Alert #76, “Alcohol and Other Drugs,” National Institute on Al-
cohol Abuse and Alcoholism, January 2006, http://pubs.niaaa.nih.gov/publica-
tions/aa76/aa76htm.
15. D. M. Dick and A. Agarwal, “The Genetics of Alcohol and Other Drug De-
pendence,” Alcohol Research and Health 31, no. 2 (2008): 111–18.
10-649_Dasgupta.indb 14 1/17/11 6:40 AM

2

How the Human Body
Handles Alcohol
A Guide to Drinking Sensibly
and Avoiding a DWI
A lcoholic beverages can be classified under three broad categories: beer,

wine, and spirits. Beer and wine are fermented beverages produced
from sugar- or starch-containing plant materials. The normal fermentation
process, which uses yeast, cannot produce alcoholic beverages with an
alcohol content higher than 14 percent. Therefore, hard liquors or spirits
are produced using fermentation followed by another process called dis-
tillation. Alcohol is full of calories, and heavy drinking is a serious health
hazard, including premature death due to liver cirrhosis. However, drink-
ing in moderation has many health benefits, including protection against
cardiovascular disease, stroke, type 2 diabetes, a lower risk of forming
gallstones, and possibly a longer life (see chapter 4). Therefore, the key
is to drink in moderation and drink sensibly. This chapter discusses how
the body handles alcohol and provides clear guidance regarding drink-
ing in moderation so that after a pleasant evening of good food and wine,
you will not be stopped by the police for a suspected DWI (driving with
impairment/driving while intoxicated; in some states DUI, driving under
the influence). The guidelines provided in this chapter are conservative
guidelines, because I believe it is better to be safe than sorry.
DEFINITION OF A STANDARD DRINK
The alcohol content of various alcoholic beverages varies widely. The av-
erage alcohol content of beer is 5 percent, wine is 10 percent, and whiskey
is 40 percent. However, the serving sizes also vary according to the type
15
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16 Chapter 2
of beverage. For example, beer usually comes in a 10- or 12-ounce bottle,

while a shot of tequila in a mixed drink is only 1.5 ounces. Therefore,
regardless of the alcoholic beverage, a standard drink contains roughly
the same amount of alcohol. In the United States, a standard drink is
defined as a bottle of beer (12 ounces) containing 5 percent alcohol, 8.5
ounces of malt liquor containing 7 percent alcohol, a 5-ounce glass of wine
containing 12 percent alcohol, 3.5 ounces of fortified wine (like sherry or
port) containing about 17 percent alcohol, 2.5 ounces of cordial or liqueur
containing 24 percent alcohol, or 1.5 ounces of distilled spirits such as gin,
rum, vodka, or whiskey. Each standard drink contains approximately the
same amount of alcohol. For example, beer contains an average 5 percent
alcohol, so the total alcohol content of 12 ounces of beer is 12 × 0.05 = 0.6
ounce of alcohol, which is equivalent to 14 gm of alcohol. In general, the
average bottle of beer contains 0.56 ounce of alcohol and a standard wine
drink may contain 0.66 ounce of alcohol, but distilled spirits may contain
up to 0.89 ounce of alcohol. Therefore, 0.6 ounce of alcohol in a standard
drink is a reasonable approximation.1
In a mixed drink or cocktail, if one shot of distilled spirits is used, the
alcohol content should be 0.6 ounce. In a bar, a bartender uses a “jigger”
for preparing mixed drinks. A jigger is a measuring device used to pour
precisely 1.5 ounces of alcohol. A jigger may also have a smaller 1-ounce
cup called a pony shot. For simple mixed drinks such as rum and coke or
gin and tonic, each cocktail comes with one shot of liquor, and consuming
one such drink is equivalent to drinking one bottle of beer, as far as blood
alcohol level is concerned. However, in some mixed drinks, two shots
are used, so the alcohol content of that mixed drink equals two standard
drinks. A cocktail usually contains one or more types of distilled spirits,
fruit juice, honey, milk, or other ingredients. If a mixed drink is prepared
from more than one distilled spirit, then one mixed drink may be equiva-
lent to two to three standard drinks. For example, a margarita is prepared
from tequila and triple sec orange-flavored liquor containing 30 percent
alcohol and is often served with salt on the glass rim. Depending on the
alcohol content, drinking a 10-ounce margarita may be equivalent to two
to three standard drinks.
Because blood alcohol level depends on the number of standard drinks,
it is often difficult to calculate blood alcohol level if you are consuming
mixed drinks prepared from more than one type of liquor. The alcohol
content may also vary from bar to bar because of the use of different
recipes. Malt liquor is a North American term referring to a type of beer
with higher alcohol content. Malt liquors are often cheaper than beer and
contain an average of 7 percent alcohol. Some malt liquors are available
in a 40-ounce bottle. Therefore, drinking one such bottle of malt liquor is
equivalent to consuming 2.8 ounces of alcohol, which is equivalent to 4.6
standard drinks, or drinking more than four bottles of beer.
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How the Human Body Handles Alcohol 17
Historically, the alcohol content of various drinks was expressed as

“proof,” which is a measure of the alcohol content. The term originated
in the eighteenth century when British sailors were paid with rum as well
as money. In order to ensure that the rum was not diluted with water, it
was “proofed” by dousing gunpowder with it and setting it on fire. If the
gunpowder failed to ignite, it indicated that the rum had too much water
and was considered “under proof.” A sample of rum that was 100 proof
contained approximately 57 percent alcohol by volume (43 percent wa-
ter). In the United States, proof to alcohol by volume is defined as a ratio
of 1:2. Therefore, a beer that has 4 percent alcohol by volume is defined
as 8 proof. In the United Kingdom, alcohol by volume to proof is a ratio
of 4:7. Therefore, multiplying alcohol by volume content with a factor of
1.75 would provide the proof of the drink.
Currently in the United States, the alcohol content of a drink is measured
by the percentage of alcohol by volume. The code of Federal Regulations
(27CFR [4-1-03 edition] §5.37 Alcohol Content) requires the label of al-
coholic beverages to state the alcohol content by volume. The regulation
permits, but does not require, the “proof” of the drink to be printed on the
label as well. In the United Kingdom and in European countries, the alcohol
content of a beverage is also expressed as the percentage of alcohol in the
drink. The alcohol content of various popular beverages is given in table
2.1. It is important to note that a standard drink contains approximately the
Table 2.1. Alcohol Content of Various Drinks

Beverage One Standard Drink Alcohol Content
Standard American beer 12 ounces (355 mL) 4–10%
Anchor Porter 5.6%
Budweiser 5%
Budweiser Light 4%
Coors 4.9%
Coors Light 4.2%
Flying Dog Horn Dog 10.5%
Michelob 5%
Michelob Light 4.3%
Michelob Ultra Light 4.1%
Miller 4.7%
Miller Light 4.2%
Table wine 5 ounces (148 mL) 7–14%
Sparkling wine 5 ounces (148 mL) 8–14%
Fortified wine 2–5 ounces (59–148 mL) 14.0–24%
Whiskey 0.6 ounce (18 mL) 40–75%
Vodka 0.6 ounce (18 mL) 40–50%
Gin 0.6 ounce (18 mL) 40–49%
Rum 0.6 ounce (18 mL) 40–80%
Tequila 0.6 ounce (18 mL) 45–50%
Brandies 0.6 ounce (18 mL) 40–44%
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18 Chapter 2
same amount of alcohol (roughly 0.6 ounces). Therefore, regardless of the

type of drink, your “body burden” of alcohol depends mostly on the num-
ber of drinks consumed, as well as your body weight, gender, and whether
or not you consume food while drinking.
HOW THE BODY HANDLES ALCOHOL
When you drink, alcohol is absorbed from your stomach and small intes-
tine. It then undergoes a chemical transformation by the liver through a
process called “metabolism,” and eventually the body gets rid of all alcohol
consumed. A small amount of alcohol that is not absorbed is found in your
breath and is the basis of breath analysis of drivers suspected of driving with
impairment. Factors that affect how your body handles alcohol include:
Age
Gender
Race and ethnicity
Body weight
Amount of food consumed
How quickly alcohol is ingested
Alcoholism
In general, alcoholics metabolize alcohol faster than a nonalcoholic per-

son. Age, gender, body weight, and genetic makeup all affect how your
body handles alcohol. Drinking faster may cause much higher blood al-
cohol levels because absorption and elimination of alcohol from the body
take place simultaneously.
Absorption
When alcohol is consumed, about 20 percent is absorbed by the stomach
and the rest is absorbed from the small intestine. When alcohol is con-
sumed on an empty stomach, blood alcohol levels peak between fifteen
and ninety minutes after drinking. Food substantially slows down the ab-
sorption of alcohol, and can even reduce the rate of absorption of alcohol
for four to six hours. Sipping alcohol versus drinking it like soda or water
also slows absorption.
Always consume food when you are drinking. Sip and enjoy your
alcohol. Do not consume more than one drink in one hour.
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The effect of food on absorption and metabolism of alcohol has been

widely studied and reported in the medical literature. In one study
(Jones and Jönsson 1994), ten healthy men drank a moderate dosage
of alcohol (0.80 gm of alcohol per kg of body weight) in the morn-
ing after an overnight fast or immediately after breakfast (two cheese
sandwiches, one boiled egg, orange juice, and fruit yogurt). Subjects
who drank alcohol on an empty stomach felt more intoxicated than the
subjects who drank the same amount of alcohol after eating breakfast.
The blood alcohol analysis revealed the cause. The average peak blood
alcohol concentration in subjects who drank on an empty stomach was
104 mg/dL (0.104 percent), which was above the legal level of intoxica-
tion (0.08 percent). In contrast, the average peak blood alcohol concen-
tration in subjects who drank alcohol after eating breakfast was 67 mg/
dL (0.067 percent). The time required to metabolize all alcohol was on
average two hours less in subjects who drank alcohol after eating break-
fast compared to subjects who drank on an empty stomach. The authors
concluded that food in the stomach before drinking not only reduces the
peak blood alcohol concentration but also boosts the rate at which the
body gets rid of alcohol.2
Studies have also been conducted using different types of food, such
as high-fat versus high-protein or high-carbohydrate, to see what effect
they have on alcohol absorption. Drinking after eating a meal, regardless
of the types of foods eaten, decreases the absorption of alcohol.3 There-
fore, drinking alcohol with any food type will reduce alcohol’s effects
and concentration in the blood. Food intake slows gastric emptying time,
and the alcohol dehydrogenase enzyme, which metabolizes alcohol in the
liver, is also present in the gastric mucosa (the mucous membrane of the
stomach). Part of the alcohol ingested is metabolized in the stomach by
this enzyme before the alcohol reaches the small intestine and duodenum
for further absorption. Food prolongs the time alcohol spends in your
stomach, giving the enzyme a chance to metabolize more alcohol.
Distribution and Metabolism

A small amount of alcohol is metabolized by the enzyme present in the
gastric mucosa; also, a small amount of alcohol is metabolized by the
liver before it can enter the main bloodstream. This process is known as
“first-pass metabolism” or “pre-systematic metabolism.” After alcohol is
ingested, it is absorbed from the gut and enters the hepatic portal system
(a portal vein carries the alcohol to the liver), and some of the alcohol is
metabolized. Then the rest of the alcohol enters the bloodstream, which
is known as systematic circulation. If a person drinks a certain amount of
alcohol, the peak blood alcohol level would be significantly lower than
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20 Chapter 2
the same amount of alcohol being injected into the same person. This is
because alcohol undergoes first-pass metabolism only when ingested.
Also, a man drinking the same amount of alcohol would have a lower
peak blood alcohol level compared to a woman with the same body
weight. This gender difference in the blood alcohol level is related to the
different body water content between a man and a woman. Alcohol loves
water and distributes into the aqueous part of the blood known as serum.
Because a woman has less body water content (52 percent on average)
than a man (61 percent average), less water is available to dissolve the
same amount of alcohol compared to a man. Some studies also report that
women are more susceptible than men to alcohol-related impairment of
cognitive functions.4
Women also metabolize alcohol more slowly than do men because the
concentration of alcohol dehydrogenase (ADH) is usually lower in women
compared to men. Hormonal changes also play a role in the metabolism of
alcohol in women, although this finding has been disputed in the medical
literature. Some studies suggest that women metabolize alcohol at a higher
rate during the luteal phase of the menstrual cycle (days 19–22 of the
cycle), but a few days before menstruating, a woman’s alcohol metabolism
may slow down.5 Though more studies need to be conducted to confirm
this, it has been well documented in medical literature that alcohol addic-
tion causes disturbances in the menstrual cycle, and that such disturbances
are more prominent during the middle part of the cycle.6
A woman may be more susceptible to the effect of alcohol right before

her menstrual cycle.
Your liver metabolizes alcohol using zero-order kinetics, which means

that no matter what amount of alcohol is present in the body, the liver
gets rid of it at a constant rate. In contrast, most drugs follow first-order
kinetics, meaning that the greater burden of a drug in the body, the faster
the liver works to transform the drug into a metabolite for excretion in the
urine. Consider this analogy: Students will usually party and enjoy life at
the beginning of the semester, and study hard before a final exam. They
will also work much harder as the deadline of a project approaches. This
is like first-order kinetics, where the liver works harder when more drugs
(stress) are present in the body. On the other hand, zero-order kinetics is
like a student who starts studying at a steady rate from day one but does
not study any harder before the finals.
In the liver, at very low (<20 mg/dL; 0.02 percent) or very high (>300 mg/
dL; 0.3 percent) concentrations, ethanol elimination follows first-order kinet-
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ics; however, for the concentrations between, metabolism is independent

of the dose due to enzyme saturation and thus follows zero-order kinetics.
Several enzyme systems are involved in the metabolism of ethanol
(ethyl alcohol, or commonly termed “alcohol”), namely, alcohol dehy-
drogenase (ADH), the microsomal ethanol oxidizing system (MEOS),
and catalase.7 These enzymes also metabolize other similar compounds,
such as methanol (wood spirit), isopropyl alcohol (rubbing alcohol), and
ethylene glycol (antifreeze).
The first and most important of these, alcohol dehydrogenase, is a fam-
ily of enzymes found primarily in hepatocytes (liver cells) (equation 2.1).
NAD: Nicotinamide adenine dinucleotide is a coenzyme that is found in all

living cells.
NADH: NADH is essential for enzymatic transformation of ethanol (alco-
hol) into acetaldehyde.
At least five classes of ADH are found in humans. ADH activity is greatly
influenced by the frequency of ethanol consumption. Adults who con-
sume two to three alcoholic beverages per week metabolize ethanol at
a rate much lower than alcoholics. For medium-sized adults, the blood
ethanol level declines at an average rate of 15 to 20 mg/dL/h (0.015 to
0.020 percent/hour) or a clearance rate of approximately 3 ounces of
ethanol per hour.
The major drug-metabolizing family of enzymes found in the liver is the
cytochrome P450 mixed-function oxidase. Many members of this family of
enzymes, most notably CYP3A4, CYP1A2, CYP2C19, and CYP2E1 isoen-
zyme, play vital roles in the metabolism of many drugs. For nonalcohol-
ics, this metabolic pathway is considered a minor, secondary route, but it
becomes much more important in alcoholics. In addition to ADH, CYP2EI
isoenzyme plays a major role in metabolizing alcohol because it helps al-
coholics rid their bodies of alcohol faster than nonalcoholics (equation 2.2).
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22 Chapter 2
The acetaldehyde produced due to the metabolism of alcohol, regardless

of the pathway, is subsequently converted to acetate as a result of the ac-
tion of mitochondrial aldehyde dehydrogenase (ALDH2). Acetaldehyde
is fairly toxic compared to ethanol and must be metabolized quickly
(equation 2.3).
Acetate or acetic acid then enters the citric acid cycle, which is a normal
metabolic cycle of living cells, and is converted into carbon dioxide and
water. From the chemical point of view, the body burns (oxidizes) alcohol
into carbon dioxide and water, and this process generates calories. There-
fore, alcoholic drinks are high in calories.
EFFECT OF AGE ON ALCOHOL METABOLISM
In general, a child will metabolize a drug faster than a younger or middle-

aged adult, and an elderly person (older than sixty-five) will metabolize
a drug more slowly than a younger or middle-aged adult. Metabolism of
alcohol changes with advancing age because the activity of the enzymes
involved in alcohol metabolism diminish with age. Water volume also re-
duces with advancing age. An elderly person would have a higher blood
alcohol level from consumption of the same amount of alcohol compared
to a younger person of the same gender. Moreover, elderly people con-
sume more medications than do younger people, and a medication may
interact with alcohol (see chapter 8). It is safe for elderly people to con-
sume one drink a day provided it does not interact with any medication
they are taking.8 If an elderly person doesn’t take medication or takes a
medication that does not interact with alcohol, drinking in moderation
has several health benefits for the elderly. Compared to abstention, con-
sumption of one to six drinks weekly is associated with a lower risk of de-
mentia among older adults.9 Moderate consumption of alcohol by elderly
people also improves cardiovascular health and social behavior. Moder-
ate alcohol consumption on a regular basis is associated with increased
quality of life and mood in both older men and women.10 Among women
undergoing menopause, moderate alcohol consumption, along with other
lifestyle factors, has a positive effect on their sense of well-being.11
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GENETIC FACTORS IN ALCOHOL METABOLISM
Alcohol is metabolized by the liver, where it is converted first to acetal-

dehyde by the enzyme alcohol dehydrogenase. Acetaldehyde is then con-
verted to acetate by the enzyme aldehyde dehydrogenase. Acetaldehyde is
the most toxic metabolite of alcohol (both alcohol and acetate are relatively
nontoxic). Acetaldehyde produces unpleasant physiological reactions even
at low concentration and is responsible for the dreaded alcohol hangover.
When acetaldehyde is not rapidly converted into acetate, the results are
dramatic: a rapid increase in blood flow to the skin of the face, neck, and
chest, rapid heartbeat, headache, nausea, and extreme drowsiness can oc-
cur. These unpleasant reactions from drinking, collectively called flushing,
may occur more frequently in certain ethnic groups. Approximately half of
the Asian population are considered deficient in the alcohol dehydrogenase
enzyme and may experience flushing even after consumption of one or two
drinks. Such unpleasant reactions also deter people from drinking and may
protect against alcoholism. The alcohol-deterrent drug disulfiram works as
a deterrent by producing a similar “flush reaction.” Disulfiram inactivates
aldehyde dehydrogenase in a person who carries the normal gene for that
enzyme, in effect producing the same situation as in the Asians who have
the inactive, mutant form of the gene. Some East Indians, American Indi-
ans, and Alaskan Natives may also have genetic variations that affect me-
tabolism of alcohol. American Indians and Alaskan Natives are five times
more likely than other ethnic groups in the United States to die of alcohol-
related causes. Caucasian populations usually do not have any significant
genetic variation that affects alcohol metabolism. Please see chapter 5 for an
in-depth discussion on this important subject.
DRINKING SENSIBLY
In order to reap the beneficial effects of alcohol, one needs to drink in

moderation. It is important to drink sensibly during a party or dinner to
avoid a DWI charge if you plan to drive home the same night.
Moderate Alcohol Consumption

The following recommendations are from the U.S. government’s “Dietary
Guidelines for Americans”:12
Men: No more than two standard alcoholic drinks per day

Women: No more than one standard alcoholic drink per day
Adults over 65 (both male and female): No more than one drink per day
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24 Chapter 2
Alcoholic beverages should not be consumed by some individuals, in-

cluding those who cannot restrict their alcohol intake, women of child-
bearing age who may become pregnant, pregnant and lactating women,
children and adolescents, individuals taking medications that can interact
with alcohol, and those with specific medical conditions. Alcoholic bever-
ages should be avoided by individuals engaging in activities that require
attention, skill, or coordination, such as driving or operating machinery.
Alcohol has beneficial effects when consumed in moderation. The low-
est all-cause mortality occurs at an intake of one to two drinks per day.
The lowest coronary heart disease mortality also occurs at an intake of
one to two drinks per day (see chapter 4). The well-established relation-
ship between regular alcohol consumption in moderation and a reduced
risk of cardiovascular disease may benefit women at a much younger age
than men. In both sexes, however, these beneficial effects of alcohol use
can be negated when alcohol is consumed in a heavy episodic drinking
pattern, especially for middle-aged and older men.13 People who are mod-
erate drinkers have friends who are also nondrinkers or moderate drink-
ers and have hobbies and other interests in common. Moderate drinkers
always have blood alcohol well below 0.05 percent (50 mg/dL) and do
not get into trouble with the law (at least due to alcohol consumption).
In the United States, a standard drink (12 ounces of beer, 5 ounces of
wine, or 1.5 ounces of 80 proof distilled spirits) contains approximately
0.6 ounces or 14 gm of alcohol. Various other countries also have guide-
lines for drinking in moderation. In Canada, a standard drink is defined
as containing approximately 13.5 gm of alcohol. Drinking in moderation
means not drinking more than seven drinks a week for both men and
women. In the United Kingdom a standard drink contains 8 gm of alco-
hol, and the guideline for drinking in moderation is 8–16 gm of alcohol
per day for both men and women (table 2.2).
Heavy Drinking
Drinking more than recommended can invite problems, because the
health benefits of drinking in moderation quickly disappear. Theoreti-
cally, drinking more than three drinks a day by men and more than two
drinks a day by women can be considered heavy drinking. For all practi-
cal purposes, the National Institute of Alcohol Abuse and Alcoholism sets
this threshold at more than fourteen drinks per week for men (or more
than four drinks per occasion) and more than seven drinks per week
for women (or more than three drinks per occasion). Individuals whose
drinking exceeds these guidelines are at increased risk for adverse health
effects. Hazardous drinking is defined as the quantity or pattern of alco-
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Table 2.2. Guidelines for Drinking in Moderation in Various Countries

Amount of Alcohol
Country (One Drink) Men Women
United States 14 gm Up to 28 gm/day Up to 14 gm/day
(2 drinks) (1 drink)
Canada 13.5 gm Up to 94.5 gm/week Up to 94.5 gm/week
(Up to 7 drinks/ (Up to 7 drinks/week)
week)
Australia 10 gm Up to 40 gm/day Up to 40 gm/day
Two days/week Two days/week
no drinking no drinking
UK 8 gm 8–16 gm/day 8–16 gm/day
(Up to 2 drinks) (Up to 2 drinks)
France 12 gm 60 gm/day 36 gm/day
(Up to 5 drinks) (Up to 3 drinks)
Japan 19.8 gm Two drinks of sake per day at the most
(39.6 gm of alcohol/day maximum)
Spain 10 gm Up to 30 gm/day Up to 30 gm/day
(Up to 3 drinks/ (Up to 3 drinks/day)
day)
Italy 10 gm Up to 40 gm/day Up to 30 gm/day
Elderly Elderly
Up to 30 gm/day Up to 25 gm/day
New Zealand 10 gm Up to 210 gm/week Up to 140 gm/week No
No more than 60 mg more than 40 mg in
in one occasion one occasion
Ireland 8 gm Up to 24 gm/day Up to 16 gm/day (Up to
(Up to 3 drinks) 2 drinks)
hol consumption that places individuals at high risk from alcohol-related

disorders. Usually hazardous drinking is defined as twenty-one or more
drinks per week by men or more than seven drinks per occasion at least
three times a week. For women, more than fourteen drinks per week or
drinking more than five drinks in one occasion at least three times a week
is considered hazardous drinking.14
Alcohol use is a leading cause of mortality and morbidity interna-
tionally and is ranked by the World Health Organization (WHO) as
one of the top five risk factors for disease. Without treatment, approxi-
mately 16 percent of all hazardous or heavy alcohol consumers will
become alcoholics.15 Heavy consumption of alcohol leads not only to
increased domestic violence, decreased productivity, increased risk of
motor vehicle and job-related accidents, but also to increased mortal-
ity from liver cirrhosis, stroke, and cancer (see chapter 5 for a more
detailed discussion).
10-649_Dasgupta.indb 25 1/17/11 6:40 AM

26 Chapter 2
Fortunately, alcohol consumption is going down in the United States.

Compared to fifty years ago, Americans consume less alcohol now. The
per capita consumption of alcohol is much higher in European countries,
such as Hungary, the Czech Republic, Germany, France, the United King-
dom, and Denmark, compared to the United States. Fortunately, the per-
ception of the mean reported number of drinks to feel drunk reduced sig-
nificantly between each survey conducted between 1979 and 2000 in the
United States. This may be explained partly by the increase in education,
the decline in per capita alcohol consumption, and changes in alcohol
policy toward lower blood alcohol levels for determining impairment.16
Binge Drinking
“Binge drinking” means heavy consumption of alcohol within a short pe-
riod of time with the intention of becoming intoxicated. Although there is
no universally accepted definition for binge drinking, usually consump-
tion of five or more drinks by males and four or more drinks by females is
considered binge drinking. Such drinking patterns always result in blood
alcohol levels above 0.08 percent, the legal limit for driving. Despite hav-
ing a legal drinking age of twenty-one in the United States, binge drinking
is very popular among college students. In one study (Naimi et al. 2004),
the authors found that 74.4 percent of binge drinkers consumed beer ex-
clusively or predominantly, and 80.5 percent of binge drinkers consumed
at least some beer. Wine accounted for only 10.9 percent of binge drinks
consumed.17 Predictably, college binge drinkers are more likely than
their nondrinking counterparts to experience one or more alcohol-related
problems while in college. In another study (Jennisom 2004), the author
observed in a ten-year follow-up of binge drinkers that such drinkers
have a much higher risk of becoming dependent on alcohol later in life.
Binge drinking also caused early departure from college and less favor-
able labor market outcomes.18
BLOOD ALCOHOL CONCENTRATION AND DWI
DWI stands for “driving with impairment.” The charge differs from state
to state in the United States and includes DUI or “driving under the in-
fluence,” OUI or “operating [a vehicle] under the influence,” and OWI
or “operating [a vehicle] while impaired.” In some states DWI stands for
“driving while intoxicated.” Although impairment may also be drug re-
lated, alcohol is the major cause of DWI, not only in the United States but
worldwide. Alcohol-related motor vehicle accidents kill approximately
17,000 Americans annually and are associated with more than $51 billion
10-649_Dasgupta.indb 26 1/17/11 6:40 AM

in total costs annually. A strong correlation exists between binge drinkers

and alcohol-impaired drivers in the United States. In one study (Flow-
ers et al. 2008), the authors found that overall, 84 percent of all alcohol-
impaired drivers are binge drinkers; non–heavy drinkers are also in-
volved in alcohol-related motor vehicle accidents.19
Currently, in all states in the United States, the legal limit for driving is
0.08 percent alcohol concentration in the blood. This translates to 80 mg of
alcohol in 100 milliliter of whole blood (80 mg/dL). Blood is composed of
an aqueous part and various blood cells. Red blood cells contain hemoglo-
bins and carry oxygen throughout the body, a biological process essential
for living, whereas white blood cells perform other important functions,
including protecting our body from invading organisms. In addition, vari-
ous other cells, such as neutrophils, eosinophils, basophils, and so on are
also found in whole blood. When blood is centrifuged for five to ten min-
utes, it separates into two levels: the upper aqueous layer (water-containing
layer) called “serum” and the bottom red blood cell (RBC) layer. Alcohol is
soluble in the aqueous part of blood. In some laboratories, blood alcohol is
measured in the serum after separating blood cells from the whole blood.
Serum concentration of alcohol is more than whole blood concentration of
alcohol. In order to calculate whole blood concentration of alcohol, the mea-
sured serum concentration must be multiplied by a factor that is generally
considered as 0.85. Therefore, if serum alcohol concentration is 100 mg/dL
(0.1 percent), then the whole blood concentration is 85 mg/dL (0.085 per-
cent). In most states, the legal limit of intoxication is defined as 0.08 percent
alcohol in whole blood rather than serum alcohol concentration. However,
for young adults, many states have a zero-tolerance policy for drivers. After
drinking, alcohol enters into the circulatory system and distributes mostly
into the aqueous component of blood. The blood alcohol level is deter-
mined by the number of drinks consumed and the time elapsed since the
beginning of drinking. In general, the blood alcohol concentration reduces
by 0.015 percent (15 mg/dL) per hour.
In the United Kingdom and Canada, the legal limit for driving is also
0.08 percent, but in other countries, lower levels of alcohol are mandated
as the acceptable upper limit of driving under the influence of alcohol. In
Switzerland, Denmark, Italy, the Netherlands, Austria, Australia, China,
Thailand, and Turkey, the upper limit is 0.05 percent alcohol. In Japan, the
upper acceptable limit is only 0.03 percent, and in certain countries, such
as various Middle Eastern countries, Hungary, Romania, and Georgia,
there is zero tolerance for blood alcohol limits in drivers.
Although the legal limit of blood alcohol in adult drivers in the United
States is 0.08 percent, some driving impairment may occur at an even lower
blood alcohol level. There is a general agreement that some impairment of
the ability to drive takes place at a blood alcohol level of 0.05 percent. Even
10-649_Dasgupta.indb 27 1/17/11 6:40 AM

28 Chapter 2
Figure 2.1. Correlation between blood alcohol concentrations and physiological effects
blood alcohol levels of 0.03 percent affect some cognitive functions that rely
on perception and the processing of visual information.20 Ingestion of one
drink generally leads to a blood alcohol level of 0.025 percent. Low blood
alcohol levels of 0.05 percent usually produce more relaxation and more
social interactions with other individuals. However, intoxication can occur
at a blood alcohol level of 0.1 percent, and levels higher than 0.5 percent are
potentially lethal (fig. 2.1). The drunkest reported driver in Sweden had a
blood alcohol level of 0.55 percent.21
CALCULATION OF BLOOD ALCOHOL CONCENTRATION:

WIDMARK FORMULA
In 1932, the Swedish scientist Eric P. Widmark developed a formula that

is still used today for the calculation of the amount of alcohol ingested
and for assessing the concentration of alcohol prior to a blood alcohol
analysis.22 The Widmark formula suggests estimating blood alcohol level
on a given amount of alcohol administration by factoring in the subject’s
10-649_Dasgupta.indb 28 1/17/11 6:40 AM

body weight and gender. By using this formula, one can estimate the
amount of alcohol consumed by a person.
A=C×W×r
The letter A represents the total amount of alcohol consumed by the per-
son in grams, C is the blood alcohol concentration in grams per liter, W is
the body weight of the person expressed in kilograms, and r is a constant,
which is assumed to be roughly 0.7 for men and 0.6 for women. Although
these values are based on a Caucasian population, Tam et al. (2005) calcu-
lated that the average r value for Chinese men is 0.68 and average r value
for Chinese women is 0.59, which are very close to average r values of
Caucasian men and women.23
The modern form of the formula to calculate blood alcohol concentra-
tion from the amount of alcohol consumed by an individual by figuring
in body weight and gender is as follows:
C = (A/W × r) – 0.015 t, where t represents time passed since the

beginning of drinking
In the United States, one standard drink of alcohol has 0.6 ounce of alco-
hol and the weight of a person is expressed in pounds. However, blood
alcohol concentration is expressed as mg per 100 mL of blood. Taking
into account all these factors, this formula can be modified for calculating
blood alcohol concentration as follows:
C = (Total amount of alcohol consumed in ounces × 5.14/weight in

pounds × r) – 0.015 t
C is the percentage of blood alcohol. Assuming each drink contains 0.6

ounce of alcohol, this equation can be further modified to:
C = (Number of drinks × 3.1/weight in pounds × r) – 0.015 t
Because most standard drinks contain approximately the same amount

of alcohol, it is only important to know how many drinks one person
consumes. The type of drink does not matter, which makes the calculation
easy. For example, if a 150-pound man drinks five beers in a two-hour
period, his blood alcohol at the end of drinking would be:
C = (5 × 3.1/150 × 0.7) – 0.015 × 2

= 0.147 – 0.030
= 0.117 percent
10-649_Dasgupta.indb 29 1/17/11 6:40 AM

30 Chapter 2
If a 150-pound woman consumes five beers in two hours, her blood alco-
hol would be:
C = (5 × 3.1/150 × 0.6) – 0.015 × 2

= 0.172 – 0.030
= 0.142 percent
The blood alcohol level in women would be higher than men of

the same weight. These calculations show that regardless of gender,
drinking five beers or any five drinks within a two-hour time frame
would result in a blood alcohol level much higher than the legal limit
for driving.
There are many Internet sites that will calculate the blood alcohol
level for you when you insert the number of drinks you have consumed,
your gender, your body weight, and the time elapsed since you started
drinking. In addition, there are also many charts available on Internet
sites that provide approximate blood alcohol levels based on your body
weight, gender, and number of drinks consumed. You need to subtract
0.015 percent per hour from that number in order to get an approximate
blood alcohol level when you are ready to go home. In table 2.3, I have
calculated the projected blood alcohol levels for men weighing between
Table 2.3. Projected Blood Alcohol in Males Consuming between 1 and 8 Drinks
Using Widmark Formula
Body Number of Drinks

Weight 1 2 3 4 5 6 7 8
Male Blood Alcohol Concentration (%)
100 lb 0.044 0.088 0.132 0.176 0.220 0.264 0.308 0.352
125 lb 0.035 0.070 0.105 0.140 0.175 0.210 0.245 0.280
150 lb 0.030 0.060 0.090 0.120 0.150 0.180 0.210 0.240
175 lb 0.025 0.050 0.075 0.100 0.125 0.150 0.175 0.200
200 lb 0.022 0.044 0.066 0.088 0.110 0.132 0.154 0.176
225 lb 0.020 0.040 0.060 0.080 0.100 0.120 0.140 0.160
250 lb 0.018 0.036 0.054 0.072 0.090 0.108 0.126 0.144
275 lb 0.016 0.032 0.048 0.064 0.080 0.096 0.112 0.128
Female
90 lb 0.057 0.114 0.171 0.228 0.285 0.342 0.399 0.456
100 lb 0.051 0.102 0.153 0.202 0.255 0.306 0.357 0.408
125 lb 0.041 0.082 0.123 0.164 0.205 0.246 0.287 0.328
150 lb 0.034 0.068 0.102 0.136 0.170 0.204 0.238 0.272
175 lb 0.030 0.060 0.090 0.120 0.150 0.180 0.210 0.240
200 lb 0.026 0.052 0.078 0.104 0.130 0.156 0.182 0.208
225 lb 0.023 0.046 0.069 0.092 0.105 0.128 0.161 0.184
250 lb 0.020 0.040 0.060 0.080 0.100 0.120 0.140 0.160
10-649_Dasgupta.indb 30 1/17/11 6:40 AM

100 and 275 pounds and women weighing between 90 and 250 pounds.
In these calculations, I assumed that all alcohol was consumed rapidly,
so these values represent blood alcohol levels at an equilibrium state. I
did not take into account any metabolism of alcohol. You need to sub-
tract 0.015 percent per hour from this number from the time you started
drinking. For example, if you are a 125-pound women who consumed
four drinks in four hours, then your estimated blood alcohol level is 0.164
percent minus 0.015 multiplied by four, which is 0.060, accounting for
the burning of alcohol. Therefore, your estimated blood alcohol level is
0.104 percent, which is above the legal limit for driving. Therefore, even
following the rule of one drink per hour is not valid if you consume more
than two drinks in one occasion and still plan to drive. For a 150-pound
man consuming four drinks in four hours, the estimated blood alcohol
level would be 0.120 minus 0.060, which is 0.060, a value below the legal
limit for driving; however, this blood alcohol level may still cause some
impairment in driving.
In general, you should not consume more than one drink per hour
(beer, wine, or dinner wine, but not a cocktail) and not more than two
drinks in one occasion. You should wait for at least two hours from the
beginning of drinking before you drive, unless your body weight is be-
low 100 pounds or you belong to an ethnic group that has difficulty in
metabolizing alcohol due to genetic predisposition. No guideline can
be provided for drinking mixed drinks and cocktails, because alcohol
content may vary widely at different bars. For example, depending on
how it is prepared, one margarita may be equivalent to two or three
standard drinks. Always consume alcohol with food.
Again, the guidelines provided are very conservative, and if you drink
no more than two standard drinks in two hours, your blood alcohol
should likely be below 0.05 percent and you should have little or no
impairment for driving. If you weigh between 175 and 200 pounds, then
you can consume up to three standard drinks in two to two and half
hours and it will probably still be safe to drive. For people between 175
and 200 pounds, one margarita or a double-shot mixed drink should not
cause blood alcohol levels over the legal limit for driving, provided at
least two hours have passed since initiating drinking and before begin-
ning to drive. A petite woman with a body weight around 100 pounds
or less who consumes one beer or one five-ounce glass of wine should
wait for two hours before driving. If you are an average woman with
a body weight between 125 and 150 pounds, drinking one margarita or
10-649_Dasgupta.indb 31 1/17/11 6:40 AM

32 Chapter 2
mixed drink is fine, provided you wait one and a half to two hours from
the initiation of drinking until you drive. For petite women, with a body
weight around 100 pounds or less, it is better not to drink mixed drinks,
such as margaritas, and then drive, unless at least two and a half to three
hours have passed from when you started drinking. Always consume
alcohol with food.
ALCOHOLIC ODOR AND BLOOD ALCOHOL
There is a perception that if your breath smells like alcohol, you must
have a blood alcohol level exceeding the legal limit for driving. In reality,
alcohol is almost odorless, and the alcoholic smell perceived by people is
due to the presence of many complex, organic, volatile compounds in al-
coholic beverages. Wine aroma is attributed to a large range of molecules
from different chemical families, including esters, aldehydes, ketones, ter-
penes, tannins, and sulfur compounds. Some of these compounds origi-
nate from grapes and others are formed during fermentation or aging. In
general, more volatile substances are present in white wine compared to
red wine.24 Therefore, there is no correlation between blood alcohol level
and alcoholic odor. Such odor may also be present in an individual drink-
ing nonalcoholic beer.
CAN OUR BODIES PRODUCE ALCOHOL?
This is a very popular DWI defense: the defendant never drank alcohol
but felt tipsy after eating a big meal, and that caused the accident. I have
encountered this defense strategy several times in my twenty years of
experience as an expert witness for the state on alcohol- and drug-related
cases. Although substantial alcohol may be produced endogenously in a
decomposed body by the action of various microorganisms, living bodies
do not produce enough endogenous alcohol to be used as a defense in the
case of accidents or impaired judgment. In healthy individuals who do
not drink, endogenous alcohol levels are usually way below the detection
level of instruments used in laboratories for measuring blood alcohol.
There are reports of measurable endogenous ethanol production in pa-
tients with liver cirrhosis. In one report (Madrid et al. 2002), after a meal
in such patients, negligible alcohol levels of 11.3 mg/dL (0.01 percent)
and 8.2 mg/dL (0.008 percent) were detected in two out of eight patients.
Small intestinal bacterial overgrowth generates such small amounts of en-
dogenous alcohol. Patients with liver cirrhosis often have small intestinal
bacterial overgrowth.25
10-649_Dasgupta.indb 32 1/17/11 6:40 AM

CONCLUSION
Drinking in moderation—two drinks a day for men, one drink a day for
women, and one drink a day for people older than sixty-five—has health
benefits, but heavy drinking is associated with many diseases and also
increases mortality from alcohol-related causes. If you drink moderately,
then you will not get into trouble with the law, because your blood alco-
hol should be significantly below the legal limit of 0.08 percent. A good
rule of thumb is to drink only one drink in one hour, not exceeding two
drinks in two hours if you plan to drive home. Drinking more than that
may get you into trouble. Certain ethnic groups, such as Asians, Ameri-
can Indians, and Alaskan Natives have a genetic predisposition that
leads to impaired alcohol metabolism. Such individuals may experience
flushing due to a buildup of acetaldehyde, a toxic metabolite of alcohol in
blood, even from a single drink.
NOTES
1. W. C. Kerr, T. K. Greenfield, J. Tujague, and S. E. Brown, “A Drink Is a

Drink? Variation in the Amount of Alcohol Contained in Beer, Wine and Spirits
Drinks in a U.S. Methodological Sample,” Alcohol Clinical and Experimental Re-
search 29, no. 11 (November 2005): 2015–21.
2. A. W. Jones and K. Å. Jönsson, “Food-Induced Lowering of Blood-Ethanol
Profiles and Increased Rate of Elimination Immediately after a Meal,” Journal of
Forensic Sciences 39, no. 4 (July 1994): 1084–93.
3. A. W. Jones, K. Å. Jönsson, and S. Kechagias, “Effect of High-Fat, High-
Protein, and High-Carbohydrate Meals on the Pharmacokinetics of a Small Dose of
Ethanol,” British Journal of Clinical Pharmacology 44, no. 6 (December 1997): 521–26.
4. S. Mumenthaler, J. L. Taylor, R. O’Hara, and J. A. Yesavage, “Gender Differ-
ences in Moderate Drinking Effects,” Alcohol Research and Health 23, no. 1 (January
1999): 55–64.
5. J. Gill, “Women, Alcohol, and the Menstrual Cycle,” Alcohol and Alcoholism
32, no. 4 (April 1997): 435–41.
6. B. Augustyńska, M. ZIółkowski, G. Odrowa˛ż-Sypniewska, A. Kiełpiński, M.
Gruszka, and W. Kosmowski, “Menstrual Cycle in Women Addicted to Alcohol
during the First Week Following Drinking Cessation: Changes in Sex Hormones
Levels in Relation to Detected Clinical Features,” Alcohol and Alcoholism 42, no. 2
(February 2007): 80–83.
7. S. Zakhari, “Overview: How Is Alcohol Metabolized by the Body?” Alcohol
Research and Health 29, no. 4 (December 2006): 245–54.
8. P. Meier and H. K. Seitz, “Age, Alcohol Metabolism and Liver Disease,” Cur-
rent Opinion in Clinical Nutrition and Metabolic Care 11, no. 1 (January 2008): 21–26.
9. K. J. Mukamal, L. H. Kuller, A. L. Fitzpatrick, W. T. Longstreth Jr., Murray A.
Mittleman, and David S. Siscovick, “Prospective Study of Alcohol Consumption
10-649_Dasgupta.indb 33 1/17/11 6:40 AM

34 Chapter 2
and Risk of Dementia in Older Adults,” Journal of American Medical Association 289,
no. 11 (November 2003): 1405–13.
10. A. M. Chan, D. von Muhlen, D. Kritz-Silverstein, and E. Barrett-Connor,
“Regular Alcohol Consumption Is Associated with Increased Quality of Life and
Mood in Older Men and Women: The Rancho Bernardo Study,” Maturitas 63, no.
3 (March 2009): 294–300.
11. R. Alati, N. Dunn, D. M. Purdie, A. M. Roche, et al., “Moderate Alcohol
Consumption Contributes to Women’s Well-Being through the Menopausal
Transition,” Climacteric: The Journal of the International Menopause Society 10, no. 6
(December 2007): 491–99.
12. “Dietary Guidelines for Americans: Chapter 9—Alcoholic Beverages,”
United States Department of Agriculture and United States Department of Health
and Human Services (Washington, D.C.: U.S. Government Printing Office, 2005),
43–46. Available at http://www.health.gov/DIETARYGUIDELINES/dga2005/
document/html/chapter9.htm.
13. W. M. Snow, R. Murray, O. Ekumo, S. L. Tyas, et al., “Alcohol Use and
Cardiovascular Health Outcome: A Comparison across Age and Gender in the
Winnipeg Health and Drinking Survey Cohort,” Age and Aging 38, no. 2 (March
2009): 206–12.
14. M. C. Reid, D. A. Fiellin, P. G. O’Connor, “Hazardous and Harmful Alcohol
Consumption in Primary Care,” Archives of Internal Medicine 159, no. 8 (August
2008): 1681–89.
15. S. Coulton, “Alcohol Misuse,” Clinical Evidence Handbook, American Family
Physician, April 15, 2009, 79(8): 692–94.
16. W. A. Kerr, T. K. Greenfield, L. T. Midanik, “How Many Drinks Does It
Take to Feel Drunk? Trends and Predictors for Subjective Drunkenness,” Addic-
tion 101, no. 10 (October 2006): 1428–37.
17. T. S. Naimi, R. D. Brewer, J. W. Miller, C. Okoro, and C. Mehrotra, “What
Do Binge Drinkers Drink? Implications for Alcohol Control Policy,” American
Journal of Preventive Medicine 33, no. 3 (August 2004): 188–93.
18. K. M. Jennisom, “The Short-Term Effects and Unintended Long-Term Con-
sequences of Binge Drinking in College: A 10-Year Follow-Up Study,” American
Journal of Drug and Alcohol Abuse 30, no. 3 (August 2004): 659–84.
19. N. T. Flowers, T. S. Naimi, R. D. Brewer, R. W. Elder, R. A. Shults, and R.
Jiles, “Patterns of Alcohol Consumption and Alcohol-Impaired Driving in the
United States,” Alcohol: Clinical and Experimental Research 32, no. 4 (April 2008):
639–44.
20. D. Breitmeier, I. Seeland-Schulze, H. Hecker, and U. Schneider, “The Influ-
ence of Blood Alcohol Concentrations around 0.03 Percent on Neuropsychological
Functions: A Double-Blind, Placebo-Controlled Investigation,” Addiction Biology
12, no. 2 (June 2007): 183–89.
21. A. W. Jones, “The Drunkest Drinking Driver in Sweden: Blood Alcohol
Concentration 0.545% W/v.,” Journal of Studies in Alcohol 60, no. 3 (May 1999):
400–406.
22. I. G. Brouwer, “The Widmark Formula for Alcohol Quantification,” South
African Dental Association Journal 59, no. 10 (November 2004): 427–28.
10-649_Dasgupta.indb 34 1/17/11 6:40 AM

23. T. W. M. Tam, C. T. Yang, W. K. Fung, K. K. Mok Vincent, “Widmark Fac-

tors for Local Chinese in Hong Kong: A Statistical Determination on the Effects
of Various Physiological Factors,” Forensic Science International 151, no. 1 (June
2005): 23–29.
24. J. Torrens, M. Riu-Aumatell, E. Lopez-Tamames, and S. Buxaderas, “Vola-
tile Compounds of Red and White Wines by Headspace: Solid-Phase Microextrac-
tion Using Different Fibers,” Journal of Chromatographic Science 42, no. 6 (July 2004):
310–16.
25. A. M. Madrid, C. Hurtado, S. Gatica, I. Chacon, et al., “Endogenous Ethanol
Production in Patients with Liver Cirrhosis, Motor Alteration and Bacterial Over-
growth,” Revista Medica de Chile 130, no. 12 (December 2002): 1329–34.
10-649_Dasgupta.indb 35 1/17/11 6:40 AM

10-649_Dasgupta.indb 36 1/17/11 6:40 AM
3

How Alcohol Affects
the Human Mind
T he human brain, the part of the central nervous system where auto-
nomic functions, such as motor responses, heartbeat, respiration, and
other activities take place, totally controls the human mind, the part of
ourselves that Webster’s defines as “the element or complex of elements in
an individual that feels, perceives, thinks, wills, and especially reasons”
(Webster’s Collegiate Dictionary, 11th ed.). In order to understand how
alcohol affects the human mind, we need to understand how alcohol af-
fects the brain. Alcohol (ethanol) is the oldest of all drugs that humans
consume for pleasure. Alcohol can affect different parts of our brain,
providing relaxation, pleasure, loss of inhibition, and euphoria. The de-
tails of the molecular mechanism of how alcohol affects the human brain
is still subject to research, but extensive study in this field for more than
fifty years has unlocked many key mechanisms by which alcohol affects
our mind. Chronic alcohol use is detrimental to brain cells and may cause
them to die.
The effect of alcohol on the human mind depends on blood alcohol
level and drinking habits. Drinking in moderation (not more than two
drinks a day for men, one drink a day for women, and one drink a day re-
gardless of gender in people older than sixty-five) can help an individual
to relax after a hard day’s work and can also enhance social interactions
with others. In addition, moderate drinking has health benefits (see chap-
ter 4 for more detail).
37
10-649_Dasgupta.indb 37 1/17/11 6:40 AM

38 Chapter 3
If you want to experience the pleasurable and beneficial effects of

alcohol, always drink in moderation. Consuming excess alcohol is
detrimental to both the human body and mind.
BLOOD ALCOHOL: EFFECT ON THE HUMAN MIND
Alcohol is a central nervous system depressant that reduces our inhibi-

tions. Therefore, after one drink a person may talk more and feel more
relaxed. In addition, alcohol releases neurotransmitters like dopamine,
which can elevate our mood through the same positive reinforcement
pathway that gives us pleasure after we eat our favorite food or enjoy in-
timate moments with our loved ones. Alcohol makes your brain feel less
inhibited, which can result in exchanging feelings on deeper levels with
friends and/or family.
Substantial research has established that the effect of alcohol on the hu-
man mind largely depends on the blood alcohol concentration. At a very
low blood alcohol level (0.02–0.03 percent) people usually feel relaxation
and mild euphoria and some loss of inhibition or shyness. At moderate
blood alcohol levels (0.04–0.06 percent), a person may experience euphoria
and the pleasurable effects of alcohol, such as being happy and satisfied.
Inhibition may completely disappear, and he or she may interact more
easily with other people. However, at higher blood alcohol levels, a person
becomes impaired with compromised reflexes and motor skills. Such im-
pairments become significant at the legal limit of blood alcohol, or 0.08 per-
cent. Significantly higher blood alcohol levels that exceed the legal limit for
driving cause depression instead of elation, complete loss of motor skills,
and impaired judgment. At a blood alcohol level of 0.3 percent and higher,
complete loss of consciousness may occur, and a blood alcohol level of 0.4
percent and higher may even cause death (see table 3.1).
People like to drink alcohol because of its ability to modify emotional
states. Alcohol has a euphoric effect at low to moderate blood alcohol
concentrations and can also cause relaxation, disinhibition, and reduced
anxiety and stress levels. Rewarding and anxiolytic effects of alcohol are
well documented in the medical literature.1 However, elation caused by
alcohol is dependent on blood alcohol concentration. At low to moderate
blood alcohol levels, a person experiences the positive stimulatory effects
of alcohol, but at higher blood alcohol levels, the negative effects of alcohol
on mood (depression) become evident.2 Alcohol is known to cause reduc-
tion in inhibition in a person, probably due to the reduction of frontal lobe
functions of the brain. A recently published article (Hoppenbrouwers et
al. 2010) concluded that loss of inhibition after drinking is more significant
10-649_Dasgupta.indb 38 1/17/11 6:40 AM

Table 3.1. Blood Alcohol Level and the Effect on the Human Body and Mind
Blood Alcohol Level % Effects on Human Body and Mind
0.01 to 0.019 (10 to 19 mg/dL) Normal appearance of an individual
0.02 to 0.039 (20 to 39 mg/dL) Feeling of mild euphoria, sense of well-being, and
decreased inhibition or shyness. Usually no loss
of muscle coordination observed at this blood
alcohol level.
0.04 to 0.059 (30 to 59 mg/dL) Euphoria with feelings of self-satisfaction and loss of
most inhibition, making a person more talkative
and interactive socially with everyone in the
group. Emotions of an individual may be more
intense and some behavior may be exaggerated.
Some mild impairment may be observed in one’s
alertness and judgment.
0.06 to 0.79 (60 to 79 mg/dL) Some impairments may be evident at this blood
alcohol level, such as self-control, motor
function, judgment, and ability to operate a motor
vehicle. Peripheral vision and glare recovery
may also be impaired and a person may lose all
inhibition.
0.08 to 0.109 (80 to 109 mg/dL) Balance, speech, hearing, and reaction time are all
affected at this blood alcohol level and ability to
drive a motor vehicle is severely impaired (legal
limit for driving is 0.08 percent blood alcohol).
Emotional swings and depression may also be
observed at this blood alcohol level.
0.11 to 0.129 (110 mg/dL to Motor function, speech, judgment, and perception
129 mg/dL) are all severely impaired at this high blood level.
Staggering and slurred speech are also common,
and a person may feel more angry and aggressive.
0.13 to 0.159 (130 mg/dL to Feelings of euphoria are totally replaced by feelings
159 mg/dL) of depression and uneasiness. At such high blood
alcohol levels a person may not be able to stand
or walk without help from others, and vision may
become totally blurry.
0.16 to 0.199 (160 mg/dL to Severe feelings of illness and depression and a
199 mg/dL) person may become nauseous. At such elevated
levels of blood alcohol, a person appears drunk.
0.20 to 0.249 (200 mg/dL to Nausea, vomiting, and some blackouts, and a
249 mg/dL) person cannot move without the assistance of
others. Some loss of consciousness may also
occur.
0.25 to 0.299 (250 mg/dL to Stupor, impaired sensation, total memory blackout,
299 mg/dL) and loss of consciousness occur at such severely
elevated blood alcohol level.
0.3 to 0.4 (300 mg/dL to Severe alcohol toxicity, coma, and even death may
400 mg/dL) occur.
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40 Chapter 3
in women than in men.3 Another study (Clarisse et al. 2004), based on 184
degree-level and postgraduate students (ninety-four females and ninety
males), indicated that alcohol at a level of approximately 50 mg/dL (0.05
percent) facilitated social interaction and communication.4 Alcohol also has
a calming effect and is capable of reducing anxiety.5
The behavioral actions of alcohol on brain neurochemistry are very
much dependent on blood alcohol levels. Genetic factors and gender play
an important role in the action of alcohol on the human mind, because
at certain modest blood alcohol levels, some individuals may feel the
pleasurable effects of alcohol, while others may not feel anything at all.6
In order to understand the mechanism by which alcohol affects our mind,
we need to understand how the human brain works.
In the level of brain chemistry, alcohol is capable of selectively af-

fecting functions of gamma-aminobutyric acid (GABA) receptors. In
addition, alcohol can also affect functions of other receptors, such as
glutamatergic, serotonergic, dopaminergic, cholinergic, and opioid
systems, thus producing a feeling of joy and well-being.
HOW HUMAN BRAINS WORK
The human brain is the control center of the human body that coordi-
nates the ability to move, touch, smell, taste, and hear. The brain also
controls mood, level of consciousness, and alertness. The brain is a very
complex organ that consists of the cerebrum, the cerebellum, and the
brain stem, which are protected by the skull and internal lining, which is
called the dura mater. The cerebrum is the largest part of the brain and
is divided into two halves, the left and right cerebral hemispheres. The
hemispheres are connected by nerve fibers that form a bridge (corpus cal-
losum) through the middle of the brain, and each hemisphere is further
divided into frontal, parietal, occipital, and temporal lobes (fig. 3.1). The
right hemisphere is believed to control emotion, creativity, and intuitive
and subjective judgment, while the left hemisphere is involved in logic,
analytical thinking, and mathematical skill.
The cerebrum consists of dense masses of tissues, and the outer layer is
called the cerebral cortex, also known as gray matter, which contains most
of the nerve cells. The human brain has approximately 100 billion neurons
that are specifically designed to receive, process, and transmit information,
and are integral for the function of the brain. Similar to the other cells of the
body, neurons have a nucleus and cytoplasm but also have characteristic
features called axon and dendrite. Axon allows a neuron to send signals to
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How Alcohol Affects the Human Mind 41
Figure 3.1. Various parts of the human brain from The Merck Manual of Medical In-
formation, home ed., edited by Robert S. Porter (Whitehouse Station, NJ: Merck, 2007).
Available at http://www.merck.com/mmhe/index.html. Reprinted with permission.
the neighboring neurons, while dendrites serve as the antenna to receive

signals from other cells. Neurotransmitters are specific chemicals found in
neurons that allow the transmission of the signal from one neuron to the
next through synapse, a small gap between neurons. Neurotransmitters are
stored in the axon part of the nerve cell (bulbous end), and when an electri-
cal signal reaches the end part of the neuron, a specific neurotransmitter is
released that travels through the synaptic gap and reaches the next neuron,
either promoting or inhibiting the electrical signal along the next neuron.
When a neurotransmitter crosses the synapse gap, it is accepted by the next
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42 Chapter 3
neuron at a specialized site called a receptor (there are specialized receptors

for different neurotransmitters), and it is the interaction between the recep-
tor and the neurotransmitter that dictates the fate of the electrical impulse.
Neurotransmitters not only transmit information throughout the brain
but are also capable of transmitting information from the brain to the rest
of the body. For example, the first neurotransmitter, acetylcholine, dis-
covered in 1921, sends information to skeletal muscle, sweat glands, and
the heart. There are more than 200 known neurotransmitters, but three
major categories of substances that act as neurotransmitters are amino
acids (primarily glutamic acid, gamma-aminobutyric acid [GABA],
aspartic acid, and glycine), peptides (vasopressin, somatostatin, neuro-
tensin, to name a few), and monoamines (norepinephrine, dopamine,
and serotonin). The major neurotransmitters of the brain are glutamic
acid (also known as glutamate) and GABA, while monoamines and ace-
tylcholine perform specialized functions. GABA is the major inhibitory
neurotransmitter, and it can inhibit the action of other neurotransmitters,
for example, dopamine. The neuropeptides, which are also categorized
as neurotransmitters, perform specialized functions in the hypothalamus.
A detailed discussion of how the brain works is beyond the scope of this
book, but in table 3.2 functions of different parts of the brain are listed.
In this chapter the reward system of the brain, which is responsible for
the pleasurable effects of alcohol and drugs, will be discussed in detail,
because this center is the key by which alcohol controls the human mind.
HOW THE BRAIN’S REWARD (PLEASURE) SYSTEM WORKS
The human mind seeks pleasure in daily life, and if certain amounts of
pleasure or reward are not experienced every day, a person can become
Table 3.2. Function of Different Parts of the Human Brain

Part of the Brain Major Functions
Frontal lobe Controls facial expression and gesture
Coordinates gestures with mood
Voluntary actions such as looking at an object
Relaxes bladder to urinate
Controls motor skills, speech, and thoughts
Parietal lobe Controls body movement and processes sensory stimulation
Controls body parts and stores spatial memory
Controls mathematical skill and language comprehension
Temporal lobe Stores information and controls memory
Comprehends sounds and images so that people can
recognize a person, object, and so on
Occipital lobe Controls vision and enables people to have visual memory
Mesolimbic system Pleasure/reward center of the brain
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depressed and may experience what is known as “reward deficiency syn-

drome.” A broad range of activities stimulate our reward pathways, in-
cluding food, positive social interactions, and/or positive feedback from
work, sex, and exercise. In addition, many chemicals, such as alcohol,
cocaine, opiates, and marijuana, can also stimulate our reward system.
Addiction to drugs or alcohol occurs when the brain’s reward system is
hijacked by excessive use of drugs or alcohol.
The main center of the brain’s reward pathway is at the ventral tegmen-
tal area (VTA) of the midbrain, and it is connected to the limbic system
through the nucleus accumbens, amygdala, hippocampus, and the medial
frontal cortex. There are two major pathways in the reward system that
are modulated by the neurotransmitters dopamine and serotonin. The
dopamine pathways produce reward, euphoria, and pleasure, while the
serotonin pathway produces mood, memory, and sleep (fig. 3.2).
When the cortex of the prefrontal lobe receives and processes a sensory
stimulus indicating reward, it sends a signal, announcing the reward to
the VTA, which then releases dopamine into the entire reward system
network. This region of the brain is also known as the pleasure or reward
Figure 3.2. Diagram of mesolimbic system, the brain’s pleasure structure

Source: Brain Pleasure Center, The Brain from Top to Bottom website, http://thebrain.mcgill.ca/flash/
index_d.html. Information in the public domain. Canadian Institute of Health Research.
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44 Chapter 3
bundle, which is part of the medial forebrain bundle (MFB), whose ac-
tivation leads to repeated feelings of gratification. This structure is also
known as the reward circuit of the brain and is distinct from the punish-
ment circuit of the brain. The punishment circuit of the brain helps an
individual with coping skills in unpleasant situations and with fighting
skills. This circuit includes various brain structures, such as the hypo-
thalamus, thalamus, and some area of the gray matter. The main neu-
rotransmitter of the punishment circuit is acetylcholine. Consequently,
the reward and punishment circuits control most of human behavior on
a daily basis. The behavioral inhibition system is the third circuit, which
comes into play when neither flight nor fight work and the person must
passively submit to the environment. Serotonin plays an important role in
this circuit. The pathophysiology of chronic depression can be explained
partly from the function of this circuit.7
ALCOHOL AND THE BRAIN’S PLEASURE SYSTEM
The brain is protected by a thin barrier known as the blood-brain barrier,

which limits the substances that can reach the brain. For example, peni-
cillin and many other drugs cannot pass the blood-brain barrier, while
alcohol, caffeine, nicotine, abused drugs, and various other drugs, such
as drugs used for treating depression, can pass the blood-brain barrier.
Both alcohol and abused drugs stimulate the pleasure center of the
brain (mesolimbic system) through similar molecular mechanisms. In
general, drugs that are not abused (but that can cross the blood-brain
barrier) do not increase dopamine levels in the brain’s pleasure circuit,
but abused drugs significantly increase dopamine levels, thus provid-
ing the euphoria following drug abuse. For example, stimulants such
as amphetamines and cocaine increase dopamine levels in the brain’s
pleasure circuit (mesolimbic system) by inhibiting reuptake of dopamine
into nerve terminals via dopamine transporters.8 Opiates act by activating
both dopamine neurons as well as specific opioid receptors on the GABA
neurons at the VTA region of the midbrain. Nicotine from tobacco exerts
its pleasurable effect by acting on the specific type of receptor for the neu-
rotransmitter acetylcholine. These receptors are known as nicotine recep-
tors. Interestingly, alcohol activates multiple neurotransmitter systems in
the brain, but dopamine release in the mesolimbic system is one of the
major pathways by which alcohol exerts its rewarding effect.9
Euphoria is experienced during the early phase of alcohol consumption
(the first ten to fifteen minutes) when the blood alcohol concentration is
on the rise. The exact mechanism of euphoria caused by alcohol is still the
subject of active investigation, but in addition to the release of dopamine
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in the mesolimbic system, other neuronal mechanisms involving GABA,

opiate, and serotonin receptors may also play some role in alcohol-induced
euphoria. Alcohol may reinforce its intake by activating GABA receptors,
thus indirectly modulating dopamine levels in the mesolimbic system.
GABA receptors are present throughout the brain, and alcohol acts on
GABA receptors to inhibit neurons. When a neuron is inhibited, it can-
not fire electrical stimulus anymore, and therefore no neurotransmitter is
released. Because alcohol inhibits GABA receptors, less neurotransmitter
GABA is released and this increases the concentration of dopamine. Be-
cause dopamine receptors are also present in the brain’s pleasure center,
these receptors become activated and fire more rapidly and also result in
the release of more dopamine. Therefore, alcohol increases dopamine con-
centrations by both direct stimulation and indirect stimulation (by inhibit-
ing GABA receptors), and with higher dopamine concentrations, a person
experiences euphoria after alcohol consumption. Although the serotonin
pathway has also been suggested as a possible factor for alcohol-induced
euphoria, Morgan and Badway (2009) demonstrated that it is unlikely that
serotonin is involved in the euphoric effect of alcohol.10
In addition to the GABA pathway, alcohol can modulate dopamine
levels in the mesolimbic system by modulating receptors for other neu-
rotransmitters such as glycine receptors and acetylcholine receptors in the
VTA area. At higher blood alcohol levels, euphoria is replaced by depres-
sion and other negative effects. Interestingly, dopamine in the mesolimbic
system is involved in both the positive and negative reinforcement effect
of alcohol depending on the blood alcohol level. Chronic abuse of alcohol
can produce functional alteration in the mesolimbic system, and thus may
cause permanent damage to this important brain function.11
MODERATE ALCOHOL CONSUMPTION

AND THE HUMAN BRAIN: BENEFICIAL EFFECTS
Although chronic heavy alcohol consumption damages the human brain

and may cause memory loss and severe dementia, light to moderate alco-
hol consumption may reduce the risk of dementia. The famous Rotterdam
Study investigated the effect of alcohol consumption in subjects fifty-five
years and older in preventing age-related dementia. The study included
7,983 individuals (3,105 men and 4,878 women) who were monitored
every few years regarding health issues. The investigators concluded that
light to moderate alcohol consumption (one to three drinks per day) was
associated with a lower risk of developing any form of dementia, and
such effects appeared to be unchanged by the type of drink consumed.12
In their study on alcohol and dementia, Pinder and Sandler (2004)
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46 Chapter 3
demonstrated that moderate alcohol consumption, especially red wine,

may lower the risk of developing Alzheimer’s disease. The specific anti-
oxidant properties of wine’s polyphenolic compounds (complex organic
molecules found in the skin of grapes) may be particularly important in
preventing Alzheimer’s disease. However, due to substantially unpre-
dictable risk of progression to problem drinking, the authors concluded
that the most sensible advice to the general public is that “heavy drinkers
should drink less or not at all, that abstainers should not be indiscrimi-
nately encouraged to initiate drinking for health reasons and the light to
moderate drinkers need not change their drinking habits for health rea-
sons except in exceptional circumstances.”13
It has been demonstrated that beta-amyloid peptide, a neurotoxic
substance, can cause the death of brain cells in Alzheimer’s disease. Res-
veratrol, a natural polyphenolic compound mostly found in red wines,
can protect neurons from amyloid-induced toxicity, which may help
protect individuals from getting Alzheimer’s disease.14 Interestingly,
light to moderate consumption of alcohol in older adults results in a
lower risk of developing age-related dementia and Alzheimer’s disease
than nondrinkers, but frequent drinkers are at high risk for developing
alcohol-related dementia. In addition, leisure time physical activities also
produce protective effects against dementia, while smoking elevates the
risk of Alzheimer’s disease. Consuming vegetables and fish has beneficial
effects in preventing dementia, but consuming foods high in saturated
fats increases the risk.15 Solfrizzi et al. (2007) studied the impact of alcohol
consumption on the incidence of mild cognitive impairment and its pro-
gression to dementia in 1,445 patients between sixty-four and eighty-four
years old. The authors observed that patients with mild cognitive impair-
ment who were moderate drinkers (one drink a day) had a lower rate
of progression to dementia than abstainers. Furthermore, wine drinkers
showed an even slower rate of progression to dementia than abstainers.16
In patients with mild cognitive impairment, up to one drink per day,

especially wine, may decrease the rate of progression to dementia.
CHRONIC ALCOHOL ABUSE AND THE HUMAN BRAIN
Chronic alcohol abuse has devastating effects on the human brain, but
there is a difference between how alcohol affects adolescent brains versus
adult brains, because in adolescence the mesolimbic system and other
parts of the brain are still developing.
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How Alcohol Affects the Adolescent Brain

Unfortunately, alcohol is one of the first choices among adolescents, and
heavy binge drinking (five or more drinks in one occasion; see chapter
2 for definition) is becoming frequent among high school students in
the United States and many other countries. Reports from the European
School Survey Project on Alcohol and Other Drugs, which was conducted
in thirty-five European countries, indicated that adolescents today drink
more in order to get drunk compared to earlier generations.17 Toum-
bourou et al. (2009), comparing alcohol use and related harm in school
students in the United States and Australia, reported that in Washington
State, 10.3 percent of boys and 5.2 percent of girls in fifth grade (age
eleven) used alcohol in the past year. In contrast, in Victoria, Australia,
34.2 percent of boys and 21.2 percent of girls used alcohol in the past year,
despite having a zero-tolerance policy in both countries for adolescent use
of alcohol. Use of alcohol at age eleven is not just shocking, it’s a serious
health hazard as well.18
Underage drinking contributes to the three leading causes of death (un-
intentional injury, suicide, and homicide) among young people between
the ages of twelve to twenty years. The most adverse health hazard of
underage drinking is binge drinking. Overall, 44.9 percent of high school
students in the United States reported some alcohol use and 28.9 percent
reported episodes of binge drinking during the past thirty days of the sur-
vey. Binge drinking rates increased with age and school grade. Students
who binge drank were more likely than those who didn’t binge drink
(or those who drank moderately) to report poor academic performance
and involvement in other risky behaviors, such as riding with drivers
who had been drinking, using illicit drugs, being sexually active, being a
victim of dating violence, and attempting suicide.19 Another study indi-
cates that the rate of lifetime alcohol dependence was 40 percent when an
individual started drinking at age fourteen or younger, whereas only 10
percent of individuals who started drinking at age twenty-one were de-
pendent on alcohol in the later part of their lives. Therefore, a long-lasting
consequence of alcohol consumption during adolescence is the higher
risk of alcohol dependence in adulthood.20
Magnetic resonance imaging (MRI) studies have indicated that the hu-
man brain continues to develop throughout adolescence and undergoes
significant structural and functional changes in synaptic plasticity (the
ability of the connection between two neurons to change under various
conditions) and neural connectivity, and such refinements with modifica-
tions in certain neurotransmitter systems are critical for normal function-
ing as an adult. Alcohol exposure during the juvenile/adolescent period
overactivates developing mesolimbic systems, which then induce certain
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48 Chapter 3
adaptations that can trigger long-term behavioral patterns of alcohol ad-

diction and abuse.21
Although, on average, juveniles take their first drink at the age of

twelve years, individuals who use alcohol before age fourteen are at
an increased risk of developing alcohol use disorders.
Underage drinkers are also susceptible to immediate ill effects of alcohol

use—such as blackouts, hangovers, and alcohol poisoning—compared
to their adult counterparts. These individuals are also at higher risk of
neurodegeneration (progressive loss of the function of neurons, includ-
ing neuron death, particularly in the regions of the brain responsible
for learning and memory), impairment of functional brain activity, and
neurocognitive deficits (impairment of cognitive function). Underage
drinking is associated with impaired intellectual development due to
brain damage, and such damage carries through to adulthood. Because
adolescent drinking induces brain structure abnormalities, these changes
lead to poor memory, impaired study habits, poor ability to learn, and
poor academic performance.22 In a ten-year study using data from 8,661
respondents, Harford et al. (2006) concluded that education beyond high
school has a protective effect against alcohol abuse and dependence. In
addition, people who do not attend college may also have a higher risk
of alcohol abuse than people who attend college.23 Studies also show that
children of alcoholics constitute a population at risk for skipping school
days, poor performance, and dropping out of school. Children of alcohol-
ics also have a higher incidence of repeating a grade.24
There is a difference between how alcohol damages the male versus
female adolescent brain and the extent of damage. In general a female
adolescent brain is more vulnerable to alcohol exposure than is a male
brain. Adolescents with alcohol abuse disorder have smaller prefrontal
cortex volumes compared to healthy adolescents. The prefrontal cortex
is located in the cortical region of the frontal lobe and is a crucial area of
the brain that is involved in planning complex cognitive behavior, such
as learning, critical thinking, working with mentally stored information,
rational judgment, expression of personality, and appropriate social be-
havior. Consistent with adult literature, alcohol use during adolescence
is associated with prefrontal volume abnormality, including differences
in white matter, but girls are more affected than boys by adverse effects
of alcohol. The prefrontal cortex volume of alcohol-dependent female
adolescents is smaller than that of alcohol-dependent male adolescents.25
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How Alcohol Affects the Adult Brain

