Obesity-code-Jason Fung
Obesity-code-Jason Fung
Obesity-code-Jason Fung
Final summary
The key message in these blinks:
Obesity is a public health problem in the developed world, and it’s on the rise. But
here’s the problem: decades of just-so stories have led us up the garden path with their
claims that the answer is rapid weight loss and avoiding dietary fats. In truth, obesity is
largely a genetic issue linked to insulin levels. The real culprit isn’t fat itself but the
wrong kinds of fat – modified trans fats – and highly refined carbohydrates and sugars
which lead to insulin resistance. Cut down on those, and you’re much less likely to be at
risk of obesity and related health issues.
These blinks put many of these old myths to bed and get to the heart of the issue. Drawing on
the latest medical research, they show that most fats are an essential part of a healthy diet and
that the real driver of obesity is refined sugar and carbohydrates. Why? Well, it all comes
down to the hormone which regulates so many of our bodily processes: insulin.
And it’s the workings of that hormone which Fung explores. Once we’ve got the science right
we can start taking steps to protect our health and avoid obesity.
what the latest evidence says about the age-old nature versus nurture debate;
why you should avoid snacking and fast between meals instead; and
what makes poorer people more prone to obesity.
We know that from scientific studies of environmental factors affecting children as they
develop. The best way of determining how important these are is to look at adopted kids and
their families. That’s just what Albert J. Stunkard did. His research on adopted children in
Denmark was published in the New England Journal of Medicine in 1986. Why Denmark?
Well, the country is pretty great at keeping accurate adoption records, which is just what
Stunkard needed to compare his subject’s adoptive and biological parents.
Stunkard showed that there was no correlation whatsoever between the weight of these
minors and their adoptive parents. This indicated that environmental factors had virtually no
bearing on whether children became obese or not. The results of the study came as a shock.
Until that point, the default assumption had been that social environment was the most
important factor when it came to obesity. The argument that early exposure to junk food led
to weight issues had been refuted.
That left genetic factors. Stunkard didn’t just dismiss an old theory, however. He also
provided evidence for a new hypothesis. When he compared adopted kids to their biological
parents, he found a strong correlation: the children of obese parents were much more likely to
become obese themselves even if they’d grown up in a family in which everyone else was
relatively thin. In 1991, Stunkard published a follow-up study which put a number to his
claims. According to his new research, genetic factors account for approximately 70 percent
of a person’s likelihood to develop obesity.
You have to look at calorie output as well as
calorie intake to understand obesity.
People often intuitively believe that weight loss is all about how much you eat. Reduce your
calorie intake, the thinking goes, and your weight will also decrease. Sounds pretty plausible,
right? Well, there’s a problem – it’s just not true. In fact, there’s no causal relationship
between calorie intake and obesity.
One of the reasons for this misconception is that there’s a correlation between greater calorie
intake and higher obesity rates. According to the Mortality and MorbidityReport by Doctors
J. D. Wright and J. Kennedy published in 2004, calorie consumption in the United States
increased by an average of 250 calories per person per day between 1971 and 2000. But that
wasn’t what was causing obesity in the country.
Take it from U. Ladabaum, the doctor who wrote a 2014 study published in the American
Journal of Medicine showing that this relationship wasn’t causal. According to Ladabaum’s
data, average calorie intake didn’t rise between 1990 and 2010. Obesity, meanwhile,
continued to increase by 0.37 percent each year.
So what’s going on here? Well, reducing your overall calorie intake isn’t enough on its own
to help you lose weight. The reason for that is simple: bodyweight isn’t only determined by
how many calories you’re consuming – it’s also about how many you’re burning. Calorie
output, in other words, is just as important.
That leads us to another misconception: the idea that the calories we consume are
automatically converted into fat. This simply isn’t backed up by the data. In reality, calories
are used for all sorts of things from producing heat, proteins, bone and muscle tissue to
fueling your brain and increasing the volume and rate of your heartbeat. Fat production is just
one of many different things your body does with the calories you consume.
Obesity, then, isn’t a problem caused by eating too much – it’s an energy usage problem.
Some people’s bodies convert calories into fat while others will simply develop bigger bones
and muscles or use that energy to boost their concentration. And here’s the thing: it’s only the
first use of calories that’s regarded as socially problematic.
We’ve known that for a while now. Take a classic study conducted in 1919 at the Carnegie
Institute in Washington, D.C. Participants were put on a strict diet and consumed between
1,400 and 2,100 calories a day – a reduction of around 30 percent compared to their usual
diets. What the researchers wanted to find out was what effect this would have on their
bodies.
The result? The participants’ energy expenditure also fell. It decreased by roughly 30 percent,
falling from 3,000 to 1,960 calories per day. Their new diet didn’t result in any significant
weight loss – it just decreased the amount of energy their bodies were expending.
One way bodies reduce energy expenditure is to cut their metabolic rates, leading to all sorts
of adverse effects on other bodily functions. That was shown in research conducted by Ancel
Keys, a Minnesota-based doctor, in 1945. Keys was interested in starvation, a problem which
scientists and policymakers believed would become acute in the post-war years. To observe
its effects, he radically reduced his subjects’ calorie intake.
