to Gary Taubes:
The Soft Science of Dietary Fat
Fat: At the Heart of the Matter
role of dietary fat in the causation of coronary heart disease (CHD) has
long been a topic of interest and dispute. In his News Focus article, Gary
Taubes discusses what he calls "The soft science of dietary fat"
(30 Mar., p. 2536). He reviews the history of the diet-heart issue and
concludes that public health recommendations regarding dietary fat have not
been based on solid science. He is primarily critical of the
"low-fat" recommendation that has long been made by authoritative
bodies to the American public. Taubes covers many aspects of the diet-heart
issue, but he focuses on the question of whether there has been an
overemphasis on fat without sufficient evidence that dietary fat is a major
cause of CHD. He points out that recent trends in heart disease mortality
both in the United States and worldwide are not well correlated with changes
in dietary fat intake. Certainly he makes several astute observations, but
in some areas, particularly in cardiovascular epidemiology, he does not
appropriately recognize several other factors that confound the role of
certain dietary fats in causation of CHD.
my view, Taubes does not rightly identify saturated fatty acids as the
predominant dietary factor contributing to the development of CHD. The
significance of saturated fatty acids has been demonstrated by an enormous
number of high-quality studies carried out with dietary fat in the fields of
animal research, epidemiology, metabolism, and clinical trials (1).
Although all questions have not been answered, a clear picture of the
metabolic and health effects of saturated fatty acids has emerged. One fact
is incontrovertible. As shown in multiple metabolic studies in humans,
saturated fatty acids as a class, compared with unsaturated fatty acids and
carbohydrate, raise serum low-density lipoprotein (LDL). Evidence is
abundant that elevated LDL is a major cause of CHD and that lowering serum
LDL levels reduces CHD risk (2).
Even moderate reductions in LDL levels, such as those obtained by reducing
dietary saturated fatty acids, are projected to substantially reduce risk of
CHD in populations (3).
Early prospective epidemiological studies gave results that are consistent
with these projections (4).
For example, in Northern and Eastern Europe, where intake of animal fats
(mostly saturated fatty acids) previously was very high, serum LDL levels
and CHD rates also were high. Conversely, in Southern Europe, where plant
oils (mostly unsaturated fatty acids) are the predominant fat source, serum
LDL levels and CHD rates were much lower. These relations were established
more than 30 years ago, before increasing social and cultural homogenization
in Europe partially obscured the relation of dietary fat to CHD (4).
These population results, which in themselves were suggestive although
perhaps not definitive, have been confirmed by results of controlled
clinical trials. Several trials reveal that substitution of unsaturated
fatty acids for saturated fatty acids lowers the incidence of CHD (1).
Taubes acknowledges the difference between saturated and unsaturated fatty
acids, he does not draw a clear enough distinction in his discussion of
dietary fats in general. Consequently, the article obscures the potential
for public health benefits of substituting unsaturated for saturated fatty
acids in the American diet. Such confusion does a disservice to the public
health effort to further reduce the incidence of CHD through a reduction in
intake of saturated fatty acids. On the other hand, Taubes does rightly note
that other nutritional factors, for example energy imbalance leading to
obesity, excessive carbohydrates, and insufficient intake of fruits and
vegetables also influence population risk for CHD (1,
casual reader of Taubes' article might conclude that the only recommendation
made by Senator George McGovern's committee in its Dietary Goals for the
United States or in the Dietary Guidelines for Americans was to reduce
dietary fat. We recommended reduced consumption of cholesterol, salt, and
sugar but increased consumption of unsaturated fat, whole cereal grains, and
fruits and vegetables. One could not recommend increasing intake of anything
without reducing intake of something else. Saturated fat was, and is, the
best thing to reduce. The recent report of the Nutrition Committee of the
American Heart Association (1)
has correctly emphasized "diet as a whole" rather than
"segmented guidance on individual dietary components." In
retrospect, we should have said, "eat less sugar and refined
cereals." Nevertheless, one version of the total diet recommended would
approximate the so-called Mediterranean diet.
raises concerns about possible adverse effects of a low-fat diet,
particularly upon brain function. However, 30% of calories as fat can
scarcely be labeled a low-fat diet. One does not note mental incompetence in
the Japanese, Chinese, and other populations who do, or did, consume a
really low-fat diet. Such populations also demonstrate that low-fat diets do
not necessarily cause obesity.
et al. (2,
have demonstrated that very low-fat diets combined with exercise actually
reverse atherosclerosis. Although this is important in demonstrating the
role of diet, there is little point in recommending such severe diets that
few will follow.
calls a 10% lowering of cholesterol "trivial." That may be true
for high-risk individuals, but not for a population. A modest reduction in
risk may accomplish little for an individual, but a 10 or 20% reduction in
risk represents a substantial gain for the population.
also says that Americans now consume 34% of calories as fat. A major problem
is that we are uncertain exactly what Americans eat. It is clear that all
methods of estimating food intake are grossly inaccurate and biased. People
generally underestimate their energy intake, and people who know, or think
they know, what they should eat are likely to shade their reported intake
toward what they consider desirable. Apparently, Americans have changed
their diet little. Nevertheless, data from the Continuing Survey of Food
Intake by Individuals by the U.S. Department of Agriculture indicate modest
benefits by those who report eating lower fat diets and those who report
consumption that approximates the Food Guide Pyramid (4).