Although the onset of drinking at an early age carries a much higher risk
of alcohol dependence and brain damage, with long-lasting effects into
adulthood, the onset of drinking at age twenty-one (legal age for drink-
ing) followed by chronic abuse of alcohol can also cause significant dam-
age to the human brain. The two major alcohol-related brain disorders
are alcoholic Korsakoff’s syndrome and alcoholic dementia. Korsakoff’s
syndrome is a brain disorder caused by a deficiency of thiamine (vitamin
B1), and major symptoms include severe memory loss, false memory,
lack of insight, poor conversation skills, and apathy. Some heavy drink-
ers may also have a genetic predisposition to developing this syndrome.
In Korsakoff’s syndrome, loss of neurons is a common feature, including
microbleeding in certain regions of gray matter.26 In an alcoholic, when
Wernicke’s encephalopathy appears along with Korsakoff’s syndrome, it
is called Wernicke-Korsakoff syndrome.
Wernicke’s encephalopathy and Korsakoff syndrome are two related
diseases, both caused by thiamine deficiency, but accompanying clinical
symptoms may be different. Alcoholics with Korsakoff syndrome always
have severe amnesic syndrome (severe memory loss) but may not have
classical symptoms of Wernicke’s encephalopathy, which include oph-
thalmoplegia (paralysis or severe weakness of one or more of the muscles
that control eye movement), ataxia (lack of coordination during voluntary
muscle movement, such as walking), and confusion. However, patients
with Wernicke-Korsakoff syndrome show most of the symptoms found
in both diseases.
Damage to the anterior nucleus of the thalamus is commonly found
in patients with Korsakoff syndrome but may also be present in patients
suffering from Wernicke’s encephalopathy. The anterior nucleus of the
thalamus is involved in learning and memory, as well as the alertness of
an individual. The Royal College of Physicians in London recommends
that patients admitted to the hospital who show evidence of chronic
misuse of alcohol and poor diet should be treated with B vitamins.27
Paparrigopoulos et al. (2010) reported a case where a fifty-two-year-old
man with a ten-year history of heavy alcohol abuse was admitted to the
hospital and was treated aggressively for Wernicke-Korsakoff syndrome
with 600 mg per day of oral thiamine in addition to 300 mg of thiamine,
which was delivered intravenously every day, and he was fully recovered
two months after therapy.28
Other than developing Korsakoff’s syndrome or Wernicke-Korsakoff
syndrome, thiamine deficiency in chronic alcohol abusers is a major cause
of alcohol-induced brain damage. Thiamine is a helper molecule (cofac-
tor) required by three enzymes involved in carbohydrate metabolism,
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50 Chapter 3
and brain cells can only use sugar as a fuel. In addition, intermediate
products of carbohydrate metabolism pathways are needed for genera-
tion of essential molecules for cellular functions (such as brain chemicals,
building blocks for proteins, and DNA), and a reduction in thiamine can
interfere with many of these important biochemical processes. Chronic
alcohol consumption can result in thiamine deficiency by causing inad-
equate nutritional thiamine uptake, reduced absorption of thiamine from
the gastrointestinal tract, and impaired thiamine utilization by the cells.29
Ke et al. (2009) indicate that although thiamine deficiency causes neuro-
degeneration (loss of neurons) in the brain, alcohol uses this effect directly
because it can cross the blood-brain barrier and diffuse in the brain.30
Alcoholics in general have a reduced brain weight compared to non-

drinkers.
Prefrontal white matter is the area in the brain that is most severely af-
fected in alcoholics, and there is a correlation between the degree of loss
and daily consumption of alcohol. Loss of white matter is a major cause
of cognitive impairment in alcoholics.31 Significant loss of neurons has
also been documented in the cortex, hypothalamus, and cerebellum of
alcoholics. The types of neurons that are damaged in chronic alcohol
users are the larger neurons from the frontal cortex. These neurons are
also damaged in patients with Alzheimer’s disease. However, there is
no direct link between alcoholic brain damage and Alzheimer’s disease.
Alzheimer’s patients are more impaired on recalling names, recognition
memory, and orientation, while subjects with alcohol-induced dementia
are impaired in fine motor control, initial letter fluency, and free recall.32
Chronic abuse of alcohol results in brain damage to both men and women,
but women are more susceptible to alcohol-induced brain damage than are
men. At the same mean daily alcohol consumption, blood alcohol levels in
women may be higher than men because the woman’s body burns alcohol
slower than the man’s. Based on a study of forty-three alcoholic men and
women, and comparing them with thirty-nine healthy controls, Hommer
et al. (2001) demonstrated that alcoholic women had a significantly smaller
volume of gray and white matter than healthy subjects. Although alcoholic
men also had lower amounts of gray matter and white matter compared
to the healthy controls, the difference in magnitude was smaller in men
than in women. Direct comparison of alcoholic men and women showed
that the proportion of the intracranial contents occupied by gray matter
was smaller in alcoholic women than alcoholic men when all other factors
were adjusted. In addition, the magnitude of difference between the brain
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volume of alcoholic women and nonalcoholic women was greater than

the magnitude of the difference of brain volume between alcoholic and
nonalcoholic men. The authors concluded that women’s brains are more
susceptible to alcohol-related damage than are men’s brains.33
Binge drinkers, both men and women, are at a higher risk of develop-
ing alcohol-related brain damage. Chronic exposure to the high amounts
of alcohol that are ingested during binge drinking leads to the stimulation
of N-methyl-D-aspartate (NMDA) and calcium receptors, which results
in increased release of glucocorticoids (stress molecules such as cortisol,
which affect carbohydrate metabolism). NMDA-mediated mechanisms
and glucocorticoid actions on the hippocampus are associated with brain
damage. In addition, ethanol withdrawal becomes more difficult for
binge drinkers.34 Interestingly, alcohol at low levels inhibits NMDA re-
ceptors instead of stimulating them and may exert some beneficial effects.
Alcohol-related brain damage and loss of cognitive functions may be
reversible, at least in part, if the brain damage is not permanent and the
alcoholic successfully completes a rehabilitation program and practices
complete abstinence. Chronic alcoholism is often associated with brain
shrinkage, but this may be partially reversed if abstinence is maintained,
as demonstrated by Trabert et al. (1995), based on a study of twenty-eight
male patients with severe alcohol dependence. Even with three weeks of
abstinence, increased brain tissue densities were observed in these sub-
jects.35 Asada et al. (2010) reported a case where a forty-year-old patient
was unable to perform his office duties because of slowly progressive
amnesia (severe memory loss). The initial evaluation of the patient in-
dicated severe verbal memory loss, and early stage Alzheimer’s disease
was suspected because the patient did not disclose his habit of heavy
alcohol consumption and no thiamine deficiency was found. Later the
patient disclosed his habit of heavy alcohol consumption in the past, and
with complete abstinence, his memory and cognitive functions improved
markedly. Initial studies with FDG-PET (fluorodeoxyglucose-positron
emission tomography), an advanced imaging technique, indicated that
glucose metabolism was slower in the brain of the patient, and, as men-
tioned earlier in this chapter, glucose is the only fuel that brain cells can
use. A five-year follow-up study using PET imaging indicated that glu-
cose metabolism in the brain was recovered to the normal level, and the
patient showed dramatically improved cognitive functions.36
CONCLUSION
Alcohol is a double-edged sword with a neuroprotective effect among low

to moderate consumers but a detrimental effect in alcoholics. Drinking in
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52 Chapter 3
moderation has many health benefits (see chapter 4) and may reduce the
risk of dementia and Alzheimer’s in the elderly. However, brain develop-
ment in adolescents is at high risk for permanent damage if exposed to
alcohol, especially at a very young age. In addition, adolescents who start
drinking around age fourteen or younger are at a very high risk of becom-
ing alcoholics in their adulthood. Underage drinking is a very serious pub-
lic health and safety concern because the lives of these adolescents may
change forever due to drinking, including poor performance in school,
dropping out of school, difficulty transitioning to adulthood, and other so-
cial adjustment problems. Therefore, no one below the age of twenty-one
(the legal age for drinking) should drink. Moderate drinking in adulthood
has health benefits, but drinking should be limited to one to two drinks per
day at the maximum for men and one drink per day for women. Drink-
ing even less than that (two to three times a week, one glass or drink per
occasion) can deliver the most beneficial effects of alcohol (which will be
discussed further in chapter 4). However, drinking more for the sake of
health is unjustified, because such a practice may cause more harm than
good. Women are more affected by adverse effects of alcohol than are
men. Fortunately, some of the brain damage caused by alcohol may be
reversible. Therefore, friends and family members of a chronic abuser of
alcohol must intervene and ensure that the person receives appropriate
help for alcohol rehabilitation. It is not too late to help an alcoholic resume
a normal life after treatment.
NOTES
1. R. J. Blanchard, L. Magee, R. Veniegas, and D. C. Blanchard, “Alcohol and

Anxiety: Ethopharmacological Approaches,” Progress in Neuropharmacology and
Biological Psychiatry 17 (2003): 171–82.
2. J. A. Tucker, R. E. Vuchinich, and M. B. Sobell, “Alcohol’s Effects on Human
Emotions: A Review of the Stimulation/Depression Hypothesis,” International
Journal of Addiction 17, no. 1 (January 1982): 155–80.
3. S. S. Hoppenbrouwers, D. Hofman, and D. J. Schutter, “Alcohol Breaks
Down Interhemispheric Inhibition in Females but Not in Males: Alcohol and
Frontal Connectivity,” Psychopharmacology (Berlin) 208, no. 3 (February 2010):
469–74.
4. R. Clarisse, F. Testu, and A. Reinberg, “Effects of Alcohol on Psycho-Technical
Tests and Social Communication in a Festive Situation: A Chronopsychological Ap-
proach,” Chronobiology International 21, nos. 4–5 (July 2004): 721–38.
5. C. A. Moberg and J. J. Curtin, “Alcohol Selectively Reduces Anxiety but Not
Fear: Startle Response during Unpredictable versus Predictable Threat,” Journal of
Abnormal Psychology 118, no. 2 (May 2008): 335–47.
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6. M. J. Eckardt, S. E. File, G. L. Gessa, K. Grant, et al., “Effects of Moderate

Alcohol Consumption on the Central Nervous System,” Alcoholism: Clinical and
Experimental Research 22, no. 5 (August 1998): 998–1040.
7. Brain Pleasure Center, The Brain from Top to Bottom website, http://
thebrain.mcgill.ca/flash/index_d.html.
8. G. F. Koob, P. P. Sana, and F. F. Bloom, “Neuroscience of Addiction,” Neu-
ron 21 (1998): 467–76.
9. D. M. Tomkins and E. M. Sellers, “Addiction and the Brain: The Role of
Neurotransmitters in the Cause and Treatment of Drug Dependence,” Canadian
Medical Association Journal 164, no. 6 (March 2001): 817–21.
10. C. J. Morgan and A. Badway, “Alcohol-Induced Euphoria: Exclusion of
Serotonin,” Alcohol and Alcoholism 36, no. 1 (January 2001): 22–25.
11. B. Söderpalm, E. Löf, and M. Ericson, “Mechanistic Studies of Ethanol’s
Interaction with the Mesolimbic Dopamine Reward System,” Pharmacopsychiatry
42, no. 1 (May 2009): S87–94.
12. A. Ruitenberg, J. C. van Swieten, J. C. M. Witterman, K. M. Mehta, et al.,
“Alcohol Consumption and Risk of Dementia: The Rotterdam Study,” Lancet 359,
no. 9303 (January 2002): 281–86.
13. R. M. Pinder and M. Sandler, “Alcohol, Wine and Mental Health: Focus on
Dementia and Stroke,” Journal of Psychopharmacology 18, no. 4 (December 2004):
449–56.
14. E. Savaskan, G. Olivieri, F. Meier, E. Seifritz, et al., “Red Wine Ingredient
Resveratrol Protects from β-Amyloid Neurotoxicity,” Gerontology 49, no. 6 (No-
vember–December 2003): 380–83.
15. Y. Lee, J. H. Back, J. Kim, S. H. Kim, et al., “Systematic Review of Health Be-
havioral Risks and Cognitive Health in Older Adults,” International Psychogeriatric
22, no. 2 (March 2010): 174–87.
16. V. Solfrizzi, A. D’Introno, A. M. Colacicco, C. Capurso, et al., “Alcohol Con-
sumption, Mild Cognitive Impairment, and Progression to Dementia,” Neurology
68, no. 1 (May 2007): 1790–99.
17. E. Kuntsche, J. Rehm, and G. Gmel, “Characteristics of Binge Drinkers in
Europe,” Social Science and Medicine 59 (2004): 113–27.
18. J. W. Toumbourou, S. A. Hemphill, B. J. McMorris, R. F. Catalano, et al.,
“Alcohol Use and Related Harms in School Students in the USA and Australia,”
Health Promotion International 24, no. 4 (December 2009): 373–82.
19. J. W. Miller, T. S. Naimi, R. D. Brewer, and S. E. Jones, “Binge Drinking and
Associated Health Risk Behaviors among High School Students,” Pediatrics 119,
no. 1 (January 2007): 76–85.
20. B. F. Grant and D. A. Dawson, “Age at Onset of Alcohol Use and Its As-
sociation with DSM-IV Alcohol Abuse and Dependence: Results from the Na-
tional Longitudinal Alcohol Epidemiological Survey,” Journal of Substance Abuse
9 (1997): 103–10.
21. M. Pascual, J. Boix, V. Felipo, and C. Guerri, “Repeated Alcohol Adminis-
tration during Adolescence Causes Changes in the Mesolimbic Dopaminergic and
Glutamatergic System and Promotes Alcohol Intake in the Adult Rat,” Journal of
Neurochemistry 108, no. 4 (February 2009): 920–31.
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54 Chapter 3
22. D. W. Zeigler, C. C. Wang, R. A. Yoast, B. D. Dickinson, et al., “The Neu-

rocognitive Effects of Alcohol on Adolescents and College Students,” Preventive
Medicine 40 (2005): 23–32.
23. T. C. Harford, H. Y. Yi, and M. E. Hilton, “Alcohol Abuse and Dependence
in College and Noncollege Samples: A Ten-Year Prospective Follow-Up in a Na-
tional Survey,” Journal of the Study of Alcohol 67, no. 6 (November 2006): 803–9.
24. M. J. Casas-Gil and J. L. Navarro-Guzman, “School Characteristics among
Children of Alcoholic Parents,” Psychology Reports 90, no. 1 (February 2002): 341–48.
25. K. L. Medina, T. McQueeny, B. J. Nagel, K. L. Hanson, et al., “Prefrontal
Cortex Volumes in Adolescents with Alcohol Use Disorders: Unique Gender Ef-
fects,” Alcoholism: Clinical and Experimental Research 32, no. 3 (March 2008): 386–94.
26. M. D. Kopelman, A. D. Thomson, I. Guerrini, and E. J. Marshall, “The
Korsakoff Syndrome: Clinical Aspects, Psychology and Treatment,” Alcohol and
Alcoholics 44, no. 2 (March–April 2009): 148–54.
27. C. Harper, “The Neurotoxicity of Alcohol,” Human and Experimental Toxicol-
ogy 26, no. 3 (March 2007): 251–57.
28. T. Paparrigopoulos, E. Tzavellas, D. Karaiskos, A. Kouzoupis, et al., “Com-
plete Recovery from Undertreated Wernicke-Korsakoff Syndrome Following
Aggressive Thiamine Treatment,” In Vivo 24, no. 2 (March–April 2010): 231–33.
29. P. R. Martin, C. K. Singleton, and S. Hiller-Sturmhofel, “The Role of Thia-
mine Deficiency in Alcoholic Brain Damage,” Alcohol Research and Health 27, no. 2
(February 2003): 134–42.
30. Z. J. Ke, X. Wang, Z. Fan, and J. Luo, “Ethanol Promotes Thiamine Defi-
ciency–Induced Neuronal Death: Involvement of Double-Stranded RNA-Activated
Protein Kinase Activity,” Alcoholics: Clinical and Experimental Research 33, no. 6 (June
2009): 1097–1103.
31. H. Mochizuki, T. Masaki, S. Matsushita, Y. Ugawa, et al., “Cognitive Im-
pairment and Diffuse White Matter Atrophy in Alcoholics,” Clinical Neurophysiol-
ogy 116, no. 1 (January 2005): 223–28.
32. J. Saxton, C. A. Munro, M. A. Butters, C. Schramke, et al., “Alcohol, De-
mentia, and Alzheimer’s Disease: Comparison of Neuropsychological Profiles,”
Journal of Geriatric Psychiatry and Neurology 13, no. 3 (Fall 2000): 141–49.
33. D. Hommer, R. Momenan, E. Kaiser, and R. Rawlings, “Evidence for a
Gender-Related Effect of Alcoholism on Brain Volumes,” American Journal of Psy-
chiatry 158, no. 2 (February 2001): 198–204.
34. W. A. Hunt, “Are Binge Drinkers More at Risk of Developing Brain Dam-
age?” Alcohol 10, no. 6 (November–December 1993): 559–61.
35. W. Trabert, T. Betz, M. Niewald, and G. Huber, “Significant Reversibility of
Alcohol Brain Shrinkage within 3 Weeks of Abstinence,” Acta Psychiatry Scandina-
via 92, no. 2 (August 1995): 87–90.
36. T. Asada, S. Takaya, Y. Takayama, H. Yamauchi, et al., “Reversible Alcohol-
Related Dementia: A Five-Year Follow-Up Using FDG-PET and Neuropsycho-
logical Tests,” Internal Medicine 49, no. 4 (April 2010): 283–87.
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4

Health Benefits of Moderate
Alcohol Consumption
H uman beings have been consuming alcohol from prehistoric times,

and there is still an ongoing debate about whether drinking is ben-
eficial or detrimental to your health. Based on our current knowledge, it
can be stated that alcohol, like any drug, is beneficial at a low dose but is
a poison if consumed in excess. The beneficial effect of alcohol in prevent-
ing heart disease came to media attention with the publication of papers
that indicated that in most countries, intake of saturated fats (animal fats)
is related to high mortality from coronary heart disease.
The situation in France is paradoxical because the French population
consumes high amounts of saturated fats but experiences low mortality
from coronary heart disease. Coronary heart disease is caused by ath-
erosclerosis, the narrowing of coronary arteries that supply blood to the
heart due to fatty buildup of plaques. This process can cause chest pain
(angina pectoris) and eventually heart attack (myocardial infarction).
Epidemiological studies have indicated that consumption of alcohol at
the level of intake in France (20–30 gm/day, with one drink containing 14
gm of alcohol) can reduce the risk of coronary heart disease by 40 percent.
Other than increasing good cholesterol, wine, which is the drink of choice
in France, may be able to inhibit platelet aggregation (preventing blood
clots from forming in arteries, which stops the flow of blood to the heart),
providing further protection against coronary heart disease.1
Cardiovascular disease is the major cause of death worldwide, claim-
ing more lives than cancer. In the United States alone, each year ap-
proximately 1 million people die from cardiovascular disease, account-
ing for approximately one-third of all deaths. Cardiovascular disease is
55
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56 Chapter 4
a broad term that includes diseases that involve the heart (cardio) and
blood vessels (coronary arteries and veins). Coronary heart disease is
a category within the broad definition of cardiovascular disease. Other
than coronary heart disease, cardiovascular diseases also include heart
failure, complications of the heart due to high blood pressure, heart fail-
ure, stroke, and related diseases. In the United States, for all categories
of major cardiovascular diseases, men had a higher age-adjusted death
rate than women. According to the latest statistics available from the U.S.
government, the death rate in men in 2007 was 42 percent higher than
women (297.7 compared to 209.9 deaths per 100,000). The death from
coronary heart disease alone was 69 percent higher in men than women
(174.5 compared to 103.4 deaths per 100,000).2
In the medical literature, moderate drinking is associated with a reduced
risk of coronary heart disease; this is also true for cardiovascular disease.
Moderate drinking appears to reduce the risk of atherosclerotic plaque
buildup, heart attack, heart failure, and stroke. Moderate drinking is de-
fined as not more than two standard drinks a day for men younger than
sixty-five, one drink per day for women, and one drink per day for men
who are older than sixty-five. A standard drink is defined as 12 ounces of
beer, 5 ounces of wine, or 1.5 ounces of an 80 proof spirit (containing 40 per-
cent alcohol). A standard drink contains 14 gm of pure alcohol (see chapter
2). The consumption of a small amount of alcohol on a regular basis is more
helpful than occasional binge drinking (five or more drinks in one occasion)
on a weekend. The benefits of moderate drinking are listed in table 4.1.
Moderate alcohol consumption may increase longevity and protect

against many diseases, including cardiovascular diseases.
Table 4.1. Benefits of Drinking in Moderation

Increased longevity
Reduced risk of coronary heart diseases (heart attack, angina pectoris)
Better survival chance after a heart attack
Reduced risk of stroke
Reduced risk of other cardiovascular diseases such as heart failure
Reduced risk of developing diabetes
Reduced risk of forming gallstones
Reduced risk of developing arthritis
Reduced risk of developing age-related dementia and Alzheimer’s disease
Reduced risk of certain types of cancer
Possibly lowers the chances of getting the common cold
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Health Benefits of Moderate Alcohol Consumption 57
In contrast, chronic heavy consumption of alcohol increases the risk of

heart disease, high blood pressure, stroke, various types of cancer, severe
liver disease (including liver cirrhosis), sudden death from heart disease,
and, for women, risk of miscarriage and fetal alcohol syndrome. Ceratin
people who have a family history of alcohol abuse or those taking certain
prescription medications, and women who are pregnant or plan to be
pregnant, should not consume alcohol at all.
MODERATE ALCOHOL CONSUMPTION AND

REDUCED RISK OF CORONARY HEART DISEASE
Although coronary heart disease is one of the leading causes of death in

developed countries, a recently published article indicates that coronary
heart diseases are a growing epidemic in developing countries too due
to longer life spans and the acquisition of lifestyle-related risk factors.3 A
review of literature up to 1999 by the National Institute of Alcohol Abuse
and Alcoholism found that with few exceptions, epidemiological studies
from at least twenty countries from North America, Europe, Asia, and
Australia demonstrated 20 to 40 percent lower incidences of coronary
heart disease among moderate drinkers than nondrinkers. In addition,
large-scale prospective studies (representing a total population of more
than 1 million men and women of different ethnicities) in which par-
ticipants provide information on their drinking habits and health-related
practices before the onset of disease also indicate a relationship between
preventing coronary heart disease and drinking in moderation. The aver-
age follow-up period for these studies was eleven years, but the longest
was the Framingham Heart Study, which was conducted over a period
of twenty-four years. The two largest of these studies, conducted by the
American Cancer Society, included one with 276,802 men and another
with 490,000 men and women.4
The relationship between alcohol consumption and coronary heart dis-
ease was examined in the original Framingham Heart Study (so named
because the study originated in Framingham, Massachusetts), which was
initiated in 1948 with a twenty-four-year follow-up exam using 2,106 men
and 2,639 women. Alcohol consumption demonstrated a U-shaped curve
over the years, with a reduced risk of developing cardiovascular diseases
with moderate drinking but a high risk of developing such diseases with
heavy drinking. While smoking is a risk factor for developing coronary
heart disease, the Framingham Study revealed that moderate alcohol
consumption may also provide protection against coronary heart disease
among smokers.5
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58 Chapter 4
In nonsmokers, beer and wine drinking provided greater reductions in

coronary heart disease mortality than drinking spirits.
Smokers who smoke one pack of cigarettes per day have twice the
risk of developing coronary heart disease than nonsmokers. Alcohol
consumption actually lowered the incidence of coronary heart disease in
participants of the Framingham Study, but in a study by Castelli (1990),
when alcohol was consumed in greater amounts than two drinks per day,
a rise in mortality from cancer and stroke was observed.6
In the American Cancer Society prospective study of 276,802 Ameri-
can men over a period of twelve years, the authors determined that the
relative risk (RR) of total mortality was 0.88 for occasional drinkers, 0.84
for those drinking one drink per day, and 1.38 in people drinking six or
more drinks per day compared to nondrinkers. However, RR of death
from coronary heart disease was lower than one in all groups of drinkers
compared to nondrinkers (table 4.2). The RR is defined as the ratio of the
chance of a disease developing among members of a population exposed
to a factor compared with a similar population not exposed to the factor.
An RR value less than one indicates that the chance of developing a dis-
ease is less in a population that is exposed to the factor than the popula-
tion not exposed to the factor, while a value higher than one indicates that
the chance of developing a disease is higher in the population exposed to
the factor than the population not exposed. In this study, the factor is alco-
hol. Interestingly, the risk of cardiovascular disease was mostly reduced
in people who consumed one alcoholic drink per day (RR: 0.79), meaning
people who drank one drink per day had a 21 percent lower chance of
death from coronary heart disease, and the risk of all causes of mortality
was also lowest (RR: 0.84) in that group, meaning that the risk of death
from all other causes was 16 percent lower in people who consumed one
alcoholic drink per day than nondrinkers.7
Table 4.2. Relative Risk Factors for Total Mortality in Drinkers and Nondrinkers
Relative Risk Factor (RR)
Number of Drinks per Day Total Mortality from Coronary Heart Disease
Occasional drinkers 0.88 0.86
One drink 0.84 0.79
Two drinks 0.93 0.80
Three drinks 1.02 0.83
Four drinks 1.08 0.83
Five drinks 1.22 0.85
Six drinks 1.38 0.92
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One drink per day is probably the best practice for obtaining health
benefits from consuming alcohol.
In another large prospective study using 490,000 men and women

(mean age 56 years, range 30 to 104 years) who reported their alcohol and
tobacco use with a nine-year follow-up (46,000 people died during that
period), the authors reported that the rate of death from cardiovascular
diseases was 30 percent lower in men and 40 percent lower in women
who consumed at least one drink per day. The overall death rates were
lowest among men and women who consumed one drink daily.8 Al-
though moderate drinking is associated with reduced risk for heart dis-
ease, this benefit disappears in individuals who consume high amounts
of alcohol. In a ten-year follow-up study in Sweden of 5,769 adults (ages
thirty-five to seventy-five) without cardiovascular disease, Foerster et al.
(2009) demonstrated that by increasing the amount of alcohol consump-
tion to more than twenty-five drinks per week, blood pressure increased
in heavy drinkers and all beneficial effects of alcohol consumption dis-
appeared. In addition, wine drinking increased good cholesterol (high-
density lipoprotein cholesterol or HDL), while drinking beer and spirits
resulted in increased concentrations of triglycerides.9 Sesso et al. (2000)
studied the risk of hypertension (high blood pressure) in 28,848 women
and 13,455 men who consumed alcohol and observed that light to moder-
ate drinking increased the risk of developing hypertension in men but ac-
tually reduced the risk of developing hypertension in women. However,
the threshold above which alcohol became deleterious for hypertension
risk emerged at four or more drinks for women and more than one drink
per day for men.10
It is beneficial to drink one drink per day or at least six drinks per week
to reduce the risk of coronary heart disease and heart attack. A study
by Sesso et al. (2000) using 18,445 men (ages forty to eighty-four) and a
seven-year follow-up, revealed that when those individuals consuming
one drink per week or less increased their consumption to more than one
to six drinks per week, a further 29 percent reduction in the risk for devel-
oping cardiovascular disease was observed compared to individuals who
did not increase their alcohol consumption at all. The authors concluded
that among men with initial low alcohol consumption (one or less drink
per week), a subsequent moderate increase in alcohol consumption may
lower their risk of developing coronary heart disease.11
Diabetic patients are at a higher risk of developing cardiovascular dis-
ease. Moderate consumption of alcohol can help these patients lower their
chances of getting heart disease. In the Physician’s Health Study of 87,938
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60 Chapter 4
U.S. physicians (2,970 diagnosed with diabetes mellitus), the authors

observed that weekly consumption of alcohol reduced the risk of heart
disease by 33 percent, while daily consumption of alcohol reduced the
risk by 58 percent among diabetics. For the nondiabetic, weekly consump-
tion of alcohol reduced the risk of heart disease by 18 percent, while daily
consumption of alcohol reduced the risk by 40 percent.12
Interestingly, women may get beneficial effects from alcohol by consum-
ing lower amounts less frequently than men. In one study (Tolstrup et al.
2006) with 28,448 women and 25,052 men between fifty and sixty-five who
were free from cardiovascular disease at enrollment in the study, during a
5.7-year follow-up, the authors observed that women who consumed al-
cohol at least one day per week had a lower risk of coronary heart disease
than those who drank alcohol less than one day a week. However, little
difference was found between women who consumed at least one drink
per week compared to women who consumed two to four drinks per
week, five to six drinks per week, or seven drinks per week. However, for
men the lowest risk was found in individuals who consumed one drink
per day. The authors concluded that for women, alcohol consumption can
reduce the risk of heart disease, and the frequency of drinking may not be
an important factor, but for men, drinking frequency, not alcohol intake,
is the determining factor in preventing heart disease.13
Studies have shown that individuals who consume one alcoholic drink
every one to two days have a lower risk of a first myocardial infarction
(heart attack) than both nondrinkers and heavy drinkers. In addition,
people who drink in moderation also have a higher chance of survival af-
ter myocardial infarction. In one study (Mukamal et al. 2001) using 1,913
adult patients who were hospitalized in forty-five different hospitals for
heart attack, it was observed that 696 patients consumed less than seven
alcoholic drinks per week, 321 consumed seven or more drinks per week,
and 896 patients were nondrinkers. Compared with nondrinkers, patients
who consumed less than seven drinks per week had a much lower death
rate (6.3 deaths per 100 patients versus 3.4 deaths per 100 patients). Those
who consumed seven or more drinks per week also showed less mortality
(2.4 deaths per 100 patients) compared to nondrinkers (6.3 deaths per 100
patients). The association was similar between men and women as well
as among different types of alcoholic beverages. The authors concluded
that moderate alcohol consumption was associated with a lower rate of
mortality after heart attack.14 A recently published European study by
Brugger-Andersen et al. (2009) using 5,477 patients who had heart failure
following myocardial infarction reported that during 2.7 years of follow-
up, 946 patients died, but patients with moderate alcohol consumption
(one to seven drinks per week) showed 24 percent lower risk of all-cause
death, 26 percent lower risk of dying from heart disease, and 8 percent
10-649_Dasgupta.indb 60 1/17/11 6:40 AM

lower risk of hospitalization compared to nondrinkers. The authors con-

cluded that there was a string of positive associations between moderate
alcohol consumption and survival after complicated myocardial infarc-
tion. However, heavy drinkers had a poor prognosis.15 In another report,
De Lorgeril et al. (2002) analyzed the relationship between drinking
wine after myocardial infarction and the risk of recurrence in a patient
population of 437. Among these patients 104 complications from heart
disease occurred over a period of four years. The authors observed that
in comparison to nondrinkers, the risk of developing complications was
reduced by 59 percent in patients who drank approximately two alcoholic
beverages per day, mostly wine.16
Congestive heart failure, another potentially lethal heart disease, occurs
when the heart cannot pump blood to the body’s organs. This may occur
due to narrowing arteries (from plaque buildup), a past heart attack with
scar tissues in the heart that interfere with normal function of the heart,
high blood pressure, primary disease of the heart, such as cardiomy-
opathy, as well as birth defects. Moderate alcohol consumption not only
reduces the risk of myocardial infarction but also provides protective
effects against heart failure. In the Cardiovascular Health Study using
5,595 subjects, Bryson et al. (2006) observed that the risk of heart failure
was reduced by 18 percent in individuals who drank one to six drinks per
week and 34 percent in individuals who drank seven to thirteen drinks
per week. In addition, the authors observed that moderate alcohol con-
sumption lowered the risk of heart failure even in individuals who had
experienced a heart attack.17
Snow et al. (2009), who conducted a study using 1,154 participants (580
men and 574 women) in Winnipeg, Manitoba, Canada, indicated that the
well-established relationship between a reduced risk of cardiovascular
disease and moderate consumption of alcohol may not be evident until
middle age (thirty-five to forty-nine) or older (fifty to sixty-four) in men.
However, women may benefit from moderate consumption of alcohol
at a much younger age (eighteen to thirty-four). The beneficial effects of
alcohol consumption are negated when alcohol is consumed in heavy
episodic drinking patterns (eight or more drinks per occasion), especially
for middle-aged and older men.18
HOW ALCOHOL PROTECTS AGAINST HEART DISEASE
There are several hypotheses on how moderate drinking can reduce the
risk of developing heart disease (table 4.3). It has been well established
that cholesterol plays a major role in the formation of plaque in coronary
arteries. Narrowing of arteries may result in disruption in blood flow to
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62 Chapter 4
Table 4.3. Hypotheses by Which Moderate Alcohol Consumption Reduces Risk of

Heart Diseases
Increasing the concentration of good cholesterol (high-density lipoprotein cholesterol)
Decreasing the concentration of bad cholesterol (low-density lipoprotein cholesterol)
Reduces narrowing of coronary arteries by reducing plaque formation
Reduces risk of blood clotting
Reduces level of fibrinogen (a blood-clotting factor)
Increases coronary blood flow
Reduces blood pressure, especially in women
the heart, causing coronary heart disease. There are two main coronary ar-
teries that branch off from the aorta. These two arteries and their branches
deliver blood to the heart. When a plaque ruptures, it triggers a complex
event of platelet aggregation (the clumping together of platelets in blood),
which is a part of the sequence of events that leads to formation of a blood
clot (thrombus) in the artery. When a thrombus is formed, it may severely
disrupt the blood flow to the heart, causing heart cells to die. This patho-
logical process is called myocardial infarction or heart attack.
It has been demonstrated that when cholesterol is associated with low-
density lipoprotein (LDL), it promotes plaque formation in the arteries.
This is the reason LDL cholesterol is called “bad cholesterol.” However,
when cholesterol is associated with high-density lipoprotein (HDL), it
prevents plaque buildup and is thus called “good cholesterol.” Blood clot-
ting also plays an important role in the pathophysiology of heart attacks.
The omega-3 fatty acids found in abundance in fish such as lake trout,
sardines, herring, salmon, albacore tuna, and mackerel can reduce the
event of blood clotting and may provide protection against a heart attack.
Research has shown that moderate consumption of alcohol reduces
the risk of heart disease by increasing blood levels of HDL cholesterol,
and that this effect is independent of the type of alcoholic beverages con-
sumed. The American Heart Association and other organizations recom-
mend limiting alcohol consumption to no more than two drinks a day for
men and one drink a day for women. Heavy consumption of alcohol, on
the other hand, causes heart disease (see chapter 5).19
In general, maximal benefit and safety from consuming alcohol ap-

pears to be at the level of approximately one drink per day.
Many studies have demonstrated that HDL cholesterol levels in drink-

ers are higher than nondrinkers. The Honolulu Heart Study showed that
men who drank alcoholic beverages had higher blood levels of HDL
cholesterol than nondrinkers. Gordon et al. (1981) reviewed data from
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ten different studies, including the Honolulu Heart Study, and observed
that there was a positive correlation between amounts of alcohol con-
sumed and the serum (aqueous part of blood) level of HDL cholesterol.
In the male population between ages fifty and sixty-nine, the average
HDL cholesterol level was 41.9 mg/dL (dL: 100 milliliters) in people who
consumed no alcohol, 47.6 mg/dL in people consuming up to 16.9 gm of
alcohol per day (a single drink is 14 gm of alcohol), 50.7 mg/dL in people
consuming between 16.9 and 42.2 gm of alcohol per day (one to three
drinks), and 55.3 mg/dL in people drinking between 42.3 and 84.5 gm of
alcohol per day (three to six drinks). Interestingly, in the Albany, Fram-
ingham, and San Francisco studies on the effect of alcohol on HDL levels,
the HDL cholesterol levels of men between the ages of fifty and sixty-
nine who consumed the highest amount of alcohol per day (42.3 to 85.5
gm/day or approximately three to six drinks per day) were 54.6 mg/dL,
50.1 mg/dL, and 57.8 mg/dL (HDL cholesterol levels among nondrink-
ers were 46.3 mg/dL, 41.4 mg/dL, and 44.4 mg/dL).20 In another study
(Hulley et al. 1981), the authors observed that the HDL cholesterol level
in blood was increased by up to 33 percent in social drinkers as opposed
to nondrinkers. A small experiment also revealed an average 15 percent
reduction in HDL cholesterol levels among social drinkers who abstained
from alcohol for a two-week period.21 In women, light drinking (one drink
or less a day) was associated with lower blood levels of bad cholesterol
(LDL) and higher levels of good cholesterol (HDL).22 A recently published
article (Wakabayashi and Araki 2010) also demonstrated that serum HDL
cholesterol was higher in drinkers than nondrinkers in all age-groups of
men and women (twenty to sixty-nine), and the atherogenic index (risk of
developing coronary heart disease), calculated by using serum total cho-
lesterol and HDL cholesterol concentrations, was also lower in drinkers
than nondrinkers in all age-groups of both men and women.23
In addition to increasing good cholesterol and reducing bad choles-
terol, light to moderate consumption of alcohol also reduces the level
of apolipoprotein-A (this lipoprotein, like LDL, increases the risk of
coronary heart disease) and prevents clot formation, as well as reducing
platelet aggregation.24 Alcohol also diminishes thrombus formation on
damaged walls of the coronary artery. This action of alcohol is due to its
ability to inhibit Phospholipase A2, an enzyme that releases fatty acids.25
THE PROTECTIVE BENEFITS OF WINE

IN CARDIOVASCULAR HEALTH
Studies have indicated that the increased level of good cholesterol in

blood may explain 50 percent of the protective effect of alcohol against
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64 Chapter 4
cardiovascular disease, while the other 50 percent may be partly related

to the inhibition of platelet aggregation, thus reducing blood clot forma-
tion in coronary arteries. It has been suggested that although alcohol can
increase good cholesterol levels and inhibit platelet aggregation, the poly-
phenolic compounds found in abundance in red wine can reduce plate-
let activity via other mechanisms further than can alcohol. In addition,
these polyphenolic compounds in red wine can also increase the level of
vitamin E, an important antioxidant, thus providing further protection
against various diseases. Therefore, it appears that red wine offers more
protection against cardiovascular disease than other alcoholic bever-
ages.26 It has been postulated that resveratrol, a polyphenolic compound
found abundantly in red wine but not in white wine, beer, or spirits,
plays an important role as an antioxidant and inhibits platelet aggrega-
tion, which may explain the cardio protection received from consuming
red wine.27 A recently published article (Klatsky 2010) also suggests that
wine, especially red wine, is more protective against coronary heart dis-
ease than beer or other liquors.28
Drinking wine, especially red wine, may provide more protection

against cardiovascular diseases than beer or other liquors.
THE CONSUMPTION OF ALCOHOL AND PREVENTING STROKE
Another beneficial effect of consuming alcohol in moderation is the

dramatic reduction in the risk of having a stroke among both men and
women regardless of age or ethnicity. The Copenhagen City Heart Study,
with 13,329 eligible men and women ages forty-five to eighty-four (with
a sixteen-year follow-up) showed that there was a U-shaped relation
between intake of alcohol and risk of stroke. People who consumed low
to moderate alcohol experienced the protective effect of alcohol against
stroke, but heavy consumers of alcohol were more prone to stroke than
moderate drinkers or nondrinkers. For moderate drinkers of wine,
monthly drinking of alcohol reduced the risk of stroke by 17 percent,
weekly drinking reduced the risk by 41 percent, and daily drinking re-
duced the risk by 30 percent. There was no association between risk of
stroke and drinking beer or spirits.29
In the second examination of the Copenhagen City Heart Study, with
5,373 men and 6,723 women (with a sixteen-year follow-up), it was ob-
served that at a high stress level, weekly total consumption of one to
fourteen drinks compared to no consumption of alcohol was associated
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with a 43 percent lower risk of stroke in both men and women, but no
clear association was observed between the risk of stroke and moderate
consumption of alcohol in individuals who were at a lower stress level. In
addition, this study also reported that only drinking beer or wine reduced
the risk of stroke in individuals with high stress. It was suggested that
alcohol may alter psychological responses to stress in addition to modify-
ing physiological responses.30
The Northern Manhattan study, consisting of individuals ages forty
and older (677 patients who had experienced a stroke were matched for
gender, age, and ethnicity with 1,139 individuals in the community who
had not), observed that moderate drinking of up to two drinks per day
had a significantly protective effect against ischemic stroke. The protec-
tive effect of alcohol against stroke was detected in both younger and
older groups of men and women in all ethnic groups (white, black, and
Hispanic). However, this protective effect against stroke disappeared
in heavy drinkers (seven or more drinks per day), and such chronic
consumption of alcohol increased the risk of having strokes by approxi-
mately three times that of nondrinkers.31 In a follow-up study, it was
demonstrated that moderate drinkers (up to two drinks per day) had a 33
percent reduced risk of ischemic stroke (all ethnic groups, both men and
women) compared to nondrinkers.32 Ischemic stroke (cerebral infarction)
is the death of an area of brain tissue due to blockage of an artery (most
commonly a branch of one of the internal carotid arteries) that supplies
blood to the brain. When consumed in moderate amounts, alcohol can
prevent blood clot formation and fibrinolysis, which may protect from
stroke, but in heavy drinkers, alcohol elevates blood pressure (a risk for
stroke), may cause the rupture of arteries that deliver blood to the brain,
and vasoconstriction (narrowing of blood vessels, which causes reduced
blood flow), thus increasing the risk of stroke. In addition, at higher con-
centrations alcohol promotes blood clotting rather than preventing blood
clotting, greatly increasing the risk of a stroke, because a blood clot in an
artery may prevent blood flow to a certain part of the brain.33
MODERATE CONSUMPTION OF ALCOHOL AND

REDUCING THE RISK OF DEVELOPING DIABETES
Diabetes mellitus, commonly referred to as diabetes, is a condition where

a person has a high blood sugar level (more than 126 mg/dL after over-
night fasting) either due to not producing enough insulin (type 1 diabetes,
insulin dependent), or not utilizing insulin properly (type 2 diabetes, in-
sulin resistant). Although either type of diabetes may develop at any age,
usually the onset of type 1 diabetes occurs at an early age and requires a
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66 Chapter 4
person to have a daily injection of insulin for maintaining normal glucose

blood levels. Type 2 diabetes, which is more common and diagnosed
later in life (thirty-five years or older), can be managed with lifestyle
changes, diet control, and medication. The prevalence of diabetes for all
age groups worldwide was estimated to be 2.8 percent in 2000 and pro-
jected to be 4.4 percent in 2030. The total number of people suffering from
diabetes is projected to rise from 171 million in 2000 to 366 million in 2030.
Most people with diabetes suffer from type 2 diabetes.34
Studies have shown that moderate consumption of alcohol reduces the
risk of developing type 2 diabetes. Based on fifteen studies conducted in
the United States, Finland, the Netherlands, Germany, the United King-
dom, and Japan with 369,862 men and women and an average follow-up
of twelve years, light drinkers (less than half a drink per day or 6 gm of
alcohol) had a 13 percent lower chance of developing type 2 diabetes,
while moderate drinkers (half a drink to four drinks per day, 6–12 gm of
alcohol per day) had a 30 percent lower risk of developing type 2 diabetes
compared to nondrinkers. It made little difference whether an individual
consumed beer, wine, or spirits, and it was best to consume alcohol fre-
quently (such as daily or several times in a week) rather than occasionally.
In contrast, heavy consumption of alcohol (more than three and a half
drinks per day or 48 gm of alcohol per day) did not have any protective
effect against developing type 2 diabetes, and these individuals were at
a slightly higher risk (4 percent more) of developing type 2 diabetes than
nondrinkers.35
The Finnish Twin Cohort Study followed 22,778 twins with different
drinking patterns over the course of twenty years and found that mod-
erate alcohol consumption (half a drink to two drinks [5–29.9 gm/day]
for men and half to one and a half drinks [5–19.9 gm/day] for women)
was associated with a lower risk of developing type 2 diabetes than light
alcohol consumption (less than half a drink or less than 5gm/day). Over-
weight subjects (body mass index equal to or greater than 25.0 kg/m2)
showed more beneficial effects from moderate alcohol consumption, as
risk of developing diabetes was 30 percent lower in overweight men and
40 percent lower in overweight women, than from no alcohol consump-
tion. On the other hand, binge drinking and high alcohol consumption
may increase the risk of type 2 diabetes in women, especially lean women,
but affected men to a lesser extent.36
After reviewing twenty studies, Balinus et al. (2009) observed a U-
shaped relationship between alcohol consumption and the risk of devel-
oping type 2 diabetes, where moderate alcohol consumption decreased
the risk and heavy alcohol consumption increased the risk. Compared
to lifetime abstainers of alcohol, those who drank an average of 22 gm of
alcohol per day (one and a half drinks) had a 17 percent lower risk of de-
10-649_Dasgupta.indb 66 1/17/11 6:40 AM

veloping diabetes. Women with the highest level of protection (40 percent
lower risk) were those who consumed 24 gm of alcohol per day. Drinking
became deleterious among men who consumed more than 60 gm of alco-
hol per day (four and a half drinks) and among women who consumed
more than 50 gm of alcohol (almost four drinks) per day.37
Alcohol at lower levels decreases insulin resistance and thus may play
a protective role against developing diabetes, but this effect is lost with
higher alcohol consumption. In a twelve-year prospective study using
nearly 47,000 men who were health care professionals, those who con-
sumed one to two drinks per day (15–29 gm of alcohol) had a 36 percent
lower incidence of diabetes compared to abstainers. In this study, con-
suming even less than one alcoholic drink five days a week provided the
greatest protection, with the risk of diabetes reduced by 52 percent. In the
Nurses’ Health study, which followed 85,000 nurses, it was shown that
consuming even less than one drink per day (10 gm of alcohol) reduced
the risk of diabetes by 46 percent.
Insulin resistance is a key factor in developing type 2 diabetes. In one
study of 883 individuals ages sixty-five and older, it was observed that
individuals who consumed alcohol daily in moderation had significantly
lower fasting glucose levels, and, after receiving a dose of 75 gm of glu-
cose, they had a lower level of blood glucose compared to nondrinkers.
Serum insulin levels were lower in drinkers compared to nondrinkers,
indicating that drinkers had lower insulin resistance, because serum insu-
lin levels are elevated in diabetics (cells do not properly take insulin from
blood to use glucose as fuel). This phenomenon was observed in both
diabetics and nondiabetics, indicating that a diabetic person may also
get benefits from moderate alcohol consumption. For example, among
diabetic drinkers, the mean fasting glucose (137.5 mg/dL) and the mean
insulin (14.5 picomole per liter) were lower compared to diabetic non-
drinkers (fasting glucose 150.6 mg/dL and insulin 31.2 picomole per li-
ter). Hyperinsulinemia (high insulin level in serum) is associated with an
increased risk of type 2 diabetes and obesity. The authors concluded that
the abstainers with their relative hyperinsulinemia appeared to be more
insulin resistant than daily moderate drinkers. The difference in insulin
sensitivity may explain the lower prevalence of diabetes in drinkers.38
Shai et al. (2007) investigated the effect of daily consumption of alcohol on
glycemic control (control of blood sugar) in patients with type 2 diabetes
using 109 patients (forty-one to seventy-four years old) who had previ-
ously abstained from alcohol. The subjects were divided into two groups.
One group received 150 mL of wine daily (one standard drink/14 gm
of alcohol) and another group received nonalcoholic beer during dinner
for three months. The fasting glucose was significantly reduced from an
average value of 139.6 mg/dL initially to 118.0 mg/dL after three months
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68 Chapter 4
in diabetics who consumed one drink during dinner for three months. In
contrast, the mean fasting glucose value did not change in diabetic pa-
tients who abstained from alcohol during the three-month period of the
study (136.7 mg/dL at the beginning to 138.6 at the end of the study). Par-
ticipants in the alcohol group reported an improvement in the ability to
fall asleep. Therefore, moderate alcohol consumption may help diabetic
patients with glycemic control.39
MODERATE ALCOHOL CONSUMPTION FOR

PREVENTING DEMENTIA AND ALZHEIMER’S DISEASE
Moderate alcohol consumption can dramatically reduce the risk of age-

related dementia and developing Alzheimer’s disease. A French study
using 3,777 community residents ages sixty-five years or older dem-
onstrated that the subjects who drank three to four glasses of alcoholic
beverages (mostly wine) per day (318 subjects) had 82 percent lower
risk of developing senile dementia and 75 percent lower risk of getting
Alzheimer’s disease compared to nondrinkers (971 subjects).40 However,
chronic abusers of alcohol are at a higher risk of developing memory loss,
dementia, and lack of appropriate motor control due to alcohol-related
brain damage. Younger people, especially underage drinkers, are also at
higher risk of alcohol-related brain damage (see chapter 3).
MODERATE ALCOHOL CONSUMPTION

AND REDUCED RISK OF CANCER
Moderate consumption of alcohol may reduce the risk of certain types

of cancer. It has been suggested that moderate drinking facilitates the
elimination of Helicobacter pylori (H. pylori), a bacteria found in the gut that
causes chronic atrophic gastritis (CAG) and gastric cancer. Gastritis com-
monly refers to inflammation of the lining of the stomach, but the term is
often used to cover a variety of symptoms, including stomach discomfort
and a severe burning sensation. Gao et al. (2009), using 9,444 subjects ages
fifty to seventy-four, observed that moderate drinkers (less than 60 gm of
alcohol per week or four drinks per week) had 29 percent lower chance
of developing CAG than nondrinkers. Both beer and wine drinking pro-
vided protection against CAG. In addition to facilitating elimination of H.
pylori, other mechanisms may also contribute to reducing the risk of CAG
in moderate drinkers.41 In the California Men’s Health Study using 84,170
men ages forty-five to sixty-nine, consumption of one or more drinks per
day was associated with approximately 60 percent reduced lung cancer
10-649_Dasgupta.indb 68 1/17/11 6:40 AM

risk, including smokers. Even heavy smokers benefited from consum-

ing red wine in moderation. No clear association was observed between
moderate drinking and alcohol in individuals who consumed white wine,
beer, or other liquors.42
Moderate consumption of red wine reduces the risk of lung cancer.
In another study, the author observed that although moderate consump-

tion of wine (one drink or less per day) was associated with approxi-
mately 23 percent reduced risk of developing lung cancer, moderate con-
sumption of beer (one or more per day) increases the risk of developing
lung cancer by 23 percent in men but not in women.43 Jiang et al. (2007)
reported that people drinking beer and wine but not spirits (hard liquor)
can reduce the risk of bladder cancer by up to 32 percent compared to
nondrinkers.44 Consumption of up to one drink per day reduced the risk
of head and neck cancer in both men and women, but consuming more
than three alcoholic beverages increased the risk of developing cancer.45
In two Italian studies, the authors observed that moderate consumption
of alcohol reduced the risk of developing renal cell carcinoma (kidney
cancer) in both men and women.46 However, chronic heavy drinkers are
at increased risk of developing many types of cancers, especially cancer
of the mouth (see chapter 5).
CAN MODERATE ALCOHOL CONSUMPTION PROLONG LIFE?
Because moderate consumption of alcohol can prevent many diseases,

including the number one killer, cardiovascular disease, it is expected
that moderate drinkers may live longer than lifetime abstainers of alco-
hol. Freiberg et al. (2009), using 10,576 African American and 105,610
Caucasian postmenopausal women and an eight-year follow-up, dem-
onstrated that moderate drinking (one to less than seven drinks per
week) was associated with lower mortality among both hypertensive
and nonhypertensive Caucasian women, but among African American
women only hypertensive women received benefits from moderate
drinking. Even those who currently started drinking (versus lifetime
drinkers) only one drink or more per month increased longevity among
Caucasian hypertensive and nonhypertensive women, as well as among
African American hypertensive women. Low mortality was also ob-
served among the African American lifetime nondrinking women with
normal blood pressure.47 Klatsky et al. (1981) studied ten-year mortality
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70 Chapter 4
in relation to alcohol in 8,060 subjects and observed that people who

consumed two drinks or fewer daily fared best and had a 50 percent
reduction in the mortality rate than nondrinkers. The heaviest drinkers
(six or more drinks per day) had double the mortality rate of moderate
drinkers, while people who drank three to five drinks per day had a
similar mortality rate as nondrinkers. Therefore, consuming two or less
drinks per day is the best practice.48
In the Physician’s Health Study, which involved 22,071 U.S. male
physicians between the ages of forty and eighty-four (with no history of
myocardial infarction, stroke, or cancer) and a ten-year follow-up, the
authors observed that men who consumed two to six drinks per week
had the most favorable results (20–28 percent lower mortality rate than
people who consumed one drink per week). In contrast, people who con-
sumed more than two drinks per day had an approximately 50 percent
chance of higher mortality than people who consumed just one drink per
week.49 A Chinese study also reported that consuming not more than two
drinks per day was associated with a 19 percent reduction in mortality
risk among Chinese men.50
It has been suggested that wine consumption increases longevity
more than drinking beer or other liquors. Klatsky et al. (2003) collected
data from 128,934 adults undergoing health evaluations in 1978–1985,
with subsequent death ascertained by an automated linkage system
with a twenty-year follow-up. The authors observed that wine drink-
ing was associated with a lower mortality risk largely because of lower
coronory disease risk. The authors concluded that those who drink any
type of wine have a lower mortality risk than those drinking beer or
other liquor.51
A nationwide survey based on 17,600 people in the United States re-
vealed that those who currently drink are hospitalized less often than
abstainers. Among men the possibility of one or more hospitalizations
among current drinkers was 26 percent lower and in women 33 percent
lower in current drinkers who consume alcohol in moderation as opposed
to lifetime abstainers.52 A study from the Netherlands reported that in
the presence of stress, moderate drinkers are less likely to be absent from
work than nondrinkers.53 The nine-year Alameda County Study (1980)
indicated that moderate consumption of alcohol was associated with
the most favorable health scores, indicating that moderate drinkers in
general enjoy better overall health quality than abstainers.54 The authors
of a study conducted in Copenhagen using 12,039 subjects reported that
light to moderate wine drinking (one to two glasses of wine per day) was
associated with good self-perceived health, whereas this was not the case
with consumers of beer or spirits. However, heavy drinkers of any type
of beverage (wine, beer, or spirits) had a higher prevalence of suboptimal
health than nondrinkers.55
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MODERATE ALCOHOL CONSUMPTION AND ARTHRITIS
Moderate alcohol consumption reduces the risk of developing rheumatoid

arthritis. Results from two Scandinavian studies indicated that among mod-
erate drinkers, the risk of rheumatoid arthritis was significantly reduced
(40–50 percent). Smokers had a higher risk of developing rheumatoid ar-
thritis. The authors advised that smokers should be advised to quit smoking
in order to reduce the risk of developing arthritis, but moderate drinkers
should not be discouraged from sensible alcohol consumption.56 Moderate
alcohol consumption not only reduces the risk of developing rheumatoid
arthritis but also may slow the progression of the disease. Based on a study
using 2,908 patients suffering from rheumatoid arthritis, Nissen et al. (2010)
reported that occasional or daily consumption of alcohol reduces the pro-
gression of the disease based on radiological studies (X-rays). Best results
were observed in men.57 However, drinking beer, even one drink per day,
increases the risk of developing gout in men. Individuals who drank spirits
(even one drink a day) also had a somewhat increased risk of developing
gout, although the risk was highest among beer drinkers. In contrast, mod-
erate wine drinking did not increase the odds of developing gout.58
CAN MODERATE ALCOHOL CONSUMPTION

PREVENT THE COMMON COLD?
Cohen et al. (1993) observed that smokers are at greater risk of develop-
ing the common cold than nonsmokers. Moderate alcohol consumption
reduced the incidence of the common cold among nonsmokers but had no
protective effect against the common cold in smokers.59 In a large study
using 4,272 faculty and the staff of five Spanish universities as subjects,
the investigators observed that total alcohol intake from drinking beer
and spirits had no protective effect against the common cold, where mod-
erate wine consumption was associated with reduced risk of the common
cold. When individuals consumed fourteen or more glasses of wine per
week, the relative risk of developing the common cold was reduced by 40
percent compared to teetotalers. It was also observed that consumption
of red wine provided superior protection against the common cold. The
authors concluded that wine drinking, especially drinking red wine, may
have a protective effect against the common cold.60
CONCLUSION
The Dietary Guideline for Americans has been published jointly every five
years since 1980 by the Department of Health and Human Services and
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72 Chapter 4
the Department of Agriculture. These guides serve as the basis for federal
food and nutritional education programs. In the latest published guide-
line (2005), it was stated that consumption of alcohol can have a beneficial
or a harmful effect on health depending on the amount consumed, age,
gender, and other characteristics of the person. In 2002, approximately 55
percent of adults living in the United States were drinking alcohol, while
the other 45 percent were abstainers. Fewer Americans drink today than
fifty or a hundred years ago. Alcohol is beneficial only when consumed
in moderation and reduces all causes of mortality at an intake of one to
two drinks a day. The lowest coronary heart disease mortality also occurs
at an intake of one to two drinks per day. In contrast, morbidity and mor-
tality are highest among those drinking large amounts of alcohol. This
guideline also defines moderate drinking as up to two drinks per day for
men and up to one drink per day for women. The definition of modera-
tion is not based on an average of alcohol consumption over several days
but rather as the amount consumed every day. Consuming more than
one drink per day for women and more than two drinks per day for men
increases the risk of motor vehicle accidents and other injuries, high blood
pressure, stroke, violence, and certain types of cancer. Alcohol must be
avoided under certain circumstances, such as for those who plan to drive,
operate machinery, or other activities requiring skill and attention. Preg-
nant women and women who plan to get pregnant should not drink at
all. It appears that only middle-aged and older people receive benefits
from moderate drinking, while benefits are few among younger people.
Alcoholic drinks supply calories but few essential nutrients. Total caloric
intake from one standard drink of various alcoholic beverages is listed in
table 4.4. Although the consumption of one to two drinks per day is not
associated with micronutrient deficiency or with overall dietary quality,
heavy drinkers may be at risk of malnutrition if the calories derived from
alcohol are substituted for those in nutritious food.61
Table 4.4. Calories in Selected Alcoholic Beverages
Alcoholic Drink Serving Size Total Calories

Regular beer 12 ounces 144
Light beer 12 ounces 108
White wine 5 ounces 100
Red wine 5 ounces 105
Sweet dessert wine 3 ounces 141
80 proof spirit 1.5 ounces 96
(Gin, rum, whiskey, vodka)
Source: Dietary Guidelines for Americans, U.S. Department of Health and Human Resources, 2005, http://
www.health.gov./dietaryguidelines/dga2005/document/default.htm.
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NOTES
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29. T. Truelsen, M. Gronbaek, P. Schnohr, and G. Boyen, “Intake of Beer, Wine
and Spirits and Risk of Stroke: The Copenhagen City Heart Study,” Stroke 29, no.
12 (December 1998): 2467–72.
30. N. R. Nielsen, T. Truelsen, J. C. Barefoot, S. P. Johnsen, et al., “Is the Effect of
Alcohol on Risk of Stroke Confined to Highly Stressed Persons?” Neuroepidemiol-
ogy 25, no. 3 (March 2005): 105–13.
31. R. L. Sacco, M. Elkind, B. Boden-Albala, I. F. Lin, et al., “The Protective Ef-
fect of Moderate Alcohol Consumption on Ischemic Stroke,” Journal of the Ameri-
can Medical Association 281, no. 1 (January 1999): 53–60.
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32. M. S. Elkind, R. Sciacca, B. Boden-Albala, and T. Rundek, “Moderate Al-

cohol Consumption Reduces Risk of Ischemic Stroke: The Northern Manhattan
Study,” Stroke 37, no. 1 (January 2006): 13–19.
33. M. Hillbom and H. Numminen, “Alcohol and Stroke: Pathophysiologic
Mechanisms,” Neuroepidemiology 17, no. 6 (June 1998): 281–87.
34. S. Wild, G. Roglic, A. Green, R. Sicree, et al., “Global Prevalence of Diabe-
tes,” Diabetes Care 27, no. 5 (May 2004): 1047–53.
35. L. L. Koppes, J. M. Dekker, H. F. Hendriks, L. M. Bouter, et al., “Moderate
Alcohol Consumption Lowers the Risk of Type 2 Diabetes: A Meta-analysis of
Prospective Observational Studies,” Diabetes Care 28, no. 3 (March 2005): 719–25.
36. S. W. Carrison, N. Hammar, V. Grill, and J. Kaprio, “Alcohol Consumption
and the Incidence of Type 2 Diabetes: 20-Year Follow-Up of the Finnish Twin
Cohort Study,” Diabetes Care 26, no. 10 (October 2003): 2785–90.
37. D. O. Balinus, B. J. Taylor, H. Irving, M. Roereke, et al., “Alcohol as a Risk
Factor for Type 2 Diabetes: A Systematic Review and Meta-analysis,” Diabetes Care
32, no. 11 (November 2009): 2123–32.
38. P. V. Kenkre, R. D. Linderman, C. Lillian Yau, R. N. Baumgartner, et al.,
“Serum Insulin Concentrations in Daily Drinkers Compared with Abstainers in
the New Mexico Elder Health Survey,” Journal of Gerontology Series A: Biological
Sciences and Medical Sciences 58, no. 10 (October 2003): M960–963.
39. I. Shai, J. Wainstein, I. Harman-Boehm, I. Raz, et al., “Glycemic Effects of
Moderate Alcohol Intake among Patients with Type 2 Diabetes: A Multicenter
Randomized Clinical Investigation,” Diabetes Care 30, no. 12 (December 2007):
3011–16.
40. J. M. Orgogozo, J. F. Dartigues, S. Lafont, L. Letenneur, et al., “Wine Con-
sumption and Dementia in the Elderly: A Prospective Study in the Bordeaux
Area,” Revue Neurologique (Paris) 153, no. 3 (April 1997): 185–92.
41. L. Gao, M. N. Weck, C. Stegmaier, D. Rothenbacher, et al., “Alcohol Con-
sumption and Chronic Atrophic Gastritis: Population-Based Study among 9,444
Older Adults from Germany,” International Journal of Cancer 125, no. 12 (December
2009): 2918–22.
42. C. Chao, J. M. Slezak, B. J. Caan, and V. P. Quinn, “Alcoholic Beverage
Intake and Risk of Lung Cancer: The California Men’s Health Study,” Cancer Epi-
demiology and Biomarkers Prevention 17, no. 10 (October 2008): 2692–99.
43. C. Chao, “Association between Beer, Wine, and Liquor Consumption and
Lung Cancer Risk: A Meta-analysis,” Cancer Epidemiology and Biomarkers Preven-
tion 16, no. 11 (October 2007): 2436–47.
44. X. Jiang, K. E. Castelao, V. K. Cortessis, R. K. Ross, et al., “Alcohol c and
Risk of Bladder Cancer in Los Angeles County,” International Journal of Cancer 121,
no. 4 (August 2007): 839–45.
45. N. D. Freedman, A. Schatzkin, M. F. Leitzmann, M. F. Hollenbeck, et al.,
“Alcohol and Head and Neck Cancer Risk in a Prospective Study,” British Journal
of Cancer 96, no. 9 (May 2007): 1469–74.
46. C. Pelucchi, C. Galeone, M. Montella, J. Polesel, et al., “Alcohol Consump-
tion and Renal Cell Cancer Risk in Two Italian Case-Control Studies,” Annals of
Oncology 19, no. 5 (May 2008): 1003–8.
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76 Chapter 4
47. M. S. Freiberg, Y. F. Chang, K. L. Kraemer, J. G. Robinon, et al., “Alcohol

Consumption, Hypertension, and Total Mortality among Women,” American Jour-
nal of Hypertension 22, no. 111 (November 2009): 1212–18.
48. A. L. Klatsky, G. D. Friedman, and A. B. Siegekaub, “Alcohol and Mortality:
A Ten-Year Kaiser-Permanente Experience,” Annals of Internal Medicine 95, no. 2
(August 1981): 139–45.
49. C. A. Camargo, C. H. Hennekens, J. M. Gaziano, R. J. Glynn, et al., “Prospec-
tive Study of Moderate Alcohol Consumption and Mortality in US Male Physi-
cians,” Archives of Internal Medicine 157, no. 1 (January 1997): 79–85.
50. L. C. De Groot and P. L. Zock, “Moderate Alcohol Intake and Mortality,”
Nutritional Review 596, no. 1, part 1 (January 1998): 25–26.
51. A. L. Klatsky, G. D. Friedman, M. A. Armstrong, and H. Kipp, “Wine, Li-
quor, Beer and Mortality,” American Journal of Epidemiology 158, no. 6 (September
2003): 585–95.
52. M. P. Longnecker and B. MacMohon, “Association between Alcoholic
Beverages Consumption and Hospitalization, 1983 National Health Interview
Survey,” American Journal of Public Health 78, no. 2 (February 1998): 1543–56.
53. R. M. Vasse, F. J. Nijhuis, and G. Kok, “Association between Work Stress,
Alcohol Consumption and Sickness Absence,” Addiction 93, no. 2 (February 1998):
231–41.
54. J. A. Wiley and T. C. Camacho, “Life-style and Future Health: Evidence
from Alameda County Study,” Preventive Medicine 9, no. 1 (January 1980): 1–21.
55. M. Gronbaek, E. L. Mortensen, K. Mygind, A. T. Andersen, et al., “Beer,
Wine, Spirit and Subjective Health,” Journal of Epidemiology and Community Health
53, no. 11 (November 1999): 731–24.
56. H. Kallberg, S. Jacobsen, C. Bengtsson, M. Pedersen, et al., “Alcohol Con-
sumption Is Associated with Decreased Risk of Rheumatoid Arthritis: Results
from Two Scandinavian Studies,” Annals of Rheumatoid Diseases 68, no. 2 (February
2009): 222–27.
57. M. J. Nissen, C. Gabay, A. Scherer, and A. Finchk, “The Effect of Alcohol
on Radiographic Progression in Rheumatoid Arthritis,” Arthritis and Rheumatology
62, no. 5 (May 2010): 1265–72.
58. H. K. Choi, K. Atkinson, E. W. Karlson, W. Willett, et al., “Alcohol Intake
and Risk of Incident Gout in Men: A Prospective Study,” Lancet 363, no. 9417
(April 2004): 1277–81.
59. S. Cohen, D. A. Tyrell, M. A. Russell, N. J. Jarvis, et al., “Smoking, Alcohol
Consumption and Susceptibility to the Common Cold,” American Journal of Public
Health 83, no. 9 (September 1993): 1277–83.
60. B. Takkouch, C. Regueira-Mendez, R. Garcia-Closas, A. Figueiras, et al.,
“Intake of Wine, Beer, and Spirits and the Risk of Clinical Common Cold,” Ameri-
can Journal of Epidemiology 155, no. 9 (May 2002): 853–58.
61. Dietary Guidelines for Americans, 2005, Chapter 9: Alcohol, U.S. Depart-
ment of Health and Human Resources, http://www.health.gov./dietaryguide
lines/dga2005/document/default.htm.
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5

Harmful Effects of Chronic
Alcohol Consumption
D rinking in moderation has many health benefits, but all such posi-
tive effects quickly disappear in people who drink heavily or who
are alcoholics. Although the majority of Americans drink sensibly, and
per capita consumption of alcohol from all alcoholic beverages in 2007
was 2.31 gallons or 289 ounces (approximately twenty-four beers a year
per person), according to the National Institute of Alcohol Abuse and
Alcoholism (NIAAA), approximately 8 percent of Americans are alcohol
dependent. The group Healthy People 2010 has set a national objective
of reducing per capita consumption to no more than 1.96 gallons of al-
cohol,1 because the average total societal cost due to alcohol abuse as a
percentage of gross domestic product (GDP) in high-income countries,
including the United States, is approximately 1 percent. This is a high toll
for a single factor and an enormous burden on public health.2 Accord-
ing to a report by Dr. Ting-Kai Li, the director of the NIAAA, in 2008,
alcohol-related problems cost the United States an estimated $185 billion
annually, with almost half the costs from lost productivity due to alcohol-
related disabilities. In the United States more than 18 million people ages
eighteen and older suffer from alcohol abuse or dependency and only
7 percent of these people receive any form of treatment. In addition,
heavy drinkers who are not alcoholics but are at high risk for developing
alcohol-related physical or mental damage are seldom identified. The
highest prevalence of alcohol dependency in the United States is observed
among younger people between the ages of eighteen and twenty-four.
77
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78 Chapter 5
The World Health Organization (WHO) lists alcohol as one of the leading
causes of disability in the world.3
According to studies conducted by the Center for Disease Control
(CDC), alcohol abuse kills approximately 75,000 Americans each year
and shortens the life of alcoholics by an average of thirty years. In 2001,
34,833 Americans died from cirrhosis of the liver, a major complication
of alcohol abuse, and another 40,933 died from car crashes and other
alcohol-related fatalities. Men accounted for 72 percent of the deaths due
to alcohol abuse and 6 percent were twenty-one years old or younger.4 In
2005, liver cirrhosis was the twelfth leading cause of death in the United
States, claiming 28,175 lives. Among all cirrhosis-related deaths, 45.9
percent were alcohol related.5 California is the largest alcohol market in
the United States, and Californians consumed almost 14 billion alcoholic
drinks in 2005, which resulted in an estimated 9,439 deaths and 921,029
alcohol-related problems such as crime and injury. The economic burden
was estimated to be $38.5 billion of which $5.4 billion was for medical and
mental health spending, $25.3 billion due to loss of work, and another
$7.8 billion in criminal justice spending.6 In the United Kingdom, alcohol
consumption was responsible for 31,000 deaths in 2005, and the National
Health Services spent an estimated 3 billion pounds in 2005–2006 for
treating alcohol-related illness and disability. Alcohol consumption was
responsible for approximately 10 percent of disabilities (male: 15 percent;
female: 4 percent).7
Many studies demonstrate the harmful effects of alcohol on a variety
of organ systems, including the liver, heart, brain, immune system, en-
docrine system, and bones. Alcoholic liver disease and alcoholic liver
cirrhosis take many lives every year worldwide. Major adverse effects of
chronic alcohol consumption include:
Decreased life span