His study found that this resulted not in weight loss as Keys had assumed but in the
participants’ constant complaints that they felt cold. That sensation was caused by the fact
that their metabolic rate – which, among other things, regulates body temperature – had
declined by 40 percent. Their heartbeat had also slowed dramatically, dropping from 54 beats
a minute to just 34. Their brain activity meanwhile showed signs of serious impairment,
accounting for their lethargy and inability to concentrate.
This just goes to show that cutting down on calories isn’t a viable solution to weight issues.
Why? Well, calorie intake isn’t the devil it’s sometimes made out to be. In the next blink,
we’ll take a closer look at the real culprit.
The key point to remember here is that your body isn’t subject to your conscious control. So
who, or rather what, is in the real driving seat? Well, in a word, hormones. It’s these
regulatory substances which determine how you feel. The hormone ghrelin, for example,
makes you feel hungry. Leptin, by contrast, tells you when you’ve had enough to eat. And
that’s where insulin comes in. Once the amount of insulin in your system rises above a
certain level, your hormonal balance is disturbed, leading to behavior such as overeating.
That said, the exact mechanism linking high insulin levels to obesity remains something of a
mystery. Robert Lustig, an endocrinologist and obesity expert based in California, suggested
in 2004 that insulin inhibits the normal functioning of leptin. That’s a pretty plausible theory.
Here’s how it works.
Leptin levels, Lustig argued, increase after a meal. That tells your brain that you’ve had
enough to eat. The same goes for when you’ve recently put on weight, and your body fat
increases: the leptin in your body suppresses your appetite and encourages weight loss. When
you look at obese patients, however, you often find the opposite is happening. Their leptin
levels decrease after meals, meaning that the feeling of satiety – the sense of being full
– eludes them. The absence of this natural feedback mechanism means that they continue
eating. But even as their body-fat levels increase, their leptin levels remain low.
Lustig’s hypothesis suggests how insulin might be related to obesity, but it remains unproven
in the absence of hard experimental evidence.
When that happens, your cells eventually become insulin resistant. That essentially means
cells become unresponsive to insulin hormone receptors and stop taking in sugar molecules
from your blood. As a result insulin-resistant people have a much harder time losing weight.
Their cells only receive a small portion of the sugars they’ve consumed and constantly cry
out for more food, resulting in weight gain. That’s also the reason even successful diets
ultimately prove unsustainable: most people eventually give in to their bodies’ demands to be
fed.
One of the chief causes of raised insulin levels is snacking between meals. Why? Well, each
small snack leads to a peak in insulin production. If you’re always grazing between
mealtimes, your body will constantly be producing medium to high levels of insulin. That’s a
problem: ideally, your body should have regular periods of low insulin levels. But that’s only
possible if you fast for around four to five hours after a meal and give your body a chance to
reduce that spike in insulin production before your next meal.
Take the Pima people, Native Americans who primarily live in southwestern American states
like Arizona. Their communities are generally very poor, and around 50 percent of all adults
suffer from obesity. It wasn’t always that way. According to the historical evidence available
to us, it seems that the Pima were fit and healthy agriculturalists and hunters for much of the
nineteenth century. Things started to go downhill for them after colonists settled on their land
and disrupted their way of life.
As they struggled to adapt to the new society that was taking shape around them, their diet
changed. White sugar and refined carbohydrates like wheat and corn found in pasta and
cereals suddenly became staples. No wonder: they’re typically cheap and easy to store.
Unfortunately, they’re also one of the leading causes of insulin resistance. As the Pima
struggled to find their place in a nation that discriminated against them, they fell into poverty
and became ever more reliant on such foodstuffs.
That’s a pattern that’s repeated itself across the United States. Marginalized communities and
groups typically find themselves struggling with poverty and become reliant on cheap,
refined food to get by. That’s why obesity is so heavily concentrated in the least affluent
states like Mississippi.
This raises the question: why are sugar, corn and wheat so much cheaper than more
nourishing alternatives? Well, partly because of the way the US government subsidizes
farmers who produce these goods. Take a 2011 study by the United States Public Interest
Research Group. It showed that a whopping 29 percent of all subsidies were directed toward
corn production while a further 12 percent were used to prop up the livelihoods of wheat
farmers.
Those subsidies have artificially lowered the price of refined foods, making them much more
affordable than, say, fresh vegetables. No wonder the diets of America’s poorest citizens are
so heavily based around these products, and obesity is so widespread in the country’s least
wealthy communities!
In fact, most dietary fats aren’t unhealthy at all. Despite the widespread assumption that fats
were to blame, the evidence that this isn’t the case has been around for a while now. Take a
1948 study conducted by Harvard scientists in the town of Framingham, Massachusetts.
