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A Changing View On Sfas and Dairy: From Enemy To Friend: Editorial

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AJCN. First published ahead of print October 29, 2014 as doi: 10.3945/ajcn.114.099986.

Editorial

A changing view on SFAs and dairy: from enemy to friend1–3


Arne Astrup

Almost all national dietary guidelines recommend a reduction in acid supplementation. In the observational studies, RRs for
SFAs as a key intervention to reduce incidence and mortality of coronary disease were no different for SFAs, n–6 PUFAs, and
cardiovascular disease (CVD). This has been translated into advice MUFAs when the top and bottom thirds of baseline dietary fatty
to reduce the intake of the major sources of SFAs, that is, dairy acid intake or circulating fatty acids were compared. The meta-
produce, meat products, and eggs. However, recent meta-analyses analysis of RCTs with hard CVD endpoints reached the same
of both observational studies and randomized controlled trials not conclusion. Another meta-analysis of RCTs even suggested that
only have raised doubts about the scientific substantiation for this replacement of SFAs with pure n–6 PUFAs might increase CVD
advice but have actually undermined it. It has become clear that risk and mortality (5).
there is a need for a completely different approach, with advice that
is based on foods rather than on nutrients. DAIRY AND RISK OF CVD AND TYPE 2 DIABETES
The evidence to support reducing SFAs rests on a 2-step argu-
ment: ‘‘A strong body of evidence indicates that higher intake of In recent years, a substantial body of research has investigated
most dietary SFA (A) is associated with higher levels of blood the effects of dairy and dairy fat on risks of CVD, type 2 diabetes,
total cholesterol and low-density lipoprotein (LDL) cholesterol and obesity. A dose-response meta-analysis of prospective stud-
(B). Higher total and LDL cholesterol levels (B) are risk factors ies indicates that milk intake is not associated with total mortality
for CVD (C)’’ (1). but may be inversely associated with overall CVD risk (6).
Most would interpret the statement above as evidence of Reliance on self-reported dietary intakes poses substantial
a causal relation between intake of SFAs (A) and CVD (C), problems with validity, and the development of objective bio-
but it is actually an assumption that increased concentrations markers to distinguish between different food-derived fatty
of LDL cholesterol (B) will always increase the risk of CVD acids represents a major advantage; pentadecanoic acid (15:0),
(C). The relation between dietary fats (and other dietary compo- heptadecanoic acid (17:0), and trans palmitoleic acid (trans
nents) and CVD is, however, much more complex, and this 16:1n–7) can be used as biomarkers for dairy intake. The liter-
assumption does not take into account the importance of LDL- ature has generated mixed results with regard to risk of stroke,
cholesterol particle size, effects on HDL cholesterol, and other but the most comprehensive study from 2 large U.S. cohorts
mediators of the atherosclerotic, thrombotic, and thrombolytic (Health Professionals Follow-Up Study: 51,529 men; Nurses’
processes (2). Health Study: 121,700 women) using biomarkers of dairy fat
(pentadecanoic acid, heptadecanoic acid, and trans palmitoleic
acid) reports results for stroke in this issue of the Journal (7).
SFAs AND CVD After relevant adjustments, no significant associations with total
More recent meta-analyses of high compared with low intakes stroke were seen for any of the 3 biomarkers. The results were
of SFAs fail to find any increased CVD risk. Siri-Tarino et al. (3) similar for ischemic and hemorrhagic stroke subtypes, and the
compared extreme quantiles of SFA intake and found RRs not results remained in sensitivity analyses.
different from 1.0. However, it has become obvious that the SFAs have also been associated with increased risk of type 2 di-
different fatty acids derived from different foods do not have abetes, which is a major risk factor for CVD. However, meta-
the same biological effects, and that the food matrix within analyses of observational studies based on self-reported dietary
which they are delivered modifies their effect. So the health intake failed to find that dairy increases the risk of type 2 diabetes
effects of any food matrix rich in SFAs cannot be predicted on (8, 9). In a meta-analysis of 17 cohort studies, there was a modest but
the basis of the content of ‘‘total SFAs’’ given on the nutrient significant inverse relation between intakes of total dairy products,
content label. There is a need to view the health effect of ‘‘whole low-fat dairy products, and cheese and risk of type 2 diabetes (9).
foods’’ and to use biomarkers to improve the validity of the 1
From the Department of Nutrition, Exercise, and Sports, Faculty of
habitual food intake registered in observational studies and ad-
Science, University of Copenhagen, Frederiksberg, Denmark.
herence in RCTs. 2
No financial support was received for this editorial.
Chowdhury et al. (4) examined the effect of SFAs based on 3
Address correspondence to A Astrup, Nørre Alle 51, Copenhagen, Denmark,
a meta-analysis of 17 observational studies with fatty acid bio- DK-2200. E-mail: ast@nexs.ku.dk.
markers and 27 randomized controlled trials (RCTs) of fatty doi: 10.3945/ajcn.114.099986.

Am J Clin Nutr doi: 10.3945/ajcn.114.099986. Printed in USA. Ó 2014 American Society for Nutrition 1 of 2

Copyright (C) 2014 by the American Society for Nutrition


2 of 2 EDITORIAL

BIOMARKERS OF DAIRY AND DIABETES RISK tional food companies/organizations, including The Danish Dairy Research
Council, Arla Foods AS, and the Global Dairy Platform. AA currently serves
A case-cohort analysis was conducted based on the European
as consultant/member of advisory boards for the Global Dairy Platform, USA;
Prospective Investigation into Cancer and Nutrition–InterAct McCain Foods Ltd., USA; and McDonald’s, USA. He is recipient of honoraria
study in 12,403 individuals with incident type 2 diabetes, and and sponsorship of congress attendance as a speaker for a wide range of Dan-
fatty acids were measured in plasma phospholipids (10). ish and international concerns.
Whereas even-chain SFAs were positively associated with in-
cident type 2 diabetes, the odd-chain SFAs pentadecanoic acid
and heptadecanoic acid were inversely associated with incident REFERENCES
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The totality of evidence does not support that dairy SFAs in- response meta-analysis. PLoS ONE 2013;8:e73965.
crease the risk of coronary artery disease or stroke or CVD 9. Aune D, Norat T, Romundstad P, Vatten LJ. Dairy products and the risk
mortality. In contrast, lean dairy is clearly associated with de- of type 2 diabetes: a systematic review and dose-response meta-analysis
of cohort studies. Am J Clin Nutr 2013;98:1066–83.
creased risk of type 2 diabetes, and this effect is partly indepen- 10. Forouhi NG, Koulman A, Sharp SJ, Imamura F, Kröger J, Schulze MB,
dent of any effect of body fat loss. In addition, lean dairy does Crowe FL, Huerta JM, Guevara M, Beulens JWJ, et al. Differences in the
not increase body fatness but tends to preserve lean body tissue. prospective association between individual plasma phospholipid saturated
There is no evidence left to support the existing public health fatty acids and incident type 2 diabetes: the EPIC-InterAct case-cohort
study. Lancet Diabetes Endocrinol 2014 Aug 6 (Epub ahead of print; DOI:
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2 diabetes. Cheese and other dairy products are, in fact, nutrient- 11. Santaren ID, Watkins SM, Liese AD, Wagenknecht LE, Rewers MJ,
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The Department of Nutrition, Exercise and Sports at the University of incident type 2 diabetes and its underlying disorders. Am J Clin Nutr
Copenhagen receives research support from numerous Danish and interna- 2014;100:1532–40.

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