Increased risk of violent behavior and tendency for substance abuse
Alcoholic liver disease
Anxiety and mood disorder
Brain damage (see chapter 3)
Damage to heart
Increased risk of stroke
Damage to immune system
Damage to endocrine system, including both male and female repro-
ductive systems
Bone damage
Increased risk of various cancers
Poor outcome of pregnancy (see chapter 10)
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Harmful Effects of Chronic Alcohol Consumption 79
DEFINITION OF HEAVY CONSUMPTION

OF ALCOHOL AND RISKY DRINKING
The definition of moderate and heavy drinking has been discussed in

chapter 2. Briefly, moderate drinking means consuming up to two al-
coholic drinks per day for men, up to one alcoholic drink per day for
women, and up to one drink per day for both men and women older
than sixty-five. For all practical purposes, the NIAAA sets this thresh-
old at no more than fourteen drinks per week for men (or more than
four drinks per occasion) and no more than seven drinks per week for
women (or more than three drinks per occasion). Individuals whose
drinking exceeds these guidelines are at increased risk for adverse
health effects. Hazardous drinking is defined as twenty-one or more
drinks per week by men or more than seven drinks per occasion at least
three times a week. For women, more than fourteen drinks per week
or drinking more than five drinks in one occasion at least three times a
week is considered hazardous drinking. Risky drinking is defined as the
consumption of five or more drinks in a single occasion or day for men
and four or more drinks for women. Risky drinking is also referred to
as binge drinking.
There is a misconception that if the number of total drinks in a week
does not exceed fourteen for men and seven drinks for women, then the
drinking practice is safe. In reality, frequency of drinking is an important
criterion for defining moderate drinking. It is wise not to consume more
than one drink a day for both men and women because the beneficial
effects of alcohol can be achieved from consuming as little as one to six
drinks per week. Consuming seven drinks on Friday and seven drinks
on Saturday and not drinking at all for the remainder of the week—thus
consuming a total of fourteen drinks per week for a male—is risky be-
havior. Risky drinking or binge drinking, even practiced occasionally, is
a dangerous behavior. For example, consuming five drinks within two
hours would certainly elevate blood alcohol level over the legal limit of
0.08 percent in a lean and moderately built person, and if stopped by the
police, a DWI charge would be extremely likely.
Risky drinking is also associated with violent behavior, mood swings,
and behavior-related problems such as self-harm and injury, risky sexual
practices and sexual victimization, spousal abuse, and risk of developing
obesity. Consuming more than five drinks just once a month may increase
the risk of developing dementia, and a study with Canadian adults ages
eighteen to sixty-four found that having ever consumed more than one
drink in a single day during the preceding year was associated with an
increased risk of heart disease and hypertension among men and an
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80 Chapter 5
increased risk of heart disease among women. Dawson et al. (2001), fol-
lowing 22,245 Americans, reported that 59.9 percent of drinkers never en-
gaged in risky drinking behavior, 16.9 percent engaged in risky drinking
less than once a month, about 9 percent did so one to three times a month,
and a small minority of 3 percent did three to four times a week or nearly
every day. Risky drinkers were younger and usually not married. Daily
or nearly daily risky drinkers were more than seven times more likely to
develop alcohol dependency compared to moderate drinkers. The odds of
developing liver disease were also high in individuals who were involved
in risky drinking just once or twice a week. Daily or near daily risky
drinking was also associated with high odds of divorce, spousal abuse,
and poor job performance. In addition, daily or near daily risky drinkers
are also prone to drug abuse, drug dependence, and nicotine abuse.8
CHRONIC ABUSE OF ALCOHOL AND REDUCED LIFE SPAN
Although moderate drinking is associated with increased longevity,

heavier drinking is associated with decreased longevity compared to
abstainers. Heavy consumption of alcohol causing reduced longevity
depends on two factors: frequency of drinking and number of drinks
consumed in one occasion. As described in chapter 4, studies that dem-
onstrated increased life span among moderate drinkers also established
that heavy drinking reduces normal life span. Moderate drinking reduces
the risk of heart disease, but excess alcohol consumption is toxic to the
heart. Similarly, moderate drinking reduces the risk of stroke but heavy
drinking increases the risk.
Even occasional heavy drinking may be detrimental to health. Dawson
reported an increased risk of mortality among individuals who usually
drink more than five drinks per occasion but who drank even less than
once a month.9 Irregular heavy drinking even once a month (five or
more drinks per occasion) increases the risk of heart disease rather than
protecting the heart as observed in moderate drinkers. The cardioprotec-
tive effect of moderate drinking also disappears when light to moderate
drinking is mixed with occasional heavy drinking episodes.10
In a British study of 5,766 men ages thirty-five to sixty-four with a
twenty-one-year follow-up, it was observed that consuming between
fifteen to twenty-one standard drinks per week increases the risk of
all causes of mortality compared to moderate drinkers (up to fourteen
standard drinks per week) and nondrinkers by 34 percent, while drink-
ing more than thirty-five standard drinks per week increases the risk
by 49 percent. The authors further observed that men drinking thirty-
five or more standard drinks per week had double the risk of stroke
10-649_Dasgupta.indb 80 1/17/11 6:40 AM

compared to nondrinkers. The authors concluded that in general the

overall association between alcohol consumption and mortality is un-
favorable for men drinking twenty-two standard alcoholic drinks per
week or more.11
Using more than 43,000 participants and a fourteen-year follow-up
(2,547 people died), Breslow and Graubard (2008) observed that men who
consumed five or more drinks on a drinking day had a 30 percent higher
risk of mortality from heart disease, a more than 50 percent higher risk
of cancer, and a more than 40 percent of all-cause mortality compared to
individuals who drank one drink on a drinking day. The risk of mortality
was also increased to some extent with just two drinks per day or more
for men. Women drinkers who consumed alcohol (two drinks or more in
a session) more often than in moderation (one drink or less a day) also
showed all-cause higher mortality than moderate drinkers. Among men
both quantity and frequency of drinking were significantly associated
with mortality from cardiovascular disease, cancer, and other causes, but
among women the quantity of alcohol was more important, and women
who drank more than in moderation showed a higher risk of mortality
from cancer than from men.12 The London-based Whitehall II Cohort
Study, using 10,308 government employees between the ages of thirty-
five and fifty-five with an eleven-year follow-up, also concluded that op-
timal drinking is one drink or less daily consumed once or twice a week.
People who consumed alcohol twice a day or more had an increased risk
of mortality compared to those drinking once or twice a week.13
Binge drinking is also dangerous. In one study (based on a population
of 1,641 men who drank beer), the authors observed that the risk of death
in men who drank six or more bottles of beer in one occasion was almost
three times higher than those who consumed less than three bottles in one
occasion.14 Another study (Anda et al. 1988) based on 13,251 adults also
reported that individuals who drank five or more drinks in one occasion
were nearly twice as likely to die from injuries than people who drank
fewer than five drinks in a single occasion. People drinking nine or more
drinks in a single occasion were 3.3 times more likely to die from injuries
than people consuming less than five drinks.15
Consuming five or more drinks in one occasion increases the risk of

fatal injuries significantly compared to individuals who consume less
than five drinks.
Other than increasing mortality from various diseases, alcohol abuse

is associated with increased risk of suicide, accidents, and violent crimes.
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82 Chapter 5
Alcohol-related traffic accidents causing fatalities are discussed in chap-

ter 6. Based on a survey of 31,953 school students, Schilling et al. (2009)
observed that both drinking while depressed and episodic heavy drink-
ing were associated with self-reported suicide attempts in adolescents.16
Swahn et al. (2008) reported that in a high-risk school district in the
United States, 35 percent of seventh graders reported alcohol use initia-
tion at age thirteen or younger. Preteen alcohol users were more involved
in violent behavior than nondrinkers. Early alcohol use was also associ-
ated with higher risk of suicide attempts among these adolescents.17
ALCOHOL ABUSE AND

INCREASED RISK OF VIOLENT BEHAVIOR
Many investigators have reported a close link between violent behavior,

homicide, and alcohol intoxication. Studies conducted on convicted mur-
derers suggest that about half of them were under the heavy influence
of alcohol at the time of the murder.18 According to the latest report on
alcohol and crime published by the U.S. Department of Justice, alcohol is
involved in many violent crimes (table 5.1).
Alcohol may induce aggression and violent behavior by disrupting
normal brain function when consumed in high doses. By impairing
the normal information-processing capability of the brain, a person
can misjudge a perceived threat and may react more aggressively than
warranted. Serotonin, a neurotransmitter, is considered a behavioral in-
hibitor. Alcohol abuse may lead to decreased serotonin activity, causing
aggressive behavior. High testosterone concentrations in criminals have
been associated with violent crimes. Adolescents and young adults with
Table 5.1. Involvement of Alcohol in Violent Crimes and Offenses in the United
States
• On average each year 183,000 rapes and sexual assaults involve alcohol abuse by
offenders.
• Approximately 197,000 robberies, 661,000 aggravated assaults, and nearly 1.7
million simple assaults are caused by heavy drinkers each year.
• Two-thirds of the victims attacked by a known individual (spouse or former spouse,
boyfriend, or girlfriend) reported that alcohol was involved. In contrast, 31 percent of
victimization by strangers is alcohol related.
• Approximately 118,000 family violences annually are alcohol related.
• Approximately 36 percent of convicted offenders abuse alcohol during committing
the crime. Male offenders are more likely to be drinking than female offenders.
• Half of the convicted murderers in state prisons abused alcohol before committing
the crime.
Source: “Alcohol and Crime,” 1998 report by the U.S. Department of Justice, Bureau of Justice Statistics.
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higher levels of testosterone compared to the general population are

more often involved in heavy drinking and consequently violent behav-
ior. Young men who exhibit antisocial behavior often “burn out” with
older age due to decreased levels of testosterone and increased levels
of serotonin. By modulating serotonin and testosterone concentration,
alcohol may induce aggressive and violent behavior when consumed
in excess.19
ALCOHOLIC LIVER DISEASE
The liver is one of the largest and most complex organs of the human
body. It synthesizes important proteins vital for life, stores some nutri-
ents, and breaks down (metabolizes) drugs and toxins, including alcohol,
thus protecting the body from harmful effects. Although the liver has an
amazing capacity for self-healing through regeneration, certain liver dis-
eases, such as cirrhosis of the liver, are irreversible and may even cause
death. Alcohol-induced liver disease can be classified under three catego-
ries: (1) fatty liver; (2) alcoholic hepatitis; and (3) liver cirrhosis.
Heavy drinking for as little as a few days may produce fatty changes
in the liver (steatosis), which can be reversed after abstinence. However,
drinking heavily for a longer period may cause severer alcohol-related
liver injuries, such as alcoholic hepatitis and cirrhosis of the liver. The
diagnosis of alcoholic hepatitis is a serious medical condition because
approximately 70 percent of such patients may progress to liver cir-
rhosis, a major cause of death worldwide. However, if a patient with
alcoholic hepatitis practices complete abstinence, this condition may be
reversible.
In general, women are more susceptible to alcoholic liver disease than

are men.
Drinking in moderation has no ill effects on the liver. One drink or less a
day for both men and women is safe, and all the health benefits of alcohol
can be enjoyed from consumption of such a moderate amount of alcohol,
but heavy drinkers are susceptible to alcoholic liver disease. Although
fatty liver may develop in approximately 90 percent of alcoholics, only
10–35 percent of them develop alcoholic hepatitis, while 10–20 percent of
them develop liver cirrhosis. In the United States it is estimated that more
than 2 million people are suffering from alcohol-related liver diseases.
Liver cirrhosis is the seventh-leading cause of death among young and
middle-aged adults and approximately 10,000 to 24,000 deaths from liver
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84 Chapter 5
cirrhosis annually may be attributable to alcohol abuse.20 The risk of de-

veloping alcoholic hepatitis and liver cirrhosis depends on several factors:
Amount of alcohol consumed per day

Length of heavy drinking
Gender
Ethnicity and genetic predisposition
Nutritional status and obesity
Type of alcoholic beverage consumed
Family history of alcohol abuse
Presence of hepatitis C
The amount of alcohol consumed is a determining factor in develop-

ing alcoholic hepatitis and liver cirrhosis. In one report (Bellentani and
Tribelli 2001) the authors commented that cirrhosis of the liver does not
develop below a lifetime ingestion of 100 kg of alcohol (one standard
drink is approximately 14 gm of alcohol; therefore, this would be a life-
time consumption of 7,143 drinks). This amount corresponds to an aver-
age of five drinks a day for about four years. The authors also commented
that consuming alcohol with food lowers the risk of developing cirrhosis
of the liver compared to consuming alcohol on an empty stomach.21
Although only a small percentage of alcoholics develop alcoholic
hepatitis and liver cirrhosis, other alcohol-related liver damage occurs at
a much lower intake of alcohol. In general, it is considered that the thresh-
old of alcohol-induced liver toxicity is 40 gm of alcohol per day (approxi-
mately three drinks a day) for men and 30 gm (more than just two drinks)
or more of alcohol a day for women. But in one report (Bellentani et al.
1997) the authors concluded—based on a study of 6,917 subjects—that
risk of any alcohol-induced liver damage (noncirrhotic liver damage) may
have a threshold of just 30 gm or more of alcohol consumption (a little
more than two standard drinks) per day for both men and women, and
the risk increases with increasing daily consumption. Drinking outside
mealtime and drinking multiple different alcoholic beverages increased
alcohol-induced liver damage.22
However, another study (Walsh and Alexander 2000) indicated that
above a threshold of seven to thirteen drinks per week for women and
fourteen to twenty-seven drinks per week for men, there is a risk of devel-
oping some alcohol-related liver problems. In general women are more
sensitive than men to the toxic effects of alcohol. One of the reasons is
that women break down alcohol more slowly than do men due to genetic
differences. In addition, toxic metabolites of alcohol tend to accumulate
more in women than in men. Consumption of coffee may protect men
against alcohol-induced liver damage, but no such data is currently avail-
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able for women.23 It has also been postulated that heavy drinkers of spirits
are more susceptible to alcoholic liver damage than wine drinkers.
Although fatty liver is common in heavy drinkers, those who develop
alcoholic hepatitis, liver cirrhosis, and other severe alcohol-related liver
diseases have usually been abusing alcohol for more than a decade. Daily
alcohol consumption of three to six drinks for men and two to three
drinks for women over a period of twelve years would most likely cause
alcoholic liver diseases. However, lower amount of alcohol consump-
tion may cause alcoholic liver disease in certain ethnic populations. One
Chinese study (Lu et al. 2004) using 1,300 alcohol drinkers indicated that
the risk threshold was only 20 gm of alcohol daily (one and a half drinks)
for five years, with a greater risk when alcohol is consumed on an empty
stomach, especially with hard liquor (spirits). In addition, obese people
showed more morbidity from alcohol-related liver diseases.24
Hepatitis C is a liver disease caused by Hepatitis C virus. This virus can
be spread by sharing needles or other equipment for injecting illicit drugs
and also through sexual contact with infected partners. It has been esti-
mated that approximately 4 million Americans are infected with hepatitis
C, and between 10,000 and 12,000 die annually. Hepatitis C infection is
common among alcohol abusers, and this infection may even accelerate
alcohol-related liver diseases, including cirrhosis of the liver and liver
cancer. How much alcohol consumption is safe for a person with hepatitis
C has not been clearly established. In one study (Hezode et al. 2003) the
authors observed that moderate alcohol consumption of 31–50 gm per
day for men (two and a half drinks to three and a half drinks) and 21–50
gm per day for women (one and a half drinks to three and a half drinks)
could adversely affect the progression of liver damage.25 Anyone with a
confirmed hepatitis C infection must consult with his or her physician
before drinking any alcoholic beverages.
DIAGNOSIS AND TREATMENT

OF ALCOHOLIC LIVER DISEASES
Common symptoms of alcoholic hepatitis are weakness, weight loss, nausea,

vomiting, diarrhea, pain in the upper abdomen, and jaundice. Laboratory
findings include increased levels of liver-specific enzymes in the blood, and
increased levels of bilirubin may correlate with the severity of the disease.
Serum bilirubin over 15 mg/dL (100 milliliters of serum) indicates a severe
case of liver damage. In general, lab tests show that the liver enzyme aspar-
tate aminotransferase (AST) is more elevated than alanine aminotransferase
(ALT). Prothrombin time is usually prolonged and the albumin level in the
blood is usually reduced. Viral hepatitis can also cause similar laboratory
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86 Chapter 5
findings, and negative tests for hepatitis combined with a prolonged history
of heavy drinking may confirm the diagnosis of alcoholic liver damage.
Hepatitis C and concurrent alcohol abuse could cause more severe liver
damage and a poor prognosis. Liver biopsy may or may not be performed
depending on the physical examination of the patient and laboratory test
results. However, liver biopsy may be helpful to rule out non-alcohol-
related liver damage. In figure 5.1, representative liver biopsies of fatty
liver, alcohol hepatitis, and alcoholic liver cirrhosis are shown. Patients
with severe liver cirrhosis have poor survival rates, and 50 percent may
die within thirty days after diagnosis of the disease, but people with a
diagnosis of alcoholic hepatitis have a much better prognosis, with only
15 percent mortality within thirty days.
The severity of alcoholic liver disease can be estimated by using the
following formula:
Risk factor = 4.6 × (prothrombin time prolongation in seconds) + serum

bilirubin (mg/dL)
A value higher than 32 indicates severe disease.
Figure 5.1. Biopsies of alcoholic liver diseases

showing how a patient may progress from benign
fatty liver to potentially life-threatening alcoholic
hepatitis and liver cirrhosis
Source: L. S. Marsano et al., “Diagnosis and Treatment of
Alcoholic Liver Disease and Its Complications,” Alcohol
Research and Health 27, no. 3 (2003): 247–56. A
publication of the National Institute of Alcohol Abuse
and Alcoholism. Information in the public domain.
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Liver transplant is the replacement of a severely diseased liver (usually

in a patient suffering from end-stage liver disease), which can no longer
perform the physiological functions required for sustaining life, with a
healthy liver, usually from a deceased donor. Live liver transplant, where
a living person donates a portion of liver to another person, is usually per-
formed in children. The first such surgery was performed in 1989 when a
child received a segment of his mother’s liver.
The most commonly used liver transplant technique is orthotopic trans-
plantation, where the damaged liver is removed and then the new liver is
placed at the same anatomic spot. The mathematical formula widely used
to assess the need for liver transplant in patients with severe end-stage
liver disease is called the MELD score (model for end-stage liver disease),
which is based on natural logarithm (ln) values of bilirubin, creatinine,
and international normalization ratio (INR), indicating the coagulation
status of blood.
MELD score = 3.8 (ln bilirubin, mg/dL) + 11.2 (ln INR) + 9.6 (ln creatinine
mg/dL) + 6.4
A value of 6 or less indicates a good prognosis, while a score higher than

26 indicates fatalities in ninety days for about 90 percent of patients after
diagnosis.
Treatment of alcoholic liver diseases includes lifestyle modification and
practicing complete abstinence. Alcoholic hepatitis can often be reversed
if complete abstinence is practiced, and even patients who have progres-
sive liver cirrhosis can benefit from practicing abstinence. Other therapies
include nutritional supplementation and medications, such as pentoxifyl-
line or steroids. Liver transplantation may greatly increase the chance of
survival in some patients (table 5.2).
Table 5.2. Therapy for Alcoholic Liver Disease
Treatment Comments
Alcohol abstinence Survival is greatly increased in patients with liver cirrhosis
and alcoholic liver disease.
Nutritional supplements Many alcoholics get almost half of their daily calories
from alcohol and experience severe vitamin and
nutritional deficiencies including thiamine deficiency.
Pentoxifylline May be beneficial in some patients
Prednisone May be beneficial in some patients
Antioxidant therapy Therapy with antioxidant including vitamin E
Liver transplant Patient must be alcohol free for a specified time prior
to transplant. This is a very effective way of treating
alcoholic liver cirrhosis with about 70 percent survival
after five years. In contrast, patients with severe forms
of alcoholic liver disease, including cirrhosis, may die
in days or months.
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88 Chapter 5
Mechanism of Liver Damage by Alcohol

The mechanism for alcohol-induced liver disease is complex. While in
moderate drinkers alcohol is mostly metabolized by alcohol dehydroge-
nase in the liver, in alcoholics CYP2E1, a member of the cytochrome P-450
drug-metabolizing family of enzymes in the liver, becomes activated. In
this process free oxygen radicals are generated, causing oxidative damage
to liver cells. In addition, acetaldehyde—a toxic product of alcohol me-
tabolism if not removed quickly by further metabolism—may cause liver
toxicity. In alcoholics, the tremendous burden of alcohol on the liver for
metabolism causes both acetaldehyde and nicotinamide adenine dinucle-
otide hydrogen (NADH) to accumulate, leading to oxidative stress to the
liver and increased production of fatty acid. Metabolism of fatty acid is
also impaired, causing fatty acid buildup, which is eventually turned into
fat (triglycerides) by the liver. Fatty liver with more alcohol consumption
may proceed to liver cirrhosis.
Another mechanism of liver damage by alcohol is the excess cytokine
production by Kupffer cells of the liver due to the release of bacterial
endotoxin in the blood by the action of excess alcohol on bacteria present
in the gut. Excess cytokine can stimulate the inflammatory process, caus-
ing further liver damage. The mechanism of liver damage by alcohol is
schematically presented in figure 5.2.
HEAVY ALCOHOL CONSUMPTION,

DEPRESSION, AND BRAIN DAMAGE
Although alcohol can cause relaxation and mild euphoria with moder-
ate consumption, these pleasurable effects of alcohol are reversed when
blood alcohol levels go above 100 mg/dL (0.1 percent). Alcohol has more
damaging effects on the adolescent brain than the adult brain. The onset of
drinking at an early age (thirteen or earlier) has devastating effects on the
brain as well as on the life of the person, and such effects follow the person
throughout his or her life. Early onset of drinking is also linked to a greater
risk of alcohol dependence in adult life. Although thiamine deficiency is one
of the major factors involved in alcohol-related brain damage, both alcohol
and its toxic metabolite acetaldehyde have direct toxic effects on neurons
(brain cells). Please see chapter 3 for an in-depth discussion on this topic.
HEAVY ALCOHOL CONSUMPTION AND

RISK OF HEART DISEASE AND STROKE
As discussed in chapter 4, if consumed in moderation, alcohol can reduce

the risk of heart disease and stroke, but if consumed chronically in excess,
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Figure 5.2. Mechanism of alcohol-induced liver damage
it increases the risk of both heart disease and stroke. Drinking more than
three drinks per day (any type of alcoholic beverage) may be harmful to
the heart. Chronic alcohol abuse for several years may result in the fol-
lowing serious medical conditions:26
• Alcoholic cardiomyopathy and heart failure

• Systematic hypertension (high blood pressure)
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90 Chapter 5
• Heart rhythm disturbances

• Hemorrhagic stroke
Alcoholics who consume 90 gm or more of alcohol per day (seven to eight

drinks) for five years are at risk of developing alcoholic cardiomyopathy,
and if they continue drinking alcohol, cardiomyopathy may proceed to
heart failure, a potentially fatal medical condition. This distinct form of
heart failure (congestive heart failure) is responsible for 21–36 percent of all
cases of nonischemic heart failure. Without complete abstinence, 50 percent
of these patients will die from heart failure within four years of diagnosis.27
A stroke occurs when the blood supply in a particular part of the brain
is interrupted or decreased, depriving brain cells from the supply of glu-
cose (fuel for brain cells), oxygen, and essential nutrients. Within a few
minutes brain cells start dying, and if not treated soon, the stroke may
lead to severe brain damage, paralysis, or even death. Fortunately, there
are many excellent options for treating stroke today if the patient receives
prompt medical attention. Today fewer Americans die from stroke than
thirty or forty years ago. Controlling high blood pressure, abstinence
from tobacco, and lowering cholesterol can all reduce the risk of stroke.
Hemorrhage means “bleeding” and a hemorrhagic stroke occurs when a
blood vessel in the brain ruptures, causing interruption in the blood flow
to a part of the brain. A blood vessel may rupture from high blood pres-
sure or a weak spot in the blood vessel wall (aneurysm). Heavy drink-
ing increases the risk of stroke, but particularly the risk of hemorrhagic
stroke. Ikehara et al. (2009) observed that the risk of hemorrhagic stroke
increases in an individual drinking 300 gm or more of alcohol weekly
(twenty-one or more drinks).28
HEAVY ALCOHOL CONSUMPTION AND

DAMAGE TO THE IMMUNE SYSTEM
Alcohol abuse is associated with increased risk of bacterial infections and

opportunistic infections (including viral infections). The increased risk of
infection in alcohol abusers is due to the impairment of the immune system
by alcohol. Exposure to alcohol can result in reduced cytokine production.
Mast cells are important immune cells that are widely distributed in tissues
that are in contact with the external environment, such as skin and the mu-
cosa of the lung and the gastrointestinal tract. Mast cells produce a variety
of compounds, including cytokines, histamine, eicosanoid, and TNF-␣ (tu-
mor narcosis factor-alpha), that play important roles in the defense against
bacteria and parasites. Therefore, mast cells are considered the first line of
defense against invading bacteria and parasites. Alcohol reduces the vi-
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ability of mast cells and may cause cell death. Alcohol-induced reduction of
the viability of mast cells could contribute to the impaired immune system
function associated with alcohol abuse.29 Alcohol also accelerates disease
progression in patients with HIV infection because of immunosuppression.
In one study using 231 patients with HIV infection who were undergoing
antiretroviral therapy, Baum et al. (2010) observed that even consumption
of two or more drinks daily can cause a serious decline in CD4+ cell count
(higher CD4+ counts indicates good response to therapy).30
Even two drinks a day may have serious consequences in the progres-
sion of HIV infection.
Adult respiratory distress syndrome (ARDS) is a severe form of lung

injury. Approximately 200,000 individuals develop ARDS in the United
States each year, and nearly 50 percent of these patients have a history of
alcohol abuse. The mortality from ARDS is high (more than 40 percent)
and for alcohol abusers approximately 65 percent. In ARDS survivors,
alcohol abuse was also associated with a longer stay under ventilation in
intensive care units. Alcohol impairs immune function and decreases the
level of pulmonary antioxidants and thus may cause ARDS.31
ALCOHOL ABUSE AND DAMAGE TO THE ENDOCRINE,

REPRODUCTIVE, AND SKELETAL SYSTEMS
Hormones are chemical messengers that control and coordinate the func-
tion of tissues and organs. Each hormone is secreted from a particular
gland and distributed throughout the body to carry out its physiological
function. The hypothalamus, located deep within the brain, is the control
center for most of the body’s hormonal system. The hypothalamus, the
pituitary gland (also located in the brain), and the adrenal glands (located
on the kidneys) function together as a well-coordinated unit, controlling
the hormonal balance of the body. The hypothalamus secretes cortico-
trophin-releasing factor, which through complex mechanisms stimulates
the adrenal glands to secrete glucocorticoid hormones, which influence
carbohydrate, lipid, protein, and nucleic acid metabolism, and play a
vital role in the cardiovascular system, bone development, and immune
function.
The major circulating glucocorticoid hormone in humans is cortisol.
Alcohol abuse may lead to a disease known as pseudo–Cushing’s syn-
drome, indistinguishable from Cushing’s syndrome, characterized by
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92 Chapter 5
excess production of cortisol, which causes high blood pressure, muscle

weakness, diabetes, obesity, and a variety of other physical disturbances.
Diminished sexual function in alcoholic men has been described for many
years. Administration of alcohol in healthy young male volunteers causes
diminished levels of testosterone. Even drinking three or more drinks a
day may cause significant problems in women, including delayed ovula-
tion or failure to ovulate and menstrual problems, but such problems do
not affect women who consume two or fewer drinks a day. This may be
related to alcohol-induced estrogen levels in women. Alcoholic women
often experience reproductive problems. However, these problems
may resolve when a woman practices abstinence from alcohol. To form
healthy bone calcium, phosphorus and the active form of vitamin D is es-
sential. Chronic consumption of alcohol may reduce bone mass through
a complex process of inhibition of the hormonal balance needed for bone
growth, including testosterone in men, which is diminished in alcohol-
ics. Alcohol abuse may also interfere with pancreatic secretion of insulin,
causing diabetes.32
ALCOHOL ABUSE AND

INCREASED RISK OF VARIOUS CANCERS
Although moderate drinking reduces the risk of certain cancers (see chap-
ter 4), chronic abuse of alcohol increases cancer risk. Cancer kills an esti-
mated 526,000 Americans annually, and ranks second only to heart dis-
ease. Cancers of the lung, large bowel, and breast are most common in the
United States, and approximately 2 to 4 percent of all cancer cases may
be linked to alcohol abuse. Epidemiological research has demonstrated a
dose-dependent relationship between consumption of alcohol and certain
types of cancers; as alcohol consumption increases, so does the risk of
cancer. The strongest link was found between alcohol abuse and cancer
of the mouth, pharynx, larynx, and esophagus. An estimated 75 percent
of all esophageal cancers are attributable to chronic alcohol abuse, while
nearly 50 percent of cancers of the mouth, pharynx, and larynx are as-
sociated with chronic heavy consumption of alcohol. Prolonged drinking
may result in alcoholic liver disease and cirrhosis of the liver, and such
diseases can progress to liver carcinoma (liver cancer). There are weak
links between alcohol abuse and cancer of the colon, stomach, lung, and
pancreatic cancer.33 Disease of the pancreas (pancreatitis) and gallstones
are common among alcohol abusers. In alcoholics, endotoxin may be re-
leased from gut bacteria and trigger progression of acute pancreatitis into
chronic pancreatitis. Chronic pancreatitis may lead to pancreatic cancer.34
Pancreatic cancer is related to a high mortality rate.
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Moderate alcohol consumption and the risk of breast cancer is debat-

able because there are conflicting reports in the medical literature. One
Spanish study of 762 women between the ages of eighteen and seventy-
five showed that even one drink a day may increase the risk of breast
cancer, and one and a half drinks or more per day results in a 70 percent
higher chance of developing breast cancer than nondrinkers.35 In contrast,
another study reported that women who consumed 10 to 12 gm of wine
per day (one glass of wine) had a lower risk of developing breast cancer
compared to nondrinkers. However, the risk of breast cancer increases in
women who drink more than one drink per day.36 Nagata et al. (based on
a review of eleven reports on the association between alcohol consump-
tion and the risk of breast cancer) concluded that epidemiological evi-
dence of the link between alcohol consumption and the risk of developing
breast cancer remains insufficient.37
In general, studies have shown that heavy drinking of more than 46–69
gm of alcohol per day (three and half drinks to five drinks) contributes
to the total cancer risk, especially among men who drink heavily.38 Vari-
ous factors may contribute to the development of alcohol-related cancer,
including the action of acetaldehyde, the toxic metabolite of alcohol. The
main liver enzymes involved in alcohol and acetaldehyde metabolism
are alcohol dehydrogenase and acetaldehyde dehydrogenase, which are
encoded by various genes. Because some of these genes demonstrate
polymorphism (a variant that may control enzymatic activities), in cer-
tain individuals, lower activity of acetaldehyde dehydrogenase may lead
to an accumulation of toxic acetaldehyde in the blood. Acetaldehyde is
carcinogenic (cancer-promoting) and can react with DNA to form cancer-
promoting compounds. In addition, the generation of reactive oxygen
free radicals when alcohol is metabolized by CYP2E1 liver enzyme can
also damage DNA, thus promoting cancer.39
ALCOHOL ADDICTION AND GENES
Research on alcohol addiction has indicated that genetics play some role
in the development of alcohol abuse, and it is not just the influence of
environment alone. Based on large well- characterized studies involving
twins, it has been established that alcoholism is a moderately inherited
psychiatric disorder, with children of alcoholic parents more prone to
alcohol abuse. The variation of gene coding that determines the activi-
ties of alcohol-metabolizing enzymes and genes that code for receptors
or transmitters of neurochemical pathways for action of alcohol on the
brain influence individuals’ response and susceptibility to alcohol con-
sumption.
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94 Chapter 5
Based on genetic variation, the liver enzymes alcohol dehydrogenase

(ADH) and acetaldehyde dehydrogenase (ALDH) can accelerate or slow
down the metabolism of alcohol. Acetaldehyde dehydrogenase exits in
two major forms, ALDH1 and ALDH2. Although both forms can con-
vert toxic acetaldehyde into acetate (which eventually breaks down into
carbon dioxide and water), ALDH2 is the major enzyme responsible for
the transformation of toxic acetaldehyde metabolite of alcohol. For both
ADH and ALDH enzymes, genetically determined variants (also called
isoforms) exist in their different levels of activity. People carrying differ-
ent ADH and ALDH isoforms metabolize alcohol at different rates. ADH
and ALDH isoforms arise from a natural variation (polymorphism) in the
structures of the genes that code these enzymes. Two alcohol dehydroge-
nase genes (ADH2 and ADH3) on chromosome 4 and one acetaldehyde
dehydrogenase gene (ALDH2) on chromosome 12 are known to exhibit
polymorphism, thus controlling the activities of both enzymes. The fre-
quency of these polymorphisms differs in different ethnic groups.
One of the best understood polymorphisms of alcohol-metabolizing
enzymes is associated with the ALDH2 enzyme. One ALDH2 isoform,
known as ALDH2*2, which is found in approximately 40 percent of
people of Far East Asian descent but rarely in Caucasians, is partially in-
active because of a specific mutation in the gene encoding this enzyme. In
people carrying the ALDH2*2 enzyme, even moderate alcohol consump-
tion results in acetaldehyde accumulation in the blood, because acetalde-
hyde is only slowly removed from the blood due to the less active form
of the enzyme. An elevated acetaldehyde level after drinking may lead to
unwanted reactions toward alcohol, such as flushing, nausea, and rapid
heartbeat, and thus deter people from drinking.
The high prevalence of alcohol abuse and alcohol dependence among
American Indians may also be mediated partly by genetic factors. Wall
et al. (2003) reported that American Indians who consumed more al-
cohol and were alcohol dependent had different polymorphism in the
ADH gene than non-alcohol-dependent subjects. This genetic difference
in alcohol dehydrogenase enzyme may be linked to alcohol dependence
in some American Indians.40 Interestingly, in some Asians genetic
polymorphism of acetaldehyde dehydrogenase enzyme may protect
them from alcohol abuse, while genetic polymorphism of alcohol de-
hydrogenase may make some American Indians more prone to alcohol
dependence.
Addiction to alcohol and drugs is related to brain function, and indi-
viduals who are addicted to alcohol may also be addicted to illicit drug
abuse. Research indicates that genes affecting the activity of the neu-
rotransmitter serotonin and gamma-aminobutyric acid (GABA) are likely
candidates to be involved in the genetic mechanism of alcohol depen-
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dence. In one study, the authors (Herman et al. 2003) found that Cauca-
sian college students with a particular variant of the serotonin transporter
gene (short variant S of the serotonin transporter promoter polymor-
phism) consumed more alcohol per occasion, drank more often to get
drunk, and also engaged in binge drinking more often than students with
another variant of the gene. A higher frequency of S homozygotes (both
parents contribute S variant, the other variant is long variant) is associ-
ated with adult alcoholics who exhibited an increased frequency of binge
drinking.41 Stacey et al. (2009) commented that heritability estimates for
alcoholism range from 50 to 60 percent, pointing out the importance of
both genetic and environmental factors in its etiology. Corticotropin-
releasing factor, glutamatergic and opioidergic systems, and the genes
regulating them may all play a role in the genetics of alcoholism.42
ALCOHOL REHABILITATION
Alcohol addiction is an illness that can be cured with proper treatment. The
most widely used definitions for alcohol use disorders are those determined
by the editions of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-IV) of the American Psychiatric Association and the International
Classification of Disease (ICD-10) of the World Health Organization (WHO).
Alcoholism treatments, as well as research studies on alcohol (including
epidemiological studies), all rely on these definitions. Currently DSM-IV
and ICD-10 criteria are widely used to determine alcohol dependence.
Alcoholism can be classified under two broad categories based on the
research of C. Robert Cloninger:
• Type 1. Less severe form with later onset of alcohol-related problems,

and the problems are more psychological than physical dependence
on alcohol. Children of type 1 alcoholism tend to develop type 1 alco-
holism in the later part of their lives but under strong environmental
influence may become type 2 alcoholics.
• Type 2. More severe form of alcoholism found most commonly in
men. The onset of alcohol dependence starts at an earlier age, and
these individuals show compulsive alcohol-seeking behavior and
are disruptive socially when drinking. Children of type 2 alcoholics
tend to be type 2 alcoholics, regardless of environment. Although
originally considered male limited, later research indicated that type
2 alcoholism may also be found in females.43
More than 700,000 Americans receive alcoholism treatment in a given

day. Self-help groups are the most commonly used source of help for
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96 Chapter 5
people suffering from alcohol-related problems. Alcoholics Anonymous

(AA), one of the most widely used self-help groups, outlines twelve con-
secutive steps that an alcohol-dependent person is encouraged to follow to
achieve continuous sobriety. There are also psychosocial treatments avail-
able for an alcohol-dependent person. These therapies include Motivational
Enhancement Therapy, Couples Therapy, Cognitive Behavioral Therapy,
and Motivational Interviewing. In addition, drug therapy can be initiated if
necessary to combat withdrawal symptoms from alcohol abuse.44
Currently there are three Federal Drug Administration (FDA)–
approved medications for treating alcohol dependence. The oldest one,
disulfiram (Antabuse), interferes with metabolism of alcohol by block-
ing the action of acetaldehyde dehydrogenase enzyme, resulting in the
accumulation of acetaldehyde. Therefore, a person undergoing alcohol
rehabilitation experiences unpleasant reactions, such as flushing, nausea,
and palpitation, if he or she drinks alcohol. Therefore, disulfiram deters
a person from drinking. This drug is given orally once a day. Naltrexone,
another drug used in treating alcohol dependence, blocks opiate receptors
that are involved in the rewarding effects of drinking alcohol. It is avail-
able in oral form (Depade, ReVia) to be taken once a day or in extended
release form (Vivitrol), which is given by injection once a month. Because
a person no longer gets the pleasurable effect from drinking, this medica-
tion acts as a deterrent. The third FDA-approved drug for treating alco-
holism is acamprosate (Campral), which acts on gamma-aminobutyric
acid (GABA) and glutamate neurotransmitter symptoms, and reduces
symptoms of protracted alcohol abstinence, including insomnia, anxiety,
restlessness, and dysphoria (unpleasant and uncomfortable mood). This
medication is given orally three times a day. Although not FDA-approved
for treating alcohol dependence, the anticonvulsant drug topiramate and
several new antidepressant agents, such as fluoxetine and ondansetron,
have been shown to increase abstinence rates and decrease drinking
among alcohol-dependent people.45
CONCLUSION
All beneficial effects of alcohol disappear if it is not consumed in modera-

tion. Interestingly, if consumed in moderation, alcohol reduces the risk
of heart disease, stroke, certain types of cancer, and even Alzheimer’s
disease, but if consumed in excess instead increases the risk of develop-
ing the same diseases. Moderate drinkers enjoy longer life, while alcohol
abuse shortens life. Chronic alcohol abuse for a longer period of time may
cause alcoholic hepatitis and even liver cirrhosis, which are potentially
fatal medical conditions. Alcoholism is part genetically controlled and
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part environmentally controlled. Fortunately, alcohol dependence is an

illness, and intervention and treatment can return an alcohol-dependent
person to a normal life again.
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30. M. K. Baum, C. Rafie, C. Lai, S. Sales, et al. “Alcohol Use Accelerates HIV
Disease Progression,” AIDS Research and Human Retroviruses 26, no. 5 (May 2010):
511–18.
31. D. M. Boe, R. W. Vandivier, E. L. Burnham, and M. Moss, “Alcohol Abuse
and Pulmonary Disease,” Journal of Leukocytes Biology 76, no. 5 (November 2009):
1097–1104.
32. N. Emanuele and M. A. Emanuele, “Alcohol Alters Critical Hormonal Bal-
ance,” Alcohol Health and Research World 21, no. 1 (1997): 53–64.
33. “Alcohol and Cancer,” Alcohol Alert No. 21, PH 345 (July 1993), National
Institute of Alcohol Abuse and Alcoholism.
34. M. Apte, R. Pirola, and J. Wilson, “New Insights into Alcoholic Pancreatitis
and Pancreatic Cancer,” Journal of Gastroenterology and Hepatology 24, no. 3, supple-
ment 3 (October 2009): S351–56.
35. J. M. Martin-Moreno, P. Boyle, L. Gorgojo, W. C. Willett, et al., “Alcoholic
Beverage Consumption and Risk of Breast Cancer in Spain,” Cancer Causes and
Control 4, no. 4 (July 1993): 345–53.
36. F. Bessaoud and J. P. Daures, “Pattern of Alcohol (Especially Wine) Con-
sumption and Breast Cancer Risk: A Case-Controlled Study among a Population
in Southern France,” Annals of Epidemiology 18, no. 6 (June 2008): 467–75.
37. C. Nagata, T. Mizoue, K. Tanaka, I. Tsuji, et al., “Alcohol Drinking and
Breast Cancer Risk: An Evaluation Based on a Systematic Review of Epidemiolog-
ical Evidence among the Japanese Population,” Japanese Journal of Clinical Oncology
37, no. 8 (August 2007): 568–74.
38. M. Inoue, K. Wakai, C. Nagata, T. Mizoue, et al., “Alcohol Drinking and
Total Cancer Risk: An Evaluation Based on a Systematic Review of Epidemiologi-
cal Evidence among the Japanese Population,” Japanese Journal of Clinical Oncology
37, no. 9 (September 2007): 692–700.
39. H. K. Seitz and P. Becker, “Alcohol Metabolism and Cancer Risk,” Alcohol
Research and Health 30, no. 1 (January 2007): 44–47.
40. T. L. Wall, L. G. Carr, and C. L. Ehlers, “Protective Association of Genetic
Variation in Alcohol Dehydrogenase with Alcohol Dependence in Native Ameri-
can Mission Indians,” American Journal of Psychiatry 160, no. 1 (January 2003):
41–46.
41. A. I. Herman, J. W. Philbeck, N. L. Vasilopoulos, and P. B. Depertrillo,
“Serotonin Transporter Promoter Polymorphism and Differences in Alcohol Con-
sumption Behavior in a College Student Population,” Alcohol and Alcoholism 38,
no. 5 (September–October 2003): 446–49.
42. D. Stacey, T. K. Clarke, and G. Schumann, “The Genetics of Alcoholism,”
Current Psychiatry Report 11, no. 5 (October 2009): 364–69.
43. A. Magnusson, M. Goransson, and M. Heilig, “Early Onset Alcohol Depen-
dence with High Density of Family History is Not ‘Male Limited,’” Alcohol 44, no.
2 (March 2010): 131–39.
44. “New Advances in Alcoholism Treatment,” Alcohol Alert No. 49 (October
2000), National Institute on Alcohol and Alcoholism.
45. J. C. Garbutt, “The State of Pharmacotherapy for the Treatment of Alcohol
Dependence,” Journal of Substance Abuse and Treatment 36, no. 1 (January 2009):
S15–23.
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10-649_Dasgupta.indb 100 1/17/11 6:40 AM
6

DWI and Alcohol Testing
Breath Analyzer versus Blood Alcohol
D rinking and driving do not mix at all. “Driving while impaired”

(DWI) and “driving under the influence” (DUI) are used inter-
changeably to describe impaired drivers. In chapter 2, detailed guidelines
have been provided regarding consumption of alcohol and estimated
blood alcohol levels based on gender and body weight. The objective of
this chapter is to reinforce the philosophy of drinking sensibly and drink-
ing in moderation.
Injury from motor vehicle crashes is the leading cause of death in the
United States among people ages one to thirty-four and approximately
40 percent of all traffic-related deaths involve alcohol. According to the
statistics released by the National Highway Traffic Safety Administration,
there were 16,694 deaths and 258,000 injuries from alcohol-related motor
vehicle crashes in 2004. The estimated annual economic cost of alcohol-
related crashes is $51 billion.1
Although injuries from alcohol-related crashes have declined over the
past two decades due to implementation of legal blood alcohol limits and
strict enforcement of DWI laws, alcohol-related fatalities from traffic ac-
cidents remained relatively stable in the last decade. In 2003 there were
17,041 alcohol-related fatalities in the United States that were attributed
in part to repeat DWI offenders.2 In 2007, nearly 13,000 alcohol-impaired
people were killed in driving accidents, and, as in 2003, many alcohol-
impaired drivers involved in fatal crashes were previously arrested for
driving while intoxicated. In 2007, drivers with a blood alcohol level ex-
ceeding the legal limit (0.08 percent or above) in fatal crashes were eight
101
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102 Chapter 6
times more likely to have a prior DWI conviction compared to drivers

with no alcohol in their blood.
According to the U.S. Department of Transportation and the National
Highway Traffic Safety Administration (NHTSA) reports, 1.46 million
drivers were arrested in the United States in 2006 for driving under the
influence of alcohol or narcotics.3 In 2008, 11,733 people were killed in
driving crashes caused by alcohol impairment, accounting for one-third
(32 percent) of all traffic-related deaths in the United States. Of the 216
child passengers ages fourteen and younger who died in driving crashes
caused by alcohol/drug impairment in 2008, 99 were riding in the vehicle
with an alcohol-impaired driver.
Although the number of deaths due to alcohol-related traffic crashes
was reduced from 2007 to 2008, alcohol-related crashes remained a major
cause of traffic fatalities. In 2008, 1.4 million drivers were arrested for
driving under the influence of alcohol or narcotics.4 However, one report
(Quinlan et al. 2005) estimated that the number of alcohol-impaired driv-
ers in the United States was 159 million annually based on surveys of self-
reported episodes of alcohol-impaired driving.5 Therefore, DWI arrests
represent only 1 percent of all drivers on the road who are driving after
consuming alcohol.
Despite continued efforts from law enforcement, deaths caused by

alcohol-impaired driving take an enormous toll in the United States:
approximately one person every forty minutes or thirty-two people a
day.
Incidents of alcohol-impaired driving increase during holidays such as

Christmas and New Year’s. On average, from 2001 to 2005, about 40 per-
cent of all fatalities during the Christmas and New Year’s holidays in the
United States have occurred in crashes where at least one of the involved
drivers was impaired due to consumption of alcohol. Compare that to
approximately 28 percent of all fatalities during the rest of December and
31 percent during the entire year being alcohol related. During 2001–2005,
the average number of fatalities per day during New Year’s was fifty-four
and during Christmas was forty-five, and both numbers were signifi-
cantly higher than the average fatality rate of thirty-three per day during
the rest of December.6
In general, alcohol involvement in fatal crashes in 2007 was more than
three times higher at night (6 pm to 6 am) than during the day (6 am to 6
pm), with 62 percent of crashes involving alcohol at night versus 19 per-
cent of crashes involving alcohol during the day. Alcohol involvement in
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DWI and Alcohol Testing 103
fatal crashes was also higher (54 percent) on the weekend compared to
weekdays (35 percent). In addition, nearly one in four drivers (23 percent)
of a personal vehicle and more than one in four motorcyclists (27 percent)
involved in fatal crashes were intoxicated with a blood alcohol level of
0.08 percent or higher. The drivers between twenty-one and thirty-two
years of age had the highest proportion of drivers with blood alcohol
levels over the legal limit, followed by drivers between twenty-five and
thirty-four. Elderly drivers (seventy-five or older) showed the smallest
percentage (only 4 percent) of driving over the legal limit. Interestingly,
only 1 percent of drivers of commercial vehicles (heavy trucks) had blood
alcohol concentrations over the legal limit.7
One of the major problems of alcohol-impaired driving is the habit of
binge drinking, which is defined as consuming more than five drinks in
one episode by a man or four or more drinks by a woman (see chapter 2).
Based on a survey of 14,085 adults, Naimi et al. (2009) reported that overall
11.9 percent of binge drinkers drove during or within two hours of their
most recent binge episode. Those drinking in licensed establishments (bars,
clubs, or restaurants) consumed an average of 8.1 drinks, and 25.7 percent
of them consumed more than ten drinks.8 These episodes are considered
heavy drinking and certainly cause serious impairment in a driver.
Consuming two standard drinks by a man and one standard drink by

a woman in one episode is considered moderate drinking, and after
such moderate consumption of alcohol driving is safe within an hour,
because blood alcohol level would be well below the legal limit of
driving. A man weighing 175 pounds or more can safely consume
three standard drinks with food and wait for at least two hours before
driving. A woman weighing 125 pounds or more can safely consume
two standard drinks with food and wait for two hours before driving.
Binge drinking may produce a blood alcohol level that is two to three
times higher than the legal limit for driving, and if the driver is stopped
by the police, it would certainly result in a DWI charge.
The legal drinking age in the United States is twenty-one, and there is
a sizable amount of literature on the effect of minimum drinking age re-
strictions on teenage drunk driving. The effect of lowering the minimum
drinking age, as has been proposed in Vermont, could lead to sizable
increases in teenage involvement in fatal accidents due to the evasion of
local alcohol restrictions.9 In addition to the legal drinking age of twenty-
one, most states have a zero-tolerance policy for underage drinking. The
role of age (youth and driving inexperience) and alcohol as major risk
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104 Chapter 6
factors for traffic accidents has been firmly established by numerous stud-
ies over the last fifty years. Some investigators have hypothesized that
there is a synergistic effect in which young drivers with less experience
and a greater tendency to take risks are more adversely affected at lower
blood alcohol concentrations compared to older, more experienced driv-
ers. Peck et al. (2008) demonstrated that positive blood alcohol in drivers
younger than twenty-one is associated with a higher relative crash risk
than would be predicted from the added effect of blood alcohol level and
age. In addition, crash-avoidance skills of young drivers are adversely af-
fected by alcohol. These results support a zero-tolerance policy for blood
alcohol level laws for minors.10
Parents and other adults also have the responsibility of influencing the
attitude of younger drivers about drinking. A study by Leadbeater et al.
(2008) found that young drivers’ risk behaviors were associated indepen-
dently with their own experiences of riding with adults and peers who
drove while under the influence of drugs and/or alcohol. The authors
concluded that prevention efforts for youth drinking and driving should
be expanded to include the adults and peers who are role models for
new drivers, and that awareness should be raised concerning their own
responsibility of not drinking and driving for their own personal safety
and the safety of others.11 Social host laws for minors aim to reduce alco-
hol consumption by imposing liability on adults who host parties. These
laws have an impact on reducing alcohol-related traffic accidents. One
study reported that among those who were eighteen to twenty, social
host liability for minors reduced the drunken driving rate by 9 percent.12
In addition to fatalities from traffic accidents, alcohol-related traffic ac-
cidents and injuries are a major public health and public safety concern.
Rosen et al. (2008) reported that alcohol consumption in California led to
an estimated 9,439 deaths and 921,029 cases of alcohol-related problems,
such as crime and injury, in 2005.13 Alcohol intoxication may confound
the initial assessment of trauma patients, even minimally injured patients,
resulting in more diagnostic and therapeutic procedures, thus increasing
the cost of care. The Uniform Policy Provision Law, which permits insur-
ance providers to deny coverage for medical treatment due to alcohol-
related injuries, exists in many states. In one report (O’Keefe et al. 2009),
the authors demonstrated that of the patients admitted to the emergency
room with similar injuries, those individuals with a positive blood alcohol
level required more procedures, such as intubation, cauterization, and so
on, at an average cost of $1,833 more than similar patients with no alcohol
in their blood. In addition, a significant amount of trauma center costs are
primarily attributable to alcohol use by patients.14
Fortunately, alcohol-related traffic fatalities are on the decline thanks to
tough DWI implementation, public education, and other prevention pro-
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grams. Mothers Against Drunk Driving (MADD), which was established

in 1980, is considered one of the most successful public health citizen
advocacy organizations in the United States. This group has been given
credit for changing the attitude of Americans regarding drinking and
driving. Alcohol-related traffic deaths in the United States declined from
an estimated 30,000 in 1980 to 16,694 in 2004, partly due to the public’s
understanding of the perils of alcohol-impaired driving.15
LEGAL BLOOD ALCOHOL POLICY IN THE

UNITED STATES AND OTHER COUNTRIES
If you are stopped by the police on suspicion that you are driving while
under the influence of alcohol or drugs, the officer first conducts a field
sobriety test and, based on his or her judgment, may ask you to take a
breath alcohol test, submit a urine specimen for drug testing, or give a
blood specimen for alcohol testing. If you have a choice, always agree to
submit to a blood alcohol test. The blood is drawn in a detention center
or a health care facility, and the blood alcohol test is more accurate than
the breath alcohol test. However, depending on the state and county, you
may not have the option of a blood alcohol test and will need to agree to
a breath alcohol test.
The officer may or may not carry an evidentiary breath analyzer
where the results produced by such analyzers can be admitted to a court
of law as evidence. If the officer uses a breath analyzer for screening
purposes, you may have to go to a police station where breath analysis
is performed by a qualified person using an evidentiary breath ana-
lyzer. For this purpose, an officer may observe you for fifteen minutes
and then ask you to blow into a disposable mouthpiece for five to ten
seconds, and when enough exhaled air is collected, the instrument usu-
ally produces a buzzing noise. Before performing the test, the officer
may perform a blank test to ensure the instrument is working properly.
Then a second test may be performed to ensure validity of the test re-
sults, and, based on the results, you may be charged with DWI and your
driver’s license may be taken.
Usually you have the right to go for an administrative hearing to get
your license back prior to trial. If you are found guilty and have a very
high blood alcohol level, such as 0.15 percent or 0.2 percent, you may
need to put an ignition lock device in your car at your own expense.
This ignition lock device does not allow you to start a car if you have
any alcohol in your blood (usually 0.02 percent or 0.01 percent). The
best policy is to have a designated driver or drink in moderation so that
your blood alcohol is half of the legal limit for driving (see later in this
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106 Chapter 6
chapter for details). Many states also have open container laws where
it is illegal to have an open bottle of an alcoholic beverage in the car,
regardless of whether the driver or the passenger is drinking while the
car is in motion.
Since 2002, the legal limit for driving in the United States in all states
is 0.08 percent blood alcohol concentration (BAC), which is equivalent
to 80 mg of ethyl alcohol in 100 mL of blood. This is more conveniently
expressed as 80 mg/dL. Although DWI conviction is based on BAC,
a BAC at or over the legal limit can be established by indirect means,
such as by using a breath analyzer, which indirectly estimates blood
alcohol by measuring alcohol concentration in the exhaled air. License
suspension or revocation traditionally takes place after a DWI convic-
tion. Under a procedure called “Administrative License Suspension,”
the license may be taken before a conviction if a driver fails or refuses
to take a breath analyzer test or a similar test to determine the blood
alcohol level.
Justification of 0.08 percent BAC Limit

The legal limit for blood alcohol is the amount of alcohol in the whole
blood that is drawn directly from an individual by puncturing a vein
on the arm. Whole blood alcohol is also commonly referred to as le-
gal blood alcohol. Sometimes the alcohol level is not determined in a
laboratory directly on the whole blood but may be determined in serum
or plasma. When a whole blood specimen is drawn, after clotting, the
blood cells settle at the bottom, leaving a yellowish liquid at the top,
which is the water component of blood, or serum. If an anticoagulant
is used, such as heparin, citrate, or ethylenediaminetetraacetic acid
(EDTA) in the blood collection tube, upon centrifugation the aqueous
(water) part of the blood is separated from the blood cells; the aqueous
layer is called plasma. If an anticoagulant is not used in the blood collec-
tion tube, the serum can also be separated from the cellular components
by centrifugation. Alcohol determined in serum or plasma is higher
than whole blood alcohol. Therefore, it is important to establish how the
alcohol level was determined in the blood (whole blood versus serum)
during a DWI trial (this is covered more thoroughly later in this chap-
ter). For our purposes here, BAC represents alcohol content in whole
blood (legal blood).
Scientific research has indicated that drivers with a BAC between 0.05
and 0.08 percent are twice as likely to have accidents as drivers with no
alcohol in their blood. Drivers with BAC from 0.1 percent to 0.14 percent
are ten times more likely to have accidents than nondrinkers. There is a
10-649_Dasgupta.indb 106 1/17/11 6:40 AM

general agreement that BAC of about 0.05 percent results in some impair-
ment of the ability to drive. Initially the legal BAC in the United States
was 0.1 percent, but it was lowered to 0.08 percent in 1998 when President
Clinton directed the secretary of transportation to work with Congress,
state agencies, and other concerned safety groups to promote the adop-
tion of 0.08 percent BAC nationwide.
In 1998, as part of the Transportation Equity Act for the 21st Century
(TEA-21), a new federal program was created to encourage states to adopt
0.08 percent BAC as the legal limit of driving. Fourteen independent
studies in the United States indicated that lowering the legal limit of BAC
from 0.1 percent to 0.08 percent has resulted in a 5 to 16 percent reduction
in alcohol-related crashes, fatalities, or injuries. Legal BAC is 0.05 percent
in numerous countries, and several studies indicate that lowering BAC
from 0.08 percent to 0.05 percent also reduces alcohol-related fatalities to
some extent.16
Legal Limit of Blood Alcohol in Various Countries

The United States, Mexico, and some other countries have a legal BAC
of 0.08 percent, but several countries in the world have a zero-tolerance
policy of blood alcohol, meaning it is illegal to drive with any detectable
alcohol in the blood. In addition, several countries in the world have a
0.02 percent and 0.03 percent BAC limit, while others have a limit of 0.05
percent BAC for driving (table 6.1). In fact, to my knowledge, 0.08 percent
BAC is the highest acceptable legal limit for driving in any country, and
in this light, a 0.08 percent limit of BAC as the legal limit of driving in the
United States can be considered very fair and generous.
Table 6.1. Legal Limits for Driving in Various Countries in the World by Blood
Alcohol Concentration (BAC) Percentage
Blood Alcohol
Concentration (BAC) % Countries
0.08 United States, Mexico, United Kingdom, New Zealand,
Ireland, Malta
0.05 Austria, Belgium, Bulgaria, Costa Rica, Denmark, Finland,
Greece, Hong Kong, Israel, Peru, Portugal, Serbia, Spain,
Switzerland, Thailand, Turkey
0.03 India, Japan, Russia
0.02 China, Poland, Norway, Sweden, Estonia
Zero tolerance Saudi Arabia, United Arab Emirates, Brazil, Bangladesh,
Hungary, Czech Republic
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108 Chapter 6
A BAC of 0.08 percent is the highest acceptable legal limit for driv-
ing in a few countries in the world, including the United States. Many
countries have a 0.05 percent BAC as the highest legal limit for driving.
DIFFERENT BIOLOGICAL MATRICES OF MEASURING ALCOHOL
For medical purposes, such as in the emergency room, alcohol is usually

measured in serum or plasma and is referred to as “medical alcohol.”
Legal blood alcohol may be measured in whole blood or in serum/
plasma. Although medical alcohol may be used in the prosecution of a
DWI trial at the discretion of the judge, there are some differences be-
tween medical and legal alcohol. Breath alcohol measurement is usually
performed by police officers in a suspected impaired driver. In addi-
tion, alcohol can be measured in the urine, but determination of alcohol
levels in urine specimens is less common than blood alcohol testing
or breath alcohol analysis. Alcohol determination in a urine specimen
may be employed in a workplace alcohol and drug testing program (see
chapter 9).
Alcohol level can also be determined in saliva, also called “oral fluid.”
In general, alcohol concentration in saliva is slightly higher than in blood.
In a study of forty-eight male volunteers, researchers demonstrated that
saliva/blood alcohol ratio was 1.082. The saliva/blood alcohol ratio was
remarkably constant throughout the absorption, distribution, and elimi-
nation of alcohol from the body, and the saliva alcohol level also reached
zero when the blood alcohol level was undetectable. Because saliva alco-
hol reflects blood alcohol level, saliva alcohol can be used as supportive
evidence in legal cases involving alcohol intoxication.17
Nevertheless, saliva alcohol measurement is less common than breath
alcohol measurement or blood alcohol measurement in determining in-
toxication in a suspected individual. In addition, saliva alcohol measure-
ment is rarely used in medical settings despite commercial availability of
saliva-collecting devices and analytical methods for measuring alcohol
concentration in a saliva specimen. Interestingly, in many European
countries saliva drug testing is employed to identify a driver suspected
of driving under the influence of illicit drugs, and there are established
guidelines for cutoff levels of various drugs in saliva specimens. How-
ever, saliva testing of alcohol is rarely performed to identify a driver driv-
ing under the influence of alcohol.
Drug testing in hair specimens is gaining popularity and is used in legal
settings. Drugs stay in hair much longer than in urine. However, alcohol
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is a small molecule that is readily soluble in water and is not deposited in

hair. Metabolites of alcohol, such as ethyl sulfate and ethyl glucuronide,
are trapped in hair and can be analyzed to determine whether an indi-
vidual is abusing alcohol (see chapter 7 for more detail).
Breath Alcohol Analysis

A very small amount of alcohol is found in human breath. Only air in the
deepest portion of the lung, known as alveolar sacs, comes in contact with
the alcohol found in blood, and there is equilibrium between the alcohol
level in the exhaled air and blood alcohol. The estimated ratio between
breath alcohol and blood alcohol is 2100:1, and this ratio is utilized in vari-
ous breath alcohol analyzers to calculate blood alcohol level based on the
concentration of ethanol in exhaled air. This process is based on Henry’s
law, which states that the ratio between alcohol in blood and alcohol in
deep lung air is constant. After measuring the concentration of alcohol in
the exhaled air, the microprocessor of the instrument automatically con-
verts the value to a calculated blood alcohol level.
Breath alcohol analysis was first developed in the 1950s, at a time when
the understanding of pulmonary physiology was limited. Over the past
fifty years, the research has revealed that the mechanism by which air
in breath comes into contact with alcohol in the lungs is very complex.
Alcohol is exchanged with the airway via diffusion from the bronchial
tubes. Therefore, depending on the breathing pattern, variation in breath
alcohol content may occur.18 Because of this complex mechanism of ex-
change of alcohol from blood to exhaled air and individual variation in
the ratio of alcohol between breath and blood, as well as interferences,
legal challenges can be made at a court of law if breath alcohol value is
just above the cutoff of the legal limit. In contrast, blood alcohol levels are
more difficult to challenge during DWI defense because they are subject
to no interferences if measured by using gas chromatography (GC), even
if the value is just above the legal limit for driving.
Blood alcohol measurement is a direct measurement and there are
established guidelines for assessing degree of impairment of an indi-
vidual based on BAC and drinking history. In contrast, breath alcohol
measurement is an indirect measurement but is considered a reason-
able estimate of blood alcohol using a noninvasive technique with an
assumption that an exhaled breath sample accurately reflects the al-
veolar air alcohol concentration, which is assumed to be in equilibrium
with blood in pulmonary circulation. Despite considerable research in
this field, forensic toxicologists still have only a very basic understand-
ing of the physiological basis of breath alcohol analysis and associated
limitations.19
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110 Chapter 6
How Breath Analyzers Work

The earliest developed breath analyzer was based on a chemical principle
in which exhaled air was allowed to pass through a cocktail of chemicals
containing sulfuric acid, potassium dichromate, silver nitrate, and water.
Silver nitrate acts as a chemical catalyst in the reaction (a catalyst remains
unchanged after a chemical reaction) where alcohol in the presence of
sulfuric acid (sulfuric acid absorbs alcohol from air and also provides
an acidic medium for facilitating the reaction) turns orange potassium
dichromate solution into green due to the conversion of potassium di-
chromate into chromium sulfate, which is green in color. The intensity of
the green color can be used to estimate the amount of alcohol in the ex-
haled air. Captain Robert Borkenstein of the Indiana State Police used this
chemical principle to develop breath analyzers in 1954, and some breath
alcohol analyzers still use this principle today.20 In general, breath alcohol
analyzers work on any of the following mechanisms:
• Analyzers that utilize color change due to a chemical reaction to

determine alcohol level
• Analyzers based on detecting ethanol in breath based on infrared
spectroscopy
• Analyzers based on fuel cell technology
• Analyzers based on mixed technology (infrared and fuel cell) and
other techniques.
Breath analyzers can be further classified into screening devices and

evidentiary breath analyzers. Screen breath analyzers can be used by a
police officer for screening a suspected alcohol-impaired driver, but for the
purpose of prosecution, a result obtained by an evidentiary breath analyzer
approved by the U.S. Department of Transportation (DOT) must be used.
Evidentiary breath analyzers are more expensive and more accurate, and
results obtained correlate well with blood alcohol values. In addition, to en-
sure proper function of such analyzers, regular calibration against known
alcohol standards are performed, and other preventive maintenances are
carried out at regular intervals. Breath analyzers, which are small pocket-
sized devices, are also available for consumers. These devices are helpful to
determine an individual’s alcohol level before driving so that a person may
decide not to drive after a party; or if you think your teenager is drinking,
the breath analyzer result can be used to verify your suspicion.
Breathalyzer (Analyzers Based on Color Change Due

to a Chemical Reaction with Alcohol)
Breathalyzer is the oldest technology of breath alcohol analyzer and is
based on the principle of color change of potassium dichromate solution
10-649_Dasgupta.indb 110 1/17/11 6:40 AM

in the presence of alcohol (as described earlier) and then analysis by us-
ing spectroscopy after a specified time to ensure complete reaction. The
analyzer contains two vials of a chemical cocktail. After a subject exhales
into the device, the air is passed through one vial, and if alcohol is pres-
ent in the exhale, a color change occurs. A system of photocells connected
to a meter to measure color change associated with the chemical reaction
by comparing the response from the second vial (where no air is passed
through) produces an electrical signal proportional to the color change in
the reaction vial. This electrical signal can move the meter (more alcohol,
more signal and a higher reading), and alcohol level in the subject can be
determined. Breathalyzer was the brand name originally developed and
marketed by Smith and Wesson, and the company then sold that brand to
a German company called Draeger. The old Breathalyzer 900 model was
replaced by newer versions, such as model 1100, but this technology is
subject to interferences from a variety of substances, and because of that,
other companies have focused on developing more robust technology for
breath alcohol analysis.
Analyzers Based on Infrared Spectroscopy

There are several evidentiary breath alcohol analyzers that are based on
the principle of infrared spectroscopy (IR spectroscopy) for quantitative
determination of alcohol (ethanol) in exhaled air. The Intoxilyzer was
originally developed by Omicron in Palo Alto, California, and later sold
to CMI, Inc., in Owensboro, Kentucky. The earlier models were 4011A
and 4011S, and then the Intoxilyzer 5000 was developed, which is used as
an evidentiary breath alcohol analyzer, and, more recently, the Intoxilyzer
8000 model was introduced, which is now commercially available. Many
states use this analyzer as their evidentiary breath analyzer. In addition
to Intoxilyzer, DataMaster cdm (National Patent Analytical System, Man-
sfield, Ohio), which is also used in many states as the evidentiary breath
alcohol analyzer, is based on IR spectrum technology.
The IR spectrum of a specimen is produced by passing a beam of infra-
red light through the specimen and then recording the transmitted light.
A spectrum is formed when a particular wavelength of infrared light is
absorbed by the specimen. This takes place when the frequency of the IR
is the same as the frequency of a particular chemical bond in the molecule,
absorption occurs, and the chemical bond vibrates due to the absorption
of the energy. If a compound has multiple different bonds, absorption at
multiple wavelengths should be observed.
In a more advanced version of IR spectroscopy, Fourier Transform IR
spectroscopy, the instrument can measure all wavelengths at once and
then perform a very complex technique of background correction to
produce the IR spectrum. IR spectrum is like a picture of the molecule,
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112 Chapter 6
indicating different chemical bonds that join various atoms together

to produce the molecule, but it is unable to show atomic structures be-
cause energy is not sufficient to excite electrons in an atom. Infrared has
less energy than the visible region of the electromagnetic spectra, and
wavelengths of infrared are much longer than the wavelengths of the
electromagnetic spectra we see visually (light and color). The infrared
beam used for obtaining IR spectra of various organic compounds has a
wavelength range between 1,500 to 16,000 nm (1.5 to 15 microns).
Alcohol breath analyzers that operate on the IR spectroscopic prin-
ciple utilize the “Lambert-Beer Law,” which states that the amount of
electromagnetic radiation absorbed depends on the concentration of the
active component that absorbs in that particular wavelength. Therefore,
the amount of infrared radiation absorbed is proportional to the concen-
tration of the alcohol in the breath; when more alcohol is present, more
absorption of the infrared radiation is absorbed.
The newer version of Intoxilyzer (Intoxilyzer 5000) uses a five-
wavelength filter at 3.36, 3.4, 3.47, 3.52, and 3.8 microns and can thus dif-
ferentiate between ethanol and common interferences in exhaled air, such
as acetone, acetaldehyde, and toluene. The 3.4 micron wavelength is used
to detect alcohol, the 3.47 wavelengths identify interfering substances,
and the 3.8 micron is used as the reference wavelength. The latest model,
Intoxilyzer 8000, uses a pulsed IR source instead of a moving wavelength
filter, and uses a dual wavelength for measuring alcohol (3.4 and 9.36
micron) in the breath. It also has more advanced computer technology
to accurately provide alcohol level results. Razatos et al. (2005) evaluated
the performance of both Intoxilyzer 5000 and 8000 by comparing results
obtained by these instruments and direct analysis of alcohol using blood
from the same subjects. Based on analysis of 700 specimens, both analyz-
ers demonstrated good comparison with direct blood alcohol determina-
tions. Based on their study, Intoxilyzer 8000 was approved as an eviden-
tiary breath alcohol analyzer in the state of New Mexico.21
However, another report (Hardings et al. 1990) based on comparison of
blood alcohol determined directly and blood alcohol determination based
on breath alcohol analysis using 395 pairs of specimens indicated that in
general, the Intoxylizer 5000 reported values 10 mg/dL less than blood
alcohol most of the time, and in only 2 percent of the cases reported an al-
cohol value that was higher than the true blood alcohol level determined
directly. The range of blood alcohol values determined directly ranged
from zero to 338 mg/dL, while blood alcohol level estimates based on the
Intoxylizer 5000 ranged from zero to 320 mg/dL.22
DataMaster cdm, an evidentiary breath analyzer widely used by police
officers in many states, is also based on the principle of IR spectra, where
alcohol is detected using two different wavelengths (3.37 and 3.44 mi-
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crons). Kechagias et al. (1999) compared blood alcohol values with values
obtained by a breath alcohol analyzer (DataMaster) in patients suffering
from gastroesophageal reflux disease (GERD) and concluded that breath
alcohol analyzers can overestimate true blood alcohol value due to the
eruption of alcohol from the stomach to the mouth from gastric reflux.23
Analyzers Based on Fuel Cell Technology

