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Old Sun, Jun-09-02, 15:14
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Default Eating fat doesn't cause body fat

Is dietary fat a major determinant of body fat?1,2
Walter C Willett
1 From the Departments of Epidemiology and Nutrition, Harvard School
of Public Health, Boston.
2 Address reprint requests to WC Willett, Department of Nutrition, Harvard
School of Public Health, 665 Huntington Avenue, Boston, MA 02115.
Am J Clin Nutr 1998;67(suppl):556S–62S. Printed in USA. ฉ 1998 American Society for Clinical Nutrition 556S

ABSTRACT
The percentage of energy from dietary fat is
widely believed to be an important determinant of body fat, and
several mechanisms have been proposed to account for such a
relation. Comparisons of both diets and the prevalence of obesity
between affluent and poor countries have been used to support a
causal association, but these contrasts are seriously confounded
by differences in physical activity and food availability. Within
areas of similar economic development, regional intake of fat and
prevalence of obesity have not been positively correlated. Randomized
trials are the preferable method to evaluate the effect of
dietary fat on adiposity, and are feasible because the number of
subjects needed is not large. In short-term trials, a modest reduction
in body weight is typically seen in individuals randomly
assigned to diets with a lower percentage of energy from fat.
However, compensatory mechanisms appear to operate because
in trials lasting ณ1 y, fat consumption within the range of 18–40%
of energy appears to have little if any effect on body fatness.
Moreover, within the United States, a substantial decline in the
percentage of energy from fat consumed during the past two
decades has corresponded with a massive increase in obesity.
Diets high in fat do not appear to be the primary cause of the high
prevalence of excess body fat in our society, and reductions in fat
will not be a solution. Am J Clin Nutr 1998;67(suppl):556S-62S.
KEY WORDS Dietary fat, obesity, adiposity, overweight,
ecologic studies, randomized trials
INTRODUCTION
Excess body fat is the largest nutrition-related problem in the
United States as well as many other affluent countries. Excess adiposity
can account for <30–40% of heart disease (1, 2), many cancers
of several types (3), most cases of adult-onset diabetes (4), and
a substantial proportion of disabling osteoarthritis (5). Whereas
genetic factors influence which individuals within a population will
develop adiposity, diet and lifestyle factors are clearly the primary
reason for the high rates of excessive body fat in our population. Evidence
for this is provided by the dramatic changes in prevalence of
overweight in migrants from countries with minimal adiposity who
come to the United States; for example, the prevalence of obesity
was threefold higher in Japanese men living in San Francisco than in
those living in Japan (6). Also, the major increases in adiposity
within many populations over time, including the general US population
(7), cannot be explained by genetic factors. Dietary fat is
among the aspects of lifestyle often said to be responsible for these
high rates of adiposity. Indeed, reduction in obesity has often been a
primary justification for recommendations to reduce dietary fat.
Several mechanisms have been proposed to explain why high
fat intake should lead to greater body fat (8, 9). Dietary fat is the
most energy-dense macronutrient, providing <38 kJ/g as
opposed to 17 kJ/g for carbohydrate or protein; this could lead to
overconsumption of energy if food weight or volume is regulated.
Also, fats are often said to lend greater flavor and palatability
to foods, which could lead to greater consumption of them.
In addition, when studied under careful metabolic conditions,
carbohydrates produce a greater thermogenic effect than fat, suggesting
that dietary fat may be utilized more efficiently and accumulate
as body fat more readily (10, 11). Finally, Flatt (12) suggested
that carbohydrate intake is regulated, but fat intake is not;
thus, individuals eating a high-fat diet will tend to consume more
total energy to gain the same amount of carbohydrate as someone
eating a low-fat diet. For all these reasons, dietary fat composition
must be considered as a possible important determinant
of body fat. If a reduction in the percentage of energy from fat in
the diet in fact has a substantial effect on body fatness, this
would be a major reason to advocate low-fat diets.
EMPIRICAL EVIDENCE
Between-population (ecologic) studies
The observation that the prevalence of overweight tends to be
higher in affluent countries with high fat intakes than in poorer
regions of the world with low fat intakes has frequently been mentioned
to support a relation between dietary fat and body fat.