The researchers knew about the correlation between heart disease and high cholesterol, but
they wanted to find out what caused cholesterol levels to rise in the first place. Their working
hypothesis? Dietary fat must be the culprit. The study quickly disproved that idea, and the
researchers couldn’t find any correlation between eating large amounts of dietary fats and
higher cholesterol levels.
But the idea that fats must be to blame was so entrenched that scientists simply refused to
accept the results of their own studies disproving this link. When another group of
researchers published a paper in the New England Journal of Medicine in 1981 once again
suggesting that there was little to no correlation, they breezily ignored their data and came to
the opposite conclusion!
Today, there’s little doubt that these earlier studies were correct, even if their authors had a
hard time accepting it. Does that mean you can eat dietary fats without worrying about your
health? Well, as always, there’s an exception that proves the rule: modified trans fats. These
really are bad for you. Let’s take a closer look at them.
You’ve probably heard of saturated fats – their name reflects the fact that their molecules are
saturated with hydrogen, which prevents them from going rancid as quickly as
polyunsaturated fats. While most vegetable oils are polyunsaturated by nature, most
vegetable oil products, like margarine, are artificially saturated to extend their shelf-life.
That’s why we call them modified trans fats or hydrogenated vegetable oils.
There’s no doubting their usefulness, but there’s plenty of evidence to suggest you’re best off
avoiding them. Take a 1990 study by Dutch researchers. Their report concluded that modified
trans fats increase bad cholesterol and reduce good cholesterol. A follow-up study
underscored these findings, showing that a two percent increase in modified trans fat
consumption increased the risk of heart disease by 23 percent.
Sugar does a couple of things that make obesity and related issues much more likely: first off,
it increases your insulin levels, and that – as we’ve seen – eventually leads to insulin
resistance, above all in your liver. That’s down to the fact that sugar or sucrose contains
something called fructose, a type of sugar which only the liver can absorb. When you
consume too much of this substance, your liver struggles to keep up and begins transforming
fructose into fat. That, in turn, increases the risk of insulin resistance and interferes with
healthy digestive functions.
The only thing worse for you than sugar is high-fructose corn syrup. Regular sugar is made
up in equal parts of glucose and fructose, but high-fructose corn syrup only contains the latter
– hence the name. That makes it even worse for your liver. So if you want to reduce your
exposure to obesity, start by cutting down on sugar. But remember, sugar is often lurking in
the unlikeliest products, so make sure to check labels. If it contains lots of sugar or any high
fructose corn syrup, leave it on the supermarket shelf!
Taking care of your health isn’t all about denying yourself treats. So here’s the silver lining:
coffee isn’t bad for you. That might seem odd given the endless discussions about caffeine’s
supposedly dangerous side-effects, but there’s hard evidence to back up that claim. Take a
2005 study published in the American Journal of Clinical Nutrition. It found that coffee had
more positive than negative effects. That’s because it’s rich in antioxidants which help slow
the aging process in cells, and also magnesium, which is good for your bones and heart.
Other studies conducted in 2008 and 2012 also link coffee to a reduced risk of type 2
diabetes, Alzheimer's and Parkinson’s disease. That said, it’s probably best not to start
chugging liters of java every day as these studies aren’t definitive.
So losing weight isn’t about drastically reducing your calorie intake and exercising more.
What really makes the difference is cutting down on foods which raise your insulin levels,
above all sugars and refined carbohydrates, and avoiding constant snacking.
Final summary
The key message in these blinks:
Obesity is a public health problem in the developed world, and it’s on the rise. But
here’s the problem: decades of just-so stories have led us up the garden path with their
claims that the answer is rapid weight loss and avoiding dietary fats. In truth, obesity is
largely a genetic issue linked to insulin levels. The real culprit isn’t fat itself but the
wrong kinds of fat – modified trans fats – and highly refined carbohydrates and sugars
which lead to insulin resistance. Cut down on those, and you’re much less likely to be at
risk of obesity and related health issues.
Actionable advice:
Fasting is often a great way of reducing your insulin levels and avoiding insulin resistance.
When and how often you should fast is something best discussed with your doctor, of course,
but here are a couple of ideas to get you started. One option is to fast one day every week,
avoiding food but making sure to keep yourself well hydrated with a liquid breakfast of water
or tea, more hot beverages and a vegetable broth for lunch. Come dinnertime, you’ll want to
eat something light – ideally, some protein and nutritious vegetables. Don’t include
carbohydrates or sugars. The next day, return to your regular diet. Keep that up for a while,
and you’ll drastically reduce your insulin levels.
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What to read next: The Body Is Not an Apology, by Sonya Renee Taylor
As we’ve seen in these blinks, myths are everywhere when it comes to a subject as sensitive
as bodyweight. But it’s not just faddish diet advice and poor science that ends up misleading
people – there’s also a ton of social pressure to conform to an “ideal” body size and shape.
Those pressures can have a toxic and ultimately deeply unhealthy effect on our relationships
with our own bodies. So before embarking on another diet plan, why not reassess that
relationship with the blinks to Sonya Renee Taylor’s radical self-love manifesto The Body is
Not an Apology?