There are several different brands of evidentiary breath alcohol analyzers
that are based on the principle of fuel cell technology, such as Alcotest
Models 6510, 6810, 7410, and so on (National Draeger, Durango, Colo-
rado), and Alco-Sensor III and IV (Intoximeters, Inc., St. Louis, Missouri),
which are evidentiary breath analyzers. The fuel cell is a porous disk
coated with platinum oxide (also called platinum black) on both sides.
The porous layer is impregnated with an acidic solution containing vari-
ous salts (electrolytes) so that charged particles such as hydrogen ions can
travel through that medium. In addition, both sides of the disk containing
platinum oxide are connected through a platinum wire. The manufacturer
mounts this fuel cell in a case along with the entire assembly so that when
a person blows into the disposable mouthpiece, the air can travel through
the fuel cell. If any alcohol is present in the exhaled air, then the alcohol is
converted into acetic acid, hydrogen ion, and electrons on the top surface
by the platinum oxide. Then hydrogen ions travel to the bottom surface
(also containing platinum oxide) and are converted into water by combin-
ing with oxygen present in the air. In this process, electrons are removed
from the platinum oxide. Because there is an electron excess on the top
surface and electron deficit on the bottom surface, electrons flow from
one surface to another, generating an electric current (the electric current
is the flow of electrons through the wire) that flows through the platinum
wire, with the intensity of the current being proportional to the amount of
alcohol present in the exhaled air. The microprocessor of the instrument
then converts that current to equivalent blood alcohol.
Some evidentiary breath analyzers are based on both fuel cell and infra-
red spectroscopy technology, giving them good sensitivity and specificity
to analyze alcohol on breath. Various models of the Intox EC/IRl desktop
evidentiary alcohol breath analyzers, also manufactured by Intoximeters,
Inc., combine reliable fuel cell analysis with real-time analytical advan-
tages of infrared technology.
Interferences in Measuring Alcohol Using Various Breath Analyzers

As mentioned before, blood alcohol determination is more accurate than
breath alcohol analysis because substances with structural similarity with
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114 Chapter 6
ethanol (alcohol) may be falsely identified as alcohol. This phenomenon,

where a compound is falsely identified as the target compound, is called
“interference,” and the substance that causes this false identification is
called an “interfering substance.” Because false identification of another
compound as alcohol has grave legal consequences, readers should be
aware of such problems. If you think you are wrongly accused of DWI
based on a false reading from an evidentiary breath analyzer, please
contact an experienced DWI attorney in your area. There are legal books
on the market that discuss this topic in detail, and an attorney special-
izing in DWI defense is very familiar with this situation. In general, if
the breath analyzer results (based on two readings after fifteen minutes
with each reading correlating very well) are just above the 0.08 percent
level, it is possible that an interfering substance may have skewed the
results. However, research indicates that when alcohol levels are sig-
nificantly above the legal limit (such as two to three times higher), the
effect of interfering substances may be insignificant. Again: do not drink
and drive.
Partition Ratio
Unlike blood alcohol determination, which is a direct measurement of the
alcohol level in a blood specimen, a breath alcohol analyzer uses a 2100:1
partition ratio between the breath alcohol level and the blood alcohol
level based on Henry’s law to calculate blood alcohol from breath alcohol.
It is assumed that 2,100 mL of breath contains the same amount of alcohol
as 1 mL blood, therefore 210,000 mL (210 liters) of breath contains the
same amount of alcohol as 100 mL (1dL) of blood. Therefore, if the breath
measures 80 mg of alcohol in 210 liters of breath, it is translated to 80 mg
of alcohol in 100 mL of blood or 0.08 percent blood alcohol.
Although this ratio of 2100:1 is a very conservative estimate and
valid for most people, variation from this partition ratio has also been
reported in medical journals. Jones and Anderson (2003) reported that
the average ratio between breath and blood alcohol levels was 2448:1,
but varied widely, between 1836:1 and 4082:1. The median value (mid-
point in the distribution) was 2351:1. Therefore, for an individual with a
ratio below 2100:1, a breath alcohol analyzer would overestimate blood
alcohol level, and for an individual with a breath-to-blood alcohol ratio
greater than 2100:1, a breath alcohol analyzer would underestimate the
true blood alcohol level. The authors concluded that breath test results
obtained with the Intoxilyzer 5000S model were generally lower than the
blood alcohol level, which gives an advantage to a suspect who provides
breath compared to blood in cases close to a legal cutoff alcohol level of
0.08 percent.24
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Mouthwash, Acetone, Propyl Alcohol, and Methanol

Sometimes a driver stopped by the police may use mouthwash to hide
any alcoholic breath. Because most mouthwash contains alcohol, use of a
mouthwash prior to taking a breath alcohol analysis may cause a falsely
elevated alcohol result. However, residual alcohol evaporates from the
mouth rapidly, and this is the reason for waiting for fifteen minutes in a
police station under supervision so that the suspect cannot take anything
by his or her mouth during the waiting period. Fessler et al. (2008) studied
the effect of alcohol-based substances such as mouthwash, cough mix-
ture, and breath spray just prior to breath alcohol measurement using the
Draeger evidentiary portable breath alcohol analyzer with twenty-five
volunteers and concluded that a fifteen-minute waiting period is neces-
sary to ensure that there is no residual alcohol in the mouth following us-
ing mouthwash and other alcohol-containing products. Otherwise mouth
alcohol interference in breath alcohol analysis may occur.25
Drinking an energy drink while driving a car is not against the law, but
some energy drinks contain very low levels of alcohol. When volunteers
drank various energy drinks, eleven out of twenty-seven drinks gave pos-
itive results using evidentiary breath analyzers when testing was done
just after drinking. However, after a fifteen-minute waiting period, all
breath alcohol analysis reports were negative. The authors concluded that
a fifteen-minute waiting period eliminates the possibility of testing false
positive after consuming an energy drink with a low alcohol content.26
Laakso et al. (2004) studied the effect of various volatile solvents for
potential interference with breath alcohol analysis using the Draeger 7110
evidentiary breath analyzer and concluded that acetone, methyl ethyl
ketone, methyl isobutyl ketone, ethyl acetate, and diethyl ether do not
influence breath alcohol measurement significantly, but propyl alcohol
and isopropyl alcohol have a significant effect on breath alcohol mea-
surement.27 Isopropyl alcohol is rubbing alcohol. If an individual abuses
isopropyl alcohol, the person may produce a false positive ethanol result
using an evidentiary breath analyzer. Jones and Rossner (2007) described
a case where a fifty-nine-year-old man undergoing a weight-loss program
using a ketogenic diet attempted to drive a car that was fitted with an
alcohol ignition interlock device, and the vehicle would not start. Because
he had completely stopped drinking, he was surprised and upset. Ke-
togenic diets used for treating obesity and controlling seizures in some
epileptic children are high in fat, very low in carbohydrate, and have
adequate protein. The goal of the diet is to burn fat to get energy rather
than getting it from glucose, which is formed by carbohydrate metabo-
lism. However, in this case, consuming the ketogenic diet led to a stage
called ketonemia, where concentrations of acetone, acetoacetic acid, and
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116 Chapter 6
beta hydroxybutyric acid are high. This high amount of acetone may be
found in exhaled air. The interlock device in the car determines alcohol by
an electrochemical oxidation method, and acetone does not interfere with
the process. However, acetone is known to be converted into isopropyl
alcohol by the action of liver alcohol dehydrogenase, and isopropyl alco-
hol can be falsely identified as alcohol (ethanol) by the ignition interlock
device. In addition, methanol and propanol can also be falsely identified
as alcohol. The authors concluded that side effects of ketogenic diets
need further evaluation by authorities, especially for people involved in
safety-sensitive positions, such as airline pilots and bus drivers who are
subjected to much tougher alcohol tolerance policies.28
Methanol poisoning is dangerous because it may cause death or blind-
ness (see chapter 12 for more detail), but drinking methanol is not against
the law. A recent article reported the case of a forty-seven-year-old man
who was found at a public park and acting intoxicated (methanol poi-
soning may cause intoxication). A breath analyzer (Intoxilyzer 5000EN)
measured 288 mg of alcohol in 210 liters of breath, which was translated to
288 mg/dL blood alcohol or 0.28 percent blood alcohol (legal limit is 0.08
percent blood alcohol). In the emergency room, the patient admitted he
drank gas line antifreeze, which contains 99 percent methanol. The patient
was subsequently treated and survived, but this case indicates that metha-
nol poisoning can be mistaken by a breath analyzer as alcohol poisoning.29
In another report (Caldwell and Kim 1997) the authors showed that
toluene, xylene, methanol, and isopropyl alcohol in exhaled air can be
mistakenly identified as breath alcohol by the Intoxilyzer 5000 eviden-
tiary breath alcohol analyzer.30 Although exposure to toluene or xylene
may occur in certain workers in the chemical industry, taking proper
protective measures to control such exposure would eliminate any pos-
sibility of being wrongly charged with DWI following an analysis by an
evidentiary breath analyzer. A small amount of methanol is produced af-
ter eating certain foods high in pectin (see chapter 12), but again, the small
amount of methanol found in the exhaled air has a negligible effect on
breath alcohol analysis. A small amount of ethanol is also produced dur-
ing normal human metabolism, but the amount is negligible and would
not interfere with a breath alcohol measurement.
BLOOD ALCOHOL MEASUREMENT
Legal limit for driving is based on whole blood alcohol content in most
states. Blood alcohol can be determined in whole blood or can be deter-
mined in serum or plasma, which is obtained after separating the aqueous
part of the blood from various blood cells. The red color of the blood is due
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to the presence of hemoglobin and serum, while plasma has a yellowish

appearance due to the absence of sufficient hemoglobin. A small amount
of hemoglobin, called plasma-free hemoglobin, may be found in plasma
but is not sufficient to produce a red color. Because alcohol is readily
soluble in water, serum or plasma alcohol content is approximately 15–20
percent higher than whole blood alcohol content. Therefore, serum or
plasma alcohol must be converted to a whole blood value by multiplying
it by a correction factor. Serum and plasma alcohol content are virtually
identical. In one report (Winek and Carfagna 1987), the authors found
that the average ratio of ethanol in serum versus plasma is 1, while the ra-
tio varied only slightly from 0.98 to 1.04 among different individuals. The
serum to whole blood alcohol ratio is 1.12, which is identical to plasma to
whole blood alcohol ratio.31
In general, a whole blood alcohol level is determined using gas chroma-
tography in a crime or forensic laboratory, while serum or plasma blood
alcohol is determined in a hospital laboratory, either by an enzymatic
method or by using gas chromatography. In one study (Barnhill et al.
2007), using 212 consecutive patients admitted to a hospital trauma center,
serum was analyzed for ethanol using an enzymatic method, while whole
blood was analyzed using gas chromatography in a forensic toxicology
laboratory. The authors observed that serum to whole blood alcohol ratio
was dependent on alcohol concentration, but the average value was 1.12
up to an alcohol concentration of 300 mg/dL (0.3 percent) and may be as
high as 1.18. Therefore, a serum blood alcohol of 90 mg/dL (0.09 percent)
corresponds to a whole blood alcohol level of 80 mg/dL (0.08 percent).32
Rainey (1993) reported that the ratio between serum and whole blood
alcohol ranged from 0.88 to 1.59, but the median was 1.15. Therefore, divid-
ing the serum alcohol value by 1.15 would calculate the whole blood alco-
hol concentration. The serum to whole blood alcohol ratio was independent
of serum alcohol concentration and hematocrit.33 Hematocrit is a measure
of the proportion of volume in blood occupied by red blood cells (erythro-
cytes) and is approximately 46 percent in men and 38 percent in women.
Gas Chromatography–Based Methods

Gas chromatography is a complex analytical technique capable of analyz-
ing volatile substances in a mixture. In forensic toxicology laboratories,
whole blood alcohol is always analyzed by a gas chromatographic method.
Gas chromatography can also be used for quantitative estimation of serum
of plasma alcohol. In gas chromatography, the stationary phase is a high
boiling point liquid coated on a tube with a thin internal bore (gas chro-
matography column), and the mobile phase is an inert gas such as helium.
A small sample (usually a few microliters) is drawn into a syringe, and
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118 Chapter 6
then the needle of the syringe is placed on a hot injector and the specimen
is injected into the gas chromatograph. The injection chamber is kept at a
higher temperature than the column, and all components of the mixture
are volatilized at the injector chamber. Then these compounds are swept
by a stream of inert carrier gas through the heated column, and as these
compounds pass through the column, they go back and forth between the
carrier gas and the high boiling liquid coating of the column. More volatile
compounds (lower boiling point) have more affinity for carrier gas and
elute from the column before high volatile components. Thus, the complex
mixture can be separated into individual compounds.
As soon as a compound in the mixture comes out of the column, it
passes through a detector. When the detector sees a compound, it sends
an electrical signal to the recorder, which recodes each compound as it
comes out of the column as a function of the time it takes to elute from the
column. Each compound thus has a specific time for which it is retained
in the column, and this time is called the retention time.
For a particular instrument and a particular set of conditions, this reten-
tion time is specific for a compound, and in gas chromatographic determi-
nation of alcohol, the compound is identified based on the retention time.
In order to measure the amount of alcohol (ethanol) in the specimen, a
fixed amount of another compound with a similar structure to alcohol, for
example, 1,2-butanediol, is added to the specimen prior to analysis. Then
the concentration of alcohol in the specimen can be determined by com-
paring the response of the detector when alcohol eluted from the column
(peak area of ethanol) to the peak area of 1,2-butanediol, which elutes
from the column after alcohol. This is possible because concentration of
1,2-butanediol in the specimen is known.
A common technique applied to the analysis of blood alcohol using gas
chromatography is called headspace gas chromatography. In this process
blood is mixed with the internal standard and a solution containing vari-
ous salts that make alcohol less soluble in blood and then placed in a sealed
sample vial. Then the vial is heated, and in this process the alcohol and the
internal standard is vaporized and an equilibrium is reached between alco-
hol in the air space above the liquid level (vapor phase) and blood. Then the
air in the space above the liquid, which is also called headspace, is drawn
into a syringe and then injected into the gas chromatograph.
There are many published methods of analysis of alcohol using gas
chromatography. One advantage of gas chromatography is that alcohol
(ethyl alcohol) along with similar compounds such as methanol, propyl
alcohol, isopropyl alcohol, and acetone can be analyzed simultaneously.
Another advantage of having a gas chromatograph in the laboratory is
that ethylene glycol can also be analyzed using this equipment.
On the other hand, an enzymatic method for analysis of alcohol (ethyl
alcohol) cannot be used to measure similar compounds, although there
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is an enzymatic method available for analysis of ethylene glycol. Because

methanol, isopropyl alcohol, and ethylene glycol poisoning also occur, es-
pecially during winter months, many university hospital–based toxicology
laboratories utilize a gas chromatographic method for analysis of alcohol,
which is capable of simultaneously analyzing similar compounds. Such
laboratories usually use a serum or plasma specimen for such analysis.
Smith (1984) reported determination of various alcohols and acetone in
human serum using capillary gas chromatography, using propanol as the
internal standard. In a 2 mL centrifuge tube containing 200 ␮l of serum, 200
␮l of internal standard solution (containing propanol in deionized water),
200 ␮l of sodium tungstate (200 mmol/L), and 200 ␮l of copper sulfate (200
mmol/L) solution were added. After mixing and centrifuging to precipitate
serum proteins, 1 ␮l of supernatant was injected into the gas chromatography
column. Helium was used as the carrier gas, and both injector and detector
(flame ionization detector) temperature was 280°C. The column temperature
was maintained at 35°C. After the injection, methanol eluted at 2.06 minutes
followed by alcohol (ethanol), acetone, and isopropyl alcohol (fig. 6.1).34
Figure 6.1. Gas chromatographic

analysis of various alcohols and
acetone, peak 1: methanol; peak 2:
ethanol (alcohol); peak 3: acetone;
peak 4: isopropyl alcohol; peak 5:
propyl alcohol (internal standard).
Number adjacent to each peak
indicates retention time of each
compound.
Source: N. B. Smith, Clinical Chemistry 30,
no. 10 (October 1984). Reprinted with
permission from the American Association
for Clinical Chemistry.
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120 Chapter 6
Enzymatic Methods
In hospital laboratories, alcohol (ethyl alcohol) is also analyzed using
enzymatic methods and automated analyzers. There are several different
automated analyzers available from various diagnostic companies that
are capable of analyzing alcohol in serum or plasma. Enzyme-based auto-
mated methods are generally not applicable for analysis of whole blood,
although modified methods are available for analysis of alcohol in urine
specimens. Commonly used automated analyzers in hospital laboratories
include Dimension Vista Platform and ADVIA Platform (Siemens Diag-
nostics), Vitros Platform (Johnson and Johnson), and SYNCHRON LX20
analyzers (Beckman Corporation) to name a few.
Enzymatic automated analysis of alcohol is based on the principle of
conversion of alcohol to acetaldehyde by alcohol dehydrogenase, and in
this process nicotinamide adenine diphosphate (NAD) is converted into
NADH (which is NAD plus one hydrogen atom). NAD has no absorption
at ultraviolet light at 340 nm wavelength, while NADH absorbs at 340 nm.
Therefore, an absorption peak is absorbed when alcohol is converted into
acetaldehyde because NAD is also converted into NADH. The intensity of
the peak is proportional to the amount of alcohol present in the specimen.
If no alcohol is present, no peak is absorbed. Usually methanol, isopropyl
alcohol, ethylene glycol, and acetone have negligible effect on alcohol
determination using enzymatic methods, but propanol, if present, may
cause 15–20 percent cross-reactivity with alcohol assay. Although isopro-
pyl alcohol, which is used as rubbing alcohol, is common in the house-
hold, propanol is used in much less frequency in household products.
Moreover, if 100 mg/dL of propanol is present in serum, the maximum
false positive alcohol level would be 20 mg/dL (0.02 percent) and would
not cause any serious problem in interpreting legal blood alcohol.
However, interference of lactate dehydrogenase and lactate in the en-
zymatic method of alcohol determination is significant and may cause
misinterpretation of alcohol value over legal limit in a patient suffering
from lactic acidosis (where high concentrations of lactate and lactate de-
hydrogenase are observed in blood), a serious medical condition requir-
ing treatment in an emergency room. In addition, enzymatic alcohol assay
is unsuitable for determination of alcohol in postmortem blood because
of high concentrations of lactate dehydrogenase (LDH) and lactate; only
gas chromatography can be used for measuring alcohol in postmortem
blood. In one report (Thompson et al. 1984), the authors observed 690
mg/dL (0.69 percent) of alcohol in serum using an enzymatic method for
alcohol in a patient, but the gas chromatography did not show any alco-
hol in the serum. This patient had end-stage renal disease and received a
kidney transplant, and at the time when blood was drawn, she had severe
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metabolic acidosis and was admitted to the hospital. Her LDH concentra-
tion was 27,000 units/L and her lactate concentration was 15.0 mmol/L.
However, the authors observed no apparent alcohol level in any speci-
men containing normal levels of LDH and lactate.35
End-stage liver disease, liver transplant (biliary atresia), Duchene mus-
cular dystrophy, and chronic myelogenous leukemia may also lead to
high LDH and lactate in living patients, which may cause false positive
ethanol readings by immunoassays. Nine et al. (1995) observed a correla-
tion between increasing lactate and LDH concentration and false positive
ethanol results. This interference was most noticeable with the EMIT assay
(enzyme multiplied immunoassay technique, Syva, San Jose, California)
for alcohol and less remarkable with Abbott (Abbott Laboratories, Abbott
Park, Illinois) and Roche (Roche Diagnostics, Indianapolis, Indiana) as-
says. With EMIT assay, false positive ethanol started at an LDH activity
of 682 U/L and lactate concentration of 14 mmol/L.36 Lactate concentra-
tions also tend to increase in trauma patients. Dunne et al. (2005) reported
that 27 percent (3536) of 13,102 patients they studied had positive alcohol
screen (mean alcohol: 141mg/dL, range: 10 mg/dL–508 mg/dL).37
In contrast, Winek et al. (2004) compared alcohol concentration ob-
tained by an enzyme assay (Dimension Analyzer, Siemens Diagnostics,
Deerfield, Illinois) and gas chromatography in trauma patients and
observed no false positives by immunoassays. Alcohol concentrations
obtained by immunoassays correlated well with GC values, and, only in
six specimens (out of twenty-seven), the difference between GC and im-
munoassay values exceeded 10 percent, and the highest difference was
22 percent. The authors concluded that immunoassay methods can be
used in hospital laboratories for determination of alcohol concentrations
in trauma patients.38
In my experience, false positive alcohol measured by an enzyme assay
in an individual with high lactate and LDH is only expected in severely ill
patients and should not be a concern in terms of being wrongly accused
of DWI. Powers and Dean (2009) described a case where a driver, a thirty-
three-year-old man, was involved in a single motor vehicle collision
(hitting a tree). He was transferred to a local hospital emergency room
where blood was drawn for various tests, including blood alcohol. The
serum alcohol level was 200 mg/dL (0.2 percent), which was more than
twice the legal limit, indicating that the driver was intoxicated during the
accident. Blood tests also revealed that the patient experienced a certain
degree of trauma following the accident because his liver enzymes were
elevated due to some liver damage. Amylase and lipase levels were also
elevated. During criminal prosecution of DWI, hospital alcohol results
were admitted as evidence by the court. Although lactate and LDH were
not measured in this patient, based on other blood tests, it was estimated
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122 Chapter 6
Figure 6.2. Chemical transformation (oxidation) of lactate to pyruvate and ethanol

(alcohol) to acetaldehyde and generation of NADH from NAD. In the absence of alco-
hol, lactate can be transformed to pyruvate by lactate dehydrogenase (LDH), and in this
process excess NAD can be converted into NADH thus providing a false alcohol mea-
surement. However, both lactate and pyruvate must be present in very high amounts
to cause this interference. Reprinted with permission from The Journal of Analytical
Toxicology (Preston).
that both lactate and LDH were not elevated sufficiently to interfere with
the enzymatic alcohol determination in this case. Both lactate and LDH
must be present in very high amounts to cause this interference, and
lactate alone cannot cause this interference. Lactate must be converted
into pyruvate catalyzed by lactate dehydrogenase enzyme in order for
NAD to be transformed to NADH. The mechanism of this interference is
explained in figure 6.2.39
FORENSIC VERSUS MEDICAL ALCOHOL
Forensic or “legal” blood refers to the sample of blood the police obtain
pursuant to their investigation of DWI. When blood is drawn for deter-
mination of forensic alcohol, a chain of custody is maintained where there
is always a written record of all personnel who had possession of the
sample until the time of analysis. The name of the analyst is also recorded
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in the chain of custody. Because of this chain of custody, integrity of the

specimen is guaranteed, and there is no possibility of misidentification of
the specimen. Moreover, most forensic toxicology laboratories determine
whole blood alcohol using a specific and sensitive gas chromatographic
technique. Therefore, a forensic alcohol level over the legal limit is diffi-
cult to challenge in a court of law unless a loophole can be discovered in
the chain of custody process during the trial.
Medical blood refers to a blood sample that was either voluntarily
given or involuntarily taken by medical personnel in the course of pro-
viding medical treatment to the patient. For an injured DWI suspect
who is transferred to an emergency room of a local hospital, and who is
incapable of providing a breath sample, a blood sample given for medi-
cal treatment purposes may be subpoenaed or obtained pursuant to a
search warrant and used against him or her in his or her criminal DWI
trial with the approval of the judge. The legal standard of causation is
usually the same when requesting medical blood as it is for forensic
blood alcohol level, but a medical alcohol may be challenged in court if
a chain of custody is not maintained and alcohol analysis is conducted
by an enzymatic method rather than a chromatographic technique.
However, maintaining a chain of custody may be practiced in a hospital
if a police officer brings in a suspect injured in a drunk-driving accident.
Modern enzymatic alcohol assays are very robust and correlate well
with the gas chromatographic methods, the gold standard for alcohol
determination.
Both forensic and medical alcohol determination is subject to a preci-
sion issue. Precision means percent variation expected if alcohol level
is measured by the same method multiple times. For example, one
determination of alcohol may be 80 mg/dL and analysis of the same
specimen by the same instrument could be 78 mg/dL or 82 mg/dL.
Most gas chromatographic methods and enzymatic alcohol determina-
tion methods have variability less than 5 percent, but depending on an
individual case, a maximum allowance of 10 percent may be granted.
For example, if the whole blood alcohol level is 84 mg/dL, a defense
lawyer could argue that the true value may be between 76 and 92 mg/
dL, and if the level was determined by another person, it could well be
below 80 mg/dL, the legal limit.
However, if an alcohol value is measured twice (as we do in our hos-
pital for any emergency room patients involved in a motor vehicle crash)
and both values are over the legal limit, the defendant may be out of
luck. Therefore, both medical and legal alcohol value can be challenged
in a court if the value is just above 80 mg/dL limit for whole blood or 90
mg/dL for serum or plasma. Higher blood alcohol values are difficult to
challenge. In a report by Chang et al. (2001) the conviction rate of trauma
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124 Chapter 6
patients involved in motor vehicle crashes was high based on alcohol

levels determined in the author’s hospital. Of 213 intoxicated drivers
studied, 172 were followed up by law enforcement personnel, and 156
were arrested and charged with DWI. Out of 156 individuals arrested, 135
individuals (93.8 percent) were convicted for DWI.40
EXTRAPOLATION OF ALCOHOL VALUE AT COURT
Reliable information about the elimination rate of alcohol from the body
is often needed in forensic science and legal medicine when alcohol-
related crimes, such as alcohol-impaired driving or alcohol-related
crimes, are being investigated. The courts usually want to know the
defendant’s blood alcohol level at the time of the accident based on a
blood alcohol level determined several hours later. After drinking on an
empty stomach, the elimination rate of alcohol from the human body
falls within the range of 10–15 mg/dL per hour. In other words, blood
alcohol level declines 0.010 to 0.015 percent per hour. If alcohol is con-
sumed with food, elimination rate tends to be 15–20 mg/dL per hour
(0.015 to 0.02 percent per hour).
In general, women tend to eliminate alcohol slower than do men. In
moderate drinkers the elimination rate of 15 mg/dL per hour (0.015
percent per hour) is used by many expert witnesses to extrapolate blood
alcohol level during testimony. Alcoholics may eliminate alcohol faster
than moderate drinkers.41 Therefore, a defendant’s blood alcohol may be
75 mg/dL (0.075 percent) two hours after an accident, which is below the
legal limit, but prosecution may argue in court that two hours prior to the
time of the accident the blood alcohol level was 75 + 2 × 15 = 105 mg/dL,
a value above the legal limit of driving.
Therefore, the best policy is to not drink and drive, and if drinking,
exercise caution. In chapter 2, I provided detailed information on how
blood alcohol levels are related to a number of drinks based on body
weight and gender. Always try to limit your drinking to one drink per
hour, and do not consume more than two standard drinks in two hours if
you are a man with no genetic defect for alcohol metabolism and weigh
at least 140 pounds or more. For a woman who weighs 120 pounds or
more, consuming one drink in a two-hour period prior to driving is safe,
and the blood alcohol level would be significantly below the legal limit
of driving. Always consume alcohol with food and be careful when you
order a margarita or a specially prepared drink, because one drink may
be equivalent to two or three standard drinks as far as alcohol content is
concerned (see chapter 2).
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CONCLUSION
As emphasized in this chapter, drinking and driving do not mix well. If you
plan to drink on a night out, find a designated driver or hire a cab for your
ride home. If you drink, drink in moderation. Information provided in this
chapter should make you familiar with current laws and blood alcohol de-
terminations. Law enforcement agencies, prosecutors, and expert witnesses
exercise extreme care to ensure that an innocent person is not charged with
a DWI. My experience is that doubts are always given in favor of defendants
in borderline cases. However, despite tough enforcement of DWI laws in all
states, fatalities from motor vehicle crashes due to alcohol-impaired drivers
claim many lives each year and are major public safety concerns. Do not
drink and drive so that you can enjoy a happy and prosperous life.
NOTES
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hol Consumption and Alcohol-Impaired Driving in the United States,” Alcoholism:
Clinical and Experimental Research 32, no. 4 (April 2008): 639–44.
2. T. H. Nochajski and P. R. Stasiewicz, “Relapse to Driving under the Influence
(DUI): A Review,” Clinical Psychology Review 26, no. 2 (March 2006): 179–95.
3. “Ignition Interlocks: What You Need to Know,” Department of Transporta-
tion (U.S.), National Highway Traffic Safety Administration (NHTSA), National
Highway Traffic Safety Administration Report, November 2009, www.nhtsa.
gov/staticfiles/nti/impaired_driving/pdf/811246.pdf.
4. “Traffic Safety Facts 2008: Alcohol-Impaired Driving,” Department of Trans-
portation (U.S.), National Highway Traffic Safety Administration (NHTSA), Wash-
ington, D.C., 2009. Available at http://www-nrd.nhtsa.dot.gov/Pubs/811155.
PDF.
5. K. P. Quinlan, R. D. Brewer, P. Siegal, D. A. Sleet, et al., “Alcohol-Impaired
Driving among U.S. Adults, 1993–2002,” American Journal of Preventive Medicine 28,
no. 4 (May 2005): 346–50.
6. “Traffic Safety Facts: Fatalities Related to Alcohol-Impaired Driving during
the Christmas and New Year’s Day Holiday Periods,” NHTSA Report Number
DOT HS 810 870, December 2007, available on the NHTSA website, http://www.
nhtsa.gov.
7. J. C. Fell, A. S. Toppetts, and R. B. Voas, “Fatal Traffic Crashes Involving
Drinking Drivers: What Have We Learned?” Annual Proceedings of the Association
for Advancement of Automobile Research 53 (2009): 63–76.
8. T. S. Naimi, D. E. Nelson, and R. D. Brewer, “Driving after Binge Drinking,”
American Journal of Preventive Medicine 37, no. 4 (October 2009): 314–20.
9. M. F. Lovenheim and J. Slemrod, “The Fatal Toll of Driving to Drink: The
Effect of Minimum Legal Drinking Age Evasion on Traffic Fatalities,” Journal of
Health Economics 29, 1 (January 2010): 62–77.
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126 Chapter 6
10. R. C. Peck, M. A. Gebers, R. B. Voas, and E. Romano, “The Relationship be-

tween Blood Alcohol Concentration (BAC), Age and Crash Risk,” Journal of Safety
Research 39, no. 3 (March 2008): 311–19.
11. B. J. Leadbeater, K. Foran, and A. Grove-White, “How Much Can You Drink
Before Driving? The Influence of Riding with Impaired Adults and Peers on the
Driving Behaviors of Urban and Rural Youth,” Addiction 103, no. 4 (April 2008):
629–37.
12. A. K. Dills, “Social Host Liability for Minors and Underage Drunk-Driving
Accidents,” Journal of Health Economics, January 15, 2010 (e-publication before print).
13. S. M. Rosen, T. R. Miller, and M. Simon, “The Cost of Alcohol in California,”
Alcohol Clinical and Experimental Research 32, no. 11 (November 2008): 1925–36.
14. T. O’Keefe, S. Shafi, J. L. Sperry, and L. M. Gentiello, “The Implications of
Alcohol Intoxication and the Uniform Policy Provision Law on Trauma Centers:
A National Trauma Data Bank Analysis of Minimally Injured Patients,” Journal of
Trauma 66, no. 2 (February 2009): 495–98.
15. J. C. Fell and R. B. Voas, “Mothers Against Drunk Driving (MADD): The
First 25 Years,” Traffic Injury Prevention 7, no. 3 (September 2006): 195–212.
16. J. C. Fell and R. B. Voas, “The Effectiveness of Reducing Illegal Blood Alco-
hol Concentration (BAC) Limits for Driving: Evidence for Lowering the Limit to
0.05 BAC,” Journal of Safety Research 37, no. 3 (March 2006): 233–43.
17. A. W. Jones, “Distribution of Ethanol between Saliva and Blood in Man,”
Clinical and Experimental Pharmacology and Physiology 6, no. 1 (January–February
1979): 53–59.
18. M. P. Hlastala, “The Alcohol Breath Test: A Review,” Journal of Applied
Physiology 84, no. 2 (February 1998): 401–8.
19. M. Hlastala, “Paradigm Shift for the Alcohol Breath Test,” Journal of Forensic
Sciences 55, no. 2 (March 2010): 451–56.
20. DataMaster Operator Information Manual Review, October 2000, Washing-
ton State Patrol, http://www.breathtest.wsp.wa.gov.
21. G. Razatos, R. Luthi, and S. Kerrigan, “Evaluation of a Portable Evidentiary
Breath Alcohol Analyzer,” Forensic Sciences International 153, no. 1 (October 2005):
17–21.
22. P. M. Hardings, R. H. Laessing, and P. H. Field, “Field Performance of the
Intoxilyzer 5000: A Comparison of Blood and Breath Alcohol Results in Wisconsin
Drivers,” Journal of Forensic Sciences 35, no. 5 (September 1990): 1022–28.
23. S. Kechagias, K. A. Jonsson, T. Franzen, L. Anderson, et al., “Reliability of
Breath Alcohol Analysis in Individuals with Gastroesophageal Reflux Disease,”
Journal of Forensic Sciences 44, no. 4 (July 1999): 814–18.
24. A. W. Jones and L. Anderson, “Comparison of Ethanol Concentrations in
Venous Blood and End-Expired Breath during a Controlled Drinking Study,”
Forensic Sciences International 132, no. 1 (March 2003): 18–25.
25. C. C. Fessler, F. A. Tulleners, D. G. Howitt, and J. R. Richards, “Determina-
tion of Mouth Alcohol Using the Dräger Evidential Portable Alcohol System,” Sci-
ence and Justice: Journal of the Forensic Science Society 48, no. 1 (March 2008): 16–23.
26. B. Lutmer, C. Zurfluh, and C. Long, “Potential Effect of Alcohol Content in
Energy Drinks on Breath Alcohol Testing,” Journal of Analytical Toxicology 33, no.
3 (April 2009): 167–69.
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27. O. Laakso, T. Pennanen, K. Himberg, T. Kuitunen, et al., “Effect of Eight

Solvents on Ethanol Analysis by Dräger 7110 Evidentiary Breath Analyzer,” Jour-
nal of Forensic Sciences 49, no. 5 (September 2004): 1113–16.
28. A. W. Jones and S. Rossner, “False Positive Breath Alcohol Test after a Keto-
genic Diet,” International Journal of Obesity (London) 31, no. 3 (March 2007): 559–61.
29. E. M. Caravati and K. T. Anderson, “Breath Alcohol Analyzer Mistakes
Methanol Poisoning for Alcohol Intoxication,” Annals of Emergency Medicine 55,
no. 2 (February 2010): 198–200.
30. J. P. Caldwell and N. D. Kim, “The Response of the Intoxilyzer 5000 to Five
Potential Interfering Substances,” Journal of Forensic Sciences 42, no. 6 (November
1997): 1080–87.
31. C. L. Winek and M. Carfagna, “Comparison of Plasma, Serum, and Whole
Blood Ethanol Concentration,” Journal of Analytical Toxicology 11, no. 6 (November
1987): 267–68.
32. M. T. Barnhill Jr., D. Herbert, and D. J. Wells Jr., “Comparison of Hospital
Laboratory Serum Alcohol Levels Obtained by an Enzymatic Method with Whole
Blood Levels Forensically Determined by Gas Chromatography,” Journal of Ana-
lytical Toxicology 31, no. 1 (January–February 2007): 23–30.
33. P. Rainey, “Relation between Serum and Whole Blood Ethanol Concentra-
tions,” Clinical Chemistry 39, no. 11 (November 1993): 2288–92.
34. N. B. Smith, “Determination of Volatile Alcohols and Acetone in Serum by
Non-polar Capillary Gas Chromatography after Direct Sample Injection,” Clinical
Chemistry 30, no. 10 (October 1984): 1672–74.
35. W. T. Thompson, D. Malhotra, D. P. Schammel, W. Blackwell, et al., “False
Positive Ethanol in Clinical and Postmortem Sera by Enzymatic Assay: Elimina-
tion of Interference by Measuring Alcohol in Protein-Free Ultrafiltrate,” Clinical
Chemistry 40, no. 8 (August 1994): 1594–95.
36. J. Nine, M. Moraca, A. Virji, and K. Rao, “Serum Ethanol Determination:
Comparison of Lactate and Lactate Dehydrogenase Interference in Three Enzy-
matic Assays,” Journal of Analytical Toxicology 19, no. 3 (May–June 1995): 192–96.
37. J. R. Dunne, J. K. Tracy, T. M. Scalea, and L. Napolitano, “Lactate and Base
Deficit in Trauma: Does Alcohol or Drug Use Impair Predictive Accuracy?” Jour-
nal of Trauma 58, no. 5 (May 2005): 959–66.
38. C. L. Winek, W. W. Wahba, R. Windisch, and C. L. Winek, “Serum Alcohol
Concentrations in Trauma Patients Determined by Immunoassays Versus Gas
Chromatography,” Forensic Sciences International 139, no. 1 (January 2004): 1–3.
39. R. H. Powers and D. E. Dean, “Evaluation of Potential Lactate/Lactate De-
hydrogenase Interference with an Enzymatic Alcohol Analysis,” Journal of Analyti-
cal Toxicology 33, no. 5 (October 2009): 561–63.
40. S. Chang, J. G. Cushman, and M. D. Pasquale, “The Injured Intoxicated
Driver: Analysis of the Conviction Process,” Journal of Trauma 51, no. 3 (September
2001): 551–56.
41. A. W. Jones, “Evidence-Based Survey of the Elimination Rates of Ethanol
from Blood with Applications in Forensic Cases,” Forensic Sciences International
200, nos. 1–3 (July 2010): 1–20.
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7

Biomarkers of Alcohol Abuse
O ne of the consequences of moderate ethanol ingestion is a reduced

risk of cardiovascular events (heart disease) with the consumption
of alcoholic products that contain specific flavonoids. This was first ob-
served in conjunction with mild to moderate wine consumption, hence
the term “French Paradox.”1 In order to get the health benefits of alcohol,
one must practice moderate drinking. Although many alcoholics often
have remarkably “clean” arteries at autopsy, chronic excessive ethanol
ingestion leads to hyperlipidemia (high lipids or fats in the blood), and
such fats tend to deposit in the liver, causing fatty livers and eventually
cirrhosis of the liver, which can be fatal. Negative effects of heavy alcohol
consumption include liver cirrhosis, esophageal cancer, pancreatitis, and
epilepsy. Alcohol also plays a role in traffic accidents, violent crimes,
sexual assaults, domestic violence, and child abuse.
It is estimated that about 5 percent of the general population drinks
heavily and about 10 percent of the general population has alcohol-
related medical problems. From 2001 to 2005, there were approximately
79,000 deaths per year attributed to excessive alcohol use. In fact, alcohol
abuse is the third lifestyle-related cause of death in the United States each
year.2 The consumer expenditure on alcohol in the United States in 1999
was roughly $116.2 billion, and $22.5 billion was attributed to underage
drinking. It has also been estimated that roughly 50 percent of underage
people (twelve to twenty years old) drink alcohol and approximately
30.4 percent of adults in the United States drink more than two drinks
a day, which is considered excessive alcohol consumption.3 Heavy alco-
hol consumption causes serious public health issues that not only affect
129
10-649_Dasgupta.indb 129 1/17/11 6:40 AM

130 Chapter 7
individuals and their families but society as a whole. Prevention of alco-

hol abuse is an important concern from both a medical and social point of
view. The biomarkers of alcohol abuse are the latest techniques available
to health care professionals to identify alcohol abusers and also to moni-
tor individuals undergoing alcohol rehabilitation.
THE BIOMARKERS OF ALCOHOL ABUSE
A biological molecule found in blood, tissue, or body fluids that is a

sign of an abnormal process or condition can be broadly termed a “bio-
marker.” These markers can be used for diagnosis of a condition or a dis-
ease. Alternatively, biomarkers can also be used to measure the success
of a particular therapy. Biomarkers are also called “molecular markers”
or “signature molecules.” In general, in the absence of a disease or a con-
dition, concentration of a biomarker is very low, but when a condition
develops further, the concentration may be increased significantly, thus
indicating an abnormal condition or disease. For example, normal con-
centration of prostate specific antigen (PSA) in blood is less than 4 nano-
gram/milliliter (4 ng/mL), but in the event of prostate cancer, this value
increases significantly over 4 ng/mL. In one report (Anai et al. 2007), the
authors concluded that a PSA value higher than 30 ng/mL is an almost
certain predictor of the presence of prostate cancer.4
Alcohol can usually be detected in blood several hours to less than a
day after consumption of the last drink. Alcohol is metabolized by the
liver, and alcohol concentration in blood is reduced by approximately
0.015 percent (15 mg/dL) per hour. For example, if a blood alcohol level
is 0.08 percent (80 mg/dL, the legal limit of driving), 0.08 divided by 0.015
hours or 5.3 hours would be needed for the blood alcohol level to become
zero. If more alcohol is consumed, then more time is needed for blood
alcohol to return to the zero value (table 7.1).
Table 7.1. Number of Hours Needed for Blood Alcohol Concentration (BAC) to
Become Zero
Percentage of Blood Alcohol Time Needed to Reach Zero Blood
Concentration (BAC) Alcohol Concentration (BAC)
0.2 (200 mg/dL) 13.3 hours
0.15 (150 mg/dL) 10 hours
0.12 (120 mg/dL) 8 hours
0.1 (100 mg/dL) 6.6 hours
0.08 (80 mg/dL) 5.3 hours
0.05 (50 mg/dL) 3.3 hours
0.03 (30 mg/dL) 2 hours
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Biomarkers of Alcohol Abuse 131
The determination of blood alcohol is not a good way to screen people

who are at higher risk of alcohol abuse. In one report (Alkan et al.
2001), the authors described a case where a drunken person had fallen
from the window of his girlfriend’s apartment and died. This person’s
parents appealed to the public prosecutor that their child did not fall
down but was murdered by his girlfriend. During the trial, the vic-
tim’s autopsy revealed no blood alcohol—in contrast to his girlfriend’s
statement—and there was a reasonable doubt that the girlfriend was
the murderer. However, later in the trial, the reason for detection of
no alcohol in the autopsy was revealed, indicating that blood alcohol
detection has many limitations in criminal cases.5 Blood alcohol level
cannot discriminate between acute and long-term alcohol consumption
and risky behavior. The detection time frame of blood alcohol is very
limited (from a few hours to twelve hours in most cases) and cannot
detect a hangover stage.
Biomarkers for alcohol use have many advantages over the deter-
mination of blood alcohol level. First, biomarkers can stay elevated
for a considerably longer period of time than blood alcohol. Although
biomarkers are often used as screens for diagnosis of alcohol abuse or
dependence, strictly speaking, alcohol biomarkers are reflections of the
physiological response of the body to heavy alcohol consumption and
have diagnostic value. Biomarkers can be broadly classified into two
categories: slate markers and trait markers. Slate markers are valuable
in addressing questions, such as evidence of recent alcohol intake versus
chronic alcohol consumption, alcohol abuse versus moderate drinking,
and whether there is any evidence of organ damage related to drink-
ing. Trait markers can address broad questions, such as whether an
individual has a genetic makeup that may make that individual more
susceptible to alcohol abuse or alcoholic liver disease. In clinical practice
physicians more often order tests that measure slate markers of alcohol,
and in this chapter only slate markers of alcohol will be discussed. Many
trait markers of alcohol abuse are in developmental and extensive re-
search stages and not commonly measured in hospital laboratories. The
slate markers of alcohol include:
Liver enzymes
Mean corpuscular volume (MCV)
Carbohydrate-deficient transferrin
Serum and urine hexosaminidase
Sialic acid
Acetaldehyde-protein adducts
Ethyl glucuronide and ethyl sulfate
Fatty acid ethyl ester
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132 Chapter 7
CLINICAL APPLICATION OF ALCOHOL BIOMARKERS
Alcohol biomarkers are primarily used for screening patients for possi-
ble alcohol abuse, mainly in primary care facilities. In addition, alcohol
biomarkers are also useful in identifying pregnant women who may be
abusing alcohol, because fetal alcohol syndrome is a totally prevent-
able disorder. Alcohol biomarkers are also used in emergency room
settings, psychiatric clinics, and internal medicine settings, because
self-reporting of alcohol use is not always accurate, as some patients
are reluctant to admit a problem with alcohol. The addition of bio-
markers may help identify individuals who need treatment for alcohol
abuse. The major clinical utilities of using biomarkers of alcohol use
include
1. Identifying patients needing intervention for alcohol abuse

2. Physiological response to alcohol abuse and whether a medical
problem exists related to heavy alcohol consumption
3. Monitoring patients undergoing alcohol rehabilitation and identify-
ing any relapse of alcohol use
4. Outcome measures in studies evaluating new medication or behav-
ior modification for intervening in alcohol abuse problems
5. Guiding patients in a positive manner to change their lifestyles and
drinking habits
6. Documenting abstinence
Monitoring alcohol biomarkers is very helpful in motivating patients to

change their habit of consuming alcohol. Giving feedback on elevations of
biomarkers and reviewing their decline levels with the patient provides
objective evidence of the patient’s treatment success, personal needs, and
the benefits of reducing alcohol consumption. Relapse is unfortunately
common in alcohol detoxification programs, and identifying such relapse
in a patient at an early stage using biomarkers is clinically very useful. In
addition, alcohol biomarkers are very useful in documenting abstinence
in these special populations: individuals younger than twenty-one, es-
pecially in the military; adolescents on probation for alcohol use or pos-
session; individuals with previous alcohol-related problems who have
custody of their children with the stipulation that they must practice ab-
stinence; motorists with DWI convictions who must document abstinence
in order to get their driving privilege back; medical professionals; pilots;
and others who need to document abstinence from drinking due to previ-
ous alcohol-related problems and any other individuals where required
by the law or company policy.
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SCREENING ALCOHOL-RELATED HEALTH

PROBLEMS IN PRIMARY CARE SETTINGS
Primary health care settings are ideal for screening patients for alcohol-
related health problems because a majority of the population visits primary
care physicians for routine annual checkups or seeks treatment for chronic
conditions at least on a yearly basis. In addition, advice by the primary care
physician regarding behavior modification in order not to consume exces-
sive alcohol is usually well received by patients. The National Institute on
Alcohol Abuse and Alcoholism recommends that all adult primary care
patients be screened for alcohol use, because valid and reliable screening
tools are available. Despite these guidelines, only 55–65 percent of physi-
cians routinely ask their patients about alcohol use and only 35 percent
screen patients during their annual visit. Together with self-reporting, al-
cohol screening tools, and using biomarkers of alcohol abuse, a reliable and
accurate estimation of alcohol consumption by a patient can be reached,
and intervention can be done by the primary care physician if needed. Un-
fortunately, there has been little translation of alcohol biomarker research
into practical guidelines for primary care physicians. Many primary care
physicians say that they will use alcohol biomarkers more often in their
clinical practice if practical guidelines are readily available, and if they have
additional knowledge regarding clinical use of such biomarkers.6
APPLICATION OF ALCOHOL BIOMARKERS IN

OTHER MEDICAL AND SURGICAL SETTINGS
The utilization of alcohol biomarkers as disease risk indicators in spe-

cialty medical and surgical settings has many advantages and is a wel-
come trend, because heavy alcohol consumption may cause or aggravate
many medical conditions, including hypertension, stroke, heart disease,
liver disease, pancreatitis, and various types of cancer. Heavy alcohol
consumption also significantly contributes to complications in trauma
and surgical patients. Approximately one-fifth of patients seen in clini-
cal practice have some alcohol use disorders, ranging from hazardous
alcohol consumption to alcohol dependence. Early intervention for
alcohol-related disorders is highly desirable because a variety of effec-
tive therapeutic options exist to treat such disorders, including behavior
modification, prophylactic stress management, and therapy for alcohol-
related complications and detoxification.
Between 16 and 39 percent of trauma victims have positive blood al-
cohol concentrations, but 11–45 percent of trauma patients may suffer
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134 Chapter 7
from alcohol-related disorders, even though they have negative blood

alcohol on admission. Therefore, blood alcohol determination is a poor
measure of establishing whether a trauma patient is also suffering from
alcohol-related disorders or not, and under such circumstances, an alco-
hol biomarker, such as carbohydrate-deficient transferrin, is very useful
in detecting alcohol-related disorders in trauma patients.
Hypertension is the leading cause of stroke and heart disease, and
heavy drinking (more than three drinks a day) increases blood pressure
in both normal and hypertensive patients. In addition, excessive drink-
ing is associated with uncontrolled treatment-resistant hypertension.
There is a correlation between serum gamma-glutamyl transferase and
carbohydrate-deficient transferrin, and these alcohol biomarkers can be
successfully employed to diagnose patients with alcohol-related disor-
ders who are also suffering from uncontrolled hypertension. A consider-
able amount of research indicates that alcohol screening and brief inter-
vention can improve clinical outcome in patients and is also very effective
in reducing medical costs.7
INDIRECT VERSUS DIRECT SLATE BIOMARKERS OF ALCOHOL
Traditional slate biomarkers of alcohol use are indirect biomarkers, which

are elevated in a person consuming moderate to heavy amounts of al-
cohol. These biomarkers are elevated due to the toxicity of alcohol on a
particular organ. For example, liver enzymes, such as gamma-glutamyl
transferase (GGT), alanine aminotransferase (ALT), and aspartate amino-
transferase (AST), are elevated after heavy alcohol consumption because
alcohol has toxic effects on the liver. Mean corpuscular volume (MCV) as
well as the first FDA-approved biomarker of alcohol abuse, carbohydrate-
deficient transferrin, are also indirect markers. Serum and urine hex-
osaminidase and sialic acid are also indirect biomarkers of alcohol abuse.
Alcohol metabolites such as ethyl glucuronide, ethyl sulfate, or biomol-
ecules derived from the interaction of alcohol with other molecules, such
as fatty acid ethyl ester and phosphatidyl ethanol, are direct biomarkers
of alcohol consumption (table 7.2).
Liver Enzymes as Alcohol Biomarkers

Liver enzymes are elevated in individuals consuming excessive amounts of
alcohol because alcohol has a direct toxic effect on the liver. Alanine trans-
aminase (ALT) and aspartate transaminase (AST) are found inside liver cells
(hepatocytes), and small amounts of these enzyme activities are detected in
the serum of healthy individuals. However, in the case of liver injury, these
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Table 7.2. Various Markers for Alcohol Abuse

Type of
Marker Slate Marker Comment
Gamma- Indirect Associated with heavy drinking; value returns
glutamyltransferase to normal 2–6 weeks after abstinence. Not
(GGT) a specific marker and may be elevated in
some diseases.
Alanine amino Indirect Also elevated in alcoholics but less sensitive
transferase (ALT)/ than GGT. Not a specific marker and may
Aspartate amino be elevated in some diseases.
transferase (AST)
Mean corpuscular Indirect Associated with heavy drinking but not a
volume (MCV) specific marker and may be elevated in
certain types of anemia.
Carbohydrate- Indirect More specific marker than MCV and liver
deficient enzymes (GGT, ALT, and AST) but more
transferrin difficult to measure in blood. Value returns
to normal 2–4 weeks after abstinence.
Serum and urine Indirect Specific marker for heavy alcohol use (60
hexosaminidase gm or more per day). Value returns to
normal 7–10 days after abstinence. This is a
complex test not readily available in small
hospital laboratories.
Sialic acid Indirect Specific marker for heavy alcohol use, but it
is a specialized test not readily available to
small hospital laboratories. Value returns to
normal after 7–10 days of abstinence.
Acetaldehyde-protein Direct Distinguishes heavy drinkers from social
adducts drinkers and nondrinkers but amounts found
in blood or urine are very small and difficult
to measure.
Ethyl glucuronide Direct Specific markers for alcohol abuse and can
and ethyl sulfate differentiate between heavy drinkers and
social drinkers. Can be measured in blood
or hair, but method of determination is
complex.
Fatty acid ethyl ester Direct Specific markers for alcohol abuse and can
differentiate between heavy drinkers and
social drinkers. Can be measured in blood
or hair, but method of determination is
complex.
enzymes can be increased three- to tenfold from their normal expected val-
ues (ALT: 10–40 units/L, ALT: 5–40 units/L). Alkaline phosphatase (ALP),
another enzyme found in the cell lining of the biliary ducts of liver, is also
elevated during liver injury but may not be significantly elevated after
heavy alcohol consumption. Gamma-glutamyl transferase (GGT) is also
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136 Chapter 7
another marker of liver injury, and this enzyme is also elevated in people
drinking alcohol.
Out of all liver enzymes, GGT is considered the most sensitive bio-
marker for alcohol consumption. GGT levels are elevated following heavy
alcohol consumption, and with complete abstinence the level returns to
normal within two to six weeks. GGT is elevated in response to alcohol
consumption due to accelerated release from damaged liver cells. GGT
levels are also high in patients suffering from severe alcoholic liver
disease. However, GGT is elevated in individuals who consume high
amounts of alcohol on a regular basis rather than individuals who con-
sume high amounts of alcohol sporadically.
GGT may also be somewhat elevated in moderate drinkers compared to
nondrinkers. In one report (Alatalo et al. 2009), the authors studied GGT
along with ALT, AST, ferritin (a protein that binds iron), and albumin
(major protein found in human blood) levels in 133 heavy drinkers (mean
alcohol consumption 110 gm per day; approximately eight drinks per day
as each standard drink contains 14 gm of alcohol), 1,504 moderate drinkers
(less than 40 gm of alcohol per day or approximately three drinks or less
a day), and 685 nondrinkers (abstainers). The heavy drinkers in this study
were admitted for alcohol detoxification. The authors reported that GGT
had the highest incidence of elevated levels in heavy drinkers compared
to moderate drinkers and abstainers, followed by AST and ALT, where
albumin was elevated in approximately 20 percent of heavy drinkers only.
Interestingly, significant differences between GGT and ALT levels were
also observed between moderate drinkers and abstainers in the male
population, but no such difference was observed in females. For example,
average GGT levels in male heavy drinkers was 193 units per liter com-
pared to 34 units per liter in moderate drinkers and 26 units per liter in
abstainers. Similarly, the average AST value in heavy male drinkers was
65 units per liter compared to 26 units per liter in moderate drinkers and
25 units per liter in abstainers. Mean ALT value in heavy drinkers was 71
units per liter compared to 29 units per liter in moderate drinkers and 26
units per liter in abstainers.8 This publication also demonstrates that GGT
is a more sensitive marker than other liver enzymes (AST and ALT) for
heavy alcohol consumption.
One limitation of GGT as a biomarker of alcohol is that it may also be
elevated in a person taking a barbiturate, in nonalcoholic liver diseases,
cardiovascular disease, individuals with high lipids, and obese individu-
als. Several epidemiological studies have indicated that there is an associ-
ation between elevated GGT values and increased risk for cardiovascular
disease, type 2 diabetes (diabetes that can be controlled without taking
insulin shots), chronic kidney disease, and cancer, and these elevations in
GGT levels are not associated with alcohol consumption.9
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Mean Corpuscular Volume (MCV) as a Biomarker for Alcohol

Alcohol and its metabolites (breakdown products of alcohol produced by
liver enzymes) have toxic effects on human red blood cells (erythrocytes).
During a blood test, mean corpuscular volume or mean cell volume of
erythrocytes (MCV) is calculated from the hematocrit (ratio of the volume
of red cells to the volume of whole blood) and red cell counts. The normal
range of MCV is 86–98 femtoliter (fl). A femtoliter is one quadrillionth
of a liter (10-15 liter), an extremely small volume indicating the volume
of an average erythrocyte. Excessive alcohol consumption is known to
increase MCV, a pathogenic process known as macrocytosis (enlarged
erythrocytes). If both GGT and MCV are elevated, it is likely that regular
heavy alcohol consumption is the cause, because an erythrocyte remains
in circulation 120 days on average; it takes MCV about three months to
return to a normal level after abstinence.
Koivisto et al. (2006) studied MCV and other parameters in 105 alcohol-
ics with a wide range of alcohol consumption (40 gm to 500 gm of ethanol
per day or three to forty drinks per day), 62 moderate drinkers (less than
40 gm a day or three or less drinks a day), and 24 abstainers, and reported
that the upper limit of MCV in moderate drinkers was 98 fl (range 82–98
fl), while the upper limit of abstainers was 96 fl (range 82–96). In contrast,
in heavy consumers of alcohol, MCV can be as high as 104 fl. The increase
in MCV due to alcohol consumption is due to the penetration of alcohol
into erythrocytes, with this altering the erythrocyte membrane and affect-
ing its stability. In addition, high concentration of acetaldehyde, the first
metabolite of alcohol, is also detected in high amounts in erythrocytes
of alcoholics. Acetaldehyde can increase erythrocyte volume by form-
ing adducts with various components on the cell membrane, including
proteins.10
Carbohydrate-Deficient Transferrin as an Alcohol Biomarker

Transferrin is a protein that is responsible for transporting iron in the
blood from the intestine to bone marrow, so that iron can be incorporated
into hemoglobin during the formation of red blood cells, also known as
erythrocytes. Transferrin consists of 679 amino acids and is also a glyco-
protein, meaning that the carbohydrate is an integral part of the trans-
ferrin structure, representing approximately 6 percent of the transferrin
molecule. Carbohydrate is an organic compound that consists of carbon,
hydrogen, and oxygen, and can be expressed as Cm(H2O)n, and glucose is
a simple carbohydrate, expressed as C6H12O6. Another common name for
carbohydrate is saccharide. Glucose is a monosaccharide (a simple sugar
that cannot be broken down further), while sucrose, or common cane
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138 Chapter 7
sugar (table sugar), is a disaccharide (contains two monosaccharide mol-

ecules and can be broken down into two simple sugar molecules: glucose
and fructose). Starch is a polysaccharide. Sialic acid, an integral compo-
nent of transferrin, is a monosaccharide. So in a broader sense, sialic acid
can also be termed as a carbohydrate.
Transferrin is found in blood in several different molecular forms called
isoforms. These molecular forms differ in the number of their carbohy-
drate groups (sialic acid and other carbohydrate residues) and carry differ-
ent electrical charges. The major form of transferrin is tetrasialotransferrin,
which has four sialic acid moieties attached to the molecule and represents
approximately 80 percent of all transferrin molecules in a healthy individ-
ual. Other transferrin molecules found in blood may have more (5–8 sialic
acid moieties) or less (0–3 sialic acid moieties) carbohydrate.
Acetaldehyde formed from alcohol by the liver enzyme aldehyde de-
hydrogenase is known to interfere with the incorporation of sialic acid
moiety to transferrin, resulting in the formation of transferrin molecules
with zero, one, or two sialic acid moieties attached to the final molecules.
In addition, these isoforms of transferrin may also have reduced carbohy-
drate residue. Chronic excess alcohol consumption (approximately 60 gm
or more alcohol per day or five or more drinks per day) for one to two
weeks causes an increase in transferrin molecules in blood with only two
sialic acid moieties (disialotransferrin) attached to the final molecule with
an accompanying lesser increase in the concentration of monosialotrans-
ferrin (one sialic acid) or asialotransferrin (no sialic acid). Because sialic
acid is a carbohydrate and usually four sialic acid moieties or more are
found in transferrin, collectively disialotransferrin, monosialotransferrin,
and asialotransferrin are called carbohydrate-deficient transferrin.
Trisialotransferrin (three sialic acid moieties) is generally thought not
to increase in response to heavy alcohol consumption. In the clinical
laboratory, various forms of transferrin can be measured by separating
them based on their electrical charges, using a complex technique known
as capillary zone electrophoresis. Carbohydrate-deficient transferrin can
also be measured in a clinical laboratory by other complex analytical
techniques, such as high-performance liquid chromatography and N-
Latex Direct carbohydrate-deficient transferrin immunoassay. The first
developed assays for measuring carbohydrate-deficient transferrin were
based on ion exchange chromatography to separate disialotransferrin,
and carbohydrate-deficient transferrin value was expressed as units/liter.
Later other assays were developed, and currently carbohydrate-
deficient transferrin in blood is reported as the percentage of total
transferrin in blood. For example, in the automated immunoassay for
transferrin (N-Latex Direct carbohydrate-deficient transferrin immunoas-
say), a specific monoclonal antibody that recognizes disialotransferrin,
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monosialotransferrin, and asialotransferrin is used in combination with a

simultaneous assay for total transferrin, and the values are expressed as
the percentage of carbohydrate-deficient transferrin.11 Usually in heavy
users of alcohol, the value of carbohydrate-deficient transferrin is above 2
percent of total transferrin.12 In another report (Sorvajärvi et al. 1996), the
authors stated that in alcohol abusers (consuming more than 80 gm of alco-
hol per day), the mean concentration of carbohydrate-deficient transferrin
is 29.2 units/liter compared to the mean value of 19.0 units/liter observed
in controls. In addition, the mean percentage of carbohydrate-deficient
transferrin was 2.2 percent in alcohol abusers compared to 0.1 percent in
controls (nondrinkers and social drinkers).13 The advantage of knowing
the percentage of carbohydrate-deficient transferrin is that it automatically
corrects any fluctuations in transferrin levels not related to alcohol abuse.
It is generally assumed that at least 60 gm of alcohol per day for a man
and at least 40 gm of alcohol per day for a woman for at least a week
is needed for carbohydrate-deficient transferrin percentage in blood to
rise above the cutoff reference value. Individuals who consume more
alcohol than the level stated here (this is equivalent to heavy alcohol
consumption) may have alcohol dependence (alcoholics), and these in-
dividuals also have a higher percentage of carbohydrate-deficient trans-
ferrin in their blood. A report by Rosalki (2004) stated that 50 percent
of heavy drinkers and 80 percent of alcoholics demonstrated elevated
carbohydrate-deficient transferrin levels in blood.
However, carbohydrate-deficient transferrin has less sensitivity for
identifying female heavy drinkers than for identifying male heavy drink-
ers. This marker is also more sensitive for identifying older individuals
who are heavy drinkers compared to younger individuals. Because some
alcohol abusers show a higher percentage of carbohydrate-deficient trans-
ferrin but normal GGT and vice versa, combining both markers is ideal to
identify individuals who abuse alcohol. After complete abstinence, carbo-
hydrate-deficient transferrin returns to normal levels within two weeks.
There are ethnic variations in carbohydrate-deficient transferrin, as val-
ues are more elevated in alcoholic Puerto Ricans than alcoholic Blacks and
alcoholic Caucasians but not when abstinent. Pregnant women, women
using oral contraceptives, and patients suffering from iron-deficient ane-
mia may also have higher percentages of carbohydrate-deficient trans-
ferrin. In addition, such increase may also be observed in people with
hypertension, smokers, and in obese people.14
Whitfield et al. (2008) reported that carbohydrate-deficient transferrin
increased in men who consumed more than seven drinks per week, and
such increases were more significant with the number of drinks consumed
per week. For women, however, a maximum value of the percentage of
carbohydrate-deficient transferrin was reached with twenty-nine to
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140 Chapter 7
thirty-five drinks per week, and then the value did not change signifi-
cantly in women who drank more than that amount. Again, the authors
used 2 percent as the cutoff concentration for the percentage of carbohy-
drate-deficient transferrin. The authors further stated that the percentage
of carbohydrate-deficient transferrin is a poor marker for alcohol abuse in
both men and women who are obese, and is also less useful in nonsmok-
ers than smokers.15
Golka and Wiese (2004) commented that carbohydrate-deficient transfer-
rin is a superior biomarker than conventional biomarkers such as GGT and
MCV, but combining all these parameters may provide superior diagnostic
value in identifying patients who are abusing alcohol, because mechanisms
of elevation of these three biomarkers are different from one another. In
addition, carbohydrate-deficient transferrin determinations are particularly
useful to identify patients with chronic alcohol dependence and relapse
after withdrawal, license reapplication after suspension for driving with
blood alcohol exceeding the legal limit, and patients treated for galacto-
semia, as well as for identifying patients suffering from a genetic disorder
called carbohydrate-deficient glycoprotein syndrome. The carbohydrate-
deficient transferrin value is not usually affected by medications except in
immunosuppressant patients who may show low carbohydrate-deficient
transferrin values. The authors also stressed that carbohydrate-deficient
transferrin values appear less elevated in women than men.16
Serum and Urine beta-Hexosaminidase as Alcohol Biomarkers

Hexosaminidase, also known as N-acetyl glucosaminidase, is a lysosomal
enzyme (lysosome is a spherical organelle, a small structure with the cell
that contains certain enzymes that can break down food) found in most
body tissues, especially in the kidneys where the concentrations are even
higher than other tissues. This enzyme breaks down carbohydrates and
gangliosides. Gangliosides are complex lipids, also known as glycosphin-
golipids, that are found in cell membranes, particularly in nerve cells, and
play an important role in cell-to-cell communication. The hexosaminidase
molecule is composed of two units, alpha and beta, and both units are
composed of amino acids (polypeptides), and variations of the arrange-
ments of these chains result in various molecular forms of hexosamini-
dase known as isoforms. The hexosaminidase S is composed of two alpha
chains, while hexosaminidase B, I, and P are composed of two beta chains.
Hexosaminidase A is composed of one alpha and one beta chain. Isoforms
B, I, and P are heat stable and collectively called beta-hexosaminidase,
while isoforms A and S are heat labile.
The heat stable form of beta-hexosaminidase is elevated after heavy
consumption of alcohol because lysosomes (small spherical structures
10-649_Dasgupta.indb 140 1/17/11 6:40 AM

inside the cell) are damaged, and subsequently enzymes are released in
blood. Beta-hexosaminidase activity is also found in elevated concen-
tration in urine. Total serum beta-hexosaminidase activity, particularly
beta-hexosaminidase B isoform (beta-Hex B) activity, as well as total
urinary beta-hexosaminidase activity, is increased in alcoholics com-
pared to moderate drinkers and nondrinkers. Wehr et al. (1991) reported
increased activity of serum and urinary beta-hexosaminidase after drink-
ing more than 60 gm of alcohol daily (five or more drinks) for at least
ten consecutive days.17 The blood beta-hexosaminidase activity returns
to normal usually after abstinence for seven to ten days, while it may
take up to four weeks for urine beta-hexosaminidase activity to return to
normal values. Serum beta-hexosaminidase B activity as a percentage of
total hexosaminidase activity, expressed as the percentage of beta-Hex B,
is also a very sensitive marker for alcohol abuse.
Stowell et al. (1997) compared carbohydrate-deficient transferrin and
beta-hexosaminidase activity along with liver enzymes and MCV in
alcoholic patients and compared the values obtained in moderate and
nondrinking subjects. The total beta-hexosaminidase activity was in gen-
eral 2.5 times higher in alcoholics compared to moderate drinkers, and
this increase was mainly due to a fivefold increase in the activity of B
isoform. The average beta-hexosaminidase activity in alcoholics was 49.6
units/liter compared to 19.4 units/liter in moderate drinkers. However,
the average concentration of B isoform was 28.4 units/liter in alcoholics
compared to 5.7 units/liter in moderate drinkers. Therefore, the percent-
age of beta-Hex B was 52.4 percent in alcoholics and 29.0 percent in mod-
erate drinkers. The mean carbohydrate-deficient transferrin activity was
60.2 units/liter in alcoholics and 16.9 units/liter in moderated drinkers
(cutoff concentration was 20 units/liter). Specimens from alcoholics were
collected during admission to the authors’ hospital for alcohol detoxifica-
tion. The authors concluded that the serum percent of Hex B is a very
sensitive and specific marker for detecting people who drink more than
60 gm of alcohol per day on a regular basis and is slightly more sensi-
tive to carbohydrate-deficient albumin as a biomarker for alcohol. Beta-
hexosaminidase activity can be measured by using inexpensive reagents
and a spectrophotometer or a fluorometer.18
In another report Kärkkäinen (1990), using thirty-two alcoholic men
admitted to the detoxification center for treatment for seven days and
twenty-seven nondrinkers, demonstrated that total serum hexosamini-
dase activities were increased in 68.8 percent of alcoholics on admis-
sion while urine total beta-hexosaminidase activities were increased in
81.3 percent of patients compared to nondrinkers. Following a week of
abstinence, serum and urine total beta-hexosaminidase activities were
increased in 37.5 percent and 71.9 percent patients, respectively. These
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142 Chapter 7
results indicate that urine beta-hexosaminidase activity may be a more

sensitive marker of heavy alcohol consumption compared to serum beta-
hexosaminidase activity.19 Although beta-hexosaminidase activities are
increased after heavy consumption of alcohol for at least ten days, a paper
published in 2008 indicated that binge drinking (heavy consumption of
alcohol in one occasion, see chapter 2 for more detail) may also signifi-
cantly increase both serum and urine activities of beta-hexosaminidase. In
this study, eight binge drinkers (reported binge drinking event one to two
times a month) who abstained from consuming alcohol and drugs for ten
days, in one occasion drank 120–160 gm of alcohol along with light meals
and fruit juices between 7 pm and 1 am while staying at home under su-
pervision. Blood, urine, and saliva specimens were collected from these
subjects 12 hours prior to drinking and also 36 and108 hours after finish-
ing drinking. The total beta-hexosaminidase activity in serum increased
from a mean value of 33.0 prior to drinking to 50.0, 108 hours after drink-
ing. At 36 hours significant increases in beta-hexosaminidase activities
were also observed in saliva and urine. The authors concluded that binge
drinking in one occasion may also increase beta-hexosaminidase activities
in serum, urine, and saliva.20
Other than heavy alcohol consumption, elevated serum hexosamini-
dase activity may occur in patients with severe liver disease (such as cir-
rhosis of liver), hypertension, diabetes, after heart attack, thyrotoxicosis
(a disorder causing very high thyroid hormones levels in the body, which
may be life-threatening), and pregnancy.21
Sialic Acid as an Alcohol Biomarker