Because such observations are exceedingly confounded by the
availability of food and the level of physical activity in the subjects,
such comparisons can be completely misleading. More relevant are
comparisons within regions of the world with similar degrees of
economic development. Among European countries, no association
was observed between the national percentage of energy from fat
and median body mass index in men, even though fat intake varied
from <25% to 47% of energy (14). However, a clear inverse relation
was observed in women (Figure 1) (14). In a study of 65 counties
in China, no correlation was found between dietary fat intakes,
which ranged from <8% to 25% of energy, and body weight (15).
Ecologic studies such as these have many limitations, including
variable quality of dietary data and confounding by unmeasured
variables such as activity levels, smoking, and cultural atti-
tudes toward body fat. Nevertheless, the failure to observe any
clear, positive association between dietary fat intake and obesity
among areas with roughly similar degrees of affluence weighs
against finding an important causal relation. Because higher fat
intake typically accompanies newly gained affluence, time
trends in dietary and body fat within countries in transition from
poverty or agrarian lifestyles to greater affluence are likely to be
confounded by changes in food availability and level of physical
activity. Thus, such correlations in time are generally not informative
regarding the causal role of dietary fat and obesity. However,
in the United States and several other northern European
countries, fat intake and affluence have been disassociated by
conscious efforts to reduce fat intake. Thus, it is notable that as
fat intake has declined as a percentage of energy over the past 25
y the prevalence of obesity has dramatically increased in the
United States (Figure 2) (3, 7, 16).
Within-population correlations
Numerous cross-sectional studies, reviewed by Lissner and
Heitmann (14), were conducted to examine the correlation
between dietary fat and body fatness within populations. Results
are inconsistent; positive associations were seen in some studies
(17–27), but not in others (20, 21, 25, 27, 28).
Unfortunately, most cross-sectional studies within populations
are also prone to confounding that is almost uniquely
intractable. In most populations studied, both dietary fat and the
desirability of avoiding overweight are strongly linked with general
health consciousness in recent years. The confounding is
particularly problematic because health-conscious persons do
have awareness and influence over the primary determinants of
body weight, specifically the amount they eat and their level of
physical activity, which are both measured imperfectly in freeliving
populations and thus difficult to control for statistically.
Therefore, it should not be surprising that the fat composition of
the diet is positively associated with body fat in many studies.
Unlike many other health-related indexes, body fatness is readily
apparent to the individual, who may alter dietary intake
because of weight or weight gain.
Prospective studies are generally considered a substantially
stronger epidemiologic design than cross-sectional studies.
However, they are similarly susceptible to severe confounding
when individuals are aware of the dependent variable (weight
status) and also have conscious control over its primary determinants
(physical activity, total energy intake, and the percentage
of energy from fat). Relatively few prospective studies of dietary
fat and weight change have been published (23, 26, 27, 29, 30),
and the findings are inconsistent.
The study of Colditz et al (23) provided indirect support for
confounding by health consciousness and an intent to lose
weight. In this large prospective cohort, weight gain was weakly
positively associated with animal fat (generally viewed as
unhealthy) but weakly negatively associated with vegetable fat
(generally viewed as healthier) even though there is little reason
to believe these two fats would be metabolically distinct in relation
to weight gain. Because of the serious potential for confounding
that is extremely difficult to control, both cross-sectional
and prospective studies are likely to be particularly
unhelpful in determining the causal relation between the fat
composition of diets and body fat.
RANDOMIZED TRIALS
Because of the potential for confounding in studies both
among populations and among individuals within populations,
randomized trials are the most desirable way to determine the
effects of dietary fat on body fatness. Although this relation has
great potential importance, surprisingly few studies have been
designed to address this issue (8).
In short-term, randomized trials (those lasting from a few weeks
up to 6 mo), modest weight losses (< 1–4 kg) are typically seen
when 10–15% of energy from fat is replaced by carbohydrate (17,
31–35). In a recent 6-mo trial in which 45 full-fat foods were
replaced with low-fat versions, fat intake was reduced by 7% of
energy and weight was reduced by 0.6 kg (36). Although the effects
WILLETT 556S
FIGURE 1. Median BMI of women taken from surveys in Europe
from 1982 to 1986 versus percentage of energy available from fat.MONICA,
World Health Organization MONICA Project [monitoring trends
and determinants in cardiovascular disease (13)]; 1, Belgium; 2, Denmark;
3, Switzerland; 4, United Kingdom; 5, France; 6, Iceland; 7, West
Germany; 8, Finland; 9, Spain; 10, Sweden; 11, Hungary; 12, Italy; 13,
East Germany; 14, Czechoslovakia; 15, Malta; 16, Poland; 17,
Yugoslavia; 18, USSR. Reproduced with permission (14).