The inadequacies of food intake data also compromise the conclusions of
studies like the Nurses' Health Study and the Women's Health Initiative.
expects research to modify dietary recommendations. In the last 25 years, we
have learned more about the n-3 fatty acids, the glycemic index, and
antioxidants, and there are additional data indicating the benefits of a
high level of consumption of fruits and vegetables. The recent
recommendations from the American Heart Association (5)
include appropriate modifications. A reduction in saturated fat, however,
remains at the core of an appropriate nutrition policy.
his article, Taubes focuses on scientists who don't believe that dietary fat
plays any important role for obesity and cardiovascular disease. The crucial
evidence linking fat to obesity and coronary heart disease (CHD) is not
discussed. The following are some examples.
phenomenon that Americans have reduced dietary fat content slightly but are
getting fatter is taken as evidence that it is easier to gain weight on
low-fat, high-carbohydrate diets than on higher fat diets. What Taubes does
not mention are the meta-analyses of intervention studies comparing ad
libitum intakes of higher fat diets with low-fat diets that clearly show
reduced caloric intake and weight loss on the low-fat diets (1).
In addition, it is well known that people underreport their energy and
especially fat intake, which makes the observed fat intake reduction
questionable. The obesity epidemic in the United States and other countries
is predominantly due to an inactive life-style, which reduces the metabolic
demand for fat as fuel.
his discussion about the importance of dietary fat and CHD, Taubes focuses
on the effect of fat on fasting blood lipids, but low-fat diets with plenty
of fruit, vegetables, and fish predominantly exert their cardioprotective
effect through other mediators such as blood pressure, thrombotic,
fibrinolytic, and arrhythmic factors. Accordingly, an increase in dietary
fat of 1% of energy intake is associated with an 8% increase in CHD (2).
A Mediterranean, fat-reduced diet includes plenty of fruits, vegetables, and
fish, and such a diet has been shown to reduce mortality by 45 to 60% in
individuals with CHD (3).
message in the article is misleading and counterproductive for public health
policy to reduce dietary fat content and increase the consumption of fruit,
vegetables, and fish, and to increase physical activity, advice based on
robust scientific evidence.
H. M. Saris
whom correspondence should be addressed.
M. De Lorgeril et al., Circulation 99, 779 (1999); R. B. Singh et al., Br. Med. J. 304, 1015 (1992).
says that my article obscures the potential for public health benefits of
substituting unsaturated fatty acids for saturated fatty acids in the
American diet. The article doesn't obscure the benefits; it simply questions
whether they are sufficiently large for healthy individuals who eat
reasonable diets (that is, sufficient fruits and vegetables) to be
concerned. It also questions whether all Americans will benefit from a
low-fat diet, or whether for some, at least, there are risks involved as
well, which is still an unanswered question. Indeed, three decades of
low-fat diet recommendations has led many Americans to replace saturated
fats with carbohydrates, not unsaturated fats. Certainly, the food industry
has responded by creating low-fat and no-fat products that do just that.
Moreover, there is suggestive but not definitive evidence both for and
against the benefits of a low-fat diet, and clinical trials have both
succeeded and failed in confirming the benefits.
discusses the trials that show a positive benefit, implying that these are
the important ones, which makes for a compelling argument but does so at the
expense of good science. Hegsted and Astrup et al. also pay attention only
to those data that support the benefits of low-fat diets and ignore or
reject as irrelevant or flawed all the copious evidence to the contrary.
Astrup et al. for example cite a case-control study with 108 patients (and
142 controls) as unequivocal evidence that increased dietary fat intake is
associated with increased heart disease rates, although such case-control
studies are virtually meaningless. They say that meta-analyses demonstrate
that low-fat diets are efficient weight loss diets, yet there are trials and
even meta-analyses--a controversial tool, in any event--that suggest the
opposite. They say that the obesity epidemic in America and elsewhere is
"predominantly due to an inactive life-style," which is a
reasonable hypothesis but unproven. There remains the complicated question
of why individuals would continue to consume more calories than they expend,
despite enormous social pressure against obesity.
suggests that small individual risk reductions represent substantial gains
for a population, but individuals are not populations. And deaths are not
prevented, as I pointed out in the article, they are only delayed. Low-fat
diets might indeed delay them, but if they do, the effect is marginal. The
key point, as Grundy
says, is that "all questions have not been answered," and so we
might not want to act as though they have been.