Sialic acids are a family of thirty-six naturally occurring acetylated de-
rivatives of neuraminic acid, which are found in carbohydrate chains of
glycoprotein (proteins with carbohydrate moieties) in biological fluids
such as blood and cell membranes. The most abundant sialic acid is N-
acetylneuraminic acid. These compounds play important roles in cell-to-
cell communication or serve as a recognition site on the cell surface. Total
sialic acid in blood can be measured after breaking down conjugated
sialic acid (hydrolysis) using either a strong acid or an enzyme and then
quantitation of total sialic acid by an analytical method such as high
performance liquid chromatography. There are also immunoassays for
estimating sialic acid in blood. In one study (Sillanaukee et al. 1999), the
authors reported that total sialic acid level in the blood of female social
drinkers (less than 30 gm of alcohol per week) and male social drinkers
(less than 50 gm of alcohol per week) were 40–79 mg/100 mL and 42 to
97 mg/100 mL, respectively. In contrast, the total sialic acid content in
female alcoholics (more than 800 gm of alcohol per week) varied from
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62 to 132 mg/100 mL, while the sialic acid content of male alcoholics
(more than 1000 gm of alcohol per week) varied from 62 to 158 mg/100
mL. The authors measured the total sialic acid level in the blood using a
radioimmunoassay. During a follow-up of twenty-eight alcoholic patients
participating in inpatient detoxifying treatment, sialic acid levels were de-
creased after three weeks. However, elevated sialic acid content may also
be encountered in patients suffering from tumor, diabetes, inflammation,
and cardiovascular diseases.22
Acetaldehyde-Protein Adducts as Alcohol Biomarkers

Acetaldehyde is the first degradation product of alcohol formed by the
metabolism of alcohol in the liver by alcohol dehydrogenase. Acetalde-
hyde is highly reactive and is rapidly converted into acetic acid by an-
other liver enzyme, acetaldehyde dehydrogenase, and then acetic acid is
rapidly converted into water and carbon dioxide by further degradation.
Acetaldehyde, being highly reactive, also rapidly forms stable adducts
with a number of compounds, including proteins such as albumin (most
abundant protein in the blood) and hemoglobin (hemoglobin is also a
protein). These adducts are found mostly in chronic heavy consumers
of alcohol because acetaldehyde levels are more significantly elevated
in these individuals than in moderate or social drinkers. Hemoglobin-
acetaldehyde adduct has received more attention in the scientific com-
munity as a biomarker of alcohol abuse. In addition to blood, this marker
is also found in elevated levels in urine.
Aldehyde hemoglobin adducts can be formed within thirty minutes
of drinking, and the first adduct formed is called reversible hemoglobin-
acetaldehyde adduct because it can break down into acetaldehyde and
hemoglobin. This adduct is formed by the reaction of hemoglobin inside
the red blood cell (erythrocyte) with acetaldehyde. These reversible ad-
ducts can be detected up to forty-eight hours after the last drink. Then
the reversible adduct is converted into irreversible adduct, which does
not break down into hemoglobin and acetaldehyde. The irreversible
(stable) hemoglobin acetaldehyde adducts accumulate in the blood of
chronic drinkers and remain detectable in blood for at least twenty-
eight days. Hemoglobin-acetaldehyde adduct concentration is higher
in men than women because men usually have higher blood levels of
hemoglobin. In addition, hemoglobin-acetaldehyde adduct concentra-
tions are significantly higher in alcohol abusers than nondrinkers.23 The
chemistry of hemoglobin-acetaldehyde adduct is complex because there
is more than one type of adduct. This is because acetaldehyde, being
very reactive, can form adducts by bonding with hemoglobin at differ-
ent parts of the molecule.24
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144 Chapter 7
Measurement of hemoglobin-acetaldehyde adduct in human blood is

difficult. Initial techniques involved high-performance liquid chromatog-
raphy with isoelectric focusing gel and affinity chromatography, but very
low levels of such adducts pose a technical challenge. A complex immu-
noassay method known as enzyme-linked immunosorbent assay (ELISA)
has been developed more recently for detecting hemoglobin-acetaldehyde
adducts in blood. However, the major advantage of this biomarker is that
it is a direct biomarker of alcohol abuse, because acetaldehyde is derived
from consuming alcohol. In addition, false positive results are rarely en-
countered. Niemela et al. (1991) reported that this is an excellent marker
for detecting pregnant women who abuse alcohol, because the highest
concentrations of hemoglobin-acetaldehyde adduct were observed in
women who delivered babies with fetal alcohol syndrome.25
Ethyl Glucuronide and Ethyl Sulfate as Alcohol Biomarkers

Ethyl glucuronide and ethyl sulfate are minor degradation products
(metabolite) of alcohol that are found in various body fluids and also in
human hair. Ethyl glucuronide is formed by direct conjugation of ethanol
and glucuronic acid through the action of a liver enzyme. Ethyl sulfate is
also formed directly by the conjugation of ethanol with a sulfate group.
These compounds are water soluble. Ethyl glucuronide can be detected
after eighty hours post-alcohol consumption and is found shortly after
drinking even small amounts of alcohol. Therefore, ethyl glucuronide is
considered a sensitive and specific marker for alcohol consumption, as
well as a direct biomarker of alcohol.
Ethyl glucuronide can be measured in urine, blood, and hair speci-
mens. Ethyl glucuronide can be determined using a variety of methods,
including gas chromatography coupled with mass spectrometry, liquid
chromatography combined with mass spectrometry, and immunoassay.
In one study (Schmitt et al. 1997) healthy moderate drinkers who ingested
one standard drink showed a maximum ethyl glucuronide level of 3.7
mg/L in serum, and ethyl glucuronide was detected eight hours after
alcohol was completely eliminated from the body and no longer detect-
able in the blood. In serum samples of nondrinkers, no ethyl glucuronide
can be detected. In thirty-seven out of fifty drivers suspected of driving
under the influence of alcohol, serum ethyl glucuronide concentration
ranged from 0.1 to 20 mg/L. The authors concluded that if serum ethyl
glucuronide level exceeds 5 mg/L, it can be assumed that the person is
misusing alcohol.26
Concentration of ethyl glucuronide and ethyl sulfate in serum is higher
than concentration in whole blood because both compounds are readily
soluble in water and therefore found in higher amounts in serum (the water
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part of the blood) than in blood cells (red blood cells, white blood cells, and
other blood cells). In general, ethyl glucuronide concentrations are higher
than ethyl sulfate concentrations. In one study using thirteen subjects
(Hoiseth et al. 2009), the ethyl glucuronide concentrations ranged from 0.63
to 9.81 mg/L in serum and 0.39 to 5.53 mg/L in whole blood. The median
serum to whole blood ratio was 1.69 and the range was 1.33 to 1.90.
Similarly, for ethyl sulfate, the serum concentration in thirteen volun-
teers ranged from 0.11 to 2.64 mg/L and whole blood ethyl sulfate con-
centrations ranged from 0.10 to 1.82 mg/L. The median serum to whole
blood ethyl sulfate concentration was 1.30 and the range was 1.08 to 1.47.
Because both whole blood and serum ethyl glucuronide, as well as ethyl
sulfate values, are determined in deceased in forensic investigations, the
authors stressed the need of understanding that serum levels of both
ethyl glucuronide and ethyl sulfate are substantially higher than whole
blood values in interpreting such results.27
Because alcohol is produced by bacterial action after death, ethyl gluc-
uronide and ethyl sulfate are postmortem markers of antemortem alcohol
ingestion. A small amount of alcohol is produced by the action of bacteria
in a deceased person not consuming any alcohol, but neither ethyl gluc-
uronide nor ethyl sulfate is formed after death. In one study (Hoiseth
et al. 2009) involving thirty-six death investigations where postmortem
ethanol production was suspected, ethyl glucuronide and ethyl sulfate
were measured in both urine and blood of the deceased. In nineteen out
of thirty-nine deceased, the range of ethyl glucuronide in blood ranged
from 0.1 to 23.2 mg/L, while urinary ethyl glucuronide concentrations
ranged from 1.9 to 182 mg/L. For ethyl sulfate, the blood concentration
ranged from 0.04 to 7.9 mg/L, while urine concentrations ranged from 0.3
to 99 mg/L. In sixteen other individuals no ethyl glucuronide or ethyl sul-
fate was detected. The authors concluded that in thirty-six cases, alcohol
consumption before death was likely in nineteen deceased who showed
positive ethyl glucuronide and ethyl sulfate concentrations in blood
and urine.28
Ethyl glucuronide is a sensitive marker for alcohol consumption and
can be detected even after small amounts of alcohol are ingested, such as
1 gm to 3 gm of alcohol where a standard drink contains 14 gm of alco-
hol. In a study (Thierauf et al. 2009) involving thirty-one volunteers who
drank either 1 or 3 gm of alcohol, maximum amount of ethyl glucuronide
in urine was 0.32 mg/L after drinking only 1 gm of alcohol. Similarly,
maximum ethyl glucuronide after drinking 3 gm of alcohol was 1.53
mg/L. The corresponding ethyl sulfate levels were 0.15 mg/L (after 1
gm of alcohol) and 1.17 mg/L (after 3 gm of alcohol). These maximum
achieved concentrations are considered positive by many laboratories
testing urine for ethyl glucuronide and ethyl sulfate for workplace alcohol
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146 Chapter 7
testing and noncompliance of patients undergoing alcohol rehabilitation

therapy.29 Therefore no alcohol consumption is safe to drink, at least for
a day or two prior to taking preemployment alcohol tests (see more on
this in chapter 9).
Determination of ethyl glucuronide in hair specimens has merit to
identify heavy drinkers because ethyl glucuronide can be determined for
a longer time in hair than in blood or urine. Morini et al. (2009) used liq-
uid chromatography combined with mass spectrometry to determine hair
concentrations of ethyl glucuronide in ninety-eight volunteers, including
nondrinkers, social drinkers, and heavy drinkers. The authors concluded
that ethyl glucuronide levels of 27 picogram/milligram of hair can be
achieved in a person drinking 60 gm or higher amount of alcohol (five or
more drinks) per day for at least three months. Age, gender, body mass
index, smoking, hair color, and cosmetic treatment appear to have no ef-
fect on ethyl glucuronide level detected in hair specimen.30
In another report (Lamoureaux et al. 2009), the authors determined
concentrations of ethyl glucuronide in hair using only 30 mg of hair
specimen and liquid chromatography combined with mass spectrometry.
The method was applied to analyze hair samples taken from four fatali-
ties with documented excessive drinking habits, twelve heavy drinkers,
and seven social drinkers. Ethyl glucuronide concentrations in hair of
social drinkers were less than 10 picogram/milligram of hair, while ethyl
glucuronide concentrations were above 50 picogram/milligram of hair
(range 54–497) in hair specimens of heavy drinkers and deceased known
to abuse alcohol.31
Fatty Acid Ethyl Esters as Alcohol Biomarkers

Fatty acid ethyl esters are direct markers of alcohol abuse because they
are formed due to a chemical reaction between fatty acids and alcohol
(ethanol). Fatty acids are an integral part of the structures of triglycerides
(fats), but a small amount of fatty acids, also known as free fatty acids,
are found in circulation. The chemical reaction between alcohol and fatty
acid is known as esterification, which is mediated by fatty-acyl-ethyl-ester
synthase (FAEE synthase), an enzyme found in abundance in the liver and
pancreas. Carboxylesterase lipase, another enzyme that liberates free fatty
acids from complex lipids, can also induce the reaction between alcohol
and fatty acids, generating fatty acid ethyl esters. Therefore, hydrolysis of
triglycerides and phospholipids generating fatty acids in the presence of
alcohol may eventually be converted into fatty acid ethyl esters. Fatty acid
ethyl esters are also known as nonoxidative metabolites of ethanol, while
acetaldehyde and acetic acid are oxidative metabolites of ethanol, which
are formed by the action of liver enzymes.
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Fatty acid ethyl esters are formed primarily in the liver and pancreas
and then are released into circulation. These compounds are also incor-
porated into hair follicle through sebum and can be used as a biomarker
of alcohol abuse. There are four major fatty acid ethyl esters: ethyl my-
ristate, ethyl palmitate, ethyl stearate, and ethyl oleate. These compounds
are measured after extraction from hair or blood and analyzed using a
sophisticated instrument known as gas chromatography/mass spectrom-
etry. Then results are usually expressed as the sum of all four fatty acid
ethyl ester concentrations.
It has long been known that ethanol abuse leads to severe damage of
the liver and pancreas. Although acetaldehyde, the oxidative metabolite
of alcohol, was long thought as the mediator of organ damage, more
recent studies indicate that fatty acid ethyl esters are also responsible for
damaging the liver and pancreas, because enzymes that facilitate forma-
tion of fatty acid ethyl esters are found in the highest concentrations in the
pancreas and liver. In addition, the total concentration of major fatty acid
ethyl esters in blood is a good marker for both acute and chronic alcohol
intake. Fatty acid ethyl esters can be detected in blood for up to twenty-
four hours after drinking. In contrast, blood alcohol level declines more
rapidly and can be undetectable even four to twelve hours after drinking,
depending on the amount consumed. A negative blood alcohol with a
positive fatty acid ethyl ester test is consistent with ethanol intake four to
twenty-four hours prior to blood collection. If fatty acid ethyl ester and
carbohydrate-deficient transferrin tests are both positive, a patient can be
suspected as a chronic consumer of alcohol.32
Analysis of fatty acid ethyl esters in hair is a good marker of alcohol
abuse because these compounds can be detected in hair for a much lon-
ger time than in blood. In one study (Auwarter et al. 2001), the authors
analyzed hair specimens from nineteen alcoholics enrolled in a treatment
program, ten fatalities with verified excess alcohol consumption, thirteen
moderate social drinkers who consumed up to 20 gm of alcohol per day
(1.5 drinks on average), and five nondrinkers for fatty acid ethyl esters
(ethyl myristate, ethyl palmitate, ethyl stearate, and ethyl oleate). The to-
tal concentration ranged from 2.5 to 13.5 ng/milligram of hair (mean 6.8)
for fatalities, 0.92–11.6 ng/milligram of hair in alcoholics (mean 4.0), 0.20
to 0.85 ng/milligram of hair in social drinkers (mean 0.41), and 0.06–0.37
ng/milligram of hair in nondrinkers (mean 0.16). The authors concluded
that despite large individual differences, fatty acid ethyl esters can be
used as markers of excessive alcohol consumption.33
In another report (Pragst and Yegles 2008), the authors suggested that
moderate and social drinkers should have hair fatty acid ethyl ester concen-
trations below 0.5 ng/milligram and ethyl glucuronide concentrations in
hair below 25 pg/milligram. Above these values, alcohol abuse is possible.34
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148 Chapter 7
Fatty acid ethyl esters can be used for evaluating drinking problems with
pregnant women and can aid in diagnosis of fetal alcohol spectrum disor-
ders. Fatty acid ethyl esters detected in meconium can be related to exposure
of the fetus to alcohol due to maternal consumption of alcohol. Fatty acid
ethyl esters may be markers for identifying newborns who are at risk of
neurodevelopmental delay due to alcohol exposure in utero.35
Phosphatidyl ethanol, which is formed due to a reaction between phos-
phatidylcholine and ethanol mediated by the enzyme phospholipase D,
is an emerging biomarker of alcohol abuse. Phosphatidylcholine is an
important lipid that plays an essential role in forming cell membranes.
CONCLUSION
Alcohol abuse is a serious public health concern, and it is important to

screen patients who are at risk of alcohol abuse by using appropriate
biomarkers so that early intervention can be achieved to treat such in-
dividuals. At present there is no unique marker for determining alcohol
abuse, and various markers have their advantages and limitations. Ethyl
glucuronide, ethyl sulfate, and fatty acid ethyl esters are valuable mark-
ers for assessing alcohol abuse because these markers are direct markers
for alcohol consumption and are specific in nature. However, determin-
ing such markers in blood or hair is technically difficult and not feasible
to perform in small hospital laboratories. In contrast, liver enzymes and
MCV are routinely determined in most hospital laboratories and are
cost-effective. However, such indirect markers are not specific for alcohol
abuse and can be elevated in certain disease conditions.
NOTES
1. A. S. St. Leger, A. L. Cochrane, and F. Moore, “Factors Associated with Car-

diac Mortality in Developed Countries with Particular Reference to the Consump-
tion of Wine,” Lancet 1979 (1): 1017–20.
2. Alcohol and Public Health, Center for Disease Control, Atlanta, Georgia,
http://www.cdc.gov/.
3. S. E. Foster, R. D. Vaughan, W. H. Foster, and J. A. Califano, “Alcohol Con-
sumption and Expenditures for Underage Drinking and Adult Excessive Drink-
ing,” Journal of the American Medical Association 289, no. 8 (February 2003): 989–95.
4. S Anai, C. S. West, M. Chang, K. Nakamura, et al., “Outcome of Men Who
Present with Elevated Serum PSA (>20 ng/ml) to an Inner City Hospital,” Journal
of National Medical Association 99, no. 8 (August 2007): 895–99.
5. N. Alkan and T. Demircan, “Determination of Blood Alcohol Level in People
Who Are Involved in a Judicial Event of Medical Importance (Case Report),”
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Ulusal Travma Dergisis [The Turkish Journal of Trauma] 7, no. 4 (October 2001):
277–81. [Article in Turkish.]
6. P. M. Miller, S. M. Ornstein, P. J. Nietert, and R. Anton, “Self-Reporting and
Biomarker Alcohol Screening by Primary Care Physicians: The Need to Translate
Research Guidelines and Practice,” Alcohol and Alcoholism 39, no. 4 (2004): 325–28.
7. P. M. Miller, C. Spies, T. Neumann, M. Javor, et al. “Alcohol Biomarker
Screening in Medical and Surgical Settings,” Alcoholism Clinical and Experimental
Research 30, no. 2 (February 2006): 185–93.
8. P. Alatalo, H. Kovistro, K. Puuka, J. Hietala, et al., “Biomarkers of Liver Sta-
tus in Heavy Drinkers, Moderate Drinkers and Abstainers,” Alcohol and Alcoholism
44, no. 2 (March–April 2009): 199–203.
9. G. Targher, “Review: Elevated Gamma Glutamyltransferase Activity Is As-
sociated with Increased Risk of Mortality, Incidence of Diabetes, Cardiovascular
Events, Chronic Kidney Disease and Cancer,” Clinical Chemistry and Laboratory
Medicine 48, no. 2 (February 2010): 147–57.
10. H. Koivistro, J. Hietala, P. Anttila, S. Parkkila, et al., “Long-Term Ethanol
Consumption and Macrocytosis: Diagnosis and Pathogenic Implications,” Journal
of Laboratory and Clinical Medicine 147, no. 4 (April 2006): 191–96.
11. J. R. Delanghe, A. Helander, J. P. Wielders, J. M. Pekelharing, et al., “De-
velopmental and Multicenter Evaluation of N-latex CDT Direct Immunonephelo-
metric Assay for Serum Carbohydrate-Deficient Transferrin,” Clinical Chemistry
53, no. 6 (June 2007): 1115–21.
12. J. R. Delanghe and M. L. De Buyzere, “Carbohydrate-Deficient Transferrin
and Forensic Medicine,” Clinica Chimica Acta 406, nos. 1–2 (August 2009): 1–7.
13. K. Sorvajärvi, J. E. Blake, Y. Israel, and O. Niemelä, “Sensitivity and Speci-
ficity of Carbohydrate-Deficient Transferrin as a Marker of Alcohol Abuse Are
Significantly Influenced by Alteration in Serum Transferrin: Comparison of Two
Methods,” Alcoholism: Clinical and Experimental Research 20, no. 3 (May 1996):
449–54.
14. S. B. Rosalki, “Carbohydrate-Deficient Transferrin: A Marker of Alcohol
Use,” International Journal of Clinical Practice 58, no. 4 (April 2004): 391–93.
15. J. B. Whitfield, V. Dy, P. A. Madden, A. C. Heath, et al., “Measuring
Carbohydrate-Deficient Transferrin by Direct Immunoassay: Factors Affecting
Diagnostic Sensitivity for Excessive Alcohol Intake,” Clinical Chemistry 54, no. 7
(July 2008): 1158–65.
16. K. Golka and A. Wiese, “Carbohydrate-Deficient Transferrin (CDT): A Bio-
marker for Long Term Alcohol Consumption,” Journal of Toxicology Environmental
Health, Part B: Critical Review 7, no. 4 (August 2004): 319–37.
17. H. Wehr, B. Czartoryska, D. Gorska, H. Matsumoto, et al., “Serum Beta-
Hexosaminidase and Alpha-Mannosidase Activities as a Marker of Alcohol Abuse,”
Alcoholism: Clinical and Experimental Research 15, no. 1 (February 1991): 13–15.
18. L. Stowell, A. Stowell, N. Garrett, and G. Robinson, “Comparison of Serum
Beta-Hexosaminidase Isoenzyme B Activity with Serum Carbohydrate-Deficient
Transferrin and Other Markers of Alcohol Abuse,” Alcohol and Alcoholism 32, no.
6 (December 1997): 703–14.
19. P. Kärkkäinen, “Serum and Urine Beta-Hexosaminidase as Markers of
Heavy Drinking,” Alcohol and Alcoholism 25, no. 4 (July–August 1990): 365–69.
10-649_Dasgupta.indb 149 1/17/11 6:40 AM

150 Chapter 7
20. N. Waszkiewicz, S. D. Szajda, A. Jankowska, A. Kepka, et al., “The Effect of

the Binge Drinking Session on the Activity of Salivary, Serum and Urinary Beta-
Hexosaminidase: Preliminary Data,” Alcohol and Alcoholism 43, no. 4 (July–August
2008): 446–50.
21. P. Karkkainen, K. Poikolainen, and M. Salaspuro, “Serum Beta-
Hexosaminidase as Markers of Heavy Drinking,” Alcoholism: Clinical and Ex-
perimental Research 14, no. 2 (April 1990): 187–90.
22. P. Sillanaukee, M. Ponnio, and K. Seppa, “Sialic Acid: A New Potential
Marker of Alcohol Abuse,” Alcoholism Clinical and Experimental Research 23, no. 6
(June 1999): 1039–43.
23. S. K. Das, L. Dhanya, and D. M. Vasudevan, “Biomarkers of Alcoholism: An
Updated Review,” Scandinavian Journal of Clinical and Laboratory Investigation 68,
no. 2 (April 2008): 81–92.
24. M. D. Gross, R. Hays, S. M. Gapstur, M. Chaussee, et al., “Evidence for the
Formation of Multiple Types of Acetaldehyde Hemoglobin Adducts,” Alcohol and
Alcoholism 29, no. 1 (January 1994): 31–41.
25. O. Niemela, E. Halmesmaki, and O. Yikorkala, “Hemoglobin-Acetaldehyde
Adducts Are Elevated in Women Carrying Alcohol-Damaged Fetus,” Alcoholism:
Clinical and Experimental Research 15, no. 6 (December 1991): 1007–10.
26. G. Schmitt, P. Droenner, G. Skopp, and R. Aderjan, “Ethyl Glucuronide
Concentration in Serum of Human Volunteers, Teetotalers, and Suspected Drink-
ing Drivers,” Journal of Forensic Sciences 42, no. 6 (November 1997): 1099–1102.
27. G. Hoiseth, L. Morini, A. Polettini, A. S. Christophersen, et al., “Serum/
Whole Blood Concentration Ratio for Ethyl Glucuronide and Ethyl Sulfate,” Jour-
nal of Analytical Toxicology 33, no. 4 (May 2009): 208–11.
28. G. Hoiseth, R. Karinen, A. Christophersen, and J. Morland, “Practical Use
of Ethyl Glucuronide and Ethyl Sulfate in Postmortem Cases as Markers of Ante-
mortem Alcohol Ingestion,” International Journal of Legal Medicine 124, no. 2 (March
2010): 143–48.
29. A. Thierauf, C. C. Halter, S. Rana, V. Auwaerter, et al., “Urine Tested Posi-
tive for Ethyl Glucuronide after Trace Amounts of Ethanol,” Addiction 104, no. 12
(December 2009): 2007–12.
30. L. Morini, L. Politi, and A. Polettini, “Ethyl Glucuronide in Hair: A Sensitive
and Specific Marker of Heavy Drinking,” Addiction 104, no. 6 (June 2009): 915–20.
31. F. Lamoureux, J. M. Gaulier, F. L. Sauvage, M. Mercerolle, et al., “Determi-
nation of Ethyl Glucuronide in Hair for Heavy Drinking Detection Using Liquid
Chromatography-Tandem Mass Spectrometry Following Solid-Phase Extraction,”
Annals of Bioanalytical Chemistry 394, no. 7 (August 2009): 1895–1901.
32. M. Laposata, “Fatty Acid Ethyl Esters: Short-Term and Long-Term Serum
Markers of Ethanol Intake,” Clinical Chemistry 43, no. 8 (August 1997): 1527–34.
33. V. Auwarter, F. Sporkert, S. Harting, F. Pragst, et al., “Fatty Acid Ethyl
Esters in Hair as Markers of Alcohol Consumption: Segmental Hair Analysis of
Alcoholics, Social Drinkers and Teetotalers,” Clinical Chemistry 47, no. 12 (Decem-
ber 2001): 2114–23.
34. F. Pragst and M. Yegles, “Determination of Fatty Acid Ethyl Esters (FAEE)
and Ethyl Glucuronide (EtG) in Hair: A Promising Way for Retrospective Detec-
10-649_Dasgupta.indb 150 1/17/11 6:40 AM

tion of Alcohol Abuse during Pregnancy?” Therapeutic Drug Monitoring 30, no. 2
(April 2008): 255–63.
35. J. Peterson, H. L. K. Kirchner, W. Xue, S. Minnes, et al., “Fatty Acid Ethyl
Esters in Meconium Are Associated with Poorer Neurodevelopmental Outcomes
to Two Years of Age,” Journal of Pediatrics 152, no. 6 (June 2008): 788–92.
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8

Pharmaceuticals, Drugs
of Abuse, and Alcohol
A Potentially Deadly Mix
W e are all aware of the warning labels of many over-the-counter

(OTC) cold and allergy medications that state, “Avoid alcoholic
beverages while taking this medication.” The reason is that many allergy
medications and cold medications contain antihistamine drugs that cause
drowsiness, and alcohol can significantly enhance this effect. Combining
alcohol and antihistamines makes driving and/or operating machinery
much more difficult and not advisable. Many prescription medications
have similar warning labels. There are many reported interactions be-
tween various drugs and alcohol. In general, drug-alcohol interactions
cause only adverse effects and can be deadly.
HOW COMMON IS DRUG-ALCOHOL INTERACTION?
More than 2,800 prescription medications are available in the United

States, and physicians write 14 billion prescriptions annually. In addi-
tion, approximately 2,000 formulations are available over the counter.1
Approximately 70 percent of the U.S. population consumes alcohol
occasionally, and about 10 percent drink daily.2 So concurrent use of
alcohol and drugs can be construed as common among Americans.
According to the Substance Abuse and Mental Health Services Admin-
istration (SAMHSA), 36 percent of all patients (1.4 million) who visited
emergency rooms in 2005 had overdosed with a combination of alco-
hol, pharmaceuticals, and/or illicit drugs.3 The rest of the patients had
153
10-649_Dasgupta.indb 153 1/17/11 6:40 AM

154 Chapter 8
overdosed with pharmaceuticals or drugs of abuse. Alcohol was most

frequently combined with cocaine (estimated 86,482 visits), marijuana
(33,643 visits), both cocaine and marijuana (22,377 visits), and heroin
(12,797 visits). Another government report indicates that in 2004, an
estimated 363,641 emergency room visits by people of all ages involved
the use of alcohol combined with a drug.4 Elderly people in particular
are at higher risk from alcohol-drug interactions. Major drug-alcohol in-
teractions are listed in table 8.1. Few drugs enhance the effect of alcohol.
These drugs are listed in table 8.2.
CAN ALCOHOL-DRUG INTERACTION CAUSE DEATH?
Fatal toxicities frequently occur from alcohol and drug overdoses. In

many instances, in the presence of alcohol, a lower concentration of drug
may cause fatality due to drug-alcohol interactions. In a Finnish study
(Koski et al. 2005), it was found that median amitriptyline (an antidepres-
sant drug) and propoxyphene (a pain medication) concentrations were
lower in alcohol-related fatal cases compared to cases where no alcohol
was involved. The authors concluded that when alcohol is present, a
relatively small overdose of a drug may cause fatality.5 Although death
is more frequently observed in people abusing both alcohol and illicit
drugs, death due to consumption of alcohol and prescription medication
has also been reported.
In general, the toxicity of a particular drug is observed at a much

lower blood concentration in the presence of alcohol. In other words,
alcohol enhances the toxic effect of a drug it interacts with. Therefore,
a person who died from a drug and alcohol overdose probably would
have survived if alcohol was not consumed.
It has been well documented that heroin abusers who drink require less
heroin to overdose. In general, postmortem blood levels of morphine are
much lower than expected in tolerant individuals who died from a com-
bined morphine and alcohol overdose.6
A combination of alcohol and drugs is also a leading cause of death
in adolescence. In one report analyzing the causes of death among an
adolescent population, the authors observed that 20.8 percent of fatalities
were related to drug and alcohol combined overdose.7
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Table 8.1. Major Drug-Alcohol Interactions
Drug Class Trade Name ) Generic Name n) Drug-Alcohol Interaction
10-649_Dasgupta.indb 155
Allergies/colds/flu Alavert loratadine Drowsiness, dizziness; increased risk for overdose
Allegra, Allegra-D fexofenadine Avoid driving or operating heavy machinery.
Benadryl diphenhydramine
Clarinex desloratadine
Claritin, Claritin-D loratadine
Dimetapp Cold & brompheniramine
Allergy
Sudafed Sinus & chlorpheniramine
Allergy
Triaminic Cold & chlorpheniramine
Allergy
Tylenol Allergy chlorpheniramine
Sinus
Tylenol Cold & Flu chlorpheniramine
Atarax hydroxyzine
Angina (chest pain), Isordil isosorbide Rapid heartbeat, sudden changes in blood pressure, dizziness,
coronary heart disease nitroglycerin fainting
Anxiety and epilepsy Ativan lorazepam Drowsiness, dizziness; increased risk for overdose; slowed or
Klonopin clonazepam difficulty breathing; impaired motor control; unusual behavior;
Librium chlordiazepoxide and memory problems
Paxil paroxetine
Valium diazepam
Xanax alprazolam
Herbal Liver damage, drowsiness
preparations
(kava kava)
Arthritis Celebrex celecoxib Ulcers, stomach bleeding, liver problems
Naprosyn naproxen
Voltaren diclofenac
(continued)
1/17/11 6:40 AM
Table 8.1. (continued)
Blood clots Coumadin warfarin Occasional drinking may lead to internal bleeding; heavier
drinking may cause bleeding or may have the opposite effect,
resulting in possible blood clots, strokes, or heart attacks
Cough Delsym, dextromethorphan Drowsiness, dizziness; increased risk for overdose
Robitussin Avoid driving
Cough
Robitussin A–C guaifenesin +
codeine
Depression Anafranil clomipramine Drowsiness, dizziness; increased risk for overdose; increased
Celexa citalopram feelings of depression or hopelessness in adolescents (suicide)
Desyrel trazodone Avoid driving
Effexor venlafaxine
Elavil amitriptyline
Lexapro escitalopram
Luvox fluvoxamine
Norpramin desipramine
Paxil paroxetine Serious episode of high blood pressure if beer or wine contains
Prozac fluoxetine tyramine, which interacts with phenelzine and other drugs of
Serzone nefazodone this class.
Wellbutrin bupropion
Zoloft sertraline
Monoamine phenelzine
oxidase inhibitor
Nardil
Diabetes Glucophage metformin Liver toxicity and possibility of lactic acidosis with metformin.
Micronase glyburide Hypoglycemia or lack of sugar control with other drugs
Orinase tolbutamide
1/17/11 6:40 AM
Enlarged prostate Cardura doxazosin Dizziness, light-headedness, fainting
Flomax tamsulosin
Hytrin terazosin
Minipress prazosin
Heartburn, indigestion, Axid nizatidine Rapid heartbeat, sudden changes in blood pressure
sour stomach Reglan metoclopramide (metoclopramide); increased alcohol effect
Tagamet cimetidine
Zantac ranitidine
High blood pressure Accupril quinapril Dizziness, fainting, drowsiness; heart problems such as changes
Capozide hydrochlorothiazide in the heart’s regular heartbeat (arrhythmia)
Cardura doxazosin
Catapres clonidine
Cozaar losartan
Hytrin terazosin
Lopressor HCT hydrochlorothiazide
Lotensin benazepril
Minipress prazosin
Vaseretic enalapril
High cholesterol Advicor lovastatin + niacin Liver damage (all medications); increased flushing and itching
Altocor lovastatin (niacin); increased stomach bleeding (pravastatin + aspirin)
Crestor rosuvastatin
Lipitor atorvastatin
Mevacor lovastatin
Niaspan niacin
Pravachol pravastatin
Pravigard pravastatin + aspirin
Vytorin ezetimibe +
simvastatin
Zocor simvastatin
(continued)
1/17/11 6:40 AM
Table 8.1. (continued)
Infections Acrodantin nitrofurantoin Fast heartbeat, sudden changes in blood pressure; stomach pain,
Flagyl metronidazole upset stomach, vomiting, headache, flushing, or redness of the
Grisactin griseofulvin face; liver damage (isoniazid, ketoconazole)
Nizoral ketoconazole
Nydrazid isoniazid
Seromycin cycloserine
Tindamax tinidazole
Muscle pain Flexeril cyclobenzaprine Drowsiness, dizziness; increased risk of seizures; increased risk
Soma carisoprodol for overdose; slowed or difficulty breathing; impaired motor
control; unusual behavior; memory problems
Nausea, motion sickness Antivert meclizine Drowsiness, dizziness; increased risk for overdose
Atarax hydroxyzine
Dramamine dimenhydrinate
Phenergan promethazine
Pain (such as headache, Advil ibuprofen Stomach upset, bleeding, and ulcers; liver damage
muscle ache, minor Aleve naproxen (acetaminophen); rapid heartbeat. Chronic alcohol user
arthritis pain), fever, Excedrin aspirin, may experience severe overdose from small dosage of
inflammation acetaminophen acetaminophen.
Motrin ibuprofen
Tylenol acetaminophen
1/17/11 6:40 AM
Seizures Dilantin phenytoin Reduced effect of phenytoin; drowsiness with other drugs
Klonopin clonazepam
phenobarbital
Severe pain from injury, Darvocet–N propoxyphene Drowsiness, dizziness; increased risk for overdose; slowed or
postsurgical care, oral Demerol meperidine difficulty breathing; impaired motor control; unusual behavior;
surgery, migraines Fiorinal with butalbital + codeine memory problems, increased risk of death from overdose
codeine
Percocet oxycodone
Vicodin hydrocodone
Sleep problems Ambien zolpidem Drowsiness, sleepiness, dizziness; slowed or difficulty breathing;
Lunesta esopiclone impaired motor control; unusual behavior; memory problems
ProSom estazolam Avoid driving
Restoril temazepam
Sominex diphenhydramine
Unisom doxylamine
Herbal Increased drowsiness
preparations Avoid driving
(chamomile,
valerian,
lavender)
Source: National Institute of Alcohol Abuse and Alcoholism (NIH Publication No. 03-5329, revised 2007), http://pubs.niaaa.nih.gov/publications/Medicine/medicine.htm.
1/17/11 6:40 AM
160 Chapter 8
Table 8.2. Drugs That May Increase Blood Alcohol Level and Prolong the Effect of
Alcohol
Drug Class Specific Drug
Cardiovascular drug Verapamil increases blood alcohol concentration and prolongs
its effect.
Antibiotic Erythromycin increases alcohol absorption when low amount
of alcohol is consumed.
Antiemetic Metoclopramide enhances the effect of alcohol.
Antiulcer drug Cimetidine increases blood alcohol level more than ranitidine.
Case Reports
Case Report 1: A twenty-eight-year-old man was found dead by his
girlfriend. The postmortem analysis of the heart blood showed 90 mg/
dL (0.09 percent) of alcohol, which was slightly above the legal limit for
driving (0.08 percent). The heart blood also showed the presence of cypro-
heptadine (0.46 mg/L), a medication prescribed to his girlfriend. Cypro-
heptadine (trade name Periactin) is an antihistamine, anticholinergic, and
antiserotonergic agent that is used in treating allergies (especially hay fe-
ver), for stimulating appetite in underweight people, and for the manage-
ment of nightmares and post-traumatic stress disorder. This drug is safe
but may cause drowsiness. The level of the drug found in this individual
was moderate, and this drug rarely causes severe toxicity. However, in
this case, the medical examiner concluded that the person died from a
combined alcohol and cyproheptadine overdose.8
Case Report 2: Pure overdose from the antidepressant moclobemide (Au-

rorix) is not considered life threatening. However, one person died from
a combined overdose of moclobemide and alcohol. This person died after
consuming half a bottle of whiskey after ingesting this medication. The
authors concluded that whiskey consumption played an important role
in this case of fatal overdose.9
MECHANISM OF ALCOHOL-DRUG INTERACTIONS
Many different classes of drugs, including antibiotics, antidepressants,

antidiabetic medications, antihistamines, antipsychotic drugs, anticon-
vulsants, antiulcer medications, cardiovascular drugs, narcotic analge-
sics, non-narcotic analgesics, and sedative hypnotic drugs, interact with
alcohol. The mechanism of interaction of these drugs with alcohol can be
classified under two broad categories: pharmacokinetic interaction and
pharmacodynamic interaction.
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Pharmaceuticals, Drugs of Abuse, and Alcohol 161
• Pharmacokinetic Interaction: In this type of drug interaction, alcohol

affects the blood level and/or distribution of an interacting drug by
altering absorption, metabolism, or excretion of the drug. Alcohol
interferes with hepatic metabolism of many drugs and may increase
or decrease its blood concentration. The increased or decreased level
of the drug in the blood alters its pharmacological effects, that is, less
therapeutic benefits for reduced concentration or drug toxicity due to
increased concentration. For example, chronic alcohol consumption
can reduce the blood level of the antibiotic doxycycline by increas-
ing its metabolism by the liver. Therefore, efficacy of doxycycline is
reduced in people who consume alcohol regularly.
• Pharmacodynamic Interaction: This interaction occurs when alcohol
increases or decreases the action of an interacting drug without al-
tering its concentration. In general, alcohol and an interacting drug
with similar pharmacological actions may have an additive effect or
synergistic effect (the combined effect is more significant than the
pharmacological actions of each drug). For example, the popular
antiallergy medicine Benadryl (generic name diphenhydramine) is
an antihistamine that causes drowsiness, and alcohol acts synergisti-
cally with Benadryl to enhance this effect.
Interaction of Alcohol with OTC Allergy/Cold Medications

Many cold and allergy medications are available over the counter, and
some of these medications also carry a warning label stating that you
should not consume alcohol if you are taking this formulation. Alcohol
interacts with many first-generation antihistamines, which are found in
both cold and allergy formulations. In addition, alcohol also interacts
with analgesics, such as acetaminophen (active component of Tylenol)
and salicylate (aspirin), which are present in many cold formulations.
If you are taking any over-the-counter cold or allergy formulations, it

is advisable to limit drinking to not more than one glass of wine or a
bottle of beer per day. If you can avoid drinking altogether during this
time, it will be in your best interest.
First-generation antihistamines, such as diphenhydramine and chlor-

pheniramine, are present in many over-the-counter allergy, cold, and
sleeping aid formulations. In addition, hydroxyzine (Atarax) is a pre-
scription medication that is widely prescribed for treating various types
of allergic reactions. All these medications cross the blood-brain barrier
10-649_Dasgupta.indb 161 1/17/11 6:40 AM

162 Chapter 8
and cause drowsiness by depressing the central nervous system (CNS).

In addition, these drugs also cause some impairment of motor function.
Therefore, caution must be exercised when driving or operating heavy
machinery when you are taking one of these drugs. Alcohol is also a
CNS depressant and enhances the drowsiness caused by these drugs. In
addition, alcohol acts synergistically with these drugs in impairing mo-
tor function. Therefore, if you are taking one of these drugs, you must
limit your alcohol consumption. In addition, it is advisable not to drive
at all if you are taking any of these drugs and consuming any amount
of alcohol.
Many cold medications contain acetaminophen or salicylate. Acet-
aminophen, when consumed in recommended dosage (not exceeding
four 500 mg capsules a day), is a safe analgesic and antipyretic agent (re-
duces fever). However, overdose of acetaminophen is dangerous because
it causes liver damage. When a person consumes excess acetaminophen,
a toxic metabolite of acetaminophen is formed, and the liver does not
have enough supply of glutathione (an endogenously found tripeptide
containing three amino acids) to detoxify that toxic metabolite. This toxic
metabolite then damages hepatocytes (cells found in the liver). If an acet-
aminophen overdose is not treated in a timely manner using a specific
antidote (N-acetylcysteine; trade name Mucomyst), acetaminophen over-
dose could cause death.
If a person is a social drinker (one or two drinks a week), the risk of
toxicity from consuming alcohol and acetaminophen is low. Some re-
ports indicate that consuming one drink after ingesting acetaminophen
may even reduce the formation of toxic metabolite of acetaminophen by
the liver. On the other hand, chronic alcoholics are at an increased risk
of developing liver toxicity from consuming even therapeutic dosages
of acetaminophen. Chronic alcohol consumption reduces the storage of
glutathione in the liver, which detoxifies the toxic metabolite of acet-
aminophen. In addition, chronic alcoholism may also trigger the liver
to produce more toxic metabolite via induction of CYP2E1, a member of
liver enzymes (cytochrome P-450 mixed-function oxidase) responsible for
drug metabolism.
If you consume more than two to three drinks a day, you should not
take any medication containing acetaminophen without consulting
your doctor.
In one study (Wootton and Lee 1990), the authors identified seven alco-
holics who had severe liver injury soon after using acetaminophen for
10-649_Dasgupta.indb 162 1/17/11 6:40 AM

therapeutic purposes. All showed markedly high serum levels of liver

enzymes indicative of severe liver injury, and three individuals died. The
authors concluded that use of acetaminophen by an alcoholic patient is
potentially lethal.10 Furthermore, the elderly population is at higher risk
from acetaminophen-alcohol interaction.
Salicylate (aspirin) is a nonsteroidal anti-inflammatory drug that is
used in many over-the-counter pain medications. It is normally safe to
drink alcohol while you are taking aspirin or ibuprofen if you drink in
moderation (up to three drinks of alcohol a day for men, and two to
three drinks for women, two to three times in one week). If you drink
every day and consume more than three drinks of alcohol, then alcohol
may increase the risk of stomach irritation and may even cause gastric
bleeding. Regular intakes of salicylate in large dosages may cause gastric
irritation, heartburn, and even an ulcer. Alcohol enhances these negative
effects of salicylate. Intake of high doses of aspirin (1 gm) increases the
blood alcohol level by inhibiting the gastric enzyme alcohol dehydroge-
nase, which metabolizes alcohol.11 This enzyme is also present in the liver.
On the other hand, low-dose aspirin (usually available in 75 or 81 mg),
which is taken by many people on a regular basis to prevent heart attack
and stroke, actually decreases one’s blood alcohol level. Low-dose aspirin
delays the gastric absorption of alcohol when consumed in moderate dos-
ages.12 Older people who mix alcoholic beverages with large amounts of
aspirin for pain relief are at high risk of experiencing an episode of gastric
bleeding.13
If you drink regularly and consume more than three alcoholic drinks
each day, consult with your physician before taking aspirin or ibuprofen.
Interaction of Alcohol with OTC Pain Medications

Other than acetaminophen and salicylate, ibuprofen, ketoprofen, and
naproxen are also available as analgesics in many over-the-counter
medications. Like salicylate, all these drugs are classified as “nonsteroi-
dal anti-inflammatory drugs” because they control pain by inhibiting
cyclooxygenase enzyme. All these drugs can cause gastric irritation.
People who drink in moderation can consume these medications safely,
but heavy drinkers should not use these medications without consult-
ing with their physicians because of increased risk of developing gastric
bleeding and ulcers. With relatively stronger medications like naproxen
and ketoprofen, it is advisable not to drink at all when taking such
medications.
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164 Chapter 8
Interaction of Alcohol with Prescription Pain Medications

Prescription pain medications can be classified under two broad catego-
ries: (1) nonsteroidal anti-inflammatory medications, such as indometha-
cin, diclofenac, mefenamic acid, and so on; and (2) narcotic analgesics,
which are natural opiates such as morphine and codeine, as well as
synthetic opiates, such as hydromorphone, oxycodone, hydrocodone,
oxymorphone, meperidine, methadone, and propoxyphene.
In general, prescription nonsteroidal anti-inflammatory drugs are
much stronger than their OTC counterparts. These drugs also cause gas-
tric irritation, bleeding, and ulcers, and consumption of alcohol increases
this risk greatly. Consuming one or two drinks occasionally is not going
to cause any harm if you take these medications, but even if you consume
two to three drinks on a regular basis, you must discuss this with your
physician when such medications are prescribed for you.
Interactions between narcotic analgesics and alcohol cause more seri-
ous adverse effects than interactions between alcohol and nonsteroidal
anti-inflammatory drugs. These drugs are prescribed in patients to control
moderate to severe pain. The combination of alcohol and these narcotic
analgesic drugs enhances the sedative and respiratory depression effects of
both substances, and may cause severe overdose, prompting a situation that
could require hospital admission. Death may occur at a much lower blood
morphine level if an individual consumes alcohol.14 Alcohol interacts with
the extended-release mechanism of many opiate narcotic analgesics, caus-
ing excessive release of the drug (dose-dumping effect). As a result, coma or
even death may occur from an excessive blood level of the opiate medica-
tion. Recently, hydromorphone extended-release capsules (Palladone) were
withdrawn from the market because of the dose-dumping effect. Alcohol
enhances the CNS depression effect of oxymorphone, and such interac-
tion may cause slow respiration, lower blood pressure, and, in some cases,
coma. Alcohol increases blood concentration of propoxyphene by reducing
its first-pass metabolism. In addition, alcohol also reduces the psychomotor
skill of a person by acting in synergy with the opiate pain medication.
If you are taking any narcotic analgesic for pain management, please
do not consume alcohol.
Interaction of Alcohol with Sleeping Aids

Insomnia is the most frequently reported sleep symptom, severely af-
fecting up to 15 percent of the U.S. population.15 Many sleeping aids are
available for treating insomnia. Over-the-counter sleeping aids some-
10-649_Dasgupta.indb 164 1/17/11 6:40 AM

times contain antihistamines, such as diphenhydramine, and interaction

of this drug with alcohol has been discussed earlier in the section dealing
with the interaction of alcohol with allergy/cold medication. The most
important class of drug in treating insomnia is the benzodiazepine class
of drugs. There are more than fifty benzodiazepines, although only about
fifteen of them are available in the United States. The most commonly
prescribed benzodiazepines in the United States are diazepam, temaze-
pam, alprazolam, lorazepam, and clonazepam.
Dosages of benzodiazepines that are sedatives may increase drowsiness if
alcohol is consumed. Nobody taking any prescription tranquilizer should be
drinking at all. It increases the risk of household and automobile accidents.
Even a glass of wine may produce enough drowsiness, dizziness, and

lack of motor coordination due to interaction with a benzodiazepine
drug to make driving a hazard.
A low dose of flurazepam (Dalmane) interacts with a low dose of alcohol

to impair driving ability even when alcohol is consumed long after tak-
ing the medication.16 The hazard of interaction between benzodiazepines
and alcohol is magnified in elderly people who demonstrate an increased
response to benzodiazepines. In the presence of enough alcohol, severe
CNS depression may occur in a patient taking any benzodiazepine
medication. Acute ingestion of alcohol combined with benzodiazepines
is responsible for several toxicological interactions that may have serious
clinical consequences. Fatal poisoning involving alcohol and benzodiaz-
epines, especially triazolam, continues to be a serious problem.17
Even non-benzodiazepine sleeping aids such as zolpidem (Ambien),
zaleplon (Sonata), and eszopiclone (Lunesta) should not be combined
with alcohol, because interaction between alcohol and any of these drugs
increases the risk of driving when not fully awake (sleep-driving).
Although with the introduction of benzodiazepines old barbiturates
are rarely prescribed, alcohol and barbiturates do not mix well at all. A
combination of barbiturate and alcohol causes excessive CNS depression
and impaired psychomotor performance. There are even reports of death
due to concomitant use of alcohol and barbiturates due to severe respira-
tory depression.18
Interaction of Alcohol with Antidepressants

Antidepressant drugs include old monoamine oxidase inhibitors, tricyclic
antidepressants, tetracyclic antidepressants, and newer antidepressants,
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166 Chapter 8
such as selective serotonin reuptake inhibitors (SSRI) and serotonin-

norepinephrine reuptake inhibitors (SNRI). Older tricyclic antidepressants
such as amitriptyline, nortriptyline, doxepin, and so on are prescribed less
frequently than newer SSRI medications. Alcohol increases the sedative ef-
fect of tricyclic antidepressants, for example, amitriptyline (Elavil), and also
inhibits psychomotor skills, thus making driving hazardous. A chemical
called tyramine, found in some beer and wine, interacts with antidepres-
sants (which are monoamine oxidase inhibitors) and can cause a dangerous
rise in blood pressure even after a single drink. Tailor et al. (1994) reported
a case of hypertensive crisis resulting from drinking tap beer in a patient
taking monoamine inhibitor antidepressant phenelzine.19
Alcohol heightens the negative side effects of SSRI drugs. The combina-
tion of alcohol and any of these drugs may produce increased drowsiness,
clouded judgment, slower reflexes, and even suicidal thoughts. Alcohol
may also interfere with the clinical efficacy of these drugs.
Just one alcoholic drink may lead to DWI (driving with impairment)
if you are taking an SSRI. Your level may be below the legal limit
for driving, but if both alcohol and any SSRI drugs are found in your
blood, you may be charged with a DWI because your driving is im-
paired.
Serotonin is a neurotransmitter that plays a role in one’s mood. SSRI

medications inhibit serotonin reuptake by presynaptic nerve cells, and
higher serotonin levels available outside the nerve cells can bind with
specific serotonin receptors to elevate our mood. However, in the pres-
ence of excess extracellular serotonin, a life-threatening medical condition
known as “serotonin syndrome” may arise. The symptoms include very
high heart rate, high blood pressure, severe twitching, and convulsion. If
untreated, this syndrome can be fatal. It is unusual to observe serotonin
syndrome in a patient receiving a single SSRI medication, but if a patient
consumes alcohol in large amounts, especially hard liquor, serotonin syn-
drome may occur even if one medication is prescribed to the patient. In
one report (Velez et al. 2004), the authors described life-threatening sero-
tonin syndrome in a fifty-seven-year-old man who was taking paroxetine
(Paxil) and who consumed a pint of hard liquor.20
Interaction of Alcohol with Antidiabetic Medications

Antidiabetic medications, also known as oral hypoglycemic agents, are
prescribed to patients with type 2 diabetes (non-insulin-dependent diabe-
10-649_Dasgupta.indb 166 1/17/11 6:40 AM

tes) in order to lower serum concentration of sugar (glucose). Metformin

(Glucophage) is a popular first-line oral hypoglycemic agent, and one
potential side effect of this medication is to increase the concentration of
lactic acid in the blood, causing a syndrome called lactic acidosis. If the
concentration of lactic acid is very high in the blood, it may even cause
a medical emergency. A person taking metformin should only drink in
moderation, because excess alcohol intake may cause lactic acidosis due
to the interaction of excess alcohol with metformin.
Alcohol may also interact with various sulfonylureas, another popular
class of oral hypoglycemic agent. The effects are sometimes opposite. For
example, a patient taking glipizide (Glucotrol) may find his or her blood
sugar concentration stays low longer (hypoglycemia), while a person
taking tolbutamide (Orinase) may find a lack of glucose control because
alcohol reduces the effectiveness of this drug. Even two to three drinks
may trigger this effect.
Alcohol also enhances the glucose-lowering effect of insulin. There-
fore, a person with diabetes taking either insulin or oral hypoglycemic
agents should only drink occasionally and limit themselves to no more
than two standard drinks. Drinking hard liquor may be dangerous for
these patients, because alcohol content may be higher than the standard
drink. Caution should also be exercised if you drink mixed drinks, be-
cause one drink may be equivalent to two to three standard drinks in
terms of alcohol content. Please tell your physician if you drink on a
regular basis, so that your doctor can properly select your medication
and guide you in how much drinking is safe when you are taking an
oral hypoglycemic agent.
Interaction of Alcohol with Antibiotics

There are many classes of antibiotics, including aminoglycosides, cepha-
losporins, macrolide antibiotics, penicillins, quinolones, sulfonamides,
and tetracycline. Each of these classes of drugs contains many members,
and there are also other classes of antibiotics with few members. Fortu-
nately, only a few antibiotics approved for use in the United States show
clinically significant drug interaction with alcohol, and drinking must be
avoided when taking any of these medications. These antibiotics carry a
warning label stating that if you are taking the medication, you should
avoid alcohol consumption altogether as long as you are taking that
medication. Even one drink may potentiate an adverse effect if you are
taking one of these specific antibiotics. Cephalosporins, such as cefaman-
dole, cefotetan, and cefoperazone, interact with alcohol even after one
drink. Symptoms include flushing, wheezing, breathing difficulty, rapid
heartbeat, and profound sweating, as well as nausea and vomiting, and
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168 Chapter 8
such symptoms may develop within fifteen to thirty minutes after drink-
ing.21 It is advisable not to drink for an additional two to three days after
you complete the course of one of these cephalosporins. Alcohol reduces
blood concentration, thus the effectiveness of doxycycline may also in-
terfere with the absorption of erythromycin. Alcohol must be avoided
if you take metronidazole (Flagyl), tinidazole (Tindamax), ketoconazole
(Nizoral), furazolidone (Furoxone), griseofulvin (Grisactin), and the anti-
malarial drug quinacrine (Atabrine).
Interaction between metronidazole and alcohol (consuming high
amounts of alcohol) may even cause fatality. In one case report, a thirty-
one-year-old woman died from taking metronidazole and drinking heav-
ily. Her blood alcohol was elevated to 162 mg/dL (more than double the
legal limit of drinking, 80 mg/dL).22
Interaction of Alcohol with Antiulcer Medications

The commonly prescribed antiulcer medications (also used in treating
acid reflux), such as cimetidine (Tagamet) and ranitidine (Zantac), may
prolong the effect of alcohol. DiPadova et al. (1992) studied the interac-
tions between alcohol and cimetidine, ranitidine, and famotidine using
human subjects. Cimetidine showed a greater effect on blood alcohol
levels compared to ranitidine, but famotidine showed no significant ef-
fect. The authors concluded that patients taking cimetidine or ranitidine
should be warned of possible impairments after consumption of alcohol
in quantities usually considered safe when not taking these medications.23
Interaction of Alcohol with Anticoagulants

Warfarin (Coumadin) is prescribed to reduce blood clotting. However,
excessive action of warfarin is dangerous, because a patient may bleed
to death (life-threatening hemorrhages). Acute alcohol consumption
increases the effectiveness of warfarin, while chronic alcohol consump-
tion reduces the effectiveness of warfarin therapy. This opposing effect
of acute versus chronic alcohol consumption on warfarin therapy is a
medical challenge.24 Warfarin therapy must be monitored very carefully
in patients who drink on a regular basis.
Interaction of Alcohol with Cardiovascular Medications

This class of drugs includes a wide variety of medications prescribed to
treat ailments of the heart and the circulatory system. Acute alcohol con-
sumption interacts with some of these drugs, causing dizziness or faint-
ing upon standing. These drugs include nitroglycerin, methyldopa (Al-
domet), hydralazine (Apresoline), and guanethidine (Ismelin). Chronic
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alcohol consumption also reduces the efficacy of propranolol. Verapamil

increases blood alcohol level and prolongs its effect.
Interaction of Alcohol with Miscellaneous Drugs

Phenytoin (Dilantin) is used to treat patients with seizure disorders.
People who drink regularly may experience a decreased effect of this
medication and may require a higher dosage. Regular drinkers may also
require a higher dosage of propofol (Diprivan). Metoclopramide (Reglan)
increases absorption of alcohol and prolongs its effect. A patient taking
this medication and consuming alcohol may experience additional seda-
tion and may be unable to drive. Methotrexate is an anticancer drug. A
low dose of methotrexate is also used in treating patients with rheuma-
toid arthritis. Alcohol consumption increases the risk for methotrexate-
induced liver toxicity. The manufacturer of this drug advises against
prescribing this drug to patients who drink alcohol excessively.
ABUSING ALCOHOL AND DRUGS

SIMULTANEOUSLY: A RECIPE FOR DEATH
A 2006 survey indicated that about 20.4 million Americans (8.3 percent)
ages twelve and older were currently illicit drug abusers, meaning they
abused drugs during the month prior to the survey. The survey also re-
vealed that marijuana was the most common illicit drug abused, followed
by cocaine, ecstasy, and methamphetamine.25 Other drugs abused include
various benzodiazepines, barbiturates, opiates (heroin, morphine, codeine,
oxycodone, and methadone), and phencyclidine. In addition, various young
people also abuse rave party drugs, mainly ecstasy (3,4-methylenedioxy-
methamphetamine), ketamine, gamma-hydroxybutyric acid (GHB), and
flunitrazepam (Rohypnol). In order to enhance the experience of abused
drugs, people also consume large amounts of alcohol.
Abusing alcohol and drugs at the same time is a recipe for death. All of
these drugs can cause death due to drug overdose. Alcohol significantly
enhances the adverse effects of these abused drugs, accelerating death from
overdose. There are numerous reports in the medical literature document-
ing significantly lesser amounts of various abused drugs present in the
postmortem blood of the victim when alcohol was also present in the blood.
Think twice before you abuse any drug, and think at least ten times be-
fore you abuse alcohol and drugs at the same time. It could be your last
night on this planet if you do not think about the possible consequences.
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170 Chapter 8
Cocaethylene: A Messenger of Death

Although a combination of any abused drug and alcohol is potentially
lethal, the combination of cocaine and alcohol is probably the most
dangerous recipe for death. The body detoxifies cocaine into a harmless
compound called benzoylecgonine. Unfortunately, when cocaine and
alcohol are consumed at the same time, this metabolic detoxification of
cocaine is altered, and a dangerous active metabolite of cocaine is formed
due to an interaction with alcohol. This dangerous metabolite is called
cocaethylene. Alcohol also increases other toxic metabolites of cocaine,
for example norcocaine. Alcohol also increases the blood level of cocaine,
thus prolonging its toxicity. In general, if a person who overdoses on co-
caine is admitted to the hospital in a timely fashion, the victim has a good
chance of survival. In contrast, later rebound toxicity causing fatality may
occur in a victim abusing both cocaine and alcohol.26
CONCLUSION
Out of almost 5,000 drugs (combining prescription and OTC drugs), only
a small fraction of drugs demonstrate a clinically significant interaction
with alcohol. However, when such an interaction is present, extreme care
must be exercised when you drink. If you are taking an over-the-counter
cold or allergy medication, the best place to start is to study the medica-
tion label and talk to the pharmacist on staff in the store. Your pharmacist
is very familiar with all drug-drug and drug-alcohol interactions. If the
advice is not to drink at all, please follow the advice—it can save you
from all sorts of trouble. If you are a heavy drinker, you may get liver
damage from simply consuming Tylenol. Consult with your pharmacist
to see if ibuprofen is more appropriate for pain relief. If you are taking
a prescription drug, consult with your physician about whether you can
drink alcohol occasionally or not when taking this medication. If you are a
heavy drinker, tell your doctor, because you may need a different drug or
a higher dosage of a drug. Again, studying the label on your medication
is a good idea. If you do your homework and study all warning labels on
medications and abide by the warnings, you can avoid almost all troubles
with drug-alcohol interactions.
Do not abuse drugs. Abusing drugs does not solve any problems or
help you get through any difficulty. It only makes matters worse. Talk
to your parents, relatives, teachers, and friends or loved ones for help.
Do not abuse drugs and alcohol at the same time—unless you have a
death wish.
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NOTES
1. B. F. Sands, C. M. Knapp, and D. A. Ciraulo, “Medical Consequence of

Alcohol-Drug Interaction,” Alcohol Health & Research World 17, no. 4 (December
1993): 316–20.
2. L. T. Midanik and R. Room, “The Epidemiology of Alcohol Consumption,”
Alcohol Health & Research World 16, no. 3 (September 1993): 183–90.
3. See http://www.samhsa.gov/newsroom/advisories/0703135521.aspx.
4. See http://www.samhsa.gov/news/newsrelease/060510_dawn2htm (ac-
cessed June 26, 2009).
5. A. Koski, E. Vuori, and I. Ojanpera, “Relation of Postmortem Blood Alcohol
and Drug Concentrations in Fetal Poisonings Involving Amitriptyline, Propoxy-
phene and Promazine,” Human and Experimental Toxicology 24, no. 8 (August
2005): 389–96.
6. M. Hickman, A. Longford-Hughes, C. Bailey, J. Macleod, et al., “Does
Alcohol Increase the Risk of Overdose Death? The Need for a Translational Ap-
proach,” Addiction 103, no. 7 (July 2008): 1060–62.
7. V. Valle, H. Gosney, and J. Sinclair, “Qualitative Analysis of Coroners’ Data
into the Unusual Deaths in Children and Adolescents,” Child Care and Health De-
velopment 34, no. 6 (November 2008): 721–31.
8. B. Levine, D. Green-Johnson, S. Hogan, and J. E. Smialek, “A Cyprohepta-
dine Fatality,” Journal of Analytical Toxicology 22, no. 1 (January–February 1998):
72–74.
9. G. S. Bleumink, A. C. van Vliet, A. van der Tholen, and B. H. Stricker, “Fa-
tal Combination of Moclobemide Overdose and Whiskey,” Netherlands Journal of
Medicine 61, no. 3 (March 2003): 88–90.
10. F. T. Wootton and W. M. Lee, “Acetaminophen Hepatotoxicity in the Alco-
holic,” Southern Medical Journal 83, no. 9 (September1990): 1047–49.
11. R. T. Gentry, E. Baraona, I. Amir, R. Roine, et al., “Mechanism of the
Aspirin-Induced Rise in Blood Alcohol Levels,” Life Sciences 65, no. 23 (October
1999): 2505–12.
12. S. Kechagias, K. A. Jonsson, B. Norlander, B. Carisson, et al., “Low-Dose
Aspirin Decreases Blood Alcohol Concentrations by Delaying Gastric Emptying,”
European Journal of Clinical Pharmacology 53, nos. 3–4 (December 1997): 241–46.
13. M. C. Dufour, L. Archer, and E. Gordis, “Alcohol and the Elderly,” Clinical
and Geriatric Medicine 8, no. 1 (February 1992): 127–41.
14. F. Johnson, G. Wagner, S. Sun, and J. Stauffer, “Effect of Concomitant Inges-
tion of Alcohol on the In Vivo Pharmacokinetics of KADIAN (Morphine Sulfate
Extended Release) Capsules,” Journal of Pain: Official Journal of American Pain Soci-
ety 9, no. 4 (April 2008): 330–36.
15. G. S. Richardson, T. Roth, and J. A. Kramer, “Management of Insomnia: The
Role of Zaleplon,” Medscape General Medicine 4, no. 1 (March 2002): 9.
16. M. Linnolia, M. J. Mattila, and B. S. Kitchell, “Drug Interactions with Alco-
hol,” Drugs 18, no. 4 (October 1979): 299–311.
17. E. Tanaka, “Toxicological Interactions between Alcohol and Benzodiaz-
epines,” Journal of Toxicology: Clinical Toxicology 40, no. 1 (January 2002): 69–75.
10-649_Dasgupta.indb 171 1/17/11 6:40 AM

172 Chapter 8
18. H. Kinoshita, M. Nishiguchi, S. Kasuda, H. Quchi, et al., “An Autopsy Case

of Poisoning with Ethanol and Psychotropic Drugs,” Soudni Lekkarstivi 53, no. 2
(April 2008): 16–17.
19. S. A. Tailor, K. I. Shulman, S. E. Walker, J. Moss, et al., “Hypertensive Crisis
Associated with Phenelzine and Tap Beer: A Reanalysis of the Role of Pressor
Amines in Beer,” Journal of Clinical Psychopharmacology 14, no. 1 (February 1994):
5014.
20. L. I. Velez, G. Shepherd, B. S. Roth, and F. L. Benitez, “Serotonin Syndrome
with Elevated Paroxetine Concentrations,” Annals of Pharmacotherapy 38, no. 2
(February 2004): 269–72.
21. H. Portier, J. M. Chalopin, M. Freysz, and Y. Tanter, “Interaction between
Cephalosporins and Alcohol,” Lancet 2, no. 8188 (August 1980): 263.
22. S. J. Cina, R. A. Russell, and S. E. Conradi, “Sudden Death Due to Metro-
nidazole/Ethanol Interaction,” American Journal of Forensic Medicine and Pathology
17, no. 4 (December 1996): 343–46.
23. C. DiPadova, R. Roine, M. Frezza, R. T. Gentry, et al., “Effects of Ranitidine
on Blood Alcohol Levels after Ethanol Ingestion: Comparison with H-2 Receptor
Antagonists,” Journal of the American Medical Association 267, no. 1 (January 1992):
83–86.
24. D. E. Havrda, T. Mai, and J. Chonlahan, “Enhanced Antithrombotic Effect
of Warfarin Associated with Low-Dose Alcohol Consumption,” Pharmacotherapy
25, no. 2 (February 2005): 303–7.
25. National Survey on Drug Use and Health, U.S. Department of Health and
Human Services, Washington, D.C., Government Printing Office, 2006, http://
oas.samhsa.gov.
26. M. B. Patel, M. Opreanu, A. J. Shah, K. Pandya, et al., “Cocaine and Alcohol:
A Potential Lethal Duo,” American Journal of Medicine 122, no. 1 (January 2009):
e5–6.
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9

Workplace Alcohol
and Drug Testing
When Not to Drink at All
B y far the most common legal substance that can affect job performance
is alcohol (ethyl alcohol). Many studies have clearly documented that
heavy drinking and misuse of alcohol over time is associated with ab-
senteeism, industrial accidents, poor job performance, job turnover, lack
of self direction, poor interpersonal relations with coworkers, and lower
level of job satisfaction, as well as theft, vandalism, and negative work
behavior.1 Historically, employers have relied on supervisors to identify
such problem employees. Later, workplace drug and alcohol testing
programs evolved to address these issues using a more rigorous, direct
approach. The anticipated effect of workplace alcohol and drug testing is
to deter employees from abusing alcohol and drugs and to prevent work-
place accidents, as well as to improve productivity and morale.
Workplace drug testing has evolved from virtually nonexistent in the
1980s to a point where there is widespread acceptance of drug testing
programs by employers, both in the public and private sector. The fed-
eral drug testing programs applied to 1.8 million employees in 2005. The
types of testing conducted have included job applicants, postaccident/
unsafe practice, reasonable suspicion, follow-up to treatment, random,
and voluntary testing.2
Private employers also embrace the practice of preemployment and
workplace drug testing in order to achieve a drug-free workplace. Work-
place drug testing deters employees from abusing drugs, as reflected in
the Drug Testing Index published by Quest Diagnostics, a reputable na-
tional reference laboratory performing workplace drug testing. Accord-
ing to the Drug Testing Index published on March 12, 2008, among the
173
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174 Chapter 9
combined U.S. workforces, only 3.8 percent of the drug tests had positive
results in 2007 compared to 13.6 percent test results that were positive in
1988. In addition, amphetamine, methamphetamine, and cocaine abuse
by American workers is also in decline.3
Nevertheless, according to a 2007 federal government report, drug and
alcohol abuse continues to be a serious problem in the United States, with
an estimated 9.4 million workers between the ages of eighteen and sixty-
four reporting illicit drug use in the past month of the survey, while an
estimated 10.6 million workers were dependent on or abused alcohol. The
prevalence of drug abuse was highest among workers who were between
eighteen and twenty-five. In addition, food service workers and construc-
tion workers showed a higher prevalence of drug abuse than other occu-
pational groups. The prevalence of alcohol use was also highest in workers
between the ages of eighteen and twenty-five. Construction workers had
the highest prevalence of past-month heavy alcohol use, followed by work-
ers in installation, maintenance, and repair businesses.4 However, it is un-
disputed that workplace drug testing deters employees from drug abuse.5
Preemployment drug testing is more common than alcohol testing. How-
ever, both alcohol and drug tests are mandated by the federal government
for personnel in safety-sensitive positions. These personnel include: avia-
tion personnel, commercial drivers and personnel working in commercial
transportation, pipeline workers and personnel involved in transporting
hazardous materials, maritime personnel, and military personnel.
Many employers in the private sector also implement both alcohol and
drug testing for employees in security-sensitive positions or jobs related
to public safety or health, such as hospital nurses and related health care
providers. Although the focus of this book is on alcohol, because work-
place alcohol and drug testing are interrelated, in this chapter, I discuss
both topics so that readers can get familiar with the current practice of
workplace alcohol and drug testing. Detailed discussions on workplace
alcohol and drug testing, including applicable laws, technical aspects of
such testing, the role of medical review officers, and the consequences of
positive alcohol and drug testing results in the workplace, is beyond the
scope of this book. This chapter provides only an overview.
HOW WORKPLACE DRUG AND ALCOHOL TESTING EVOLVED
On September 15, 1986, President Reagan issued Executive Order No.