FIGURE 2. Changes in dietary fat (as percentage of energy) and the
percentage of population that is overweight (3, 7, 16).
of fat reduction on body weight in short-term studies were modest,
these could potentially be important if they were cumulative over
periods of years. Thus, long-term studies are critical.
Long-term, randomized trials studying fat reduction and body
weight are few, and most data are secondary observations from
studies in which body weight was not the primary outcome. Most
were pilot studies of fat reduction for the prevention of cancer or
cardiovascular disease (Table 1) (30, 37–41).
The only double-blind, long-term study of fat reduction appears
to be the National Diet-Heart Study (37) conducted in 900 individuals,
in which foods with variable fat content were provided to
participants. The difference in fat intake between groups was 30%
compared with 35% of energy and after <1 y the difference in
weight was only 0.8 kg (Figure 3) (37). Although the difference
in fat intake was not large, this is similar to the difference between
current US diets and US dietary goals.
Two long-term trials of fat reduction were pilot studies for
interventions targeting breast cancer. In the Women’s Health
Trial (30), fat intake was to be reduced from <38% to 20% of
energy. Reported compliance was nearly perfect by 6 mo and
decreased only modestly by 24 mo. Women in the low-fat group
lost 3.2 kg of body weight by 6 mo; however some of this was
regained so that by 24 mo they had lost only 1.9 kg, and the difference
between the intervention and control group was 1.8 kg.
This study strongly suggests that weight losses with low-fat diets
are not cumulative over time and indeed seem to be transient, at
least in part. In a trial of fat reduction in the prevention of skin
cancer (40), the reduction in body fat with a low-fat diet relative
to the control diet was only <1 kg.
The study of Kasim et al (39) included only overweight
women, and thus, presumably those who would be susceptible to
higher-fat diets. Fat intake was reduced to 17.6% of energy at 1
y, therefore providing a major contrast in diets. This study
included more detailed data on body composition than most
other investigations (Table 2) (39). The difference in weight
change between intervention and control groups was somewhat
greater than in the other studies, being 2.6 kg. However, lean
mass as well as fat mass was lost so that the difference in change
between treatment groups in percentage of body fat at 1 y was
only 0.7%, and no effect was observed on the waist-to-hip circumference
ratio. Thus, despite a large contrast in diet, the
change in adiposity was minimal. Importantly, the maximum difference
in weight was seen at 3 mo, with no subsequent divergence
between groups.
A major limitation of most long-term studies of fat reduction
is that the control groups did not receive dietary instruction and
motivation comparable to the intervention groups. In these studies
the intervention subjects were generally given state of the art
individual and group instruction and support to increase consciousness
about dietary fat, sometimes including the provision
of scales to weigh food and control portion sizes. Thus, changes
in body weight, to the extent that they occurred, could have been
the result of greater attention to intake of total energy rather than
just attention to fat. To determine whether dietary fat reduction
reduces body fatness, an appropriate control group would receive
dietary instruction and counseling of similar intensity but
directed at the reduction of carbohydrate or total energy. Such a
study was recently reported by Jeffery et al (41). Participating
women, who were initially moderately obese, received counseling
either to reduce fat to 20 g/d or to reduce overall energy
intake to 5000 kJ/d. Both groups lost weight initially but after 6
mo they also gained weight in parallel (Figure 4) (41). By 18 mo
558S IS DIETARY FAT A DETERMINANT OF BODY FAT?
TABLE 1
Long-term trials studying fat reduction and body weight
Study Duration Fat in Greatest Change in weight
diet weight loss at end trial Comments
mo % kg
National Diet-Heart
Study Research Group (37)
Intervention (n = 450) 12–20 30 22.8 22.3 The only double-blind study.
Control (n = 450) 12–20 35 22.3 21.5
Sheppard et al (30)
Intervention (n = 171) 24 20 23.2 21.9 A somewhat large difference at 6 mo became smaller
Control (n = 105) 24 38 20.4 20.1 with time.
Boyd et al (38)
Intervention (n = 100) 12 21 22.0 21.0 —
Control (n = 106) 12 37 0 0
Kasim et al (39)
Intervention (n = 34) 12 17 — 23.4 Weight differences reflect changes in lean as well as fat
Control (n = 38) 12 36 — 20.8 mass as there were no differences between groups in
changes in percentage body fat, BMI, or waist-to-hip
ratio.