12564, which directed all federal employees involved in law enforcement,
national security, protection of life and property, and public health and
safety, as well as other functions requiring a high degree of public trust,
to be subjected to mandatory drug testing. Following this executive order,
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Workplace Alcohol and Drug Testing 175
the U.S. Department of Health and Human Services developed guidelines

and protocols on testing for drugs of abuse. The overall testing process
under mandatory drug testing guidelines consists of proper collection
of specimens, initiation of a chain of custody (record of personnel who
have possession of the specimen from the time of collection to the time of
analysis), and analysis of the specimen by a Substance Abuse and Mental
Health Services Administration (SAMHSA) certified laboratory.
Commercial motor vehicles make up about 4 percent of police-reported
crashes and 12 percent of traffic fatalities. The role of alcohol in commercial
motor vehicle accidents was first recognized in 1970, and then subsequent
studies showed that a blood alcohol level of 0.1 percent (100 mg/100ml of
blood: 100 mg/dL) was consistently associated with fatally injured drivers.
Prompted by some highly publicized alcohol-related commercial transpor-
tation accidents, including the 1989 Exxon Valdez oil spill in Alaska, the
1990 conviction of three Northwest Airlines pilots for having significant
blood alcohol while on duty, and a 1991 New York subway derailment,
the U.S. Congress passed the Omnibus Transportation Employee Testing
Act in 1991, which requires drug and alcohol testing of safety-sensitive
employees working in aviation, trucking, railroads, mass transit, pipeline,
and other transportation industries.6 The U.S. Department of Transporta-
tion (DOT) publishes rules on who must conduct drug testing, what proce-
dures to use, and when such testing should be done. These regulations are
applicable to roughly 12.1 million people and are encompassed in 49 Code
of Federal Regulations Part 40 (49CFR40). The Office of Drug and Alcohol
Policy and Compliance (ODAPC) publishes, implements, and provides
authoritative interpretations of these results.
The Department of Defense also developed its own regulations for
contractors working in the national security arena (Section 48 CFR 252,
223-7004). Under these regulations defense contractors must maintain a
drug-free workplace that includes a comprehensive employee assistance
program, provision for self-referral and supervisory referrals for drug
testing, supervisory training on detecting and responding to illegal drug
use, and a carefully controlled and monitored employee drug testing
policy. The U.S. Department of Energy, the National Aeronautics and
Space Administration (NASA), and the Nuclear Regulatory Commission
(NRC) all have drug testing requirements for safety-sensitive contractors.
In addition to federal laws and regulations, many states have their own
drug laws. In general, three types of state legislation may affect work-
place drug testing policy:
1. State and local laws regulating drug testing

2. State worker’s compensation laws
3. State unemployment insurance laws
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176 Chapter 9
In the interest of promoting a safer work environment, some states offer

employer discounts on their workers’ compensation insurance premium,
and many states deny workers’ compensation where injuries are deter-
mined to be related to substance abuse. In addition, some states have
policies to deny unemployment benefits to people who are fired due to
positive drug testing results or drug abuse.
CURRENT PRACTICES OF WORKPLACE

DRUG AND ALCOHOL TESTING
Preemployment drug testing is the most common type of workplace drug

testing; alcohol testing along with drug testing is less common, unless the
position is security sensitive. In general, a person undergoing preemploy-
ment drug testing has few legal rights, and in most cases, employment is
denied if the drug test is failed. An employer may also conduct drug test-
ing and alcohol testing under the following circumstances, especially for
employees who are working in safety-sensitive positions:
• Annual physical test

• Pre-promotion test
• Postaccident drug testing
• Treatment follow-up test
• Return to duty drug testing
• Random, unannounced drug testing
Usually five drug classes are tested, including amphetamine and meth-
amphetamine, cocaine, marijuana, opiates, and phencyclidine, in feder-
ally mandated workplace drug testing programs. Private employers may
also test for additional drugs, such as benzodiazepines, barbiturates,
methadone, methaqualone, and propoxyphene.
The Federal Motor Carrier Safety Administration (FMCSA) issues
guidelines regarding alcohol and drug testing rules for people required to
obtain a commercial driver’s license. The Department of Transportation
(DOT) rules include procedures for urine drug testing and breath alcohol
testing. Initially, the agency issued urine drug testing rules in December
1989, and then in 1994 the rules were amended to add breath alcohol
testing procedures because alcohol is widely consumed by the general
population in the United States.
In December 2000, modification of the initial guidelines was published
in order to incorporate input from the public sector concerning the final
rules. In August 2001, the FMCSA revised modal-specific drug and alcohol
testing regulations (published in 49 Code of Federal Regulations Part 382)
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to reflect the revisions made in 2000. Finally, in 2008 the DOT amended
certain provisions of its drug and alcohol testing procedures to change in-
structions to collectors, laboratories, medical review officers, and employ-
ers regarding adulterated, substituted, diluted, and invalid urine specimen
results. These changes were intended to create consistency with specimen
validity requirements established by the U.S. Department of Health and
Human Services. The final rule was published in the Federal Register on
June 25, 2008.7 Although meant for drug and alcohol testing for appropriate
federal employees, many private corporations also use these guidelines to
develop their own workplace drug and/or alcohol testing policies.
Who Is Tested?
In general, any person seeking employment in the public or private sec-
tor may be subjected to preemployment drug testing. However, only
certain personnel hired for security-sensitive positions are subjected to
both alcohol and drug testing. The FMCSA rules apply to safety-sensitive
employees. Those who operate commercial motor vehicles that require a
commercial driver’s license may be subjected to both alcohol and drug
testing. These personnel are listed in table 9.1.
Use of alcohol is prohibited while working in such security-sensitive
jobs. In addition, alcohol should not be consumed for at least four hours
before reporting for such jobs. Abuse of any illicit drug is not permitted
under any circumstances.
Table 9.1. Personnel Subjected to Workplace Alcohol and Drug Testing

Commercial Motor Vehicle–Related Personnel
Anyone who owns or leases commercial motor vehicles
Anyone who assigns drivers to operate commercial motor vehicles
Federal, state, and local governments
For-hire motor carriers
Private motor carriers
Civic organizations (disabled veteran transport, Boy/Girl Scouts, etc.)
Church bus drivers
Aviation Personnel
Flight crew, including pilots
Flight attendants
Flight instructors
Aircraft dispatch personnel
Aircraft maintenance and preventive maintenance personnel
Ground security coordinators
Aviation screening personnel
Air traffic controllers
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178 Chapter 9
The Federal Aviation Administration (FAA) determines drug and

alcohol testing guidelines applicable to airline personnel and air traffic
controllers. The guidelines were published in the DOT’s workplace drug
and alcohol testing programs (Title 49, CFR Part 40).
HOW WORKPLACE ALCOHOL AND

DRUG TESTING ARE CONDUCTED
The current guidelines allow for screening tests to be conducted using saliva
devices or appropriate breath analyzers approved by the National Highway
Traffic Safety Administration in order to determine the blood alcohol level
of the person being tested. Direct determination of blood alcohol by draw-
ing blood from the arm of a person is not done. Two tests are required to
determine if a person has a prohibited alcohol concentration. A screening
test is conducted first. Any result less than 0.02 percent (20 mg/dL) alcohol
concentration is considered a “negative” test. If the alcohol concentration is
0.02 percent or greater, a second confirmation test must be conducted after a
waiting period of at least fifteen minutes, but the confirmation must be per-
formed within thirty minutes of the initial screening test. A new mouthpiece
and an evidential breath testing device must be used to assure proper regis-
tering of the results. The person undergoing drug testing and the individual
conducting the confirmation breath test (called a breath alcohol technician
or BAT) must complete the alcohol testing form to ensure that the results
are properly recorded. It is also important to print out the results, including
date and time, a sequential test number, and the name and serial number of
the instrument to ensure the reliability of the results. The confirmation test
results determine if any actions must be taken.
In the United States, Intoximeter, Alcosensor, Alcotest, Intoxilyzer, and
DataMaster are commonly used breath analyzers. A person being tested
blows into a breath analyzer, and the results are reported as blood alcohol
concentration. Breath analyzers do not directly measure the blood alcohol
level, but rather estimate blood alcohol levels indirectly by measuring
the amount of alcohol in one’s breath (see chapter 6 for a more in-depth
discussion on breath analyzers).
Drug testing is conducted by analyzing urine specimens. The analysis
is performed at laboratories certified and monitored by the SAMHSA, an
agency under the Department of Health and Human Services (DHHS). The
specimen collection procedures and chain of custody ensure that the speci-
men’s security, proper identification, and integrity are not compromised.
The Omnibus Transportation Employee Testing Act of 1991 requires that
drug testing procedures for commercial motor vehicle drivers include
split specimen procedures. Each urine specimen is subdivided into two
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bottles labeled as a “primary” and a “split” specimen. Both bottles are

sent to a laboratory. Only the primary specimen is opened and used for
the urinalysis. The split specimen bottle remains sealed and is stored at
the laboratory. If the analysis of the primary specimen confirms the pres-
ence of illegal, controlled substances, the driver has seventy-two hours to
request the split specimen be sent to another DHHS-certified laboratory for
analysis. This split specimen procedure essentially provides the driver with
an opportunity for a “second opinion.” All urine specimens are analyzed
for marijuana, cocaine (as benzoylecgonine, a cocaine metabolite), amphet-
amines, opiates, and phencyclidine. The testing is a two-stage process.
First, a screening test is performed. If it is positive for one or more of the
drugs, then a confirmation test is performed for each identified drug using
state-of-the-art gas chromatography/mass spectrometry (GC/MS) analy-
sis. GC/MS confirmation ensures that over-the-counter medications or
preparations are not reported as positive results. After conducting the drug
test, the laboratory reports the result to the appropriate agency personnel.
All drug test results are reviewed and interpreted by a physician (medical
review officer [MRO]) before they are reported to the employer. If the labo-
ratory reports a positive result to the MRO, the MRO contacts the person
and conducts an interview to determine if there is an alternative medical
explanation for the drugs found in the driver’s urine specimen.
All alcohol and drug testing results are confidential. Employees failing
workplace alcohol and/or drug testing may be given an opportunity to
undergo drug or alcohol rehabilitation. After successful drug rehabilita-
tion, a person is eligible to work again depending on the position under
the Americans with Disabilities Act.
LEGAL GUIDELINES FOR WORKPLACE

ALCOHOL AND DRUG TESTING
The legal limit for driving in all states in the United States is 0.08 per-
cent blood alcohol (80 mg/dL) or less. However, personnel involved in
safety-sensitive positions are subjected to more stringent requirements. As
implemented on January 1, 1995, the mandatory alcohol testing program
for commercial motor vehicle drivers includes preemployment testing,
random testing, reasonable suspicion testing, and postaccident testing.
Random testing requires that randomly sampled employees report to the
job site immediately before, during, or after their driving shift to be tested
for the presence of drugs and/or alcohol. Commercial drivers with a blood
alcohol level of 0.04 percent (40 mg/dL) or higher should be suspended im-
mediately. Those who register a blood alcohol between 0.02 to 0.03 percent
should be removed from their duties for twenty-four hours. In the case of
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180 Chapter 9
an accident, all involved drivers are required to submit to alcohol testing

within two hours. Reasonable suspicion testing allows an employer to test
an employee if appearance, behavior, speech, or breath/body odor shows
signs of alcohol use.8 The employee’s refusal to be tested for blood alcohol
or not cooperating with the testing proposal is considered a violation of
the rule, and under such circumstances the breath analyzer test should be
considered positive and appropriate action taken against the person refus-
ing to take the test.
According to a news report published recently in the St. Petersburg
Times, a school superintendent recommended that the school board
fire a bus driver who failed an alcohol breath test. On the evening of
September 17, 2009, the driver sat down for dinner with her husband
and consumed a couple of 16-ounce beers. After the meal she had three
or four cocktails, the last one at 11 pm. Bus drivers are forbidden from
consuming alcohol within twelve hours of getting behind the wheel. The
driver started her pre-trip preparation at 5:55 am and admitted that she
violated the twelve-hour rule. She was selected for a random alcohol test,
and when she returned to the bus depot, her first test showed a blood
alcohol concentration of 0.057 percent (57mg/dL). A second test a few
minutes later showed a blood alcohol level of 0.053 percent, and, finally,
another test at 10:17 am showed a level of 0.043 percent. Two more tests
on a second breath testing machine tested within the next forty-five min-
utes demonstrated blood alcohol levels of 0.029 percent and 0.028 percent,
respectively. The driver was suspended and the school superintendent
recommended that the school board terminate her employment.9
The Federal Aviation Administration also has strict guidelines for alco-
hol consumption for security- and safety-sensitive personnel involved in
the aviation industry. Airline pilots must abide by the current regulations
governing alcohol use, and the FAA can even take emergency revocation
action against a pilot’s airman certificate when a pilot is in violation of the
agency’s alcohol and drug policy. The FAA has a long-standing policy of
eight hours of prohibition against pre-duty alcohol consumption. Differ-
ent airlines may have policies where pilots must refrain from consuming
alcohol longer than eight hours. Because of extremely low acceptable
limits for blood alcohol in pilots, it is possible that a pilot may not be able
to fly the airplane despite not consuming alcohol for eight hours. The cur-
rent regulation prohibits pilots from performing safety-sensitive duties
with a blood alcohol level of 0.02 percent or higher. A reported alcohol
level between 0.02 and 0.039 percent, while not a rule violation, may re-
sult in the pilot being grounded for an additional eight hours, or until the
alcohol level is reduced below the 0.02 percent limit. Reporting for duty
or being on duty with a blood alcohol level of 0.04 percent or higher as
measured by a breath analyzer or other method is a serious violation of
FAA regulations, and the pilot may be subject to stiff penalties.
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A United Airlines pilot was pulled from his transatlantic flight from Lon-
don to Chicago after a coworker suspected him of being drunk. He failed
the breath test, and a subsequent blood alcohol test showed a level of 0.05
percent (50 mg/dL), well above the acceptable limit of 0.02 percent (20 mg/
dL), at or below which a pilot is eligible to fly the aircraft. The United flight
carrying 124 passengers was canceled, and passengers were put on differ-
ent carriers. The pilot was remorseful and pleaded guilty to the charges
against him. Washington lawyer Chris Humphreys commented that an
American Airlines pilot who recorded a blood alcohol level of 0.039 per-
cent (39 mg/dL) was given a fine in July 2009. Another pilot with a blood
alcohol level of 0.06 percent (60 mg/dL) was given a suspended sentence.10
Legal limits for blood alcohol levels in pilots, commercial drivers, and
other personnel involved in safety-sensitive positions, such as miners, mari-
ners, and so on, are extremely low, and consuming just one drink prior to re-
porting for duty is enough to get a blood alcohol level above the acceptable
limit. Even consuming moderate to high amounts of alcohol the night before
(eight to twelve hours prior to reporting to duty) may be problematic. Cau-
tion must be exercised by these personnel regarding alcohol consumption
prior to reporting for duty. Any presence of illicit drugs in the urine of a per-
son undergoing workplace alcohol or drug testing is a violation. However,
some prescription drugs, such as narcotic analgesics, may cause a positive
workplace drug testing result. The person must establish during his or her in-
terview with the medical review officer (MRO) that such prescription drugs
are being taken under the supervision of a licensed medical practitioner.
In addition, the MRO may verify that information independently with the
individual’s physician in order for that individual to pass the drug test.
The U.S. Department of Homeland Security also enforces a strict policy
to ensure military personnel are not affected by alcohol and drug abuse.
Individuals applying for active duty in the U.S. Army, U.S. Army Re-
serves, Army National Guard, U.S. Navy, U.S. Marines, or the U.S. Air
Force are given a drug and alcohol test as a part of their initial physical
exam at the Military Entrance Processing Station. If any individual tests
positive for alcohol or marijuana, he or she cannot join the military and,
at the discretion of the commander, may receive a waiver for being tested
after waiting for forty-five days. If still testing positive, a final waiver
may be granted again at the discretion of the commander. After waiting
for one year, if the individual fails the test, the person is permanently dis-
qualified from joining the military. If a person tests positive for cocaine, a
waiver may be granted and the person must wait for a year before being
retested. If the second test is positive, that person is permanently disquali-
fied from joining any active duty. However, during the first test, if a per-
son tests positive for any drug other than alcohol, marijuana, or cocaine,
that person is permanently disqualified. The Department of Defense man-
dates that several drugs must be tested for, including marijuana, cocaine,
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182 Chapter 9
amphetamine, and opiates, while tests for barbiturates, phencyclidine,

and LSD (lysergic acid diethylamide) are done on a random rational basis.
Steroids can also be tested for if indicated.
Active duty members are not allowed to consume any alcohol if below
the age of twenty-one. In addition, alcohol cannot be consumed twelve
hours prior to joining active duty, while in uniform, within twelve hours
of operating a motor vehicle, and any other time as restricted by the com-
mander. Possession or sales of illegal drugs, as well as abuse of prescrip-
tion medications, are not tolerated in the military, and active duty person-
nel are subjected to regular alcohol and drug testing, at least once a year.
Failure to pass an alcohol or drug test may lead to disciplinary action.
Military personnel are usually younger than the general U.S. population,
and there are more men than women. However, due to strict drug and
alcohol testing policies in place since December 1981, drug abuse among
military personnel is much lower than the general U.S. population. Ac-
cording to the latest report available, in 2005, 4.6 percent of military
personnel admitted drug abuse based on an anonymous survey by the
Department of Defense, while in the general American population, 8.3
percent admitted drug abuse based on an anonymous survey conducted
by the federal government. Drug abuse is also higher among the younger
population (ages eighteen to twenty-five). In that group, 6.8 percent of
military personnel admitted abuse of a drug compared to 18.8 percent of
people in the general population.11
Alcohol Testing in Urine

Federal workplace alcohol and drug testing programs use breath tests for
alcohol and urine tests for drugs of abuse. However, an extensive number of
commercial international maritime workplace alcohol and drug testing pro-
grams utilize urine samples for both alcohol and drugs (amphetamines, bar-
biturates, benzodiazepines, buprenorphine, marijuana, cocaine, methadone,
opiates, and propoxyphene).12 In addition, administrators of many hospitals
use urine specimens for both alcohol and drug testing. Alcohol may ap-
pear in the urine within two hours of consumption and may be detected in
the urine longer than in the blood, up to twelve to twenty-four hours after
consumption of alcohol. Just after drinking, in the early absorption phase,
the urine alcohol concentration (UAC) to blood alcohol concentration (BAC)
ratio is less than in the late absorption phase when the UAC to BAC is be-
tween 1.0 and 1.2. After absorption is complete, UAC to BAC ratio is around
1.3 to 1.4.13 Urine concentrations of ethanol, as reported by some laborato-
ries, can be convertible to blood levels by the following formula: divide the
urine concentration by 1.3, provided alcohol is not in the early absorptive
stage. For instance, the urine concentration of 0.08 percent is equivalent to
a blood concentration of 0.06 percent. There is, however, some individual
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variation in this ratio, and urine alcohol measurement can only provide an
approximate level of blood alcohol. Ethanol is screened in urine using an
automated alcohol dehydrogenase–based enzymatic assay and confirmed
by quantitative gas chromatography. This method also allows the separa-
tion and quantitation (amount present) by many volatile substances such
as methanol, isopropyl alcohol, and ethylene glycol, if present in the urine.
However, false positive results in urine alcohol tests may be encoun-
tered in patients suffering from diabetes, because sugar present in the
urine specimen can be converted into alcohol by bacteria or yeast. Jones
et al. (2000) reported high urinary alcohol concentrations of 82 mg/dL
and 102 mg/dL in two victims of date rape who denied any alcohol
consumption. Both girls (ages fifteen and eighteen) suffered from diabe-
tes mellitus. The presence of glucose in urine and the high risk of yeast
(fungus) infection in female diabetics suggests that ethanol was produced
by fermentation after the collection of the urine specimens, and positive
ethanol results in their urine specimens was an artifact. Therefore, it is
important to add a preservative like sodium fluoride to the collection cup
in order to avoid such false positive urine alcohol results.14
In another report (Helander et al. 2009), one subject demonstrated a
urine ethanol concentration of 10.8 gm/L (1080 mg/dL), a concentration
not physiologically possible. Low levels of ethyl glucuronide and ethyl
sulfate, minor metabolites of ethanol, were also detected, raising suspi-
cion regarding unexpectedly high urine alcohol level. The urine tested
positive for Candida albicans, fermenting yeast causing yeast infection in
humans, thus further raising the suspicion that the alcohol level detected
in the urine was due to postcollection formation of ethanol by the yeast
found in the specimen. In order to investigate this false positive case of
urinary ethanol determination, the authors analyzed another twenty-four
specimens collected from other individuals and observed the presence of
ten of fifteen ethanol positive specimens and four of nine ethanol nega-
tive specimens where yeast and/or bacteria were present. In four ethanol
positive specimens, no ethanol metabolite was found (ethyl glucuronide
or ethyl sulfate), indicating that these urine specimens had false positive
results for ethanol. When yeast negative but bacteria positive specimens
were supplemented with glucose and stored for a week, ethanol was
formed in some of these specimens, indicating that even bacteria such as
E. coli and P. aeruginosa can produce ethanol from sugar. The authors con-
cluded that false positive ethanol urine tests may result if urine specimens
are collected without using proper preservatives.15
Drug Testing Using Urine

The majority of workplace drug testing is carried out using urine. As men-
tioned earlier, federally mandated drug testing requires testing for five
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184 Chapter 9
drugs, including amphetamines, cocaine, marijuana, opiates, and phen-

cyclidine, which are commonly referred to as the five SAMHSA drugs.
In addition to these five drugs, private employers at their discretion may
test for additional drugs, such as barbiturates, benzodiazepines, metha-
done, oxycodone, propoxyphene, and methaqualone. These drugs are
generally referred to as non-SAMHSA drugs. Among the five SAMHSA
drugs, the amphetamine class of drugs includes both amphetamine and
methamphetamine, while opiates include morphine, codeine, and heroin.
Similarly, among non-SAMHSA drugs, the barbiturate class includes
various drugs, including secobarbital, pentobarbital, phenobarbital, and
butalbital. There are more than fourteen approved benzodiazepines in the
United States, but the most commonly abused benzodiazepines are alpra-
zolam, diazepam, clonazepam, halazepam, lorazepam, and oxazepam.
Most drugs stay in the urine for two to three days, while some drugs,
such as marijuana metabolite, may stay for up to thirty days in chronic
abusers. The window of detection of various illicit drugs is given in table
9.2. Some drugs, such as amphetamines, are detected unchanged in urine
drug tests. However, some drugs are detected in urine as their metabolite;
Table 9.2. Window of Detection of SAMHSA and Commonly Monitored Non-

SAMHSA Drugs
Drug Detection Window in Urine
SAMHSA drugs
Amphetamine 2 days
Methamphetamine 2 days
Cocaine (as benzoylecgonine) 2 days after single use; 4 days
after repeated use
Morphine 2–3 days
Codeine 2 days
Heroin (as morphine) 2 days
Phencyclidine 14 days
Marijuana 2–3 days after single use
(as marijuana metabolite 30 days in chronic abuser
11-nor-⌬9-tetrahydrocannabinol- 9-
carboxylic acid; THC-COOH)
Non-SAMHSA drugs
Barbiturates
Short-acting (pentobarbital, secobarbital etc.) 1 day
Long-acting (phenobarbital) 21 days
Benzodiazepines
Short-acting (alprazolam, lorazepam, etc.) 3 days
Long-acting (diazepam, lorazepam, etc.) 30 days
Methadone 3 days
Methaqualone 3 days
Oxycodone 2–4 days
Propoxyphene 6 hours–2 days
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Table 9.3. Cutoff Concentrations of Various SAMHSA and non-SAMHSA drugs

Drug or Drug Class Immunoassay (ng/mL) GC-MS Confirmation (ng/mL)
SAMHSA Drugs
Amphetamines 1000 Amphetamine 500
Methamphetamine 500
Cannabinoids 50 THC-COOH 15
Cocaine metabolites 300 Benzoylecgonine 150
Opiates 2000 Morphine 2000
Codeine 2000
6-Acetylmorphine 10*
Phencyclidine 25 Phencyclidine 25
Non-SAMHSA Drugs
Barbiturates 200 Barbiturates 150^
Benzodiazepines 200 Benzodiazepines 150^
Methadone 300 Methadone 200
Methaqualone 300 Methaqualone 200
Propoxyphene 300 Propoxyphene 300
Oxycodone 100 or 300 ng/mL Oxycodone 100
*6-monoacetyl morphine is a specific metabolite indicating heroin abuse.
^Individual drug in this class of drug can be confirmed at 150 ng/mL cutoff concentration.
for example, cocaine is determined as benzoylecgonine, a major cocaine

metabolite. Similarly, marijuana is determined as 11-nor-⌬9-tetrahydro-
cannabinol- 9-carboxylic acid or THC-COOH, the major metabolite of
marijuana.
Like alcohol testing where most tests cannot accurately determine
blood alcohol level below 0.02 percent (20 mg/dL), assays employed for
detection of various drugs in urine specimens also have detection limits.
Usually screening assays are done using immunoassays and automated
analyzers, and if a screening assay is positive, the presence of a particular
drug in the urine specimen must be confirmed by a second analytical
method. The gold standard for confirmation of drugs in urine specimens
is gas chromatography/mass spectrometry (GC/MS). This is a very so-
phisticated analytical instrument costing between $75,000 and $100,000.
In general, GC/MS is capable of confirming drug concentrations in much
lower levels than immunoassays. Screening and confirmation cutoff con-
centrations of various drugs are given in table 9.3. If the screening test
is positive but the confirmation test is negative, the drug testing result
should be considered negative.16
LIMITATIONS OF ALCOHOL AND DRUG TESTING
Breath analyzers are widely used for determination of alcohol use

among employees working in security- and safety-sensitive positions.
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186 Chapter 9
Breath analyzers, although based on robust analytical principles, are

occasionally subject to certain limitations, including false positive and
false negative test results. Derogis et al. (1995) reported that out of 204
patients studied using the breath analyzer, three patients showed false
positive ethanol levels and another three patients showed false nega-
tive results.17 Blood alcohol determination using gas chromatography
is very accurate and is the method of choice in laboratories performing
legal alcohol determinations (please see chapter 6 for more in-depth
discussion on breath analyzers and various methods for determining
blood alcohol concentrations).
Workplace drug testing also has certain limitations. For example, im-
munoassays are used for screening tests and such assays are subject to
interferences, meaning that another drug may trigger a positive result.
Amphetamine immunoassays are subject to interferences from many
over-the-counter cold medications, such as brompheniramine, ephedrine,
phentermine, phenylpropanolamine, pseudoephedrine, and phenyleph-
rine.18 Fortunately, such false positive test results can be eliminated in the
GC/MS confirmation step.
Consuming food containing poppy seeds is legal, but poppy seeds
contain both morphine and codeine, and urine opiate drug testing can
be positive after consuming such foods (depending on the amount
consumed and the time elapsed after eating). Because the GC/MS con-
firmation step also targets morphine (heroin abusers also show mor-
phine in their urine because heroin is finally metabolized to morphine)
and codeine, eating poppy seeds may result in a positive drug test. A
morphine concentration of 5,880 ng/mL after ingestion of poppy seed
cake in one subject was reported by Thevis et al. (2003). Other subjects
in this study also showed significant amounts of morphine, which was
confirmed in the urine by the GC/MS method.19 Although in November
1998, SAMHSA increased the cutoff concentration for screening (as well
as the GC/MS confirmation cutoff) for opiates to 2000 ng/mL, it is still
possible to get positive test results from consuming poppy seed prod-
ucts, especially if the opiate concentrations (morphine and codeine) are
relatively high in the seeds. Australian, Turkish, and Dutch poppy seeds
are available in the market, and Australian poppy seeds usually have
high amounts of opiates (90 to 200 microgram of morphine per gram of
poppy seeds), while Turkish and Dutch poppy seeds contain only 4 to
5 microgram of morphine per gram of seeds.20 Some private employers
still use the old 300 ng/mL cutoff for both screening and confirmation of
opiates in workplace drug testing. Such levels of morphine and codeine
can be easily achieved by eating one poppy seed muffin prior to a pre-
employment drug test. After eating food containing poppy seeds, urine
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may test positive at 300 ng/mL cutoff level for a day or two. Therefore,
it is important not to consume such food several days prior to taking a
preemployment drug test.
Although less common than positive workplace drug testing results
due to eating food containing poppy seeds, certain herbal teas originat-
ing from South America, especially mate de coca tea and health Inca
tea, may be contaminated with cocaine. Usually one tea bag contains 1
gm of dried plant material and may contain between 1.4 and 5 mg of
cocaine. Drinking such tea prior to workplace drug testing may result
in a positive cocaine test because sufficient amounts of cocaine are usu-
ally present in the tea for urinary concentrations of benzoylecgonine
(cocaine metabolite) to exceed the cutoff concentration of 300 ng/mL.
Although U.S. customs regulations require that no cocaine should be
present in any herbal tea, literature references indicate that some health
Inca tea sold in the United States contains cocaine. Jackson et al. (1991)
reported urinary concentration of benzoylecgonine after ingestion of
one cup of health Inca tea by volunteers. Benzoylecgonine was detected
up to twenty-six hours postingestion. Maximum urinary benzoylec-
gonine concentration ranged from 1400 ng/mL to 2800 ng/mL after
ingestion of health Inca tea. The total excretion of benzoylecgonine in
thirty-six hours ranged from 1.05 to 1.45 mg, which correlated with
59–90 percent of the ingested cocaine dose from drinking such tea pre-
pared using one tea bag.21
In addition, taking certain prescription medications, such as a narcotic
analgesic, may cause positive workplace drug testing. Common prescrip-
tion medications that result in positive workplace drug testing are listed
in table 9.4. It is important to disclose use of any such medication prior to
submitting urine specimen for workplace drug testing.
Table 9.4. Prescription Drugs that May Cause a Positive Result in Workplace Drug
Testing
Positive Workplace Test Generic Name of the Drug
Amphetamines amphetamine, amphetaminil, clobenzorex,
ethylamphetamine, fenoproporex, mefenorex,
prenylamine, methamphetamine, benzphetamine,
famprofazone, furfenorex, selegiline
Opiates codeine, morphine, hydromorphone
Benzodiazepine estazolam, flurazepam, temazepam, triazolam, midazolam,
alprazolam, chlordiazepoxide, clorazepate, clonazepam,
diazepam, halazepam, lorazepam, nitrazepam, prazepam,
oxazepam quazepam
Author’s Note: Oxycodone does not interfere with workplace opiate testing.
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188 Chapter 9
TIPS TO PASS WORKPLACE ALCOHOL AND DRUG TESTS
For passing alcohol tests, do not drink at all for at least twelve hours and
do not consume more than two standard drinks between twelve hours
and twenty-four hours before testing. Most workplace alcohol tests have
very strict requirement and even a single drink a few hours prior to
alcohol testing can push blood alcohol over the acceptable limit of 0.02
percent (20 mg/dL) or less.
To pass preemployment drug tests do not drink too much water before
testing due to being nervous. Because people try to beat drug tests by
diluting urine so that drug concentrations can be pushed below the detec-
tion threshold, all drug testing facilities follow strict criteria to determine
which specimens are not acceptable for analysis. Creatinine below 20 mg/
dL and specific gravity below 1.003 may be considered an indication of
intentionally diluted urine. Drinking too much water (more than 3 liters
in twenty-four hours) may cause such dilution of urine. Therefore, drink
normal amounts of fluid before workplace drug testing and do not con-
sume too much caffeine. In addition, do not eat any poppy seed–contain-
ing food at least three to four days prior to drug testing and do not drink
any herbal tea, especially any herbal tea coming from South America,
because it may be contaminated with cocaine.
CONCLUSION
Workplace alcohol and drug testing are common practice in today’s

work environment in order to achieve a drug- and alcohol-free work-
place. Workplace drug testing is more prevalent than combined alcohol
and drug testing. Usually personnel employed in security- and safety-
sensitive positions are subjected to both alcohol and drug testing. As a
result of implementing such programs, alcohol- and drug-related work-
place injuries are declining in the United States.
There are very strict criteria for blood alcohol limits in personnel work-
ing in security-sensitive positions, and it is advisable not to drink at all
before reporting for such work. For workplace drug testing, any positive
test may cause adverse action against the person, and abusing drugs is a
bad idea. Although there are many products advertised on the Internet
as effective to beat drug tests, in reality none of them work because drug
testing facilities routinely screen for such adulterants, and if detected, the
drug testing may be considered positive.
10-649_Dasgupta.indb 188 1/17/11 6:40 AM

NOTES
1. T. C. Blum, P. M. Roman, and J. K. Martin, “Alcohol Consumption and

Work Performance,” Journal of Studies on Alcohol 44 (1993): 61–70.
2. D. Bush, “The U.S. Mandatory Guidelines for Federal Workplace Drug
Testing Programs: Current Status and Future Considerations,” Forensic Science
International 174 (2008): 111–19.
3. Drug Testing Index, Quest Diagnostics, March 12, 2008.
4. Substance Abuse and Mental Health Services Administration, News 15, no.
5 (September/October 2007).
5. C. S. Carpenter, “Workplace Drug Testing and Worker Drug Use,” Health
Services Research 42, no. 2 (April 2007): 795–810.
6. J. E. Brady, S. P. Baker, C. Dimaggio, M. L. McCarthy, et al., “Effectiveness
of Mandatory Alcohol Testing Programs in Reducing Alcohol Involvement in Fa-
tal Motor Carrier Crashes,” American Journal of Epidemiology 170, no. 6 (September
2009): 775–82.
7. “Procedures for Transportation Workplace Drug and Alcohol Testing Pro-
grams: Final Rule,” Federal Register 73, no. 123 (June 25, 2008): 35961–75.
8. J. E. Brady, S. P. Baker, C. Dimaggio, M. L. McCarthy, et al., “Effectiveness
of Mandatory Alcohol Testing Programs in Reducing Alcohol Involvement in Fa-
tal Motor Carrier Crashes,” American Journal of Epidemiology 170, no. 6 (September
2009): 775–82.
9. T. Marrero, “Hernando Superintendent Recommends School Board Fire
Bus Driver Who Failed Alcohol Breath Test,” St. Petersburg (Florida) Times, Octo-
ber 16, 2009.
10. Associated Press, “United Pilot Charged with Being over Alcohol Limit,”
New York Times, January 5, 2010.
11. J. F. Jemionek, C. L. Copley, M. L. Smith, and M. R. Past, “Concentra-
tion Distribution of the Marijuana Metabolite Delta 9-Tetrahydrocannabinol-
9-Carboxylic Acid and Cocaine Metabolite Benzoylecgonine in the Department
of Defense Urine Drug Testing Program,” Journal of Analytical Toxicology 32, no. 6
(July–August 2008): 408–16.
12. A. Helander, C. A. Hagelberg, O. Beck, and B. Petrini, “Unreliable Alcohol
Testing in a Shipping Safety Program,” Forensic Science International 189, nos. 1–3
(August 2009): e45–47.
13. A. W. Jones, “Urine as a Biological Specimen for Forensic Analysis of Al-
cohol and Variability in the Urine to Blood Relationship,” Toxicological Review 25,
no. 1 (January 2006): 15–35.
14. A. W. Jones, A. Eklund, and A. Helander, “Misleading Results of Ethanol
Analysis in Urine Specimens from Rape Victims Suffering from Diabetes,” Journal
of Clinical and Forensic Medicine 7, no. 3 (September 2000): 144–46.
15. A. Helander, C. A. Hagelberg, O. Beck, and B. Petrini, “Unreliable Alcohol
Testing in a Shipping Safety Programme,” Forensic Science International 189, no. 10
(August 2009): e45–47.
10-649_Dasgupta.indb 189 1/17/11 6:40 AM

190 Chapter 9
16. A. Dasgupta, A Health Educator’s Guide to Understanding Drugs of Abuse Test-

ing (Sudbury, MA: Jones and Bartlett, 2009), 55–91.
17. V. Derogis, P. Bourrier, O. Douay, A. Turcant, et al., “Ethyl Alcohol Levels
in Expiratory Air vs. Blood Alcohol Levels in 204 Cases in an Emergency Unit,”
Presse Medicale 24, no. 23 (June 1995): 1067–70.
18. A. Dasgupta, S. Saldana, G. Kinnaman, M. Smith, et al., “Analytical Per-
formance Evaluation of EMIT II Monoclonal Amphetamine/Methamphetamine
Assay: More Specificity than EMIT D.A.U. Monoclonal Amphetamine/Metham-
phetamine Assay,” Clinical Chemistry 39, no. 1 (January 1993): 104–8.
19. M. Thevis, G. Opfermann, and W. Schanzer, “Urinary Concentrations of
Morphine and Codeine after Consumption of Poppy Seeds,” Journal of Analytical
Toxicology 27, no. 1 (January 2003): 53–56.
20. M. G. Pelders and J. J. W. Ross, “Poppy Seeds: Difference in Morphine and
Codeine Content and Variation in Inter- and Intra-individual Excretion,” Journal
of Forensic Sciences 41 (1996): 209–12.
21. G. F. Jackson, J. J. Saady, and A. Poklis, “Urinary Excretion of Benzoylec-
gonine Following Ingestion of Health Inca Tea,” Forensic Sciences International 49
(1991): 57–64.
10-649_Dasgupta.indb 190 1/17/11 6:40 AM

10

Why Not to Drink at All
When You’re Pregnant
P regnancy and drinking do not mix at all. Alcohol use among women
of childbearing age is a leading preventable cause of birth defects and
developmental disabilities. Ethyl alcohol, which is commonly referred to as
alcohol, is a well-documented teratogen. A teratogen is an agent that can
cause birth defects if the mother is exposed to that agent during pregnancy.
After conception (when the egg is fertilized), it takes about six to nine days
for the embryo to anchor to the uterus, and then a common blood supply
line is developed (placenta) between the mother and the embryo so that
nutrients can flow to the embryo for its development into a fetus. This
supply line lasts until delivery of the baby when the placenta is cut from
the newborn after birth. A teratogen can cross over from the mother to the
developing embryo (or fetus) and cause birth defects. Alcohol is a small
molecule, so it can easily pass through the placenta to the embryo and
cause birth defects. These defects are collectively called “fetal alcohol spec-
trum disorders.” If more severe signs of these birth defects are present in a
newborn, the condition may be called “fetal alcohol syndrome.” Drinking
alcohol during pregnancy may cause stillbirth, and a newborn may even
die from fetal alcohol syndrome shortly after birth. Poor outcomes associ-
ated with drinking alcohol during pregnancy include but are not limited to
• Stillbirth/death of the baby shortly after birth

• Preterm baby
• Smaller birth weight/growth retardation of the baby
• Neurological abnormality/intellectual impairment
• Facial abnormalities
191
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192 Chapter 10
DRINKING DURING PREGNANCY

AND STILLBIRTH/INFANT MORTALITY
Drinking during pregnancy, especially heavy drinking (for women seven

drinks per week or three or more drinks per occasion) or binge drinking
(drinking alcohol in order to get intoxicated—four drinks in two hours
for a female; see also chapter 2), is associated with very poor outcomes of
pregnancy, including stillbirth and high infant mortality. A study by Mar-
bury et al. (1983) involving 12,440 pregnant women clearly established
that drinking fourteen or more drinks per week was associated with still-
birth, low birth weight, and preterm babies (gestational age under thirty-
seven weeks).1 A recent epidemiological study involving 79,216 mothers
concluded that intake of four drinks of alcohol per week or binge drink-
ing on more than three occasions during pregnancy is associated with an
increased risk of infant mortality among full-term infants, especially soon
after birth.2
Despite the risk associated with binge or heavy drinking with poor
pregnancy outcomes, a double-digit percentage of women in the United
States are involved in binge drinking during their childbearing years. In
a study based on women between the ages of eighteen and forty-four
who participated in the CDC Behavioral Risk Factors Surveillance System
(58,431 women in 2001, 64,181 in 2002, and 65,678 in 2003), the authors
reported that the percentage involved in binge drinking was 11.9 per-
cent, 12.4 percent, and 13.0 percent in 2001, 2002, and 2003. The authors
concluded that health care providers must identify and intervene with
these binge drinkers who engage in alcohol use in pregnancy, in order to
reduce the risk of alcohol-exposed pregnancy.3 Although the percentage
of pregnant women involved in binge drinking is substantially lower than
the percentage of women in childbearing age involved in binge drinking,
the average annual percentage of alcohol use among pregnant women
was 12.2 percent in one report (Denny et al. 2007), and 1.9 percent of
pregnant women were involved in binge drinking according to the same
report. Surprisingly, the highest percentages of pregnant women report-
ing alcohol use during the survey period of 2001–2005 were women ages
thirty-five to forty-four (17.7 percent), college graduates (14.4 percent),
employed (13.7 percent), and unmarried (13.4 percent), and average alco-
hol use among these groups was higher than the overall average of 12.2
percent of pregnant women who used any alcohol during pregnancy.4
Although binge drinking and heavy drinking are dangerous practices
during pregnancy, some studies have discovered that even moderate
or infrequent drinking during pregnancy may cause adverse outcomes,
including death of the baby. In one study (Kesmodel et al. 2002), the
authors investigated 24,768 pregnant women and found that the risk of
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Why Not to Drink at All When You’re Pregnant 193
stillbirth among women who consumed five or more drinks per week was
three times higher than women who consumed less than one drink per
week. The rate of stillbirth was 1.37 per 1,000 births among women who
consumed less than one drink per week to 8.83 per 1,000 births among
women who consumed five or more drinks per week.5
A recent study (Aliyu et al. 2008) reported that mothers who consumed
any alcohol during pregnancy were 40 percent more likely to have
stillbirths compared to nondrinking mothers. In addition, mothers who
consumed five or more drinks per week during pregnancy experienced a
70 percent elevated risk of stillbirth compared to pregnant women who
did not consume any alcohol during pregnancy. These findings reinforce
current counseling strategies toward pregnant women—and women
who intend to get pregnant—of the detrimental effect of drinking during
pregnancy.6 In addition, women giving birth to children with fetal alcohol
syndrome also have a higher risk of early mortality.7
FETAL ALCOHOL SYNDROME, FETAL ALCOHOL

SPECTRUM DISORDERS, AND EPIDEMIOLOGY
Fetal alcohol syndrome due to prenatal alcohol exposure was first re-
ported by Jones and Smith in 1973.8 Since then many publications have
documented the teratogenic effect of alcohol in both human and animal
studies. This syndrome is the most common noninherited (nongenetic)
cause of mental retardation in the United States. “Fetal alcohol spectrum
disorders” was a term described in 2004 to convey that exposure of the fe-
tus to alcohol produces a continuum of effects, and that many babies who
do not fulfill all criteria for a diagnosis of fetal alcohol syndrome may nev-
ertheless be profoundly impacted negatively throughout their lives due to
exposure to alcohol. Therefore, fetal alcohol spectrum disorders include
a wide range of permanent birth defects due to maternal consumption of
alcohol during pregnancy, which also includes all serious complications
found in babies born with fetal alcohol syndrome.
Other medical terminology related to birth defects in babies caused by
maternal alcohol consumption during pregnancy include partial fetal al-
cohol syndrome, fetal alcohol effect, alcohol-related neurodevelopmental
disorders, and alcohol-related birth defects. Approximately 1 to 4.8 of
every 1,000 children born in the United States has fetal alcohol syndrome,
while as many as 9.1 babies out of 1,000 babies born have fetal alcohol
spectrum disorder. This is an alarming statistic because nearly 1 in every
100 babies born in the United States is born with fetal alcohol spectrum
disorders. Therefore, fetal alcohol spectrum disorders are a major public
health issue, affecting up to 1 percent of the U.S. population.9 Recent
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194 Chapter 10
school studies indicate that the prevalence of fetal alcohol syndrome in

the United States is at least 2 to 7 per 1,000 babies, and current prevalence
of fetal alcohol spectrum disorders may be as high as 2 to 5 percent in
the United States among school population. Such prevalence of alcohol-
related complications in newborns is higher among school populations
than in the general population.10
IS ANY AMOUNT OF ALCOHOL SAFE DURING PREGNANCY?
Drinking is a risk factor for poor outcome of pregnancy, including the pos-
sibility of a child born with fetal alcohol syndrome or a related disorder. A
risk factor means that chances of adverse outcome is high if such a factor
is present in a person. For example, if an individual has an elevated cho-
lesterol level (over 200 mg/100 milliliter of blood; 200 mg/dL), that person
has an increased risk of myocardial infarction (heart attack). That does not
mean that every person with a cholesterol value over 200 mg/dL has a
higher chance of a heart attack than a person with a desirable cholesterol
level (less than 200 mg/dL). Because heart attacks are not desirable, physi-
cians always advise their patients to keep cholesterol levels below 200 mg/
dL by changing their diet and lifestyle and, if necessary, taking medication.
Similarly, not every woman who drinks alcohol during pregnancy will
have a poor outcome. However, it is impossible to predict which women
will be affected by drinking and which women will not be affected by
drinking based on any laboratory tests or any other means. In addition, it
is also impossible to predict if even one episode of drinking during preg-
nancy is going to hurt the fetus. Although fetal alcohol syndrome and less
severe fetal alcohol spectrum disorders are strongly associated with higher
levels of alcohol consumption during pregnancy, animal studies have sug-
gested that even a single episode of alcohol consumption equivalent to two
standard drinks during pregnancy may lead to loss of fetal brain cells. Ma-
ternal factors that increase the risk of a baby being born with fetal alcohol
spectrum disorders include maternal age (thirty and older), history of binge
drinking, and low socioeconomic status.11
Adverse pregnancy outcomes due to use of alcohol have been noted
very early in history, and Aristotle’s warning of adverse effects of alcohol
associated with pregnancy was probably one of the earliest observations
regarding alcohol and pregnancy. However, the majority of documented
adverse outcomes of pregnancy associated with alcohol use began with
the eighteenth-century London Gin Epidemic (ca. 1720–1750), when
newer distillation techniques entered into England from the Netherlands
with the ascent of William and Mary to the throne of England. At that
time a ban was placed on imported French wine, and plenty of distilled
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liquor in the form of gin was available in England at low cost because
taxes were lowered on the sale of such liquors. Crime rates were high in
England, probably due to increased drinking of gin, and physicians in
London also blamed alcohol for a higher death rate compared to birth
rate. By 1725 the damage caused by alcohol was so significant that the
London College of Physicians presented their concerns to the House of
Commons and commented that the frequent use of several sorts of dis-
tilled liquors resulted in the birth of weak, feeble, distempered children
who became burdens to society rather than assets. Fearing the loss of
their workforce, combined with poor pregnancy outcomes due to alcohol
use and related factors, the elites of London became vocal on the abuse
of distilled alcohol and caused the eventual repeal of the law that helped
increase the production of cheap alcohol.12
Modern research on understanding fetal alcohol syndrome started in the
1970s. Although earlier publications indicated that fetal alcohol syndrome
was associated with heavy drinking, and modest drinking during preg-
nancy may be relatively safe, more recent in-depth studies indicate that at
this point we do not know for sure how much alcohol is safe for a preg-
nant woman to consume to avoid adverse effects on the developing fetus
or newborn. A 2002 study found that fourteen-year-old children whose
mothers drank as little as one drink a week were significantly shorter and
leaner and had a smaller head circumference than children of women who
were nondrinkers.13 This research is in contrast to the earlier studies that
reported that up to two drinks per day were safe during pregnancy.
Based on the body of literature on poor pregnancy outcomes associated
with alcohol use, the American Academy of Pediatrics (AAP) and the
American College of Obstetricians and Gynecologists (ACOG) have for
many years recommended alcohol abstinence for both pregnant women
and women trying to become pregnant, because no safe threshold for
drinking during pregnancy can be established. In 1994, the AAP and
the ACOG released a joint statement advising physicians to question
all pregnant women at their first visits regarding their current and past
consumption of alcohol. Because drinking during pregnancy is associated
with a negative social stigma, denial is not uncommon, especially among
minority women. Fortunately, screening tools have been developed to
help clinicians accurately identify pregnant women who consume alcohol
during pregnancy. One such tool is a four-item questionnaire called T-
ACE, which is validated for use with pregnant women, including minor-
ity women. The T-ACE is the tool that is recommended by the ACOG and
the National Institute on Alcohol Abuse and Alcoholism for screening
pregnant women for potential alcohol consumption. The questions asked
in this test are given in table 10.1. A total score of two or more is consid-
ered positive for risk of drinking.14
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196 Chapter 10
Table 10.1. T-ACE Scoring Tool for Assessing Risk of Drinking in a Pregnant Woman
Question Scoring
How many drinks does it take to make you feel high? Score 2 if more than 2 drinks,
or 1 for 1 drink
Have people annoyed you by criticizing your Yes answer score 1
drinking?
Have you felt you need to cut down on your drinks? Yes answer score 1
Have you ever had a drink first thing in the morning Yes answer score 1
to steady your nerves?
A total score of 2 or more is indicative of drinking risk in pregnancy.
The 2005 U.S. surgeon general, Dr. Richard H. Carmona, issued an advi-
sory warning to pregnant women and women who may become pregnant
to abstain from alcohol consumption in order to eliminate the chance of
giving birth to a baby with any harmful effects of fetal alcohol spectrum
disorders. This updates a 1981 surgeon general’s advisory that suggested
that pregnant women should limit alcohol consumption. Dr. Carmona said,
We must prevent all injury and illness that is preventable in society, and
alcohol-related birth defects are completely preventable. We do not know what,
if any, amount of alcohol is safe. But we do know that the risk of a baby being
born with any of the fetal alcohol spectrum disorders increases with the amount
of alcohol a pregnant woman drinks, as does the likely severity of the condition.
And when a pregnant woman drinks alcohol, so does her baby. Therefore, it’s
in the child’s best interest for a pregnant woman to simply not drink alcohol.
In addition, studies indicate that a baby can be affected by alcohol

consumption within the earliest weeks after conception, even before a
woman knows she is pregnant. The surgeon general also recommended
that women who plan to become pregnant should abstain from consum-
ing alcohol.15 The Healthy People 2010 objectives include increasing the
percentage of pregnant women who report abstinence from alcohol use
to 95 percent and increasing the percentage who report abstinence from
binge drinking to 100 percent, because binge drinking is particularly
harmful to the fetal brain.
FETAL ALCOHOL SYNDROME AND FETAL ALCOHOL

SPECTRUM DISORDERS: CLINICAL FEATURES
Fetal alcohol syndrome usually presents with three major features:

growth retardation; some degree of brain damage, such as small head size
at birth; and characteristic facial features.
Diagnosis of fetal alcohol syndrome and related disorders are based on
the following criteria:16
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• Category 1: Confirmed maternal consumption of alcohol

• Category 2: Fetal alcohol syndrome may be confirmed without es-
tablished maternal alcohol consumption if major features of fetal al-
cohol syndrome, including growth retardation, facial abnormalities,
and neurodevelopmental abnormalities are observed.
• Category 3: Partial fetal alcohol syndrome with confirmed maternal
exposure to alcohol
• Category 4: Alcohol-related birth defect if maternal alcohol con-
sumption is confirmed and one or more congenital defects character-
istic of fetal alcohol syndrome is present in the newborn
• Category 5: Alcohol-related neurodevelopmental disorders if ma-
ternal consumption of alcohol is confirmed and neurodevelopmen-
tal abnormalities or cognitive disorders are present. Any obvious
physical characteristics of fetal alcohol syndrome may be absent.
The most common deformity seen in fetal alcohol syndrome is mod-

erate to severe growth retardation during pregnancy and also after the
birth of the newborn. This is manifested by the crown-rump length of
the infant (measurement of the infant from the top of the head to the
bottom of the buttocks), head circumference, and body weight due to
irreversible change in body structure from fetal exposure to alcohol.
Other facial abnormalities observed in these babies include microceph-
aly (small head, a neurodevelopmental disorder where the circumfer-
ence of the head is significantly smaller than the head of the average
person in the same age-group and gender), long and narrow forehead,
frontal bossing (unusually prominent forehead), and a variety of other
deformities (table 10.2). Facial abnormalities common in fetal alcohol
Table 10.2. Abnormalities Present in Babies with Fetal Alcohol Syndrome

Abnormality Comments
Growth retardation Low birth weight, lack of weight gain over time,
low weight-to-height ratio
Facial abnormalities Small head circumference, small eye opening,
small midface, flat midface, flat upper lip, low
nasal bridge, short nose
Neurodevelopmental problems Abnormalities of central nervous system, small
head size at birth, impaired motor skills, poor
eye-hand coordination, hearing loss
Behavioral and cognitive problems Mental retardation, learning disability, poor
memory, language deficiency, poor judgment,
problem with reasoning and math
Cardiac malfunctions Atrial septal defect, ventricular septal defect, and
other malfunctions
Other organ problems Renal insufficiency, endocrine disorders, various
problems with eyes
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198 Chapter 10
syndrome are shown in figure 10.1. Mental retardation is the major

complication of fetal alcohol syndrome due to impaired neurodevelop-
ment of the fetus associated with the maternal use of alcohol during
pregnancy. The brain of the fetus is the organ that is most vulnerable
to prenatal alcohol across a wide range of regions. However, other com-
plications found in babies born with fetal alcohol syndrome include
cardiac malformations, bone and joint problems, endocrine disorders,
and eye and hearing problems. Some of these complications may also
be found in babies born with fetal alcohol spectrum disorders.
Alcohol can easily cross the placenta and enter fetal circulation and can
also easily cross the fetal blood-brain barrier. Alcohol has a direct toxic
effect on the developing brain of the fetus, including developing neurons.
The hippocampus is one of the major targets for alcohol to exert its toxic
effect on the developing brain. The hippocampus is a major part of the
limbic system of the brain (“limbic” can be loosely translated to “belt,”
and the limbic system has a beltlike structure) and plays an important role
in forming long-term memory and orientation. The limbic system is a ma-
jor part of the brain structure that controls emotion, behavior, long-term
memory, and olfaction (sense of smell). Ethanol can release L-glutamate,
an amino acid that also acts as a neurotransmitter, in the hippocampus
of the fetal brain, and toxicity of ethanol may be mediated through the
release of L-glutamate. In addition, acetaldehyde, a metabolite of alcohol,
may play a role in the teratogenic effect of alcohol on the fetus.17 Ethanol
also triggers widespread suicide by developing neurons (neurodegenera-
Figure 10.1. Facial features associated with fetal alcohol syndrome

Source: Alcohol Research and Health Journal, reference 20. The National Institute of Alcohol Abuse and
Alcoholism (NIAAA) website. Information in the public domain.
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tion due to neural apoptosis), thus causing degeneration of the develop-

ing fetal brain. Based on rat experiments, it has been postulated that neu-
ral apoptosis is due to the blockage of N-methyl-D-aspartate glutamate
receptors and excessive activation of GABA (gamma-aminobutyric acid)
receptors.18
In addition, alcohol impairs placental blood flow to the fetus by con-
stricting blood vessels, causing fetal hypoxia (lack of oxygen) and malnu-
trition. Oxidative stress normally experienced by the fetus may also be
increased due to the maternal use of alcohol. Major problems associated
with fetal alcohol syndrome and fetal alcohol spectrum disorders are
discussed below.
Mental Health Issues and Fetal Exposure to Alcohol

Mental retardation is the major complication associated with fetal alco-
hol syndrome, as well as fetal alcohol spectrum disorders. In addition, a
variety of behavioral problems may be associated in children where the
fetus was affected to a lesser degree by the maternal use of alcohol dur-
ing pregnancy. Fetal alcohol syndrome is a devastating developmental
disorder, and it is now a leading cause of mental retardation. In addition
to structural abnormalities and growth deficit, fetal alcohol syndrome
is associated with a broad spectrum of neurobehavioral abnormalities,
including lower IQ, hyperactivity, attention deficit disorder, learning
disabilities, memory and language problems, and reduced visuospatial
ability (mental capacity to visualize objects and their spatial arrangement)
in children born with this syndrome.19
In addition, children with fetal alcohol spectrum disorders also have
significant impairments in memory that negatively affect their academic
performance and daily functioning. Verbal memory is one of the main
areas of memory affected by gestational alcohol exposure, especially in
forming memory, as well as recall. Spatial memory is also impaired, and
such impairment is found among children, adolescents, and adults who
were exposed to alcohol in utero. Animal research has documented that
key areas of the brain involved in memory functioning are affected by
alcohol if the fetus is exposed to alcohol due to maternal drinking.20 In
addition, the odds of appearance of many psychiatric illnesses, includ-
ing substance abuse, depression, anxiety, paranoid behavior, antisocial
behavior, obsessive-compulsive disorders, and psychotic disorders are
higher in adults whose mothers were involved in one or more episode
of binge drinking while pregnant.21 Mental health issues associated with
fetal alcohol syndrome are listed in table 10.3.
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200 Chapter 10
Table 10.3. Mental Health Issues Associated with Fetal Alcohol Syndrome
Mental retardation
Attention deficit disorder/hyperactivity disorder
Memory impairment
Learning disability
Behavior/learning problems causing dropping out of school
Depression/anxiety
Paranoid behavior
Obsessive-compulsive disorders
Alcohol/substance abuse problems
Inappropriate sexual behavior
Antisocial trends/trouble with the law
Cardiac Malformations and Fetal Exposure to Alcohol

The common cardiac malfunctions associated with fetal alcohol syndrome
are ventricular septal defects (VSD) and atrial septal defects (ASD). Both
defects are due to the presence of a hole or holes in the heart. The human
heart has four chambers, two upper chambers known as the left and right
atria and two lower chambers known as the left and right ventricles. Ven-
tricular septal defect means that one or more holes are present in the wall
that separates the right and left ventricles of the heart. Ventricular septal
defect is one of the most common congenital (present from birth) heart
defects. In the fetus, the right and left ventricles of the heart are not sepa-
rate, but as it grows to a full-term baby, a wall is formed to separate these
two ventricles. If the wall formation is incomplete, VSD occurs, while in
ASD the wall between the left and right atrium is incomplete. If the hole
is small (both VSD and ASD), it may close as the baby grows, but if the
hole is large, both defects may cause the heart to work harder, causing
heart failure. Major symptoms of VSD are shortness of breath, fast breath-
ing, hard breathing, and pounding heart. Similar symptoms may also be
observed in patients with ASD. Although VSD and ASD are the major
congenital heart defects associated with fetal alcohol syndrome, other
cardiac malfunctions may also be observed with fetal alcohol syndrome.22
Other Problems Associated with Fetal Alcohol Syndrome

Alcohol is capable of causing deformation of all cells and organs. Sig-
nificant skeletal deformity, such as cervical spine fusion (developmental
deformity of vertebrate), microcephaly (small head size), and abnormal
thoracic cage development are frequently associated with fetal alcohol
syndrome.23 A delayed bone age (delayed bone development) has been
observed in children with fetal alcohol syndrome. The effect is more
significant in the long bones, which explains the shorter height of chil-
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dren born with fetal alcohol syndrome compared to normal children of

the same age-group. The eyes may also be affected by fetal alcohol syn-
drome. The cornea may be smaller and cloudy at birth. Other eye prob-
lems include nystagmus (involuntary eye movement), microphthalmos
(abnormal smallness in the dimensions of one or both eyes), coloboma (a
hole in the structure of the eye, such as in the eyelid, iris, retina, or other
structure), and epicanthus (skin fold of the upper eyelid).
Renal abnormality or renal impairment may also be present in a child
with a history of maternal drinking during pregnancy. Some hearing
impairment may also be present in these children.24 Prenatal alcohol ex-
posure also causes abnormalities in endocrine functions. Alcohol abuse
is known to result in abnormalities of endocrine function. Alcohol is not
only able to cross the placenta and directly affect fetal cells; it can also
cause disruption in the mother’s endocrine function, thus disrupting
maternal-fetal hormonal interactions, which may affect the ability of the
mother to maintain a successful pregnancy.
Alcohol-induced endocrine imbalance may play a major role in
the mechanism by which alcohol harms the fetus. The hypothalamic-
pituitary-adrenal (HPA) axis is programmed during fetal development,
and alcohol can reprogram this axis, causing hyperactivity of this axis in
the baby born with fetal alcohol syndrome; such effects may last for the
lifetime of the child. Fetal reprogramming of the HPA axis due to fetal
alcohol exposure may be responsible for many problems, including be-
havior, endocrine, cognitive, and immune deficiencies.25
The hypothalamic-pituitary-adrenal (HPA) axis is a complex set of
direct influence and feedback mechanisms between the hypothalamus
(a funnel-shaped part of the brain), the pituitary gland (a small gland
located below hypothalamus in the brain), and the adrenal glands (small
conical-shaped glands on top of kidneys), which control many essential
body functions, including the immune system, digestion, sexuality, mood,
and stress level. This system also controls the level of various hormones
and cortisol in the body. Reprogramming of this axis during fetal growth
may cause many problems throughout the life of an affected individual.
HOW DOES PRENATAL EXPOSURE TO ALCOHOL

AFFECT THE CHILD THROUGH ADULTHOOD?
Exposure of the fetus to alcohol affects the newborn throughout its entire
life. A newborn baby may be born with a small head and be fussy and
may also suffer from feeding problems (poor sucking). In addition, such a
baby may bond poorly with the mother and have an abnormal sleep cycle,
frequently waking up during the night. The baby may also have poor
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202 Chapter 10
muscle tone and may appear floppy. As a toddler, language delays, poor
coordination and balance, poor memory, head banging, and hyperactivity
may be observed. As the baby grows older (ages four to twelve) learning
disabilities, short attention span, frequent temper tantrums, and aggres-
siveness are commonly observed features. At this stage, a baby born with
fetal alcohol syndrome may also experience difficulty in getting along
with others. As an adolescent, poor judgment, memory impairment,
poor problem-solving ability, and poor social skills are common among
children born with this syndrome. Dropping out of school, trouble with
the law, developing drug and alcohol dependence, and a variety of other
problems may develop when these children reach adulthood.
Exposure of the fetus to alcohol results in lifelong consequences that
affect physical development, intellectual development, behavior, social
development, occupation, independent living, and sexual behavior. Babies
born with fetal alcohol syndrome or fetal alcohol spectrum disorders may
even need lifelong assistance and are often prone to suicide.26 The devastat-
ing effects of exposure of the fetus to alcohol last a lifetime, and abstinence
from alcohol consumption during pregnancy is the best way to prevent
such detrimental effects. There is no good therapy that is able to reverse
the ill effects of fetal alcohol syndrome or fetal alcohol spectrum disorders.
SMOKING, DRINKING, AND DRUG ABUSE

DURING PREGNANCY AND POOR OUTCOME
Smoking is hazardous to health, and maternal smoking during preg-

nancy is associated with several adverse developmental outcomes in the
offspring. These include preterm delivery, spontaneous abortion, growth
restriction, and increased risk of sudden infant death syndrome, as well
as long-term behavioral and psychiatric disorders in the offspring.27 An
increase in congenital abnormalities (birth defects) associated with ciga-
rette smoking and the use of alcohol during pregnancy has been reported
in many scientific studies. Smoking and drinking during pregnancy also
increases the risk of many complications in pregnancy, including pla-
cental abruption, unexplained stillbirth, preterm labor, and intrauterine
growth restrictions. In one report (Odendaal et al. 2009), the authors
concluded that preterm labor leading to delivery of premature babies oc-
curs more frequently in women who smoke and drink during pregnancy,
and the risk was more than the sum of the effects of either smoking or
drinking. Therefore, smoking and drinking have synergistic effects that
greatly increase the risk of preterm labor. Smoking and drinking also
have synergistic effects for delivering babies with low birth weight and
growth restriction.28
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Substance abuse during pregnancy has devastating effects on preg-

nancy outcome, including stillbirth, preterm labor, and various birth
defects. Babies born to cocaine-addicted mothers often have congenital
abnormalities and low birth weight. One of the most devastating effects
of fetal cocaine exposure is damage to the developing heart. In addition,
substance abuse during pregnancy is associated with significant maternal
and fetal morbidity.29 In some states exposure of a fetus to illicit drugs
due to maternal abuse is considered a form of child neglect and abuse and
can lead to losing custody of the child and the potential for prosecution.
Concurrent abuse of illicit drugs and alcohol has synergistic effects associ-
ated with poor outcomes in pregnancy. Detailed discussion of the effect of
substance abuse on poor pregnancy outcome is beyond the scope of this
book, but many studies are available on this subject.
IS IT SAFE TO DRINK DURING BREAST-FEEDING?
Ample evidence indicates that drinking alcohol during pregnancy is associ-

ated with severe risks of poor pregnancy outcome, which is preventable by
abstinence, but the risks of consumption of alcohol during breast-feeding
are not as well defined. Alcohol is a small molecule and can easily pass
from the mother’s blood into her milk. A nursing infant is exposed to only
a fraction of the alcohol that the mother drinks, but the infant detoxifies
alcohol at a much slower rate than the mother. Adverse effects of alcohol
on suckling infants include changes in sleep pattern with much-reduced
sleep and waking up more frequently, decrease in milk intake, and risk
of developing low blood sugar (hypoglycemia). When alcohol appears in
breast milk, it alters the natural flavor of the milk and may explain why an
infant might consume less milk. Currently, there is no known benefit of
exposing the infant to alcohol. In contrast, most likely no level of alcohol in
breast milk is safe for the infant. Drinking water and pumping and dump-
ing breast milk will not accelerate elimination of alcohol from the breast
milk, because alcohol is not trapped in the breast milk but is constantly
removed as it moves back into the bloodstream. Therefore, the only way to
ensure that there is no alcohol in breast milk is to wait long enough after
consumption of alcohol before the next breast-feeding.
Elimination of alcohol from the body depends on body weight and
number of drinks consumed. For example, if a 90-pound woman drinks
two drinks in an hour, it will take approximately five hours and forty
minutes for the body to clear all of the alcohol. However, if the woman’s
weight is 150 pounds, it will take four hours and thirty minutes for
alcohol elimination after consuming two standard drinks in an hour.
Nursing mothers who choose to consume alcohol should carefully plan
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204 Chapter 10
a breast-feeding schedule by storing milk before alcohol consumption

and then waiting for complete elimination of alcohol from the breast
milk before resuming breast-feeding.30 Contrary to popular belief,
which encourages women to drink alcohol as an aid to lactation, alcohol
consumption in reality disrupts breast milk production.31
CONCLUSION
Due to devastating and lifelong effects of maternal consumption of alco-

hol on the offspring, pregnant women must abstain from drinking alco-
hol. In addition, smoking and substance abuse are also associated with
stillbirth, spontaneous abortion, and other poor outcomes in pregnancy.
Contrary to earlier guidelines where moderate alcohol consumption dur-
ing pregnancy was considered relatively safe, in 2005 the U.S. surgeon
general issued an advisory strongly recommending pregnant women to
refrain from consuming alcohol because no safe limit of alcohol during
pregnancy has been established. Fetal alcohol syndrome and less severe
fetal alcohol spectrum disorders are completely preventable if pregnant
women practice total abstinence.
NOTES
1. M. C. Marbury, S. Linn, R. Monson, S. Schoenbaum, et al., “The Association

of Alcohol Consumption with Outcome of Pregnancy,” American Journal of Public
Health 73, no. 10 (October 1983): 1165–68.
2. K. Strandberg-Larsen, A. Gronboek, A. M. Anderson, P. K. Andersen, et al.,
“Alcohol Drinking Pattern during Pregnancy and Risk of Infant Mortality,” Epi-
demiology 20, no. 6 (November 2009): 884–91.
3. J. Tsai, R. L. Floyd, and J. Bertrand, “Tracking Binge Drinking among U.S.
Childbearing Age Women,” Preventive Medicine 44, no. 4 (April 2007): 298–302.
4. C. H. Denny, J. Tsai, R. L. Floyd, P. P. Green, et al., “Morbidity and Mortality
Weekly Report,” 58, no. 19 (May 2009): 529–32.
5. U. Kesmodel, K. Wisborg, S. F. Olsen, T. B. Henriksen, et al., “Moderate
Alcohol Intake during Pregnancy and the Risk of Stillbirth and Death in the First
Year of Life,” American Journal of Epidemiology 155, no. 4 (February 2002): 305–12.
6. M. H. Aliyu, R. E. Wilson, R. Zoorob, S. Chakrabarty, et al., “Alcohol Con-
sumption during Pregnancy and the Risk of Early Stillbirth among Singletons,”
Alcohol 42, no. 5 (August 2008): 369–74.
7. J. P. Berg, M. E. Lynch, and C. D. Coles, “Increased Mortality among Women
Who Drank Alcohol during Pregnancy,” Alcohol 42, no. 7 (November 2008):
603–10.
8. K. L. Jones and D. W. Smith, “Recognition of the Fetal Alcohol Syndrome in
Early Infancy,” Lancet 302, no. 7836 (November 1973): 999–1001.
10-649_Dasgupta.indb 204 1/17/11 6:40 AM

9. P. D. Sampson, A. P. Streissguth, and F. L. Bookstein, “Incidence of Fetal

Alcohol Syndrome and Prevalence of Alcohol-Related Neurodevelopmental Dis-
order,” Teratology 56, no. 5 (November 1997): 317–26.
10. P. A. May, J. P. Gossage, W. O. Kalberg, L. K. Robinson, et al., “Prevalence
and Epidemiological Characteristics of FASD from Various Research Methods
with an Emphasis on Recent in School Studies,” Developmental Disability Research
Review 15, no. 3 (2009): 176–92.
11. D. J. Wattendorf and M. Muenke, “Fetal Alcohol Spectrum Disorders,”
American Family Physicians 72, no. 2 (July 2005): 279–82.
12. K. R. Warren and B. G. Hewitt, “Fetal Alcohol Spectrum Disorders: When
Science, Medicine, Public Policy, and Laws Collide,” Developmental Disabilities and
Research Reviews 15, no. 3 (September 2009): 170–75.
13. N. L. Day, S. L. Leech, G. A. Richardson, M. D. Cornelius, et al., “Prena-
tal Alcohol Exposure Predicts Continued Deficits in Offspring Size at 14 Years
of Age,” Alcohol Clinical and Experimental Research 26, no. 10 (October 2002):
1584–91.
14. B. A. Bailey and R. J. Sokol, “Pregnancy and Alcohol Use: Evidence and
Recommendations for Prenatal Care,” Clinical Obstetrics and Gynecology 51, no. 2
(June 2008): 436–44.
15. “U.S. Surgeon General Releases Advisory on Alcohol Use in Pregnancy,”
U.S. Department of Health and Human Services, Washington D.C., 2005, http://
www.surgeongeneral.gov/pressreleases/sg02222005.html.
16. D. J. Wattendorf and M. Muenke, “Fetal Alcohol Spectrum Disorders,”
American Family Physicians 72, no. 2 (July 2005): 279–82.
17. J. D. Reynolds and J. F. Brien, “Ethanol Neurobehavioral Teratogenies and
the Role of L-glutamate in the Fetal Hippocampus,” Canadian Journal of Physiology
and Pharmacology 73, no. 9 (September 1995): 1209–23.
18. C. Ikonomidou, P. Bittigau, M. J. Ishimaru, D. F. Wozniak, et al., “Ethanol-
Induced Apoptotic Neurodegeneration and Fetal Alcohol Syndrome,” Science 287,
no. 5455 (February 2000): 1050–60.
19. S. N. Mattson and E. P. Riley, “A Review of the Neurobehavioral Deficits in
Children with Fetal Alcohol Syndrome or Prenatal Exposure to Alcohol,” Alcohol
Clinical and Experimental Research 22, no. 2 (April 1998): 279–94.
20. S. Manji, J. Pei, C. Loomes, and C. Rasmussen, “A Review of the Verbal and
Visual Memory Impairments in Children with Foetal Alcohol Spectrum Disor-
der,” Developmental Neurorehabilitation 12, no. 4 (October 2009): 239–47.
21. H. M. Barr, F. L. Bookstein, K. D. O’Malley, P. D. Connor, et al., “Binge
Drinking during Pregnancy as a Predictor of Psychiatric Disorders on the Struc-
tured Clinical Interview for DSM-IV in Young Adult Offspring,” American Journal
of Psychiatry 163, no. 6 (June 2006): 1061–65.
22. L. Burd, E. Deal, R. Rios, E. Adickes, et al., “Congenital Heart Defects and
Fetal Alcohol Spectrum Disorders,” Congenital Heart Disease 2, no. 4 (July 2007):
250–55.
23. D. F. Smith, G. G. Sandor, P. M. MacLeod, S. Tredwell, et al., “Intrinsic De-
fects in the Fetal Alcohol Syndrome: Studies on 76 Cases from British Columbia
and the Yukon Territory,” Neurobehavioral Toxicology and Teratology 3, no. 2 (Sum-
mer 1981): 145–52.
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206 Chapter 10
24. J. D. Chaudhuri, “Alcohol and the Developing Fetus: A Review,” Medical

Science Monitor 6, no. 5 (2000): 1031–41.
25. X. Zhang, J. H. Sliwowska, and J. Weinberg, “Prenatal Alcohol Exposure
and Fetal Programming: Effects on Neuroendocrine and Immune Function,” Ex-
perimental Biology and Medicine (Maywood) 230, no. 6 (June 2005): 376–88.
26. J. Merrick, E. Merrick, M. Morad, and I. Kandel, “Fetal Alcohol Syndrome
and Its Long-Term Effects,” Minerva Pediatrica 58, no. 3 (June 2006): 211–18.
27. A. K. Shea and M. Steiner, “Cigarette Smoking during Pregnancy,” Nicotine
and Tobacco Research 10, no. 2 (February 2008): 2657–78.
28. H. J. Odendaal, D. W. Steyn, A. Elliott, and L. Burd, “Combined Effects of
Cigarette Smoking and Alcohol Consumption on Perinatal Outcome,” Gynecologic
and Obstetric Investigation 67, no. 1 (January 2009): 1–8.
29. K. M. Kuczkowski, “The Effects of Drugs Abuse on Pregnancy,” Current
Opinion in Obstetrics and Gynecology 19, no. 6 (December 2007): 578–85.
30. G. Koren, “Drinking Alcohol While Breastfeeding: Will It Harm My Baby?”
Canadian Family Physician 48, no. 1 (January 2002): 39–41.
31. J. A. Mannella and M. Y. Pepino, “Biphasic Effects of Moderate Drinking
on Prolactin during Lactation,” Alcohol Clinical and Experimental Research 32, no. 11
(November 2008): 1899–1908.
10-649_Dasgupta.indb 206 1/17/11 6:40 AM

11

Dangers of Moonshine
Whiskey and Related
Illegally Produced Liquors
M oonshine” is an old term for smuggled liquor because such liquors

were transported at night under moonlight to avoid detection by
any law enforcement agents. In a broad sense, moonshine whiskey or
moonshine liquors are defined as alcoholic drinks that are produced il-
legally without proper license and sold to consumers without paying any
taxes. The people involved in producing such liquors are called “moon-
shiners.” In the United States, moonshine whiskeys have been prepared
since the late eighteenth century, mostly in the Appalachian Mountains
region and the South. At that time, fermentation of mostly corn, but also
apples and peaches, followed by distillation to produce whiskey and
other alcoholic beverages became a cottage industry among farmers who
profited from selling such liquors when corn prices were relatively low
and it was unprofitable to sell corn.
The federal government first implemented taxes on liquors in 1790.
Farmers producing moonshine whiskey protested and resentment fi-
nally exploded in 1794, with angry farmers seizing the city of Pittsburgh,
Pennsylvania. At that time, President Washington sent troops to control
the volatile situation and arrested leaders of the uprising. During the
Civil War (1861–1865), the federal government imposed taxes on liquor
production to collect extra revenue in order to help pay for the war. How-
ever, after the Civil War was over, the federal government continued to
collect revenue on alcohol and tobacco, and many small farmers produc-
ing moonshine whiskey and related liquors refused to pay such taxes.
Thus, the production of moonshine whiskey was performed at night un-
der moonlight using equipment known as a still, and wood fire was used
207
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208 Chapter 11
for distillation. In order to avoid detection of the smoke, such production

was carried out in remote areas.
Production of such illegal liquors increased during the 1920s when al-
cohol consumption was illegal in the United States. Although producers
of moonshine whiskey and related liquors were called “moonshiners,”
people who smuggled such products were called “bootleggers,” because
they often concealed the liquor in their long boots. In the 1920s and later,
bootleggers used cars for transportation of illegally produced alcohols
and drove at night at high speed to escape detection by law enforcement
agencies. This created a culture of car racing, which eventually evolved
into the popular National Association for Stock Car Auto Racing (NAS-
CAR). Although a ban on alcohol consumption was no longer present in
1933, the moonshine whiskey culture continued, and even today, moon-
shine liquors are produced in the United States and the rest of the world.
Although moonshine whiskey is the most popular term, it is also called
mountain dew, hooch, white lightning, rotgut, happy Sally, stump, and
white mule.
Current U.S. laws permit home production of beer and wine by fermen-
tation for personal use. An individual may produce up to 100 gallons of
beer or wine per year for personal use, and a family of two can produce
up to 200 gallons of such alcoholic beverages per year. No permit or re-
cord is needed, and no tax is payable to either state or federal authorities.
However, selling such alcoholic beverages is not permitted, and federal
law does not permit production of distilled liquor such as whiskey with-
out a valid permit, because distillation of alcohol requires skill, and if not
done properly, it can cause harm to consumers. Despite legal sanctions,
illegal whiskey production and subsequent consumption, mostly by
people with low incomes, continues to occur even today.
Not all moonshine whiskeys are illegal. Certain brands produced by
local distillers with proper licensing may be legally available in certain
states, such as Virginia. Today, moonshine liquors are defined as any
illegally produced alcohol worldwide. In addition, the broader term
“surrogate alcohol” is used to define moonshine liquors, as well as any
alcoholic product not designated for human consumption. Consumption
of such products may cause severe toxicity and even death.
MOONSHINE WHISKEY: CURRENT STATUS
When the prohibition of alcohol was repealed in 1933, illegally produced

moonshine whiskey was on the decline. Nevertheless, in the 1960s and
1970s, moonshine continued to be a problem to federal authorities. Pro-
duction and consumption of moonshine whiskey has been on decline in
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Dangers of Moonshine Whiskey and Related Illegally Produced Liquors 209
the United States since 1990, but such illegally produced liquors are still
encountered in the United States. Currently, consumption of moonshine
whiskey is mostly found in rural populations in Alabama, Georgia, South
Carolina, and Mississippi. However, consumption of moonshine whiskey
has also been reported in the urban populations of the District of Colum-
bia, Michigan, Pennsylvania, and Virginia.1 The main reason for the de-
cline in production of illegally produced alcohol is that large commercial
breweries can buy raw material in bulk at such a cheap price that even
after paying taxes, the cost of such liquors is not that much higher than
illegally produced moonshine liquors. However, moonshine whiskey is
still cheaper than legal alcohol, and many consumers of moonshine whis-
key simply do it to get a kick.
According to a March 23, 2000, report by the New York Times, 130 proof
alcohol was produced for three dollars a gallon, bottled in six-pack plastic
jugs, and sold for ten to twelve dollars a gallon in the back rooms of bars
known as “nip joints” or “shot houses” in big mid-Atlantic cities such as
Richmond, Virginia, Washington, D.C., Baltimore, Maryland, and Phila-
delphia, Pennsylvania. Such illegally produced alcohol was sold for one
dollar per shot, which was much lower in price than legal whiskey. The
major manufacturing places for such illegal liquors were Rocky Mount,
Virginia, and the surrounding areas. Since the federal excise tax on a gal-
lon of whiskey at that time was $13.50, the U.S. Bureau of Alcohol, To-
bacco, Firearms and Explosives (ATF) estimated a loss of $19.6 million in
tax revenue between 1992 and 1999 that was related to the sale of moon-
shine liquors. The task force of state and federal agents applying federal
law rather than weaker anti-moonshiner state laws made its first arrest
in March 2000.2 Federal agents also closed illegal moonshine whiskey
production facilities in Virginia and North Carolina. Since moonshining
carries a sentence of five years in prison, federal agents often use other
charges, such as tax evasion and money laundering, which carry stiffer
(longer) sentences.
WHY ARE MOONSHINE WHISKEY AND

RELATED ALCOHOLS DANGEROUS?
Like any whiskey production, moonshine whiskey is produced by the

fermentation of sugar using yeast followed by distillation using a still.
Moonshine whiskey is mainly made from corn. After the corn is ground
into meal, sugar is sometimes added, and then it is soaked in hot water.
Malt may also be added in order to convert cornstarch into sugar. Then
yeast is added to start the fermentation process; this mixture is called
“mash.” The mash is heated in a still for a set amount of time (usually
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210 Chapter 11
two days) where the fermentation process is nearly complete. The still is
heated (in the past by using wood fire, but today moonshiners may use
propane gas) a final time to distill the alcohol, which is collected as clear
liquid. Commercial liquors often have a golden or amber color, which is
due to the aging and storage process in oak barrels. Moonshine whiskey
is always clear like water, because it is not aged prior to sale. Moonshine
and related alcohols are dangerous for the following reasons:
• Poor production conditions and lack of quality control

• High alcohol content
• Presence of various harmful contaminants, including lead
• Harmful substances added to these products to increase “kick”
Because moonshine whiskeys and related liquors are produced ille-

gally, there is no federal inspector who can ensure that proper sanitary
conditions are met to produce such products. Often impure water is used
for production, and insects may even get into the product. Moreover, the
distillation process requires skill, and it usually takes two to three passes
through the still to remove impurities from distillated liquors. Moonshin-
ers may not be careful in the manufacturing process, so contaminants may
be present in such products. Some moonshiners add harmful substances
such as manure, embalming fluid, bleach, rubbing alcohol (isopropyl al-
cohol), and even paint thinner to increase the kick from consumption of
such liquors (see table 11.1).
Serious toxicity and even death may occur from consuming moonshine
whiskey and related illegally produced liquors. The major dangers of
Table 11.1. Potential Contaminants Found in Moonshine Liquors

Heavy Metals
Mostly lead,* but arsenic, zinc, and copper may also be found in high amounts.
Other Contaminants
Methanol^
Formaldehyde
Acetaldehyde
Ethylene glycol
Embalming fluid
Insecticide
Herbicide, such as paraquat
Paint thinner
Manure
*Most commonly encountered contaminant.

^ Not commonly encountered in the United States but major contaminant added to illegally produced
liquors in many countries.
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moonshine whiskey and related products are high alcohol (ethanol) con-
tent—sometimes as high as 75 percent (150 proof)—and lead contamina-
tion. Methanol, a harmful alcohol, is sometimes added (a more common
practice in third world countries because it is cheap) as a contaminant in
moonshine liquors to reduce the cost as well as to increase the kick. Meth-
anol is dangerous and may cause death or total blindness (see chapter 12).
The alcohol content of moonshine whiskey is usually quite high, but it
may vary widely. In one report (Holstege et al. 2004), the authors found
that ethanol content of various moonshine whiskey specimens (forty-
eight samples analyzed) varied from 10.5 percent to 66 percent, with a
mean alcohol content of 41.2 percent. In addition, lead was found as a
contaminant in forty-three out of forty-eight samples analyzed. Toxic
methanol was found in one specimen.3 In another report (Morgan et
al. 2004), the alcohol content of 115 moonshine samples seized by the
authorities from nine states showed alcohol content between 3.85 per-
cent and 65.80 percent, with a median alcohol content of 44.75 percent
(middle value). The lead content in these moonshine liquor specimens
varied from 5302 micrograms/100 milliliter (dL), and in thirty-three
samples (28.7 percent of all samples), lead concentrations exceeded 300
micrograms/dL, the limit designated potentially hazardous by the Food
and Drug Administration. Drinking one liter of such liquor per day may
cause lead toxicity.4
Lead toxicity is the major complication of consuming moonshine

whiskey and related illegally distilled liquors.
The elevated lead content in moonshine whiskey and other illegally

produced liquors is related to the stills being made from automobile
radiators. Multiple copper tubes are attached to the unit and sealed with
lead soldering. An automobile radiator often contains lead, and the lead
leaches out into the moonshine during the production process, especially
when the radiator is taken from an older used car.5 Although lead is the
main contaminant found in moonshine whiskey and related illegally pro-
duced liquors, other contaminants may also be present in such products
(see table 11.1).
Moonshine Liquors and Lead Poisoning

Lead is a heavy metal that has been used by humans for a long time. The
early victims of lead poisoning were workers involved in lead mining or
lead-related work, as well as wine drinkers. Lead’s sweet taste made it
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212 Chapter 11
useful in winemaking in ancient days to counteract the astringent flavor

of tannic acid found in grapes. Lead-sweetened wine containing high
amounts of lead was an important staple of upper-class Romans and may
have caused decreased fertility and an increase in psychosis among Ro-
man aristocrats.6
In modern times, major environmental exposures to lead were due to
tetraethyl lead, a volatile and flammable organic lead derivative used
in gasoline to improve octane numbers and in lead-based paints. In the
United States, lead-based paint was banned in 1978. However, deterio-
rated lead-based paint in older housing remains the most common source
of lead exposure in American children today. In 1986, leaded gasoline
was phased out. Despite such efforts, Americans are still exposed to
environmental lead through old house paint, contaminated soil, lead-
contaminated water due to the use of lead pipes and solder, and food
(lead-lined containers and pottery glazes made with lead).7
Lead enters the body either through inhalation or ingestion. Lead is
distributed in the body in three main compartments: blood, soft tissue,
and bone. Lead stored in bones may be resident for twenty-five to thirty
years or more. Lead toxicity is serious and may be life threatening. Lead
affects hematological (blood), renal, and neurological systems, with the
hematological system being one of the most important targets of lead tox-
icity. Lead inhibits the production of hemoglobin, the major component
of red blood cells that carry oxygen. Many of lead’s toxic properties are
due to its ability to mimic or compete with calcium, thus affecting the
neurological system. Lead can also cause acute or chronic renal failure, as
well as hypertension (high blood pressure). The acceptable level of lead
in blood is less than 10 micrograms/dL of blood, and a blood lead level
higher than 50 micrograms/dL is considered clinically significant and
requires medical intervention. Blood lead concentration higher than 100
micrograms/dL may even cause death if not promptly treated.
There are many reports of lead toxicity due to consumption of moonshine
whiskey and other home-brewed liquors. Morgan et al. (2003) reported four
adult cases of potentially lethal lead toxicity in moonshine drinkers who
were admitted in February and March 2000 to the Grady Memorial Hospital
at Atlanta. The blood lead levels of these patients were 81 micrograms/dL,
190 micrograms/dL, 312 micrograms/dL, and 230 micrograms/dL. These
patients were treated and eventually survived. In addition, the authors in-
terviewed 581 patients who visited their hospital and found that 8.6 percent
of these patients consumed moonshine in the past five years. Moonshine
drinkers were predominantly men between the ages of forty and fifty-nine.
The authors then analyzed blood specimens from the moonshine drinkers
and observed that the median blood lead level among moonshine drinkers
was 11.0 micrograms/dL, which was substantially greater than the median
blood level of lead of 2.5 micrograms/dL among nondrinkers. The authors
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concluded that moonshine consumption was more prevalent than expected

in their patient population. Furthermore, moonshine consumers were more
likely to report heavy alcohol consumption, and such consumption was
strongly associated with elevated blood levels of lead.8
Fatal lead poisoning due to the consumption of moonshine whiskey has
also been reported in medical literature. Pegues et al. (1993) reported that
blood lead concentration ranged from 16 to 259 micrograms/dL in nine
patients with lead poisoning due to consumption of moonshine liquor.
One patient died from lead poisoning.9 In another report (Kaufmann et
al. 1991), the authors noted that death related to lead poisoning in the
United States has been rare since removing all lead-based paints and
lead products from gasoline. Between 1979 and 1998, an estimated two
hundred lead poisoning–related deaths occurred in the United States, but
alcohol-related lead poisoning occurred in 28 percent of the adults who
died from lead poisoning. Among these adults, twenty were reported to
have consumed illegally produced moonshine alcohol.10
Although illegally produced moonshine whiskey consumption is usu-
ally associated with lead toxicity, such toxicity may also be encountered
from drinking homemade wine. A potentially lethal blood lead level of
98 micrograms/dL was reported in a sixty-six-year-old man who con-
sumed homemade red wine. A detailed investigation revealed that the
wine specimen contained 14 milligrams of lead per liter of wine, a very
high amount. The source of the lead was the highly corroded surface of a
bathtub that was used for grape crushing, and the juice was stored there
for up to one week before bottling. The homemade wine was very acidic
(pH of 3.8), which would have greatly contributed to the solubilization of
lead from the corroded bathtub.11
A moderate level of lead in blood may cause chronic lead toxicity,
which in turn may lead to the development of hypertension and gout.
People who consume moonshine whiskey are at higher risk of a body
burden of lead, and even if they do not experience acute, life-threatening
lead toxicity, they may experience many complications of lead poisoning.
Symptoms of lead poisoning are listed in table 11.2.
Table 11.2. Symptoms of Lead Poisoning

Confusion
Fatigue
Impairment of verbal skills
Impaired memory
Impaired motor skills
Peripheral neuropathy
Hematological problem
Endocrine (hormone) problem
Psychiatric problem
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214 Chapter 11
Moonshine Liquors and Poisoning with Other Heavy Metals

Gerhardt et al. (1980) reported twelve sequential cases of arsenic poison-
ing, where a significant number of such cases were due to consumption
of contaminated moonshine whiskey. Some specimens of confiscated
whiskey demonstrated high amounts of arsenic as a contaminant.12 In
another report by Gerhardt et al. (1980), in addition to lead, the authors
found copper, zinc, and arsenic in potentially toxic ranges in some
samples of moonshine whiskey (a total of twelve samples analyzed). One
whiskey specimen had a potentially toxic concentration of arsenic (41.5
micrograms/dL), and copper was found in a high amount (1.4 mg/dL)
in another specimen. As expected, seven specimens contained lead, with
amounts varying from 3.5 to 530 micrograms/dL.13 Although copper tox-
icity from consuming moonshine whiskey has not been well documented
in the medical literature, consuming moonshine whiskey may put an
individual at a much higher risk of getting copper toxicity.
Miscellaneous Toxicity Due to Consumption of Moonshine Whiskey

Conradi et al. (1980) reported a case where a person died from paraquat
poisoning, presumably from paraquat being mixed into illicit moonshine
alcohol. During an autopsy investigation, this herbicide was found in ma-
jor organs of the victim.14 Methanol contamination of moonshine liquors
is not commonly encountered in the United States, but cheap methanol
is added to illegally produced liquors in many countries of the world.
Consumption of such liquors may cause epidemics, including blindness
and death. Similarly, ethylene glycol, rubbing alcohol (isopropyl alcohol),
and other alcohols with higher molecular weight may also be present in
moonshine liquors (the toxicity of such substances is described in detail
in chapter 12). In a report by Lachenmeier et al. (2009), additives like
sulfites, sorbic acid, saccharin, and artificial colors were detected in cheap
fruit wine products collected from local markets in Poland. In addition,
the authors also detected ethyl carbamate, a human carcinogen, in some
cheap unrecorded alcohol products and concluded that the harmful effect
of unrecorded alcohol products on the health of people with poor socio-
economic status should be investigated in detail.15
MOONSHINE LIQUORS IN OTHER NATIONS
Although research on moonshine liquors focused on lead poisoning in the

United States, in Eastern Europe and other countries research on moon-
shine focused on volatile components other than ethanol (alcohol) in such
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products. Cheap, illegally produced alcohols are often adulterated with

methanol, an inexpensive product, and death may occur from consuming
such products. There are many reports of mass poisoning from consum-
ing such products.
Methanol poisoning due to consumption of moonshine liquors is a

major public health concern in many third world countries.
Although methanol poisoning is the major public health safety issue

related to consumption of moonshine liquors in other countries, lead poi-
soning from drinking such products has also been reported.
Mass Methanol Poisoning from Consuming

Moonshine Liquors: World Reports
A report in the New York Times on May 21, 2008, indicated that consump-
tion of contaminated moonshine claimed 110 lives among poor people in
Bangalore, India, nearby rural areas, and across the state border of Tamil
Nadu. A vast majority of the dead lived in slums and got sick after con-
suming contaminated cheap moonshine. The police chief, Srikumar, stated
that the liquor was spiked with camphor and tobacco and was suspected
to have toxic amounts of methanol. In addition, the liquor also contained
a high amount of alcohol (40 percent) according to Venugopal, the state’s
top liquor enforcement official.16 In Kenya, Kabir Ahmad reported that on
November 22, 2000, Kenyan courts charged 6 people with manslaughter
for illegally brewing alcoholic liquor that claimed 140 lives in Nairobi and
the neighboring Kiambu district around November 15. Another 20 people
became irreversibly blind, and more than 400 people were admitted to the
hospital. This was one of the worst poisoning incidents in Kenya from
consumption of illicitly produced alcohol. Police reported that the brew
had been laced with methanol to increase its potency. In 1998, a similar
brew killed 100 people and in 1999, another 23 died and 5 became blind
after consuming contaminated alcohol.17
The number of deaths due to methanol poisoning between October 1992
and May 2001 in Turkey was 271; 241 of these victims were men. In this
report (Yayci et al. 2003), the authors determined that twenty-nine victims
died from methanol poisoning due to the consumption of cologne, and three
men died from drinking an alcoholic beverage named “Raki.” The authors
concluded that in order to decrease mortality due to methanol poisoning,
some precautions should be developed that would help prevent the produc-
tion and consumption of illegally produced alcoholic beverages.18 Cheap
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216 Chapter 11
eau de cologne was the major source of methanol poisoning and death in
Turkey, and the authors commented that public education about colognes
and legislative control of cologne production are important in preventing
methanol poisoning.19 In the Adana region of Turkey, methanol contamina-
tion occurs during home production of Raki from grapes, figs, and plums.
Villagers often use wooden materials and reed pipes during the distillation
process, and methanol (wood alcohol produced during wood burning) is
produced automatically by the equipment during the production of alcohol.
Thus, villagers unknowingly sell contaminated Raki to consumers, and se-
vere methanol toxicity may occur after consuming such products. Gulmen
et al. (2006) reported that seventeen deaths occurred in Adana, Turkey, due
to consumption of such alcoholic drinks.20
Higher Alcohols Found in Moonshine Liquors in Other Countries

Although methanol adulteration is the major cause of mass poisoning
from consumption of moonshine liquors in countries other than the United
States, contamination of such products with higher alcohols (alcohols with
molecular weight greater than ethyl alcohol) is another public safety con-
cern, because some of these higher alcohols are toxic. In one study, Szucas
et al. (2005) determined that in addition to methanol, isobutanol, propanol,
butanol, and isoamyl, alcohol concentrations found in illegally produced
spirits in Hungary were significantly higher compared to levels found in
spirits produced legally. The authors concluded that their results suggest
that the consumption of such homemade spirits is an additional risk factor
for developing alcohol-induced cirrhosis of the liver and may have contrib-
uted to higher levels of mortality from liver cirrhosis in Central and Eastern
Europe. Therefore, restriction of the supply and sale of alcohol from illicit
sources is urgently needed to significantly reduce mortality from chronic
liver disease.21 Although higher alcohols are found in legally produced
alcoholic beverages, much higher amounts of higher alcohols may be en-
countered in illegally produced alcoholic drinks, because the process of
production is crude and not standardized. Narawane et al. (1998) investi-
gated 328 patients from a public hospital in Mumbai, India, and concluded
that although illicit liquors in general contain less alcohol than legally pro-
duced alcoholic drinks, alcoholic liver disease occurs more commonly with
consumers of illicit liquors, and such liver diseases appear earlier than in
people drinking legally produced liquors.22
Surrogate Alcohol
“Surrogate alcohol” is a broad term that includes illegally produced
moonshine and all nonbeverage alcohols, that is, alcohols not intended
10-649_Dasgupta.indb 216 1/17/11 6:40 AM

for human consumption. Denatured alcohol (methylated spirit in which

methanol is added to alcohol to make it nondrinkable) is a major sur-
rogate alcohol that is sometimes consumed by alcoholics (see chapter 12
for methanol toxicity). Aftershave lotion, mouthwash, windshield wiper
fluid, antifreeze, and fire lighting liquids can all be considered surrogate
alcohol. In Russia, there are two types of surrogate alcohol: (1) true surro-
gate alcohol, that is, solutions and liquids manufactured from ethanol or
containing large amounts of ethanol, and (2) false surrogate alcohol, such
as methanol, propanol, and ethylene glycol.23
McKee et al. (2005) determined the composition of surrogate alcohols
consumed in Russia, where an estimated 7.3 percent of the population
drink such product. The authors identified three broad ranges of prod-
ucts, including samogon (home-produced spirits), medicinal compounds,
and other alcohols not produced for human consumption (mostly after-
shave). Although samogon contains less alcohol than commercially pro-
duced vodka, certain toxic higher alcohols were present in such illegally
produced liquors in Russia. Medicinal compounds, however, contained
more alcohol than vodka, and other nonbeverage alcohol products also
contained high amounts of alcohol (ethanol). The authors concluded that
a significant number of Russian men are drinking products that have
either very high concentrations of ethanol or contaminants known to be
toxic to humans. These products are untaxed and thus much less expen-
sive than vodka, but consumption of such products by a significant num-
ber of people is a serious public health and safety concern.24
In Estonia, a wide range of nonbeverage alcoholic products are con-
sumed by individuals. These products include aftershave lotions, fire
lighting fluid, medicinal compounds, and illegally produced spirits.
Lank et al. (2006) determined that the medicinal compounds contained
an average 67 percent alcohol, while aftershaves contained slightly less.
The illegally produced liquors contained an average of 43 percent alcohol
(range 32–53 percent), but also contained detectable quantities of toxic
higher alcohols. However, these products were sold at roughly half the
price of commercially available vodka, and fire lighting fluids were very
inexpensive. The presence of higher amounts of alcohol in these products,
as well as the presence of toxic higher alcohols, can cause serious toxicity
or illness and is thus a major public health concern.25
Surrogate alcohol use is a potential threat to public health. In general,
there are two pathways by which such products exert their toxicity. First,
the presence of components other than alcohol, most commonly methanol
and lead, in significant amounts in such products have caused significant
outbreaks of toxicity and even death after mass consumption. Methanol,
the major culprit, has caused massive outbreaks of alcohol-related death
and toxicity in various parts of the world after consumption of such
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218 Chapter 11
contaminated products. Second, high alcohol content in these surrogate

products, especially medicinal alcohol, is responsible for organ damage,
especially liver cirrhosis and other diseases from chronic consumption of
such products. Leon et al. (2007) reported that in Russia there is a strong
link between consumption of surrogate alcohol and all-cause mortality
among men. In addition, almost half of all deaths in working-age men in
a typical Russian city may be accounted for by hazardous drinking (non-
beverage alcohol consumption, problem drinking, or both).26
CONCLUSION
Moonshine whiskey and related illegally produced alcohol is a public

safety concern even today, although production of such illegally produced
liquors is on the decline at the present. The major problem of consuming
such alcohol is lead toxicity. In addition, other harmful substances, such as
methanol, higher alcohols, herbicides, pesticides, and various heavy met-
als, may also be present in such products. In other countries, adulteration
of illegally produced alcohol with methanol is a major public health haz-
ard. There are many reports of massive alcohol poisoning and death after
consuming such illegally produced alcoholic products, mostly among poor
people, in various parts of the world. Strict regulation and public education
is urgently needed to overcome these important public safety issues.
NOTES
1. R. Montgomery and R. Finkenbine, “A Brief Review of Moonshine Use,”

Psychiatric Service 50, no. 8 (August 1999): 1088.
2. P. Kilborn, “U. S. Cracks Down on Rise in Appalachia Moonshine,” New York
Times, March 23, 2000.
3. C. P. Holstege, J. D. Ferguson, C. E. Wolf, A. B. Baer, et al., “Analysis of
Moonshine Whiskey,” Journal of Toxicology: Clinical Toxicology 42, no. 5 (August
2004): 597–601.
4. B. W. Morgan, C. S. Parramore, and M. Ethridge, “Lead Contaminated
Moonshine: A Report of Bureau of Alcohol, Tobacco and Firearms Analyzed
Samples,” Veterinary and Human Toxicology 46, no. 2 (April 2004): 89–90.
5. B. W. Morgan, K. H. Todd, and B. Moore, “Elevated Blood Lead Levels in
Urban Moonshine Drinkers,” Annals of Emergency Medicine 37, no. 1 (January
2001): 51–54.
6. S. C. Gilfillan, “Lead Poisoning and the Fall of Rome,” Journal of Occupational
Medicine 7, (February 1965): 53–60.
7. M. Czachur, M. Standbury, M. Gochfield, G. G. Rhoads, and D. Wartenberg,
“A Pilot Study of Take-Home Lead Exposure in New Jersey,” American Journal of
Industrial Medicine 28 (1995): 289–93.
10-649_Dasgupta.indb 218 1/17/11 6:40 AM

8. B. W. Morgan, L. Barnes, C. S. Parramore, and R. B. Kaufmann, “Elevated

Blood Lead Levels Associated with the Consumption of Moonshine among Emer-
gency Department Patients in Atlanta,” Annals of Emergency Medicine 42, no. 3
(September 2003): 351–58.
9. D. A. Pegues, B. J. Hughes, and C. H. Woernle, “Elevated Blood Lead Levels
Associated with Illegally Distilled Alcohol,” Archives of Internal Medicine 153, no.
12 (June 1993): 1501–4.
10. R. B. Kaufmann, C. J. Staes, and T. D. Matte, “Deaths Related to Lead Poi-
soning in the United States, 1979–1998,” Environmental Research 91, no. 2 (February
1991): 78–84.
11. S. Mangas, R. Visvanathan, and M. van Alphen, “Lead Poisoning from
Homemade Wine: A Case Study,” Environmental Health Perspective 109, no. 4
(April 2001): 433–35.
12. R. E. Gerhardt, E. A. Crecelius, and J. B. Hudson, “Moonshine-Related Ar-
senic Poisoning,” Archives of Internal Medicine 140, no. 2 (February 1980): 211–13.
13. R. E. Gerhardt, E. A. Crecelius, and J. B. Hudson, “Trace Element Content
of Moonshine,” Archives of Environmental Health 35, no. 6 (November–December
1980): 332–34.
14. S. E. Conradi, L. S. Olanoff, and W. T. Dawson, “Fatality Due to Paraquat
Intoxication: Confirmation by Postmortem Tissue Analysis,” American Journal of
Clinical Pathology 80, no. 5 (November 1980): 771–76.
15. D. W. Lachenmeier, S. Granss, B. Rychak, J. Rehm, et al., “Association
between Quality of Cheap and Unrecorded Alcohol Products and Public Health
Consequences in Poland,” Alcohol Clinical and Experimental Research 33, no. 10
(October 2009): 1757–69.
16. S. Sengupta, “Poison Moonshine Kills 110 of India’s Poor,” New York Times,
May 21, 2008.
17. K. Ahmad, “Methanol-Laced Moonshine Kills 140 in Kenya,” Lancet 356, no.
9245 (December 2000): 1911.
18. N. Yayci, H. Agritmis, A. Turla, and S. Koc, “Fatalities Due to Methyl Al-
cohol Intoxication in Turkey: An 8-Year Study,” Forensic Science International 131,
no. 1 (January 2003): 36–41.
19. S. Kalkan, A. A. Cevik, C. Cavdar, O. Aygoren, et al., “Acute Methanol Poi-
soning Reported to the Drug and Poison Information Center in Izmir,” Veterinary
and Human Toxicology 45, no. 6 (December 2003): 334–37.
20. M. K. Gulmen, D. Meral, A. Hilal, R. Akcan, et al., “Methanol Intoxication
in Adana, Turkey,” Toxicology Mechanism and Methods 16, no. 7 (September 2006):
508–14.
21. S. Szucas, A. Sarvary, A. McKee, and R. Adany, “Could the Higher Level of
Cirrhosis in Central and Eastern Europe Be Due Partly to the Quality of Alcohol
Consumed? An Exploratory Investigation,” Addiction 100, no. 4 (April 2005): 536–42.
22. N. M. Narawane, S. Bhatia, P. Abraham, S. Sanghani, et al., “Consumption
of Country Liquor and Its Relation to Alcoholic Liver Disease in Mumbai,” Journal
of the Association of Physicians in India 46, no. 6 (June 1998): 510–13.
23. D. W. Lachenmeier, J. Rehm, and G. Gmel, “Surrogate Alcohol: What Do
We Know and Where Do We Go?” Alcoholism: Clinical and Experimental Research
31, no. 10 (October 2007): 1613–24.
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220 Chapter 11
24. M. McKee, S. Suzcs, A. Sarvary, R. Adany, et al., “The Composition of Sur-

rogate Alcohols Consumed in Russia,” Alcohol: Clinical and Experimental Research
29, no. 10 (October 2005): 1884–88.
25. K. Lank, M. Vali, S. Szucs, R. Adany, et al., “The Composition of Surrogate
and Illegal Alcohol Products in Estonia,” Alcohol and Alcoholism 41, no. 4 (July–Au-
gust 2006): 446–50.
26. D. A. Leon, L. Saburova, S. Tomkins, E. Andreev, et al., “Hazardous Al-
cohol Drinking and Premature Mortality in Russia: A Population-Based Case-
Controlled Study,” Lancet 369, no. 9578 (June 2007): 1001–2009.
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12

More Dangerous than Alcohol
Methanol and Ethylene Glycol
M ethanol and ethylene glycol are sweeter tasting than ethyl alcohol
but not suitable for human consumption. Both methanol and eth-
ylene glycol are more dangerous than alcohol because the body converts
both of them into very toxic compounds (metabolites), and if ingested or
even inhaled for a prolonged period of time (especially methanol) serious
poisoning and even death may result. According to a 2002 report by Davis
et al., the average methanol exposure reported to the American Associa-
tion of Poison Control Centers between 1993 and 1998 was 2,254 cases
annually, and one death occurred in every 183 exposures. In this report,
the authors concluded that 90.3 percent of cases of methanol toxicity were
due to unintentional exposure, while 8.3 percent of cases were due to
intentional exposure.1
In the most recent report of the American Association of Poison Control
Centers (2007), substances involved in a majority of the exposures were
analgesics. For children younger than six, most exposure was from cos-
metics and personal care products. In 2007, 2,252 cases of methanol and
5,395 cases of ethylene glycol poisonings were reported to the U.S. Poison
Control Centers. Of those intoxicated with methanol, twenty-six patients
were classified as experiencing “major” disability, and eleven patients died.
For those patients who were intoxicated with ethylene glycol, 135 patients
were classified as having “major” disability, and sixteen patients died.
Interestingly, there were more reports of exposure to isopropyl alcohol
(7,447 cases) than methanol or ethylene glycol poisoning in the same year,
but only thirty-six patients experienced major complications and only one
patient died, because isopropyl alcohol causes less toxicity in general than
221
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222 Chapter 12
either methanol or ethylene glycol. It is important to recognize that these

numbers probably underestimate the true incidence of exposure, however,
due to not recognizing the ingestion or failing to report the suspected or
known ingestion to a poison control center.2
In chemical terminology alcohol is any organic compound that contains
a hydroxyl group (-OH). A hydroxyl group is composed of one oxygen
atom and one hydrogen atom and this group (also known as a functional
group) is responsible for many properties of this class of organic com-
pounds. There are many organic compounds that contain the hydroxyl
group, and all are classified under the general term “alcohol.” The sim-
plest compound in this series is methyl alcohol or methanol, which is also
referred as “wood spirit” or “wood alcohol.” Methanol contains only one
carbon, one oxygen, and four hydrogen atoms. The next alcohol in this
series is ethyl alcohol or ethanol, which is widely referred to as “alcohol”
and is the active ingredient of alcoholic beverages as well as hard liquor.
Next in the series is propyl alcohol, a more complex structure that is
found in two distinct forms: propyl alcohol and isopropyl alcohol. Both
compounds have the same number of carbon, hydrogen, and oxygen but
differ slightly in structure. Propyl alcohol and isopropyl alcohol have
antiseptic properties. Propyl alcohol is used in many household prod-
ucts, such as shampoo, hair spray, aftershave, mouthwash, and so on.
Isopropyl alcohol is also referred to as rubbing alcohol, and a 70 percent
solution of isopropyl alcohol is widely used as a disinfecting agent. Iso-
propyl alcohol evaporates very quickly and is also used in many cleaning
solutions, such as paint thinner and antifreeze. Chemical structures of
common alcohols are given below.
CH3-OH Methanol (one carbon, four

hydrogens, and one oxygen)
CH3-CH2-OH Ethyl Alcohol (two carbons, six
hydrogens, and one oxygen)
CH3-CH2-CH2-OH Propyl Alcohol (three carbons,
eight hydrogens, and one
oxygen)
CH3
|
CH-OH Isopropyl Alcohol (three
| carbons, eight hydrogens,
CH3 and one oxygen)
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More Dangerous than Alcohol 223
Ethylene glycol is also an alcohol and contains two hydroxyl groups. This
compound is widely used as automobile antifreeze and for manufactur-
ing plastic and polymers. Alcoholics tend to drink methanol or ethylene
glycol, especially in winter, as a substitute for ethanol. The chemical struc-
ture of ethylene glycol is given below.
CH2-OH Ethylene Glycol (two carbons, six

| hydrogens, and two oxygens)
CH2-OH
METHANOL: PRODUCTION
Methanol is produced when wood is burned, a process chemically

termed “dry distillation of wood” or “pyrolysis.” Pure methanol was
first prepared in 1661 by Robert Boyle from boxwood, and later, in 1834,
the chemical structure of methanol was described by Dumas and Peligot.
Because methanol can be prepared from burning wood, it is also called
wood alcohol or wood spirit. Today, methanol is no longer prepared
from wood but is manufactured primarily from methane, which is found
in natural gas or during the burning of coal. However, natural gas is
preferred over burning coal to get methane because of environmental
concerns, and it is the major source of raw material (methane) for indus-
trial production of methanol. In this process, methane is converted into
synthetic gas (which primarily contains carbon monoxide and hydrogen
and may also contain some carbon dioxide) using steam, pressure, and
high temperature with the aid of a nickel catalyst in methanol manufac-
turing plants. Then synthetic gas is converted into methanol using high
pressure and temperature with the aid of another catalyst, such as zinc
oxide or chromium oxide. A catalyst is an agent that accelerates a chemi-
cal reaction but is not consumed in the process, and it can be used over
and over again.
Methane is a greenhouse gas, second only to carbon dioxide for the
greenhouse effect. Methane is found in landfills, and landfills are one of
the major sources of atmospheric methane.3 Methane is the most abun-
dant hydrocarbon in the atmosphere and has contributed to an estimated
20 percent of postindustrial global warming.
Only three types of bacteria regulate the fluxes of methane on Earth:
methanotrophic bacteria, methanogenic archaea, and methanotrophic
archaea.4 Methanogenic archaea found in wetlands converts carbon di-
oxide and hydrogen into methane, while methanotrophic bacteria con-
verts methane to methanol in the first step of their metabolic pathway
using a specific enzyme called methane monooxygenase. One form of
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224 Chapter 12
this enzyme is soluble, while another form is bound to cell membranes.5

Methanol can be prepared from biogas using specific bacteria and us-
ing tools of genetic engineering. Such bacteria can be fine-tuned for the
development of economically competitive bioprocesses based on metha-
nol.6 “Biogas” is defined as gas produced by the biological breakdown
of organic matter, such as manure, municipal waste, cow dung (gobor
gas in India), green waste, and farm waste, which are all rich in meth-
ane. Landfill gas is also a type of biogas.
On November 5, 2008, Professor Tsang and his group at Oxford Uni-
versity announced that they had successfully developed a novel method
by which glycerol, the main by-product of biodiesel and oleochemical
(chemicals produced from plant and animal fat) production, could be
turned into methanol. For every 9 kg of vegetable oil processed, 1 kg of
glycerol is produced as an unwanted by-product, and in the United States
approximately 350,000 tons of glycerol are incinerated each year.7 In this
method, using a novel catalyst, conversion of glycerol to methanol can be
achieved under relatively mild conditions (100°C and 20 bar of pressure).
ISIS Innovation, a subsidiary of the University of Oxford, has patented
this technology.
METHANOL: COMMERCIAL USE AND

USE IN HOUSEHOLD PRODUCTS
Methanol is biodegradable and is widely used in the manufacturing of

a variety of chemicals including formaldehyde, which then can be used
for manufacturing plastics, paints, synthetic textiles, adhesive, and foam
cushions (table 12.1). Methanol is also used for producing the gasoline ad-
ditive methyl-tertiary-butyl ether (MTBE, which is no longer used in the
United States but is common in other parts of the world). Methanol can be
used as a fuel, and during the Second World War was used in rocket fuel.
Methanol is the most versatile fuel available, and its use may substitute
for petroleum. If 5–15 percent methanol is added to gasoline in internal
combustion engines (such as automobiles), there is an immediate reduc-
tion in atmospheric pollution, as well as improvement in the performance
of the engine. Methanol can also be used in electrical power plants and for
heating and other fuel applications.8
Pure methanol has been used as a fuel for racing cars for a long time,
because methanol fire can be extinguished using water but petroleum-
induced fire cannot be controlled as easily. In 1964, following a devas-
tating crash and explosion at an Indianapolis car race, fuel for Indy cars
was switched to methanol. In 2006, the fuel used in these racing cars was
a blend of 90 percent methanol and 10 percent ethanol (ethyl alcohol),
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Table 12.1. Methanol and Ethylene Glycol: Commercial Applications and Domestic
Products
Compound Common Sources
Methanol
Domestic use Windshield washer fluid, carburetor cleaner, windshield deicer,
paint and varnish remover, gas line antifreeze, paint thinners,
cleaning products, and Canned Heat; also used in making
denatured alcohol (methylated spirit)
Commercial use Fuel additive, fuel, preparation of formaldehyde (formalin, a
tissue preservative that is 40 percent solution of formaldehyde),
acetic acid, methyl methacrylate, methyl chloride, synesthetic
resins, synthetic textiles, polymers, plastics, paints, adhesives,
and foam cushions; also used as a solvent in chemical
laboratories and industry
Ethylene glycol
Domestic use Automobile antifreeze (major use), hydraulic brake fluid coolant
Commercial use Deicing fluid for aircrafts; preparation of polyester fibers, resins,
polymers, dye and plastic bottles containing polyethylene
tetraphthalate
while in 2007 the fuel was completely switched to 100 percent ethanol.9
One disadvantage of methanol in its use as a fuel is its corrosive nature
toward some metals, including aluminum.
Another application in producing energy is the methanol fuel cell,
where methanol can be used to generate electricity. The methanol fuel
cell is ideal where a small amount of electricity is required for powering
a device for a long time, such as cell phones, laptops, and digital cameras.
Several companies, including the Japanese company Toshiba, are actively
involved in developing such fuel cells. On October 22, 2009, Toshiba
Corporation announced the launch of its first direct methanol fuel cell
product: Dynario, which is an external power source for mobile digital
consumer products. This device, a small palm-sized product, when fueled
with an injection of methanol from its dedicated cartridge can generate
enough electricity to charge two mobile phones.10
Methanol is also found in many household products, including wind-
shield washer fluid, carburetor cleaner, paints, varnishes, paint thinners,
and various cleaning products (see table 12.1). Methanol is used in prepar-
ing denatured alcohol, because the addition of methanol to ethanol makes
it toxic and undrinkable. In addition, denatured alcohol is cheap because
it is exempted from the excise duty, which is applicable to ethanol. De-
natured alcohol is used as a fuel for spirit burners, camping stoves, and
Canned Heat, which is designed to be burned directly from its can. A popu-
lar brand is Sterno (Candle Corporation of America, a subsidy of Blyth,
Greenwich, Connecticut). Denatured alcohol, which usually contains 5–10
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226 Chapter 12
percent methanol, is also referred to as “methylated spirit” in many coun-

tries in the world. Although not a household chemical, embalming fluid
contains methanol, along with formaldehyde, ethanol, and other chemicals.
HUMAN EXPOSURE TO METHANOL
As you can see, methanol is used in a variety of commercial and con-

sumer products. As a result, human exposure to methanol may occur
through different routes, including inhalation, cutaneous exposure
(which is through the skin), and ingestion. Methanol is well absorbed
through all three routes and may cause toxicity regardless of the route of
exposure. In one report (Givens et al. 2008), the authors studied all cases
of methanol exposure from January 2003 to May 2005 using the Texas
Poison Center Network database. The authors reported that eighty-seven
cases of methanol exposure were through inhalation, while eighty-one
cases were through ingestion. Carburetor cleaner was responsible for
the majority of inhalation cases (seventy-nine out of eighty-seven), while
ingestion involved mostly windshield washer fluid (thirty-nine out of
eighty-one) and carburetor cleaner (twenty out of eighty-one). While
most of the inhalation exposure to methanol (78 percent) was intentional,
most ingestion of methanol cases were either accidental (65 percent) or in
suicide attempts (24 percent). A majority of these patients (56 percent of
patients in the inhalation group and 46 percent of patients in the inges-
tion group) were admitted to the hospital, and some patients experienced
vision loss in both groups.11 This recent report indicates that exposure to
methanol through inhalation may cause serious toxicity, although some
of the previous reports indicated that individuals who abuse methanol-
containing products by inhalation are at low risk of developing methanol
toxicity.12 In a report by Frenia and Schauben (1993), out of seven cases
of methanol toxicity due to inhalation abuse of carburetor cleaner, one
person died from methanol inhalation, while another person experienced
vision loss.13 However, such serious methanol toxicity only results from
abuse of methanol-containing products. Routine occupational exposure
to methanol-containing products is relatively safe. Methanol is also ab-
sorbed through the skin and may cause methanol toxicity as reported in
the following case.
A Case Study
In the 1980s methanol production was introduced at a new petrochemical
complex in the port of Jubail, Saudi Arabia. A consultant who was super-
vising tank cleaning prior to methanol loading wore a positive-pressure
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breathing apparatus but no protective clothing. After working for two to

three hours in the tank, he came out and worked on deck, but unfortu-
nately he wore his methanol-soaked clothing, which had eventually dried
out because methanol is very volatile, with a boiling point of only 65°C.
He developed visual disturbances, a typical symptom of methanol toxic-
ity, eight hours after exposure, but recovered fully in the hospital.14
METHANOL EXPOSURE AND PREGNANCY
Exposure to both ethanol and methanol is dangerous during pregnancy be-

cause these low molecular weight substances can cross the placenta and af-
fect the fetus. Hantson et al. (1997) reported a case where a twenty-six-year-
old in her thirty-eighth week of pregnancy drank 250 to 500 mL methanol
voluntarily. She was admitted to the hospital five hours after examination
but gynecological examination and fetal monitoring failed to detect any fetal
distress. The mother was treated for methanol poisoning and after six days
delivered her baby. At that point no methanol was detected in the blood of
the mother and no further complications were noted in the mother and her
newborn.15 However, in another report where a twenty-eight-year-old preg-
nant woman was poisoned with methanol (route of exposure not reported)
and was treated aggressively, including using hemodialysis, methanol was
also detected in the blood of the newborn baby. Despite aggressive therapy,
both the mother and her newborn died from methanol poisoning.16
METHANOL CONTENT OF
ALCOHOLIC BEVERAGES AND FRUIT JUICES
A small amount of methanol is found in alcoholic beverages as a part of

the natural fermentation process, and this small amount does not cause
any harm because the ethanol present in the drink protects the human
body from methanol toxicity. However, illicit drinks prepared from
methylated spirit cause severe and even fatal illness. Illegally prepared
moonshine whiskey may contain much higher amounts of methanol and
cause severe toxicity (see chapter 11). In the European Union, 0.04 percent
methanol at 40 percent alcohol (10 gm of methanol in one liter of ethanol)
is considered the upper limit of safety.17
Pectin is a natural product found in plants and in many fruits. Apples,
bananas, oranges, and strawberries contain significant amounts of pectin.
Pectin is a polysaccharide (carbohydrate) that is often found in methyl-
ated form. When plant enzymes break down pectin, a process that occurs
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228 Chapter 12
during the ripening of fruit, methanol is released. During the processing

of fruits, especially when preparing freshly squeezed juices, pectin may
be hydrolyzed, thus producing methanol. Often manufacturers treat
cloudy apple juice with pectin esterase in order to get rid of the cloudi-
ness (which is due to soluble and colloidal pectin), and slightly higher
amounts of methanol can be found in processed apple juice compared to
other juices. Humans cannot metabolize pectin, but bacteria in the gut can
break down pectin, producing a small amount of methanol. However, the
amount of methanol consumed by humans when drinking fruit juices or
eating fruits is so small that it does not cause any toxicity. In a recently
published article, Hang and Woodams (2010) reported that the methanol
content of apple eau-de-vie (a traditional alcoholic beverage produced in
France by fermented apple juice, also known as hard cider) made from
apples grown in the Finger Lakes region of New York had a minimum
methanol content of below 200 mg and maximum methanol content of
400 mg in 100 mL of 40 percent ethanol. The United States’ legal limit of
methanol for fruit brandy is 0.35 percent by volume of alcohol or 280 mg
per 100 mL of 40 percent methanol. Although the methanol content of ap-
ple eau-de-vie may exceed the upper limit set by the U.S. government, the
methanol content of hard cider varied from 0.037 percent to 0.091 percent,
which was significantly below the upper limit of methanol content set
by the U.S. government. Pasteurization of apple juice prior to preparing
apple cider and the alcoholic beverage significantly reduced the methanol
content of the drink.18 In general, methanol content of processed fruit juice
is lower than freshly squeezed juice.
Aspartame Controversy
Aspartame is a synthetic artificial sweetener (NutraSweet, Equal, and other
brands) that is a methyl ester of a dipeptide (contains two amino acids:
phenylalanine and aspartic acid). This compound has no nutritional value
but is used in many diet drinks, including Diet Coca Cola. It has been es-
timated that aspartame is used in more than ninety countries in the world
and in more than 6,000 food products. Aspartame is not absorbed and is
completely broken down in the intestine into phenylalanine, aspartic acid,
and methanol. Current use of aspartame, even by high user groups, remains
well below the aspartame level of 50 mg/kg of body weight/day (U.S. Food
and Drug Administration) and 40 mg/kg of body weight/per day (Euro-
pean Food Safety Authority). A critical review of all studies did not find any
credible information that regular use of aspartame at recommended levels
causes cancer, learning disabilities, or neurological diseases. The epidemiol-
ogy and toxicological studies published so far indicate that aspartame is safe
at current levels of consumption as a nonnutritive sweetener.19
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Another controversy based on various Internet blogs regarding aspar-

tame use is the generation of methanol, which is a toxic compound. It
is true that aspartame contains 11 percent by volume of methanol, and
complete breakdown of aspartame leads to methanol production in the
body. Drinking a standard can of diet soda (330 mL) sweetened with as-
partame will yield 20 mg of methanol; a similar amount of fruit juice will
produce 40 mg of methanol; and an alcoholic beverage consumed in the
same amount will produce 60–100 mg of methanol.
In addition to methanol, aspartame also produces phenylalanine, and
many products containing aspartame have a warning level that the prod-
ucts contain phenylalanine so that an individual with phenylketonuria
can be careful in consuming such products. Nevertheless, the yield of
phenylalanine after drinking a can of diet soda is 100 mg compared to
500 mg of phenylalanine from consuming a glass of milk or 300 mg of
phenylalanine from an egg.
Therefore, an amount of methanol and phenylalanine generated from
consumption of aspartame-containing food is safe. Clinical studies have
shown no evidence of toxic effect and no increase in blood methanol or
phenylalanine with daily consumption of 50 mg/kg of body weight/per
day (equivalent to seventeen cans of diet soft drink daily for a 70 kg adult)
as documented in a report by Zehetner and McLean (1999) that was pub-
lished in the prestigious medical journal the Lancet.20
ENDOGENOUS PRODUCTION OF METHANOL
A very small amount of methanol is produced in our body along with

ethanol. Human blood typically contains 0.2 to 0.8 mg of methanol per
liter of blood. A typical human body produces 0.3 to 0.6 gm of metha-
nol per day and up to 30 gm of ethanol per day. Methanol is produced
in trace amounts during mammalian metabolism, and ethanol may be
produced in the gut by bacterial activity, but the complete mechanism by
which the body produces methanol and ethanol is not fully elucidated.
Methanol has also been detected in human breath in 0.2 to 0.6 parts per
million (ppm). After consuming certain fruits, methanol levels in breath
may increase. After eating 1 kg of apple, a total of approximately 0.5 gm
of alcohol is released in the body. Therefore, daily consumption of a few
apples or oranges may increase daily endogenous methanol production
from 0.3 gm to 0.6 mg/per day, but such increases have no demonstrated
harmful effects to the body such as nonalcoholic liver disease.21
A more recent study (Turner et al. 2007) demonstrated that methanol is
present in the exhaled breath of all people, and its concentration is further
increased after consumption of ripe fruits and fruit juices, as well as after
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230 Chapter 12
consumption of alcoholic drinks. Methanol may remain in the body long

after ethanol following heavy alcohol consumption. However, authors
of this study reported that increases in methanol content of breath after
consumption of fruit or fruit juice was small and less than expected based
on earlier studies.22
How the Body Handles Methanol

Methanol is readily absorbed after ingestion or inhalation and enters into
the bloodstream. A small amount of methanol is excreted unchanged in
urine and also through exhaled breath, but the majority of methanol is
metabolized by the same enzyme in the liver that metabolizes ethanol,
namely, alcohol dehydrogenase. In this process formaldehyde is gener-
ated and further metabolized by another liver enzyme, acetaldehyde
dehydrogenase, to formic acid (fig. 12.1).
Although methanol is relatively nontoxic, both methanol metabolites
(formaldehyde and formic acid) are toxic and responsible for the toxicity
Figure 12.1. Metabolism of methanol
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of methanol. Although both rodents and primates metabolize methanol

into formic acid, rodents can rapidly metabolize formic acid into carbon
dioxide so this end toxic metabolite of methanol metabolism does not
accumulate in them and spares them from many toxic manifestations of
methanol, as observed in primates. The metabolism of formaldehyde into
carbon dioxide is a folate-dependent enzymatic reaction. Primates also
metabolize formaldehyde into formic acid through a folate-dependent
pathway; the rate of metabolism of methanol by primates is much slower
than the rate observed in rodents.23 Therefore, methanol toxicity is ob-
served in monkeys and humans but not in rodents. Johlin et al. (1987)
demonstrated that total folate was 60 percent lower in human liver than
in rat liver, and tetrahydrofolate (a form of folate that is crucial for con-
version of formaldehyde into carbon dioxide) is also 50 percent in human
liver compared to rat liver. Additionally, the activity of 10-formyltetra-
hydrofolate dehydrogenase, a key liver enzyme that catalyzes the final
step of conversion (oxidation) of formaldehyde into carbon dioxide, was
markedly reduced in both human and monkey livers, thus explaining
low-formate conversion into carbon dioxide in humans and monkeys,
who are susceptible to methanol toxicity.24
METHANOL TOXICITY
Methanol itself is relatively nontoxic, and methanol toxicity is a classic

example of “lethal synthesis,” where metabolites of methanol in the body
are the major cause of methanol toxicity. Formaldehyde, the end product
of methanol metabolism, is the key factor in causing toxicity from metha-
nol, including blindness and death. Because of this, methanol toxicity is
not initially characterized by distinct symptoms, and manifestation of
toxicity may be noticeable anywhere from one to seventy-two hours after
exposure but typically twelve to twenty-four hours after exposure. Visual
disturbances, including blurred vision, sensitivity to light, witnessing a
snowstorm, and in some cases partial or total loss of light perception, are
commonly present in an individual presented in the emergency room
with suspected methanol toxicity. Nausea and vomiting may also be pres-
ent but may not be seen in all patients.
The major complication of methanol poisoning is loss of vision, includ-
ing partial or total blindness. Methanol toxicity may also be fatal. The
lethal dose of methanol in humans is not fully established. Although it
is assumed that ingestion of anywhere from 30 to 100 mL of methanol
may cause death, fatality from methanol may occur even after ingestion
of 15 mL of 40 percent methanol. In contrast, there is a published report
that neither death nor blindness occur after the consumption of even 500
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232 Chapter 12
mL of methanol. However, cases of visual impairment and blindness are

more common with methanol ingestion, and blindness may result from
consuming at little as 4 mL of methanol.25
How methanol causes blindness is not fully understood. Animal exper-
iments indicate that formic acid, a metabolite of methanol, is responsible
for most of the damage. An enzyme very similar to alcohol dehydroge-
nase, known as retinol dehydrogenase, is present in the human retina,
and the metabolism of methanol inside the retina, producing formic acid,
causes major methanol-induced retinal toxicity.26
Blood methanol levels may vary widely among individuals poisoned
with methanol. In general if blood methanol concentration exceeds 20 mg/
dL (20 mg of methanol per 100 mL of blood), treatment should be initiated.
Wallage and Watterson (2008) reviewed twelve fatal cases of methanol poi-
soning. Six of the individuals who were found deceased had postmortem
methanol concentrations between 84 and 543 mg/dL, and postmortem
formic acid levels between 64 and 110 mg/dL. Six other individuals who
received therapy prior to death showed blood methanol levels between 68
and 427 mg/dL and formic acid levels between 37 and 91 mg/dL during
hospitalization, but their postmortem levels of both methanol and formic
acid were significantly lower due to hospital treatment of formic acid toxic-
ity.27 However, Lushine et al. (2004) described a case where a patient with a
blood methanol level of 692 mg/dL on admission was treated with 4-meth-
ylpyrazole (fomepizole) and dialysis without any aftereffects.28
Methanol is metabolized to formic acid, which makes the blood more
acidic by reducing its pH (the measurement of hydrogen ion in a fluid,
where pH 7 is neutral). Blood is slightly alkaline in nature, and a delicate
balance of a pH between 7.35 and 7.46 is needed for normal physiologi-
cal function of the human body. Because formic acid is acidic in nature,
it lowers blood pH, and the process is an example of metabolic acidosis,
where metabolism of the body is responsible for a decrease in the pH of
blood, which may be very significant clinically and even life threatening.
Metabolic acidosis is secondary to methanol poisoning and is a serious
complication of methanol poisoning. Meyer et al. (2000) reported that
there was no correlation between blood methanol level and clinical out-
come of methanol poisoning, but blood pH of 7 or lower was a strong
predictor of death or poor outcome from methanol poisoning.29
Another complication of methanol poisoning is lactic acidosis, which
may also become life threatening. Lactic acid, a product that is gener-
ated in our body during exercise and other activities, is found in small
amounts in our blood. The muscles of trained athletes can even use lactic
acid as a fuel. Although lactic acid levels in blood may be elevated after
exercise, our body can readily convert lactic acid into other products, and
lactic acid levels return to normal levels within an hour. However, if lactic
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acid builds up in our body, it can be harmful, because it can reduce the
pH of our blood and cause acidosis (often termed lactic acidosis), which
may severely disrupt the body’s normal functions. If untreated, severe
lactic acidosis may cause death.
Laboratory Diagnosis of Methanol Toxicity

In the clinical laboratory a patient with suspected methanol poisoning is
tested for the presence of methanol in the blood. In addition, sometimes
formic acid levels are also analyzed along with other volatiles—such as
ethanol, acetone, and ethylene glycol—in a single analytical step using a
sophisticated technique known as headspace gas chromatographic analy-
sis. Although blood is usually collected from a vein for analysis of blood
methanol levels and other tests, a blood sample from an artery (arterial
blood) may also be collected to measure the pH of the blood to see if pH is
below the normal range. Another indirect indication of methanol poison-
ing is the increased anion gap in the serum, which can be easily separated
from blood cells by centrifugation. The anion gap is defined as the differ-
ence between the measured level of positively charged ions (cations) in
the blood and negatively charged ions (anions) in the blood.
Anion Gap = Concentration of sodium − (Concentration of chloride +

Concentration of bicarbonate)
The concentration of potassium is often ignored because it is very small.

The normal anion gap is 8 to 16 mmol/L (millimolar per liter), but in
methanol poisoning this anion gap may increase significantly. Anion
gap may increase in many pathological conditions, such as renal failure,
lactic acidosis, and also in common poisoning, such as salicylate poi-
soning. Methanol poisoning also increases serum osmolality, another
complex analytical measurement of total amounts of dissolved chemicals
in serum. In serum, sodium, potassium, chloride, bicarbonate, urea, and
glucose together make up 95 percent of total osmolality. Serum osmolal-
ity is measured by a principle called “freezing point depression” using an
osmometer and is called “measured osmolality.” Osmolality can also be
calculated from measured concentrations of sodium, potassium, chloride,
glucose, and urea.
Osmolar gap = Measured osmolarity − calculated osmolarity
Measured osmolarity should be close to calculated osmolality unless

compounds like methanol, ethanol, acetone, ethylene glycol, or related
compounds are present in serum. These compounds would increase
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234 Chapter 12
serum osmolality. For example, if methanol is present in 50 mg/dL, it

would increase serum osmolality by 15.6, and in the case of methanol
poisoning, osmolar gap would be increased. However, poisoning with
ethanol, isopropyl alcohol, ethylene glycol, acetone, and other organic
solvents could also increase osmolar gap.
Treatment of Methanol Toxicity

Methanol poisoning can be treated using a variety of agents, such as etha-
nol, 4-methylpyrazole (fomepizole), and sodium bicarbonate, as well as
dialysis. The outcome of methanol poisoning appears to be related more
to the interval of time between exposure and initiation of treatment and
to degree of acidosis rather than to the initial blood methanol level. Early
and aggressive therapy with bicarbonate and ethanol and subsequent ini-
tiation of hemodialysis are strongly recommended whenever methanol is
detected in blood, especially in patients who also have metabolic acidosis
and demonstrated anion gap.30 Sodium carbonate is a basic compound (a
basic compound can neutralize an acid) and can bring the blood pH back
to normal in the case of metabolic acidosis. Intravenous administration of
sodium bicarbonate, which reduces the acidity of blood, is often initiated
if the pH of blood is 7.2 or below. Intravenous administration of ethanol
using a 10 percent solution of ethanol is also initiated if blood methanol
concentration is more than 20 mg/dL or when ingested methanol amount
is 30 mL or more.31 Ethanol is an effective antidote for methanol poison-
ing, and the sooner the therapy can be initiated, the better the outcome.
Ethanol is a preferred substrate for alcohol dehydrogenase, and in the
presence of ethanol, metabolism of methanol to toxic formic acid metabo-
lite is greatly reduced. Because the human body can effectively handle
small amounts of formic acid, converting it to carbon dioxide, methanol
toxicity can be greatly reduced by ethanol therapy.
Another effective therapy for methanol overdose is hemodialysis.
Methanol is a small molecule with a molecular weight of only thirty-two.
Methanol can be effectively removed from circulation using hemodi-
alysis. Usually hemodialysis, along with ethanol therapy for methanol
poisoning, should be initiated if the blood methanol level is 50 mg/dL or
more. Hemodialysis may also be initiated if an individual has ingested 30
mL or more of methanol or based on other clinical indications as deter-
mined by the physician treating such overdose.32
Recently, fomepizole (4-methylpyrazole), a potent competitive in-
hibitor of alcohol dehydrogenase has been used as an antidote to treat
methanol poisonings. This antidote has the capability of slowing down
the formation of formaldehyde from methanol. Formaldehyde is toxic
and responsible for toxic effects due to methanol ingestion, and small
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formaldehyde buildup can be secreted in urine. Bicarbonate therapy can

also be used with fomepizole therapy to correct metabolic acidosis caused
by methanol.33
Case Report
An adult male presented to the emergency room with central blindness
after ingesting methanol. His blood pH was 7.19, indicating severe meta-
bolic acidosis, and his blood methanol level was 97 mg/dL. The patient
was treated aggressively with ethanol, fomepizole, and hemodialysis.
Further methanol metabolism was totally blocked by fomepizole and the
patient recovered from this life-threatening methanol poisoning; fourteen
days after this episode he recovered his vision completely.34
ETHYLENE GLYCOL: COMMERCIAL USE

AND HOUSEHOLD PRODUCTS
Ethylene glycol is a colorless and relatively nonvolatile liquid that has a

high boiling point of 193.7 °C. It has a sweet taste, which is why children
and pets tend to ingest it, causing ethylene glycol toxicity. An adult may
drink ethylene glycol as a substitute for ethanol or in a suicide attempt.
Because of the low melting point and high boiling point, ethylene glycol
is used as a major ingredient in automobile antifreeze. Ethylene glycol is
also an ingredient in several domestic products and is also widely used
for commercial purposes. Ethylene glycol is used in deicing fluid and as
a starting material for preparing various polyester products in industry
(see table 12.1). In Germany ethylene glycol was used in the explosives
industry during wartime.
Currently ethylene glycol is commercially prepared from ethylene. In
the first step, ethylene, a hydrocarbon, is converted into ethylene oxide,
and then ethylene oxide is converted into ethylene glycol by using silver
as a catalyst and a high temperature, usually 250°C.
Human Exposure to Ethylene Glycol

Because ethylene glycol is relatively nonvolatile, inhalation exposure
to it is not generally considered an occupational health hazard. In one
study (Gerin et al. 1997), the authors measured ethylene glycol levels in
154 breathing zone air samples and 117 urine samples from thirty-three
aviation workers exposed to deicing fluid (basket operators, deicing
truck drivers, leads, and coordinators) during forty-two workdays over
a winter period of two months at a Montreal airport. Ethylene glycol
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236 Chapter 12
concentrations in air samples were relatively low, and measurable

amounts of ethylene glycol in urine were only found in basket operators
and coordinators, but some of them did not wear masks or were ac-
cidently sprayed with deicing fluid. However, acute or chronic renal
toxicity, the major complication of ethylene glycol exposure, was not
found in any of the aviation workers. The authors concluded that health
hazards from exposure to ethylene glycol in the form of inhalation is not
significant, but other routes of exposure such as the percutaneous route
(absorption through the skin) may cause health hazards.35
Absorption of ethylene glycol through the skin may cause serious toxic-
ity, especially if there are any skin lesions. Bouattar et al. (2009) reported a
case of toxicity in a thirty-eight-year-old man who presented at the hospi-
tal with nausea, vomiting, abdominal pain, and worsening of his mental
status. The patient also experienced renal failure and was treated with
hemodialysis. The renal biopsy revealed the presence of calcium oxalate
crystals, a characteristic of ethylene glycol poisoning. It was later discov-
ered that the patient worked in a cement factory and handled ethylene
glycol without protective gloves. In addition, the patient had had cutane-
ous psoriasis for ten years. (Normal skin cells mature and replace dead
skin every twenty-eight to thirty days, but in psoriasis, skin cells some-
times mature in less than a week. Because the body can’t shed old skin
as rapidly as new skin, cells rise to the surface and patches of dead skin
develop on the arms, back, chest, elbows, legs, nails, and in other parts
of the body and appear as red skin lesions. Psoriasis is a noncontagious
autoimmune disease.) The authors concluded that cutaneous contact with
ethylene glycol may cause poisoning in the presence of skin lesions.36 The
major route of exposure to ethylene glycol is ingestion of fluids contain-
ing ethylene glycol. Ethylene glycol is rapidly and completely absorbed
from the intestinal tract after oral ingestion.
How the Body Handles Ethylene Glycol

Ethylene glycol itself is relatively nontoxic, like methanol. But when the
body metabolizes it, it produces toxic compounds, which are respon-
sible for its adverse effects. The peak blood ethylene glycol concentra-
tion (highest ethylene glycol level) occurs within one to two hours after
ingestion. Ethylene glycol is also metabolized by the same enzyme
systems that metabolize ethanol and methanol. The half-life of ethylene
glycol in blood (half-life is the time required for blood concentration to
reduce half of its initial concentration) is three to five hours. Ethylene
glycol is primarily metabolized in the liver (approximately 80 percent)
while another 20 percent is excreted in the urine unchanged. Metabo-
lism of ethylene glycol by the liver is a four-step process. Ethylene gly-
col is first metabolized to glycoaldehyde by alcohol dehydrogenase, and
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Figure 12.2. Metabolism of ethylene glycol to glycolic acid
then glycoaldehyde is further metabolized by aldehyde dehydrogenase

into glycolic acid (fig. 12.2).
The conversion of ethylene glycol in two steps to glycolic acid occurs
relatively rapidly, but then glycolic acid is further transformed to gly-
oxalic acid and then further transformed to the metabolite oxalic acid.
Oxalic acid binds with calcium-forming calcium oxalate, the end toxic
metabolite of ethylene glycol. The mechanism of conversion of glycolic
acid to oxalic acid is not fully understood, but it has been established that
lactate dehydrogenase enzymes present in hepatocytes (major cells in the
liver) catalyzes this transformation (fig. 12.3).37
Figure 12.3. Conversion of glycolic acid to oxalic acid
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238 Chapter 12
ETHYLENE GLYCOL TOXICITY
Ethylene glycol toxicity in humans occurs in several stages. The first stage
is the neurological stage where mild euphoria, like ethanol poisoning,
may be observed within thirty minutes of ingestion of ethylene glycol.
Other neurological symptoms may include nystagmus, ataxia, seizure,
and even coma, and these symptoms may be observed between thirty
minutes and up to twelve hours after ingestion of ethylene glycol. The
next stage of ethylene glycol poisoning is cardiac symptoms, including
mild hypertension and tachycardia. Finally, between twenty-four to
seventy-two hours after exposure, symptoms of renal failure may be ob-
served, especially in patients who are not treated (table 12.2).
Major complications of ethylene glycol poisoning are metabolic acido-
sis and renal failure, and these complications may be fatal. The lethal dose
of ethylene glycol is usually assumed as 100 mL, but there are reports of
fatality from ethylene glycol poisoning even from ingestion of only 30
mL.38 Death from ethylene glycol poisoning may follow if symptoms are
untreated within eight to twenty-four hours after poisoning. On the other
hand, prognosis of ethylene glycol poisoning is good if treated in a timely
fashion. A thirty-six-year-old man with a history of depression consumed
a massive amount of ethylene glycol (3 liters) in a suicide attempt. On
admission, his blood ethylene glycol level was 1889 mg/dL, a very high
ethylene glycol level that is potentially fatal. Despite ingesting a lethal
amount of ethylene glycol, this patient survived due to prompt medical
attention and aggressive treatment using hemodialysis.39
The blood level of ethylene glycol in fatal poisoning may vary widely
among different individuals. Rosano et al. (2009) reviewed twelve medi-
Table 12.2. Common Symptoms of Methanol and Ethylene Glycol Toxicity

Compounds Symptoms of Toxicity
Methanol
Early symptoms Inebriation (appear drunk/intoxicated), drowsiness
Delayed symptoms (12–24h) Vomiting, dyspnea (difficulty in breathing),
Kussmaul respiration (deep, slow, and labored
breathing characteristic of metabolic acidosis),
vertigo, blurred vision, absent light perception,
partial to total blindness
Ethylene glycol
Early symptoms (Neurological; Euphoria, appear intoxicated, stumbling,
30 min–6 h) increased thirst
Intermediate symptoms Vomiting, decreased body temperature,
(Cardiopulmonary; 6 h–24 h) tachycardia, deep, slow, and labored breathing
Late symptoms (Renal: 24–72 h) Low urine output, renal failure, coma
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cal examiners’ cases where fatality was due to ethylene glycol poisoning
and observed that the ethylene glycol concentrations ranged widely from
only 5.8 to 779 mg/dL with a mean value of 183 mg/dL. The concentra-
tion of glycolic acid, a metabolite of ethylene glycol, varied from 81 mg/
dL to 177 mg/dL. Calcium oxalate crystals were detected in renal tis-
sues.40 In another case report, an adult male died from ethylene glycol
poisoning with a blood ethylene glycol level of 25 mg/dL. Acute renal
failure was the cause of death, and calcium oxalate crystals were identi-
fied in renal cells (tubular epithelial cells) using confocal laser scanning
microscopy.41 Garg et al. (2009) reported a case where a person who died
from ethylene glycol poisoning showed a very high level of ethylene gly-
col in postmortem blood (2340 mg/dL) but without elevated concentra-
tion of any ethylene glycol metabolites. In addition, oxalic acid crystals
were not detected in the urine.42
Although most cases of ethylene glycol poisoning are due to accidental
ingestion or suicidal attempts, there is an interesting case where ethylene
glycol was used in a homicide in which a thirty-six-year-old female care-
giver poisoned a seventy-five-year-old man suffering from both diabetes
and hypertension. On postmortem investigation, the causes of death were
established as acute poisoning by ethylene glycol and recent blunt impact
injuries to the head, trunk, and extremities. A trial by jury involving the
female caregiver resulted in her conviction, and she was sentenced to
twenty-three years to life in prison.43
Ethanol protects the human body from the toxic effect of ethylene gly-
col unless a person injects both ethylene glycol and ethanol at the same
time. Usually laboratory findings of ethylene glycol poisoning, such as os-
molality and anion gap, are not present and may obscure the diagnosis of
ethylene glycol poisoning.44 However, concurrent ingestion of methanol
and ethylene glycol is dangerous. Arai et al. (1983) reported a fatal case
of poisoning by a mixture of methanol (80 percent) and ethylene glycol
(20 percent) in a seventy-two-year-old man who was found semicomatose
and subsequently hospitalized. It was estimated that he drank between
150 to 200 mL of fluid containing both methanol and ethylene glycol. De-
spite aggressive therapy, the man died from the complications of toxicity
from both of these agents.45
Ethylene glycol poisoning often results in acute renal failure, especially
if treatment by doctors at a medical facility is delayed. The mechanism of
ethylene glycol toxicity was thought to be due to accumulation of toxic
metabolites, such as glycoaldehyde, glyoxylate, and oxalic acid. However,
more recent investigations reveal that the accumulation of calcium oxa-
late crystals—mostly calcium oxalate monohydrate—accounts for most
major toxicity and acute renal failure due to ethylene glycol poisoning.
Calcium oxalate crystals are found in both calcium oxalate monohydrate
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240 Chapter 12
(one molecule of water is incorporated in the structure of calcium oxalate)

or calcium oxalate dihydrate (two molecules of water are incorporated).46
However, another major complication of ethylene glycol poisoning is
caused by glycolic acid.
Oxalic acid is found in high amounts in some poisonous plants and is
also present in significant amounts in various foods, such as beets, spin-
ach, and certain fruits (table 12.3). Our bodies also produce oxalic acid on
their own, for example, from degradation of vitamin C (ascorbic acid).
It is assumed that more than 80 percent urinary excretion of oxalic acid
is due to endogenous production (the body’s production of oxalic acid),
while another 20 percent derives from food. Some individuals have a
genetic defect in producing more oxalic acid endogenously and also have
a higher rate of intestinal absorption of oxalic acid. These individuals are
at greater risk of developing kidney stones, because almost 80 percent
of all kidney stones are due to the formation of calcium oxalate crystals.
Intestinal absorption of oxalic acid makes a substantial contribution to ox-
alic secretion in urine, and this absorption can be modified by decreasing
oxalate intake or increasing the intake of calcium, magnesium, or fiber.47
Laboratory Diagnosis of Ethylene Glycol Poisoning

Treatment for ethylene glycol poisoning is an important issue because
early diagnosis based on symptoms (central nervous system depression,
cardiopulmonary complications, and renal insufficiency) and laboratory
tests are crucial for treatment. Early diagnosis can prevent mortality as
well as avoid complications from ethylene glycol poisoning. Laboratory
findings of ethylene glycol poisoning include increased anion gap, meta-
bolic acidosis (blood pH significantly lower than 7.35), increased osmolar
gap, oxalic acid crystals in the urine, and detectable ethylene glycol level
in the blood.48 For example, if ethylene glycol is present in the blood in an
amount of 50 mg/dL, it would increase the measured serum osmolality
by 8.1, thus increasing the osmolar gap.
Table 12.3. Food Containing High or Moderate Amount of Oxalic Acid

Oxalic Acid Content Food
High oxalic acid Beets, coca, figs, parsley, poppy seeds, spinach, lime peel,
nuts, Brussels sprouts
Moderate oxalic acid Green beans, blackberry, blueberry, carrot, celery, strawberry,
green onions, okra, green peppers, sweet potatoes, lettuce,
carrots, cauliflower, broccoli
Low oxalic acid Corn, tomato, squash, peas, onion, potato, kale, apple,
asparagus, apricots
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Blood levels of ethylene glycol are usually measured by headspace gas

chromatography, either singly or in combination with other volatile com-
pounds, such as methanol, acetone, and isopropyl alcohol. In addition,
there are some enzymatic methods available for rapid determination of
blood ethylene glycol levels using an automated analyzer in the clinical
laboratory setting.
Treatment of Ethylene Glycol Poisoning

Toxicity from ethylene glycol is mostly due to ingestion, because unlike
methanol, ethylene glycol is relatively nonvolatile and inhalation is not a
route of exposure that may cause toxicity. Many ethylene glycol poison-
ings are the result of using ethylene glycol as a cheap alcohol substitute or
in attempted suicide. Children and animals often consume large amounts
of ethylene glycol because of its sweet taste. In an attempt to prevent eth-
ylene glycol poisoning, denatonium benzoate may be added to ethylene
glycol, because this agent has a bitter taste. In eight states the addition of
a bittering agent to antifreeze formulations containing ethylene glycol is
compulsory (table 12.4).
Ethylene glycol poisoning is treated by using bicarbonate, ethanol,
fomepizole, and hemodialysis. The sooner the treatment is initiated, the
better the outcome. If treatment can be started early enough after ingestion,
simple administration of ethanol intravenously may be sufficient for full
recovery from ethylene glycol poisoning. In one report (Karlson-Stiber and
Persson 1992), the authors treated four patients with ethylene glycol poi-
soning and ethylene glycol blood levels varying from 62 mg/dL to 124 mg/
dL with ethanol alone. These patients demonstrated minimal metabolic
acidosis, and none of them developed any kidney damage.49 In another
report (Velez et al. 2007), the authors treated a thirty-three-year-old man
who drank half a gallon of antifreeze and an unknown amount of beer with
fomepizole alone. His blood ethylene glycol level was 70.6 mg/dL, but
fortunately this patient presented to the hospital within one hour of inges-
tion of ethylene glycol and beer. Over the next three days the patient was
treated, but no further complications, such as metabolic acidosis or renal
insufficiency, developed in this patient. This report indicates that early ini-
tiation of treatment has a favorable outcome in ethylene glycol poisoning.50
Table 12.4. States Where the Addition of a Bittering Agent

Is Compulsory in Antifreeze Containing Ethylene Glycol
Arizona New Mexico Virginia
California Oregon Washington
Maine Tennessee
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242 Chapter 12
Hemodialysis to correct metabolic acidosis, along with ethanol or

fomepizole infusion and bicarbonate therapy, may also be needed in
treating patients with more serious ethylene glycol toxicity. This is a
clinical decision made by the attending physicians based on symptoms,
laboratory values, and many other factors. In general, patients with se-
vere metabolic acidosis, high serum potassium values, seizure, or coma
during admission show poor outcomes from ethylene glycol poisoning.
A patient may also die from ethylene glycol poisoning despite aggressive
therapy, including hemodialysis.51
Propylene glycol, which is similar to ethylene glycol, is used as an in-
dustrial solvent and can also be used in antifreeze formulations. Propyl-
ene glycol is significantly less toxic than ethylene glycol and is preferred
for antifreeze used in motor homes and recreational vehicles. Propylene
glycol is also used as a diluent for oral, topical, or intravenous pharma-
ceutical preparations so that active ingredients can be dissolved properly
in the formulation.
TOXICITY WITH ISOPROPYL ALCOHOL,

ACETONE, AND RELATED COMPOUNDS
Although less common, toxicity may result from other organic solvents
used in many domestic products. Isopropyl alcohol is also known as rub-
bing alcohol, which is a 70 percent aqueous solution of isopropyl alcohol.
Isopropyl alcohol is slowly metabolized by alcohol dehydrogenase to ac-
etone. Acetone is also found in many domestic products, for example, nail
polish remover. Neither isopropyl alcohol nor acetone can cause metabolic
acidosis, and poisoning from these compounds may be less life threaten-
ing than methanol or ethylene glycol poisoning, but there are reports
of death from isopropyl alcohol poisoning. The lethal dose of isopropyl
alcohol in an adult is estimated to be 240 mL, which is significantly higher
than the lethal dose of either methanol or ethylene glycol. Acetone concen-
tration is often higher than isopropyl alcohol in patients, and acetone can
cause ketosis, a life-threatening illness. Using sponges soaked in rubbing
alcohol to clean neonates can cause burning and even death in premature
neonates following excessive cleaning. A twenty-one-day-old baby boy
was presented to the hospital with isopropyl alcohol poisoning secondary
to the mother applying gauze pads or cotton balls soaked with isopropyl
alcohol to the umbilicus with every diaper change. The isopropyl alcohol
concentration in the serum was 8 mg/dL and acetone concentration was
203 mg/dL. The patient was discharged from the hospital after three
days.52 An eighteenth-month-old child was wrapped in towels soaked
with isopropyl alcohol by her mother to control a high fever (104°F). The
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towel was wrapped around the child’s waist for approximately four hours
and the child became lethargic. She was admitted to the ICU in a comatose
condition and had a high serum osmolar gap. Eight hours after exposure,
her serum isopropyl alcohol level was 162 mg/dL and her acetone level
was 180 mg/dL. She responded to supportive care and was discharged
from the hospital after three days in stable condition.53
Sometimes isopropyl alcohol is used along with propyl alcohol in
topical antiseptic solution. Propyl alcohol is also metabolized by alcohol
dehydrogenase to propyl aldehyde and then to propionic acid by acet-
aldehyde dehydrogenase. Because propionic acid can lower blood pH,
ingestion of propanol may cause metabolic acidosis. Blanchet et al. (2007)
reported a case where a hospitalized patient drank two 100 mL bottles of
a topical antiseptic solution containing both isopropyl alcohol and propyl
alcohol on two separate days. Eight hours after the second ingestion, his
blood isopropyl alcohol concentration was 37 mg/dL, propyl alcohol
concentration was less than 10 mg/dL, and acetone concentration was
227 mg/dL. The patient was treated with fomepizole. This case points
out the need to limit access to alcohol containing antiseptic solutions on
wards where alcoholic or psychotic patients are hospitalized.54 There are
other reports of similar ingestion of isopropyl alcohol and propyl alcohol.
Death may even occur from such solvent ingestion. Alexander et al. (1982)
reviewed fifty-seven cases of fatality from isopropyl alcohol poisoning.55
SOLVENT AND GLUE SNIFFING
Although it is not within the scope of this book to discuss solvent and
glue abuse, because of the gravity of the problem, a brief description is
provided here. Solvent (inhalant) abuse is common among adolescents,
not only in the United States but also worldwide. In the United States,
approximately 20 percent of adolescents have tried inhalants at least
once by the time they reach eighth grade. Abused inhalants include sol-
vents, glues, adhesives, paint thinners, fuels, and propellants (petroleum
products). Inhalant abuse includes breathing directly from a container
or soaking a rag with the solvent and then placing it over the nose and
mouth, as well as pouring the solvent in a plastic bag and then breathing
the fumes. Abuse of inhalant can produce euphoria, just like other abused
drugs. When an abuser becomes hypoxic by rebreathing from a bag, the
euphoric effect may even intensify.56
Various easily available household products that are abused include
glue, adhesives, nail polish, nail polish remover, cigarette lighter fluid, bu-
tane gas, gas (petrol), air fresheners, deodorant, hair spray, pain-relieving
spray, typewriter correction fluid, paint thinners, paint removers, and a
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244 Chapter 12
variety of other agents. These household and office products contain toxic
solvents such as toluene (paint, spray paint, adhesives, paint thinner, shoe
polish), acetone (nail polish remover, typewriter correction fluid, and
markers), hexane (glue, rubber cement), chlorinated hydrocarbon (spot
and grease removers), xylene (permanent markers), propane gas (gas to
light the grill, spray paints), butane gas (lighter fluid, spray paint), and
fluorocarbons (hair spray, analgesic spray, and refrigerator coolant such
as Freon).
Solvent abusers often present with nonspecific symptoms, but long-
term abusers may come to the hospital with a wide range of neuropsychi-
atric symptoms. The most serious consequence of solvent abuse is death,
which may occur after aspiration or asphyxia. Nearly 50 percent of deaths
from solvent abuse are due to sudden sniffing death syndrome. Steffee
et al. (1996) reported two cases of fatal volatile solvent inhalation abuse;
gasoline sniffing in a twenty-year-old man and aerosol air freshener inha-
lation in a sixteen-year-old girl.57 Pfeiffer et al. (2006) reported two cases
where individuals sniffed cigarette lighter fluid containing isobutane
for euphoria and hallucinations and died due to cardiac arrhythmia and
other complications. Isobutane was detected in heart blood and brain tis-
sue of both individuals.58 Although death from solvent vapor inhalation
in most cases is intentional abuse to get high, there is a case report of an
adult male who unintentionally inhaled excessive amounts of paint thin-
ner vapor and then died due to multiple organ failure.59
CONCLUSION
Methanol, ethylene glycol, and related alcohols are not made for human
consumption but are widely used in domestic products. Such products
must be kept completely out of reach of children, because ingestion of
these products by children may cause life-threatening toxicity and may
even be fatal. Ethylene glycol, in particular, should be kept out of reach
of children and animals, because both children and animals (especially
dogs, because cats do not have sweet taste buds) are drawn to ethylene
glycol due to its sweet taste. Intentional or accidental poisoning of metha-
nol or ethanol glycol require prompt medical attention because the sooner
the therapy can be initiated, the better the outcome. Although symptoms
of methanol toxicity, especially neurologic symptoms, may appear within
thirty minutes of ingestion of ethylene glycol, symptoms of methanol
toxicity may not be apparent for a period of twelve to twenty-four hours.
Both methanol and ethylene glycol are relatively nontoxic, but severe
toxicity from both these agents are due to their toxic metabolites: formic
acid for methanol and calcium oxalate for ethylene glycol. Both methanol
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and ethylene glycol poisoning can be effectively treated with sodium

bicarbonate, ethanol, fomepizole, and hemodialysis. Isopropyl alcohol,
which is commonly used as rubbing alcohol, is less toxic than methanol or
ethylene glycol, but excessive use of pads soaked with rubbing alcohol in
cleaning newborn babies may cause significant toxicity or may burn the
delicate skin of a newborn. Solvent abuse is a significant problem among
adolescents, and such abuse is dangerous because it may cause severe
toxicity, multiple organ failures, and even death.
NOTES
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31. B. R. Ekins, D. E. Rollins, D. P. Duffy, and M. C. Gregory, “Standardized

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248 Chapter 12
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Index
Note: Page numbers of figures and tables are italicized.
Abbott Laboratories, Abbott Park, Ill., adolescents, 24, 132, 154, 156, 243, 245;
121 brain, alcohol’s effect on, 10–11,
absorption, alcohol, 18–19 47–48, 52, 88
abstinence, 51, 83, 87, 90, 92, 96; adrenal glands, 91, 201
biomarkers and, 132, 135–37, 139, adult respiratory distress syndrome
141; during pregnancy, 195–96, (ARDS), 91
202–4 adults, 49–51. See also guidelines for
abuse of alcohol. See chronic alcohol alcohol consumption
consumption ADVIA Platform (Siemens
acamprosate, 96 Diagnostics), 120
acetaldehyde, 11, 22, 33, 93–94; as African Americans, 65, 69, 139
moonshine contaminant, 210; as aftershave, 217, 222
toxic metabolite, 11, 23, 33, 88, agave, 9
93–94, 137, 146–47, 198 age-groups, 63, 66, 197, 201. See also
acetaldehyde dehydrogenase (ALDH), guidelines for alcohol consumption
93–94, 96, 138, 143, 230, 243. See also AIDS (HIV) infection, 91
liver enzymes airline pilots. See aviation workers
acetaldehyde-protein adducts, 131, 135, Alameda County Study, 70
143–44 alanine aminotransferase (ALT), 85,
acetaminophen, 2, 158, 161–63 134–36
acetone, 115–16, 242–43 Alaskan Natives, 23, 33
acetylcholine, 42, 44–45 Alavert (loratadine), 155
addiction, alcohol. See alcoholism albumin, 85, 136, 141, 145
“Administrative License Suspension,” alcohol. See ethanol; ethylene glycol;
106 methanol
249
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250 Index
Alcohol, Tobacco, Firearms and Alzheimer’s disease, 11, 46, 50–51, 56,
Explosives, Bureau of (ATF), 209 68, 96
alcohol addiction/dependence. See Ambien (zolpidem), 159, 165
alcoholism American Academy of Pediatrics
alcohol consumption, chronic (abuse). (AAP), 195
See chronic alcohol consumption American Association of Poison
alcohol consumption, moderate. See Control Centers, 221–22
moderate alcohol consumption American College of Obstetricians and
alcohol dehydrogenase (ADH), Gynecologists (ACOG), 195
19–23, 88, 93–94, 116, 120, 143, 163; American Council for Drug Education,
ethylene glycol and, 236; isopropyl 11
and propyl alcohol, 242–43; American Indians, 23, 33, 94
methanol and, 230, 232, 234. See also Americans with Disabilities Act, 179
liver enzymes amino acids, 42, 137, 140, 162, 198, 228
alcohol-drug interaction. See drug- aminoglycosides, 167
alcohol interaction amitriptyline, 154, 156, 166
alcoholic beverages: alcohol content amphetamine, 44, 174, 176, 179, 182–87
of, 17; calories in, 9–10, 15, 22, 72, amygdala, 43
87; fermenting materials used, 9; amylases, 6
standard, definition of, 15–18, 24, 56 Anafranil (clomipramine), 156
Alcoholics Anonymous (AA), 96 angina pectoris, 55–56, 155
alcoholism (alcohol addiction/ anion gap, 233–34, 239–40
dependence), 1–2, 10–12, 18, 77, Antabuse (disulfiram), 23, 96
80, 133, 139–40, 162; and brain antibiotics, 160, 167–68
damage, 51–52; genetic factors/ anticoagulants, 156, 168
heritability, 12, 23–24, 48, 93–95, 97; antidepressants, 44, 96, 154, 156, 160,
intervening to help, 52; treatment 165–66
and rehabilitation, ix, 95–97; type 1 antifreeze, x, 21, 217, 222–23, 225,
and type 2, 95; underage drinking 235; bittering agent added, 241;
and, 11, 47–49, 88 poisoning, 116, 241. See also ethylene
alcohol poisoning, 48, 116, 218 glycol
alcohol tolerance (by age, sex, body antihistimines, 153, 160–62, 165
weight). See guidelines for alcohol anti-inflammatory drugs, 163–65
consumption antipyretic agent (reduces fever), 162
Alcosensor, 178 antiretroviral, 91
Alco-Sensor III and IV, 113 antiulcer medications, 160, 168
Alcotest (models 6510, 6810, 7410, etc.), anxiety, 11, 38, 40, 78, 96; medications
113, 178 for, 1, 155
Aldomet, 168 apolipoprotein-A, 63
all-cause mortality, 24, 60, 81, 218 apple juice, fermented, 228
Allegra (fexofenadine), 155 Apresoline (hydralazine), 168
allergies; allergy medications, 153, 155, arthritis, 11, 56, 71, 155, 158, 169
161–63, 165, 170 ascorbic acid, 240
alprazolam, 1, 155, 165, 184, 184, 187, asialotransferrin, 138–39
187 Asians, 23, 33, 94
alveolar sacs, 109 aspartame, 228–29
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Index 251
aspartate aminotransferase (ALT), 85, adducts as, 143–44; carbohydrate-

134–36 deficient transferrin, 137–40;
aspartic acid, 42, 228 clinical application of, 132; ethyl
aspirin, 161–63, 233 glucuronide and ethyl sulfate, 144–
Atabrine (quinacrine), 168 46; false positive results, 143; fatty
Atarax (hydroxyzine), 155, 158, 161 acid ethyl esters, 146–48; indirect vs.
ataxia, 49, 238 direct slate, 134–48; liver enzymes,
atherogenic index, 63 134–36; mean corposcular volume
atherosclerosis, 55 (MCV), 137; primary care/medical/
Ativan, 155. See also lorazepam surgical settings, 132–34; serum and
atorvastatin (Lipitor), 157 urine beta-hexosaminidase, 140–42;
atrial septal defects (ASD), 200 sialic acid, 142–43; two categories of,
Aurorix (antidepressant), 160 131; various, 135
auto accidents. See motor vehicle biomolecule, 134
accidents birth-control pills, 139
aviation workers, 174, 177–78, 180, birth defects, 61, 191, 193, 196, 202–3
235–36 blackouts, 39, 48
axons, 40–41 Blacks (African Americans), 65, 69,
Ayurvedic doctors, 12 139
bladder cancer, 69
barbiturates, 136, 165, 169, 176, 182, blindness, 116, 211, 214–15, 231–32, 235,
184–85 238
barley, 3, 6, 9 blood, composition of, 27. See also red
basophils, 27 blood cells
Beckman Corporation, 120 blood alcohol concentration (BAC),
beer, 4, 6–7, 12, 70–72. See also specific 108–22; and alcoholic odor, 32; body
topics/health conditions, e.g., coronary and mind, effects on, 28, 38–40;
heart disease calculation of (Widmark formula),
Benadryl (diphenhydramine), 155, 161 28–32; detection time frame, 131;
benzodiazepine, 1, 165, 169, 176, 182, and DWI, 26–28; the legal limit, 33,
184–85, 187 105–8, 116. See also breath alcohol
benzoylecgonine, 170, 179, 184–85, 187 analysis
beta-amyloid peptide, 46 blood-brain barrier, 44, 50, 161–62, 198
beta-hexosaminidase, 140–42 blood clots, 55, 62, 64–65, 168;
beverages, alcoholic. See alcoholic anticoagulants, 156, 168
beverages blood pressure, high. See hypertension
bicarbonate therapy, 235, 242 Blyth (Sterno manufacturer), 225
bilirubin, 85–87 body, alcohol’s effect on, 15–33;
binge drinking, 26–27, 51, 56, 66, 79, 81, absorption, 18–19; blood alcohol
95; definition of, 103; and driving, level, 39; distribution and
27, 103; pregnancy and, 192, 194, metabolism, 19–22
196, 199; underage drinking and, 10, “body burden” of alcohol, 18
26–27, 47 body weight, guidelines for. See
biogas, 224 guidelines for alcohol consumption
biomarkers of alcohol abuse, bones, 78, 91–92, 137, 198, 200, 212
129–48; acetaldehyde-protein “bootleggers,” 208
10-649_Dasgupta.indb 251 1/17/11 6:40 AM

252 Index
Borkenstein, Captain Robert, 110 carbohydrate, 137

bourbon, 9 carbohydrate-deficient transferrin, 131,
bowel cancer, 92 134, 137–41, 147
Boyle, Robert, 223 carboxylesterase lipase, 146
brain, 40–46 carburetor cleaner, 225–26
brain, alcohol’s effect on, 37–52; cardiomyopathy, 61, 89–90
adolescent, 47–48; adult, 49–51; cardiovascular disease, ix, 15, 24, 55–61,
blood alcohol, 38–40; heavy 69, 81, 136, 143; men/women and,
drinking, 46–52, 88; low/moderate 60–61; red wine and, 64. See also
drinking, 45–46, 51–52; reward coronary heart disease; heart failure;
(pleasure) system, 44–45 stroke
brain cells. See neurons Cardiovascular Health Study, 61,
brain damage, 11, 48–52, 68, 78, 88, 90, 63–64
196 cardiovascular medications, 168–69
brandy, 9, 17, 228 Carmona, Richard H., 196
breast cancer, 92–93 Carter, Jimmy, 4
breast-feeding, 24, 203–4 catalyst, 110, 223–24, 235
breath alcohol analysis, 109–16; Caucasians, 23, 29, 65, 69, 94–95, 139
acetone, 115–16; Breathalyzer, 110– CD4+, 91
11; and false identification, 113–14; CDC Behavioral Risk Factors
fuel cell technology, 113; infrared Surveillance System, 192
spectroscopy, 111–13; methanol, Celebrex (celecoxib), 155
115–16; mouthwash, 115–16; Celexa (citalopram), 156
partition ratio, 114; propyl alcohol, Centers for Disease Control and
115–16 Prevention (CDC), 78, 192
breath alcohol technician (BAT), 178 central nervous system (CNS), 37–38,
Breathalyzer, 110–11 162, 164–65, 197, 240
brompheniramine, 155, 186 cephalosporins, 167–68
bupropion (Wellbutrin), 156 cerebral infarction (ischemic stroke), 65
Bureau of Alcohol, Tobacco, Firearms champagne, 8
and Explosives (ATF), 209 children of alcoholics, 12, 48, 93
B vitamins, 49. See also thiamine China, 3–4, 27, 29, 70, 85, 107
chlordiazepoxide, 155, 187
caffeine, 44, 188 chlorpheniramine (antihistamine), 155,
calcium, 92, 212, 240 161
calcium oxalate, 236–37, 239–40, 244 cholesterol, 55, 59, 61–64, 90, 194;
California Men’s Health Study, 68 medications for, 157
calories, 9–10, 15, 22, 72, 87 chronic alcohol consumption (abuse),
Campral (for alcoholic treatment), 96 10–11, 24–26, 46–52, 77–97; brain,
cancer, 68–69, 72, 92–94, 96. See also effect on, 46–52, 88; and cancer,
specific cancers, e.g., breast cancer 92–93; and heart disease, 88–90;
Candle Corporation of America immune system and, 90–91; life
(Sterno), 225 span, reduced, 80–82; and liver
cannabis. See marijuana disease, 83–88; reproductive system
Canned Heat, 225 and, 91–92; skeletal system and,
capillary gas chromatography, 119 91–92; and stroke, 88–90; and violent
capillary zone electrophoresis, 138 behavior, 82–83. See also binge
10-649_Dasgupta.indb 252 1/17/11 6:40 AM

Index 253
drinking; biomarkers of alcohol crime, 11, 78, 81–82, 104, 129, 194; blood
abuse testing and, 117, 124
chronic atrophic gastritis (CAG), 68 Cushing’s syndrome, 91–92
cimetidine (Tagamet), 157, 160, 168 cyclooxygenase enzyme, 163
cirrhosis of the liver. See liver cirrhosis CYP2E1 (a member of the cytochrome
citalopram (Celexa), 156 P-450), 21, 88, 93, 162
citrate, 106 cyproheptadine (Periactin), 160
citric acid cycle, 22 cytokines, 88, 90
Civil War, 4, 207
Clarinex (desloratadine), 155 Dalmane (flurazepam), 165, 167, 187
Claritin (loratadine), 155 Darvocet-N, 159. See also propoxyphene
Clinton, Bill, 107 DataMaster cdm (breath analyzer),
clomipramine (Anafranil), 156 111–13, 178
clonazepam, 155, 159, 165, 184, 187 date rape; dating violence, 47, 169
Cloninger, C. Robert, 95 Deerfield, Ill., 121
CMI, Inc. (owner of Intoxilyzer), 111 Delsym (dextromethorphan), 156
Coca Cola, Diet, 228 dementia, ix, 11, 22, 45–46, 52, 56, 68,
cocaethylene, 170 79; alcoholic dementia, 49–50
cocaine, 4, 43–44, 154, 169–70, 174, 176, Demerol (meperidine), 159, 164
179; cocaethylene, 170; drug testing denatonium benzoate (bittering agent),
and, 181–85; mothers addicted to, 241
203; as tea contaminant, 187–88 denatured alcohol, 226–27
cocktails, 16, 31 dendrites, 40–41
codeine, 156, 159, 164, 169, 184–87 Depade (for alcoholic treatment), 96
coffee, 84–85 Department of Health and Human
cognac, 9 Services (DHHS), 71, 175, 177–79
cold, common, 56, 71; medications for, Department of Transportation (DOT),
153, 155, 161–63, 165, 170 102, 110, 175–78
college students, 26. See also underage depression, 11, 38–39, 44–45, 88; and
drinking “reward deficiency syndrome,”
colon cancer, 92 42–43. See also antidepressants
congestive heart failure, 61, 90 desipramine (Norpramin), 156
contaminants, 210–11, 214, 217 desloratadine (Clarinex), 155
Copenhagen City Heart Study, 64–65 Desyrel (trazodone), 156
corn, 6, 9, 207, 209, 240 detoxification programs, 132–33, 136,
coronary heart disease, 11, 24, 55–64, 141, 143
72; angina pectoris, 55–56, 155; dextromethorphan, 156
heart attack, 55, 60–62, 70, 194; diabetes, 11, 56, 60, 65–68, 92, 142–43,
medications for, 155 183; antidiabetic medications, 156,
corpus callosum, 40 166–67; non-insulin-dependent,
corticotropin-releasing factor, 91, 95 166–67; type 1, 65–66; type 2, 15,
cortisol, 51, 91–92, 201 65–67, 136, 166
cough medicines, 115, 156 Diagnostic and Statistical Manual of
Coumadin, 156, 168 Mental Disorders (DSM-IV), 95
court/legal system, 32, 105–6, 108–9, dialysis, 232, 234
114, 121–25, 131 diazepam, 1, 155, 165, 184, 187, 187
Crestor (rosuvastatin), 157 diclofenac, 155, 164
10-649_Dasgupta.indb 253 1/17/11 6:40 AM

254 Index
Dietary Guideline for Americans, 23, 168; cardiovascular medications,

71–72 155, 168–69; cocaethylene, 170; as
Diet Coca Cola, 228 common, 153–54; death caused
Dilantin (phenytoin), 159, 169 by, 154, 169–70; and drug toxicity,
Dimension Vista Platform, 120 154; list of major drug-alcohol
Dimetapp (brompheniramine), 155, 186 interactions, 155–59; mechanism
diphenhydramine (antihistamine, of, 160–69; miscellaneous drugs,
Benadryl), 155, 159, 161, 165 155–59, 169–70; OTC allergy/cold
Diprivan, 169 medications, 155, 161–63; pain
disaccharides, 5, 138 medications, 158, 163–64; sleeping
disialotransferrin, 138 aids, 159, 164–65
distillation, 5–9, 12 Drug Education, American Council
distilled spirits (hard liquor), ix, 4, 8–9, for, 11
15–16, 69–70; fermenting materials drugs, x, 1–2, 11–12, 37
used for, 9. See also specific topics/ drug testing, workplace. See workplace
health conditions, e.g., arthritis alcohol/drug testing
disulfiram (Antabuse), 23, 96 drunken monkey hypothesis, 2–3, 12
divorce, 80 drunkenness, 3–4
dopamine, 38, 42–45 Dudley, Robert (University of
dose-dumping, 164 California, Berkeley), 2–3, 12
doxepin, 166 DUI (driving under the influence), 26.
doxycycline (antibiotic), 161, 168 See also driving with impairment/
doxylamine (Unisom), 159 driving while intoxicated
Draeger (owner of Breathalyzer), 111, Dumas, 223
113, 115 dura mater, 40
drinks, alcoholic. See alcoholic DWI. See driving with impairment/
beverages driving while intoxicated
driving, 31, 33, 72; designated driver,
105, 125; ignition lock devices, 116, ecstasy, 169
195; motor vehicle accidents, x, 10, Effexor (venlafaxine), 156
26–27, 72, 175 Egypt, 3
driving with impairment/driving eicosanoid, 90
while intoxicated (DWI), 32; and Elavil, 156, 166. See also amitriptyline
alcohol testing, 101–25; and blood elderly adults, 1, 22, 23, 25, 33, 37, 52,
alcohol concentration, 26–28; false 103; and alcohol-drug interactions,
positive results, 115, 120–21; under 154, 163, 165
the influence (DUI), 26; the legal embalming fluid, 210, 226
limit, 33, 105–8 encephalopathy, Wernicke’s, 49
drug abuse, 12, 44, 80, 94, 169; endocrine system, 91–92
during pregnancy, 202–3; and the endogenous alcohol production, 32,
workplace, 174, 176, 181–82 229
drug-alcohol interaction, 153–70; endotoxin, 88, 92
antibiotics, 160, 167–68; energy drinks, 115
anticoagulants, 156, 168; enzymatic methods of blood alcohol
antidepressants, 156, 165–66; analysis, 117–23, 241
antidiabetic medications, 156, enzyme-linked immunosorbent assay
166–67; antiulcer medications, (ELISA), 144
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Index 255
enzyme multiplied immunoassay famotidine, 168

technique (EMIT assay), 121 fatty acid ethyl esters, 131, 134–35,
enzymes, liver. See liver enzymes 146–48
eosinophils, 27 fatty acids, 8, 62–63, 146
epilepsy, 115, 129, 155 fatty-acyl-ethyl-ester synthase (FAEE),
Equal, 228 146
erythrocytes (red blood cells), 27, 117, fatty liver, 83, 85–86, 88, 129
137, 212 FDG-PET (fluorodeoxyglucose-positron
erythromycin, 160, 168 emission tomography), 51
escitalopram (Lexapro), 156 Federal Aviation Administration
esophageal cancer, 92, 129 (FAA), 178, 180
esterification, 146 Federal Drug Administration (FDA),
Estonia, 107, 217 96, 134
eszopiclone (Lunesta), 159, 165 Federal Motor Carrier Safety
ethanol (ethyl alcohol), 2, 5, 37, 234; Administration (FMCSA), 176–77
body’s handling of, 15–33; in femtoliter, 137
chemical terminology, 222; as fermentation; fermenting materials,
drug, 1–2, 11–12, 37; fermentation 5–9
and distillation, 5–9; historical ferritin, 136
perspective (past and present), 1–13; fetal alcohol spectrum disorders, 148,
metabolism of, 21. See also specific 191, 193–94, 196–201, 204
topics, e.g., acetaldehyde; health fetal alcohol syndrome, 57, 132, 144,
benefits of moderate drinking 191–204; clinical features, 196–201
ethnic groups, 23, 31, 33, 65, 85, 94, fever medications, 158
139. See also specific groups, e.g., fexofenadine (Allegra), 155
American Indians fiber, 240
ethyl carbamate, 214 fibrinolysis, 65
ethylenediaminetetraacetic acid Finnish Twin Cohort Study, 66
(EDTA), 106 fire lighting fluids, 217
ethylene glycol, x, 21, 118–20, 183, Flagyl, 158, 168
235–42, 244–45; body’s handling of, Flomax (tamsulosin), 157
236–37; commercial/household use, flu, 155
235–37; as contaminant, 210, 214, flunitrazepam (Rohypnol), 169
217; human exposure to, 235–36; fluorodeoxyglucose-positron emission
toxicity and treatment, 238–42; toxic tomography (FDG-PET), 51
metabolites, 237, 239, 244 fluoxetine, 96, 156
ethyl glucuronide, 109, 134–35, 144–48, flurazepam (Dalmane), 165, 167, 187
183 flush reaction/flushing, 23, 33, 94, 96,
ethyl sulfate, 109, 134–35, 144–45, 148, 157–58, 167
183 fluvoxamine (Luvox), 156
euphoria, 37–39, 43–45, 88, 238, 243–44 fomepizole, 232, 234–35, 241–43, 245
European School Survey Project on food (with alcohol), x, 3, 18–19, 31–32,
Alcohol and Other Drugs, 47 84–85, 103, 124
evidentiary breath analyzer, 105, forensic or “legal” blood, 122–24
110–16 formaldehyde, 210, 224–26, 230–31,
exercise, 43 234–35
Exxon Valdez oil spill, 175 formic acid, 230–34, 244
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256 Index
10-formyltetrahydrofolate glycoprotein, 137, 140, 142

dehydrogenase, 231 glyoxalic acid, 237
Fourier Transform IR spectroscopy, 111 glyoxylate, 236
Framingham Heart Study, 57–58, 63 gout, 71, 213
France, 25–26, 55, 68, 129, 194, 228 Grady Memorial Hospital (Atlanta),
“freezing point depression,” 233 212
French Paradox, 129 grains, 9
Freon, 244 grapes, 4, 7–9, 9, 32, 46, 212, 216
fructose, 5, 138 Greece, 3, 12, 107
fruit juice, 16, 227–30 Grisactin (griseofulvin), 158, 168
fruit ripening, 2–3 gross domestic product (GDP), 77
furazolidone (Furoxone), 168 guanethidine (Ismelin), 168
guidelines for alcohol consumption,
gallstones, 15, 56, 92 23–24, 25, 31, 33, 59; standard drink,
gamma-aminobutyric acid (GABA), 40, definition of, 15–18, 24, 56
42, 44–45, 94, 96, 199
gamma-glutamyl transferase (GGT), hair analysis, 108–9, 135, 144, 146–48
134 hair spray, 222, 243–44
gamma-glutamyl transpeptidase hallucinations, 244
(GGT), 135–36 hangovers, 23, 48, 131
gamma-hydroxybutyric acid (GHB), hard cider, 8, 228
169 hard liquor. See distilled spirits
gas chromatography, 117–19 hazardous drinking, 24–25. See also
gas chromatography/mass chronic alcohol consumption
spectrometry (GC/MS) analysis, HDL (good) cholesterol, 55, 59, 62–64
147, 179, 185–86 headache medications, 158–59
gastric cancer, 68 headspace gas chromatography, 118,
gastric reflux, 113 233, 241
gastritis, 68 health benefits of moderate drinking,
gastroesophageal reflux disease 11–12, 45–46, 52, 55–72. See also
(GERD), 113 specific topics/health conditions, e.g.,
gender, 18, 20, 22, 29–30, 37, 40, 72, 124 diabetes; stroke
genes/genetic factors, 23, 33, 93–94 Health Inca tea, 187–88
gin, 9, 16–17, 72, 194–95 Healthy People 2010, 77, 196
glipizide (Glucotrol), 167 heart, 57–64; cardiovascular
glucocorticoid hormones, 51, 91 medications, 168–69; disease, 61–63,
Glucophage (metformin), 156, 167 88–90, 96; wine and, 63–64. See also
glucose, 5–6, 51, 67–68, 90, 115, 137–38, specific topics, e.g., cardiovascular
167, 233 disease
Glucotrol (glipizide), 167 heart attack, 55–56, 59–62, 70, 156, 163,
glue sniffing, 243–44 194
glutamatergic system, 40, 95 heartburn, 157, 163
glutamic acid, 42 heart failure, 56, 60, 89–90, 200
glutathione, 162 heavy drinking. See chronic alcohol
glycerol, 224 consumption
glycoaldehyde, 236, 237, 239 Helicobacter pylori (H. pylori), 68
glycolic acid, 237, 239–40 hematocrit, 117, 137
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Index 257
hemodialysis, 227, 234–36, 238, 241–42, hypothalamic-pituitary-adrenal (HPA)

245 axis, 201
hemoglobin, 27, 117, 137, 143–44, 212 hypothalamus, 42, 44, 50, 91, 201
hemoglobin-acetaldehyde adduct,
143–44 ibuprofen, 158, 163, 170
hemorrhage, 90, 168 illegally produced liquors. See
hemorrhagic stroke, 90 moonshine liquor
heparin, 106 immune system, 78, 90–91, 201
hepatitis, alcoholic, 96 immunosuppression, 91, 140
Hepatitis C, 85–86 impairment levels. See driving
herbal preparations, 159, 187–88 with impairment/driving while
heritability of alcoholism. See under intoxicated; guidelines for alcohol
alcoholism: genetic factors/ consumption; legal limit
heritability of Inca tea (health Inca tea), 187–88
heroin, 154, 169, 184–85, 186 India, 3–4, 12, 107, 215–16, 224
hexosaminidase, 131, 134–35, 140–42 Indiana State Police, 110
high blood pressure. See hypertension Indians, American. See American
high-density lipoprotein (HDL) Indians
cholesterol, 59, 62–63 indigestion, 157
higher alcohols, 8, 216–18 indomethacin, 164
high school students, 47–48. See also infant mortality, 192–93
adolescents; underage drinking infections, 6, 90–91, 158, 183
hippocampus, 43, 51, 198 inflammation medications, 158
Hippocrates, 3 infrared (IR) spectroscopy, 110–13
Hispanics, 65, 139 inhalant abuse, 243–44
histamine, 90 insomnia, 1, 96, 164–65
history of alcohol/drinking, 2–4 insulin, 65–67, 92, 136, 166–67
HIV infection, 91 interference/interfering substance, 109,
homicide, 10, 47, 82 111–15, 120–22, 186
Honolulu Heart Study, 62–63 International Classification of Disease
hops, 6 (ICD-10), 95
hormones, 91, 142, 201 Intox EC/IRI, 113
Humphreys, Chris (lawyer), 181 Intoxilyzer, 111–12, 114, 116, 178
hydralazine (Apresoline), 168 Intoximeter; Intoximeters, Inc., 113, 178
hydrocodone, 1, 159, 164 ischemic stroke (cerebral infarction), 65
hydromorphone (Palladone), 1, 164, ISIS Innovation, 224
187 Ismelin (guanethidine), 168
hydroxyzine (Atarax), 155, 158, 159, isoforms, 94, 138, 140
161 isopropyl alcohol, 21, 115–16, 118–20,
hyperinsulinemia, 67 183, 210, 214, 234, 241–45
hyperlipidemia, 129 Isordil (isosorbide), 155
hypertension, 59, 72, 134, 139, 142, 157,
212–13; alcohol abuse and, 57, 72, 79, Jefferson, Thomas, 4
89, 133; and cardiovascular disease, Jesus, 4
56, 61, 134; drug interactions and, “jigger,” 16
156–57, 166; men/women and, 59; job, alcohol/drug testing for. See
and stroke, 90, 134 workplace alcohol/drug testing
10-649_Dasgupta.indb 257 1/17/11 6:40 AM

258 Index
jobs, safety-sensitive. See safety- liver damage, 11, 83–86, 88–89, 121;
sensitive jobs drug interactions and, 155, 157–58,
Jubail, Saudi Arabia, 226 162, 170
juniper berry, 9 liver enzymes, 11, 93–94, 121, 131, 141,
146, 162–63; as alcohol biomarkers,
Kärkkäinen, P., 141 134–36, 148; major family of, 21;
kava kava, 159 and metabolites, 137. See also
ketamine, 169 acetaldehyde dehydrogenase;
ketoconazole (Nizoral), 158, 168 alcohol dehydrogenase
ketogenic diet, 115–16 London College of Physicians, 195
ketonemia, 163 London Gin Epidemic, 194–95
ketoprofen, 163 longevity. See life span/longetivity
kidneys, 91, 120, 136, 140, 201, 240–41; loratadine (Alavert, Claritin), 155
kidney stones, 240; renal cell lorazepam, 1, 155, 165, 184, 187
carcinoma, 69 low-density lipoprotein (LDL)
Klonopin (clonazepam), 155, 159 cholesterol, 62–63
Korsakoff’s syndrome, 49 low-dose aspirin, 163
Kupffer cells, 88 LSD (lysergic acid diethylamide), 182
Lunesta (eszopiclone), 159, 165
lactic acid, 167, 232 lungs, 90–92, 109
lactic acidosis, 120, 156, 167, 232–33 lung cancer, 68–69, 92
“Lambert-Beer Law,” 112 Luvox (fluvoxamine), 156
larynx, cancer of, 92 lysosomes, 140–41
law/legal system, 32, 105–6, 108–9, 114,
121–25, 131 macrocytosis, 137
LDL (bad) cholesterol, 61–63, 90 macrolide antibiotics, 167
lead poisoning, 211–13 magnesium, 240
legal drinking age, 49, 52, 103 magnetic resonance imaging (MRI), 47
“legal” (forensic) blood, 122–24 malt, 3, 6, 9, 209
legal limit (blood alcohol policy), 33, malt liquor, 16
105–8, 116 Mansfield, Ohio, 111
legal system, 32, 105–6, 108–9, 114, margaritas, 16, 31, 124
121–25, 131 marijuana, 4, 43, 154, 169, 176, 179,
“lethal synthesis,” 231 181–85
Lexapro (escitalopram), 156 “mash,” 6, 209–10
Li, Ting-Kai, 77 mast cells, 90–91
Librium (chlordiazepoxide), 155, 187 mate de coca tea, 187–88
life span/longevity, 69–70, 80–82 mead, 8
light beer, 72 mean corpuscular volume (MCV), 131,
lighting fluids, 217 134–35, 137, 140–41, 148
limbic system, 43, 198 “measured osmolality,” 233
Lincoln, Abraham, 4 medial forebrain bundle (MFB), 44
Lipitor (atorvastatin), 157 medial frontal cortex, 43
liver, 19, 23, 83–88, 130; transplant, 87, medical blood, 122–24
121. See also fatty liver medical review officer (MRO), 174, 177,
liver cirrhosis, 32, 57, 83–88, 92, 96, 129, 179, 181
142; death from, 15, 25, 78; surrogate medical settings, alcohol biomarkers in,
alcohol and, 216, 218 133–34
10-649_Dasgupta.indb 258 1/17/11 6:40 AM

Index 259
medications. See drug-alcohol “methylated spirit,” 226–27

interaction; over-the-counter methyldopa (Aldomet), 168
(OTC) medications; prescription metoclopramide, 157, 160, 169
medications; specific medications metronidazole (Flagyl), 158, 168
mefenamic acid, 164 microcephaly, 197, 200
MELD score, 87 midbrain, 43–44
memory, 39, 42–43, 45, 48–51, 68, migraine medications, 159
155, 158–59. See also specific topics, Military Entrance Processing Station,
e.g., fetal alcohol syndrome; lead 181
poisoning military personnel, 132, 174, 181–82
men, 20, 70, 84; guidelines/ mind, human. See brain
recommendations for, 23, 28–33, 52, mixed drinks, 16, 31–32, 167
72; Widmark formula projections, moclobemide (antidepressant), 160
30. See also specific topics, e.g., moderate alcohol consumption
hypertension (sensible drinking), ix, 23–26, 56,
menopause, 22, 69 72; guidelines for, 23–24, 25, 31, 33.
menstrual cycle, 20, 92 See also health benefits of moderate
mental health issues: externalizing drinking
psychopathy, 13; from fetal alcohol molasses, 9
exposure, 199–200. See also specific monkeys, 231; drunken monkey
topics, e.g., depression hypothesis, 2–3, 12
mental retardation, 199–200 monoamine oxidase inhibitors, 156,
meperidine (Demerol), 159, 164 165–66
mesolimbic system, 42–47 monoamines, 42
metabolic acidosis, 232, 234–35, 238, monosaccharides, 5, 137–38
240–43 monosialotransferrin, 138–39
metabolism, 18–23, 23, 33 mood, 22, 38, 40, 42–43, 78–79, 166, 201
metabolites, nonoxidative, 146 moonshine liquor, 207–18, 227; anti-
metabolites, toxic. See toxic metabolites moonshiner state laws, 209; current
metformin (Glucophage), 156, 167 status, 208–9; danger of, 209–14;
methadone, 164, 169, 176, 182, 184–85, higher alcohols in, 216–18; and lead
184–85 poisoning, 211–13; mass methanol
methamphetamine, 169, 174, 176, poisoning from, 215–16; other heavy
184–85, 187 metals/miscellaneous toxicity
methane, 223–24 in, 214; in other nations, 214–18;
methanol (methyl alcohol), x, 115–16, potential contaminants found in,
221–45; in alcoholic beverages, 227– 210; “surrogate alcohol,” 216–18
28; aspartame and, 228–29; body’s morphine, 154, 164, 169, 184–87
handling of, 230–31; commercial/ mortality, 24, 60, 72, 81, 218; infant,
household use, 224–26; endogenous 192–93. See also life span/longevity;
production of, 229–31; in fruit juices, specific topics, e.g., smoking
227–28; human exposure to, 226–27; Mothers Against Drunk Driving
moonshine, poisoning in, 215–16; (MADD), 105
and pregnancy, 227; production, motion sickness medications, 158
223–24; toxicity and treatment, 231– Motivational Enhancement Therapy, 96
35, 238; toxic metabolites, 231, 244 Motivational Interviewing, 96
methaqualone, 176, 184–85 motor vehicle accidents, x, 10, 25–27,
methotrexate, 169 32, 72, 78, 81–82, 101–6, 129;
10-649_Dasgupta.indb 259 1/17/11 6:40 AM

260 Index
commercial motor vehicles, 175; nonsteroidal anti-inflammatory drugs,

drug-alcohol combinations, 165 163
mouth cancer, 69, 92 norcocaine, 179
mouthwash, 115–16 norepinephrine, 42, 166
MRI (magnetic resonance imaging), 47 Norpramin (desipramine), 156
Mucomyst (N-acetylcysteine), 162 Northern Manhattan study, 65
muscle pain medications, 158 nortriptyline, 166
Muslims, 12 nucleus accumbens, 42
myocardial infarction. See heart attack Nurses’ Health study, 67
NutraSweet, 228
N-acetylcysteine (Mucomyst), 162 nutritional supplements, 9, 49, 87
NAD. See nicotinamide adenine nutritional value, 9–10, 72
diphosphate
NADH. See nicotinamide adenine odor, alcoholic, 32
dinucleotide hydrogen Office of Drug and Alcohol Policy and
naltrexone, 96 Compliance (ODAPC), 175
naproxen (Naprosyn), 155, 158, 163 omega-3 fatty acids, 62
narcotic analgesics, 102, 160, 164, 181, Omicron (Intoxilyzer manufacturer),
187 111
National Association for Stock Car Omnibus Transportation Employee
Auto Racing (NASCAR), 208 Testing Act (1991), 175, 178
National Highway Traffic Safety ondansetron, 96
Administration, 101–2, 178 operating [a vehicle] under the
National Institute of Alcohol Abuse influence (OUI), 26
and Alcoholism (NIAAA), 10, 24, 57, operating [a vehicle] while impaired
77, 79, 133, 195 (OWI), 26
National Patent Analytical System, 111 ophthalmoplegia, 49
National Survey on Drug Use and opiates, 1, 4, 43–45, 164, 169, 176, 179,
Health Report, 10 182, 184–87; opiate receptor, 45, 69
Native Americans. See American opioidergic system, 95
Indians opioids, 1, 40
nausea medications, 158 oral contraceptives, 139
neurodegeneration, 48, 50, 199 “oral fluid” (saliva), 108, 142, 178
neurons, 40–41, 44, 88, 198–99 oral hypoglycemic agents, 166–67
neurotransmitters, 11, 38, 41–45, 47, 82, oral surgery medications, 159
96, 198. See also serotonin Orinase (tolbutamide), 156, 167
nicotinamide adenine dinucleotide Osiris (wine god), 3
hydrogen (NADH), 5, 21, 88, 120, osmolality, 233–34, 239–40
122 OUI (operating [a vehicle] under the
nicotinamide adenine diphosphate influence), 26
(NAD), 5, 21, 120, 122 over-the-counter (OTC) medications,
nicotine, 44, 80 161–63
“nip joints,” 209 Owensboro, Kentucky, 111
nitroglycerin, 155, 168 OWI (operating [a vehicle] while
Nizoral, 158, 159, 168 impaired), 26
N-methyl-D-aspartate (NMDA), 51 oxalic acid, 237, 239–40
nonoxidative metabolites, 146 Oxford University, 224
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Index 261
oxycodone, 1, 159, 164, 169, 184–85, 187, Poland, 107, 214

187 polyphenolic compound (resveratrol),
oxymorphone, 164 46, 64
pony shot, 16
pain medications, 158–59, 163–64. See poppy seeds, 186–88, 240
also specific types, e.g., narcotic port wine, 8–9, 16
analgesics; Tylenol post-traumatic stress disorders, 160
paint thinner, 210, 222, 225, 243–44 potassium dichromate, 110
Palladone (hydromorphone), 164 potatoes, 9, 240
Palo Alto, California, 111 prednisone, 87
pancreas, 92, 146–47; pancreatic cancer, prefrontal cortex, 43, 48
92; pancreatitis, 92, 129, 133 pregnancy, 72, 132, 191–204; and fetal
paraquat, 210, 214 alcohol syndrome/fetal alcohol
paroxetine (Paxil), 155–56, 166 spectrum disorders, 193–94,
pectin, 116, 227–28 196–201; lifelong effects of prenatal
Peligot, 223 exposure, 201–2; methanol exposure,
penicillin, 44, 167 227; and stillbirth/infant mortality,
pentobarbital, 184 192–93
pentoxifylline, 87 prescription medications, 57, 153–54,
Percocet, 159. See also oxycodone 161, 164–65, 170, 181–82, 187
Periactin, 160 primary care settings, 132–33
PET imaging, 51 primates, 2–3, 12, 231
pharmaceuticals. See drugs Prohibition, 4, 208
pharmacodynamic interaction, 160–61 “proof” (alcohol content), 17
pharmacokinetic interaction, 160–61 propanol, 116, 119–20, 216, 217, 243
pharynx, cancer of, 92 propionic acid, 243
phencyclidine, 169, 176, 179, 182, propoxyphene, 154, 159, 164, 176, 182,
184–85 184–85
phenobarbital, 159, 184 propyl alcohol, 115–16, 118–19, 222,
phenylalanine, 228–29 243
phenylketonuria, 229 propyl aldehyde, 115, 118–19, 222, 243
phenytoin (Dilantin), 159, 169 propylene glycol, 242
phosphatidylcholine, 148 prostate medications, 157
phosphatidylethanol, 148 prostate specific antigen (PSA), 130
phospholipase A2, 63 protein (dietary), 9, 19, 115
phospholipase D, 148 protein (in blood), 50, 83, 91, 119, 131,
Physician’s Health Study, 59, 70 135–37, 142–43
picomole, 67 prothrombin, 85–86
pituitary gland, 91, 201 Prozac (fluoxetine), 96, 156
plasma, 106, 117 pseudo-Cushing’s syndrome, 91–92
platelet aggregation, 55, 62–64 psoriasis, 236
platinum oxide/platinum black, 113 Pure Food and Drug Act, 4
pleasure center (mesolimbic system), “pyrolysis,” 223
42–47 pyruvate, 5–6, 122
Poison Control Centers, American
Association of, 221 quinacrine (Atabrine), 168
poisoning, alcohol, 48, 116, 218 quinolones, 167
10-649_Dasgupta.indb 261 1/17/11 6:40 AM

262 Index
race. See ethnic groups schnapps, 9

Raki, 63, 215–16 seizures, 115, 158–59, 169, 238, 242
ranitidine (Zantac), 157, 160, 168 selective serotonin reuptake inhibitors
rape, 82 (SSRI), 166
Reagan, Ronald, 174 self-harm or injury, 79
recreational drugs, x senior adults. See elderly adults
red blood cells, 27, 117, 137, 212 sensible drinking. See moderate alcohol
red wine, ix, 7–9, 32, 69, 71–72, 213; consumption
resveratrol in, 46, 64. See also specific serotonin, 42–45, 82–83, 94–95, 166
topics/health conditions, e.g., lung serotonin-norepinephrine reuptake
cancer inhibitors (SNRI), 166
Reglan, 157, 169 sertraline (Zoloft), 156
Reglan (metoclopramide), 157, 160, 169 serum, 20, 27, 63, 67, 85–86, 106–8,
rehabilitation, 95–97 116–23; as alcohol biomarker, 131,
relative risk (RR), 58 134–35, 140–42, 144–45; serum and
relaxation, 28, 37, 88 urine beta-hexosaminidase, 135,
renal cell carcinoma (kidney cancer), 69 140–42; serum gamma glutamyl
reproductive systems, 78, 91–92 transferase, 134; serum osmolality,
resveratrol, 46, 64 233–34, 240
retention time, 118–19 sex/sexuality, 43, 201
retinol dehydrogenase, 232 sexual assault, 82, 129
ReVia (for alcoholic treatment), 96 sexual function, diminished, 92
“reward deficiency syndrome,” 42–43 sexual practices, risky, 47, 79, 85, 200
rheumatoid arthritis, 71, 155, 169 sherry, 8–9, 16
risky drinking. See binge drinking S homozygotes, 95
Robitussin, 156 “shot houses,” 209
Roche Diagnostics, Indianapolis, shots, 16
Indiana, 121 sialic acid, 131, 134–35, 138, 142–43
Rohypnol (flunitrazepam), 169 Siemens Diagnostics, 120–21
rosuvastatin (Crestor), 157 silver nitrate, 110
Rotterdam study, 45 simvastatin, 157
rubbing alcohol. See isopropyl alcohol skeletal system, 91–92
rum, 9, 16–17, 72 sleep, 43, 68; infants and, 201, 203
Russia, 107, 217–18 sleep-driving, 165
rye, 6 sleeping aids, 1, 159, 164–65
smoking, 1, 44, 57–59, 90, 139–40, 146;
saccharide, 137 during pregnancy, 202–4; red wine’s
Saccharomyces cerevisiae, 6–7 benefits, 69. See also specific health
safety-sensitive jobs, 116, 174–77, 179– conditions, e.g., Alzheimer’s disease
81, 185, 188 solvents, 115, 225, 234, 243–44
salicylate (aspirin), 161–63, 233 somatostatin, 42
saliva/saliva drug testing, 108, 142, 178 Sominex, 159. See also
SAMHSA. See Substance Abuse diphenhydramine
and Mental Health Services Sonata (zaleplon), 165
Administration sorghum, 6
samogon, 217 South American tea, 187–88
San Jose, California, 121 spirits (hard liquor). See distilled spirits
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Index 263
spousal abuse, 79–80 tea, 4, 187–88

Srikumar (police chief), 215 temazepam, 1, 159, 165, 187
standard drink, definition of, 15–18, tequila, 9, 16–17
24, 56 teratogen, 191, 193, 198
steatosis, 83 testing, alcohol. See biomarkers
Sterno, 225 of alcohol abuse; driving with
steroids, 87, 182 impairment/driving while
stillbirth, 192–93 intoxicated; workplace alcohol/drug
stills, 9, 207, 209–11 testing
stomach, 18–19, 68, 163; medications testosterone, 82–83, 92
for, 157–58. See also specific topics, tetracyclic antidepressants, 165
e.g., ulcers tetracycline, 167
stress, 38, 64–65, 70, 133, 201 tetraethyl lead, 212
stroke, 56, 70, 72, 163; Coumadin tetrasialotransferrin, 138
(warfarin) and, 156; heavy drinking thalamus, 44, 49
and, 25, 57–58, 65, 78, 80–81, thiamine, 49, 51, 87–88
88–90, 133; leading cause of, 134; thrombus, 62–63
prevention of, ix, 11, 15, 56, 64–65, thyrotoxicosis, 142
80; treatment for, 90 tinidazole (Tindamax), 158, 168
Substance Abuse and Mental Health TNF-α (tumor narcosis factor-alpha),
Services Administration (SAMHSA), 90
11, 153, 175, 178, 186; drugs, 184–85 tobacco, 207. See also smoking
sucrose, 5, 137–38 tolbutamide (Orinase), 156, 167
Sudafed (chlorpheniramine), 155 tolerance (by age, sex, body weight).
sudden sniffing death syndrome, 244 See guidelines for alcohol
sugarcane, 9 consumption
sugars: converted to ethanol (alcohol), toxic metabolites, 84, 162, 170, 231, 239,
2, 5–7, 9. See also specific sugars, e.g., 244; of ethylene glycol, 237, 239,
glucose 244; of methanol, 231, 244. See also
suicide, 156, 200, 226, 235, 238, 241; acetaldehyde
adolescents and, 10, 47, 81–82 traffic accidents. See motor vehicle
sulfonamides, 167 accidents
sulfonylureas, 167 transferrin, 137–39. See also
sulfuric acid, 110 carbohydrate-deficient transferrin
supplements, nutritional, 9, 49, 87 Transportation Equity Act for the 21st
“sura,” 3 Century (TEA-21), 107
surgical settings, alcohol biomarkers in, trazodone (Desyrel), 156
133–34 Triaminic (chlorpheniramine), 155
“surrogate alcohol,” 208, 216–18 triazolam, 165, 187
SYNCHRON LX20 analyzers, 120 tricyclic antidepressants, 165–66
Syva (EMIT), 121 Tsang, Edman, 224
twin studies, 12, 66, 93
T-ACE questionnaire, 195–96 Tylenol (acetaminophen), 2, 155, 158,
Tagamet (cimetidine), 157, 160, 168 161, 170
Tamil Nadu, 215 Tylenol Cold/Allergy/Flu
tamsulosin (Flomax), 157 (chlorpheniramine), 155
taxes, 4, 195, 207–9, 217 tyramine, 156, 166
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264 Index
ulcers, 155, 158, 163–64; antiulcer Wernicke-Korsakoff syndrome, 49

medications, 160, 168 Wernicke’s encephalopathy, 49
underage drinking, 1, 10, 47–48, 52, 68, whiskey, 9, 15–16, 17, 72, 208
103, 129 “whiskey tax,” 4
Uniform Policy Provision Law, 104 Whitehall II Cohort Study, 81
Unisom (doxylamine), 159 white wine, ix, 7, 9, 32, 64, 69, 72
United Airlines, 181 Widmark, Eric P., 28
urine, 108, 120, 141, 143–45, 179, Widmark formula, 28–32
182–85; serum and urine beta- windshield wiper fluid, 217, 225, 226
hexosaminidase, 135, 140–42; urine wine, 7–9, 12, 59, 63–64, 70–72. See also
alcohol concentration (UAC), 182; red wine; white wine; specific topics,
urine hexosaminidase, 131, 134–35 e.g., cardiovascular disease
women, 20, 22, 50–51, 60–61, 69, 84–85;
Valium, 155. See also diazepam guidelines/recommendations for,
vasopressin, 42 23, 28–33, 52, 72. See also specific
venlafaxine (Effexor), 156 topics, e.g., hypertension; menopause
ventral tegmental area (VTA), 43–45, “wood spirit”/ “wood alcohol,” 222–
200 23. See also methanol
ventricular septal defects (VSD), 200 work, safety-sensitive. See safety-
Venugopal (enforcement official), 215 sensitive jobs
Verapamil, 160, 169 workplace alcohol/drug testing, 174–
Vicodin (hydrocodone), 1, 159, 164 79, 182–85; false positive/negative
violence; violent behavior, 11, 25, 47, results, 183, 186; legal guidelines
72, 78–79, 82–83, 129. See also crime for, 179–85; limitations of, 185–87;
vitamin C, 240 “negative” test, 178; tips for passing,
vitamin D, 92 188
vitamin E, 64, 87 World Health Organization (WHO), 25,
Vitros Platform (Johnson and Johnson), 78, 95
120
Vivitrol (for alcoholic treatment), 96 Xanax, 155. See also alprazolam
vodka, 9, 16–17, 72, 217
Voltaren (diclofenac), 155, 164 yeast, 2–7, 15, 209
vomiting, 39, 85, 158, 167, 231, 236, 238 yeast infections, 6, 183
warfarin (Coumadin), 156, 168 zaleplon (Sonata), 165

War of 1812, 4 Zantac (ranitidine), 157, 160, 168
Washington, George, 207 zero-order kinetics, 20–21
weight, guidelines for. See guidelines Zocor (simvastatin), 157
for alcohol consumption Zoloft (sertraline), 156
Wellbutrin (bupropion), 156 zolpidem (Ambien), 159, 165
10-649_Dasgupta.indb 264 1/17/11 6:40 AM

About the Author
Amitava Dasgupta, PhD, DABCC, FACB, is professor of pathology and

laboratory medicine at the University of Texas Health Sciences Center at
Houston. He is also the director of the Clinical Chemistry and Toxicology
Laboratory of Memorial-Hermann Laboratory Services, the major clinical
teaching hospital of the University of Texas, and the medical director of
Memorial-TIRR Hospital laboratory services. He has published over 185
scientific papers, two books on drugs of abuse, and one book on herbal
medicine and has edited three professional reference books. He is on
the editorial board of five major medical journals including American
Journal of Clinical Pathology, Archives of Pathology and Laboratory Medicine,
Therapeutic Drug Monitoring, and others. He lectures both nationally and
internationally on drug and alcohol testing and acts as an expert witness
for the State of Texas for alcohol and drug related criminal prosecutions.
In 2009, he recently received the prestigious Irvine Sunshine Award from
the Internal Association for Therapeutic Drug Monitoring and Clinical
Toxicology (IATDMCT) for his outstanding contribution in the field of
research in clinical toxicology.
265
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What is the book about?

What is the book about?

What are some of the health effects of alcohol discussed in the book?

What are some of the health effects of alcohol discussed in the book?

10-649_Dasgupta.indb i 1/17/11 6:40 AM

ROWMAN & LITTLEFIELD PUBLISHERS, INC.

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Estover Road, Plymouth PL6 7PY, United Kingdom

Copyright © 2011 by Amitava Dasgupta

British Library Cataloguing in Publication Information Available

Library of Congress Cataloging-in-Publication Data

Printed in the United States of America

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10-649_Dasgupta.indb v 1/17/11 6:40 AM

10-649_Dasgupta.indb vii 1/17/11 6:40 AM

10-649_Dasgupta.indb ix 1/17/11 6:40 AM

present these scientific facts in a more accessible fashion that everyone

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A lcohol is a drug (pharmaceutical) with medicinal value. One of the

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Tylenol (acetaminophen) regularly for pain control, even if that individual

FRUIT RIPENING AND HISTORICAL ORIGINS

Originally proposed by Professor Robert Dudley of the University of

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ALCOHOL FROM A HISTORICAL PERSPECTIVE

The first historical evidence of alcoholic beverages came from an ar-

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SCIENCE OF FERMENTATION AND DISTILLATION

Fermentation is a process by which yeasts convert sugar into alcohol in

Figure 1.1. Fermentation of glucose by yeast-producing alcohol

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Brewers classify yeasts for beer manufacturing into “top-fermenting”

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Preparation of Distilled Spirits

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NUTRITIONAL VALUE OF ALCOHOLIC BEVERAGES

Alcoholic drinks consist primarily of water, alcohol, and variable

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burning carbohydrate. Therefore, drinking one can of beer provides ap-

CURRENT USE AND ABUSE OF ALCOHOL

According to a survey by the U.S. government of adults ages eighteen

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WHY ALCOHOL IS A DRUG

According to the American Council for Drug Education, alcohol is the

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Many individuals with a genetic makeup susceptible to alcohol abuse are

1. R. Dudley, “Ethanol, Fruit Ripening, and the Historical Origins of Human

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Figure 1.2. A schematic representation illustrating common influences of genetic

2. D. Stephens and R. Dudley, “The Drunken Monkey Hypothesis: The Study

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9. C. S. Liber, “Relationships Between Nutrition, Alcohol Use and Liver Dis-

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A lcoholic beverages can be classified under three broad categories: beer,

DEFINITION OF A STANDARD DRINK

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