Black et al (40)
Intervention (n = 38) 24 21 23.0 22.0 No significant difference in weight at anytime during
Control (n = 38) 24 40 21.0 21.0 the 24 mo.
Jeffrey et al (41)
Intervention (n = 39) 18 26 24.6 +0.4 Fat counseling for < 20 g/d, energy reduction to
Control (n = 35) 18 33 23.7 +1.8 1000–1200 kcal/d (4184–5021 kJ/d). Thirty three
percent of original participants failed to finish trial.
Adherence to both fat and energy reduction regimen
was poor after 6 mo.
there was no significant or material difference between groups.
It is notable in this trial that women eating the low-fat diet indicated
greater palatability of the low-fat food, which could presumably
enhance compliance. Nevertheless, this was not
reflected in long-term lower weight, and might have contributed
to overeating of low-fat foods.
An important concern in any long-term study of dietary
change is that compliance may deteriorate with time so that the
lack of a substantial effect on body weight could simply be the
result of a lack of difference in diets. In general, studies of fat
reduction have been hindered by a lack of a well-documented
measure of compliance. However, reduced concentrations of
HDL cholesterol occur consistently with low-fat diets (42).
Although depression of HDL cholesterol is not specific to fat
reduction on a group basis, it does appear to be reasonably sensitive
to changes in dietary fat (depressed HDL cholesterol can
also result from reduced physical activity, cigarette smoking,
abstinence from alcohol, and weight gain). Thus, it is notable
that the studies by Kasim et al (39) and Lee-Han et al (43) both
showed reductions in HDL concentrations that were maintained
over time. Using the data on changes in HDL concentrations at
12 mo in the Kasim study (Table 2) and the Mensink and Katan
meta-analysis of metabolic studies on dietary fat and blood lipids
(42), it can be back-calculated that the difference in fat intake at
12 mo was <20% of energy, which is similar to the reported difference
(Appendix A). Thus, these studies do not support the
notion that failure to observe a substantial weight loss with longterm,
low-fat diets is simply the result of noncompliance.
SHORT-TERM WEIGHT-LOSS TRIALS
One hypothesized reason to expect lower body fat with a diet
with a lower percentage of energy from fat is the difference in
metabolic efficiency of processing fat compared with carbohydrate
or protein. Three studies of weight loss are germane to this
proposed mechanism (44–46). In the larger of these studies,
Powell et al (44) provided 5000-kJ diets to women randomly
assigned to consume 10%, 20%, 30%, or 40% of energy from fat.
No significant differences were seen in weight change, although
the magnitude of reduction was actually somewhat less with the
lowest fat intake (Table 3). The studies by Alford et al (45) and
Lehmann et al (46) also found no effect of the fat composition of
the diet on weight loss. These data indicate that under realistic
circumstances the theoretical differences in metabolic efficiency
associated with different levels of fat intake do not account for
important differences in rate of weight loss.
DISCUSSION OF INTERVENTION TRIALS
The long-term randomized trials of fat reduction published
thus far provide strong evidence that the effect of dietary fat over
a range of 18–40% of energy on body fatness is, at most, small.
The findings are particularly inconsistent with the hypothesis
that body fat is proportional to dietary fat (47, 48). The lack of
major effects is particularly notable because, with the exception
of the National Diet-Heart study (37) and the study by Jeffery et
al (41), the designs of the other trials were seriously biased in
favor of finding an effect of fat reduction.
Other issues in many studies, in addition to the lack of an
appropriate control group, complicate what would seem to be a
simple hypothesis to test. One of these issues is that fat reduction
may be confounded by differences in the fiber content or the
energy density of the diet. For example, in most of the fat reduction
trials, subjects were generally counseled to consume high
amounts of fruit and vegetables as well as whole grains and
legumes. In one trial of fat reduction in elderly individuals (35),
subjects continuing a baseline high-fat diet (35% of energy from
fat) were compared with subjects consuming an isoenergetic
low-fat diet. No weight loss was observed over a 12-wk period,
again arguing against any important difference in efficiency of
energy utilization. However, when subjects were allowed to eat
the low-fat diet ad libitum for another 12 wk, a modest weight
reduction was observed. This diet was exceptionally high in fiber
and had a low energy density, and subjects complained of fullness
and abdominal discomfort with the isoenergetic low-fat
diet. Thus, in this study, and potentially in other studies, low-fat
diets might be confounded by high fiber or low energy density.
It might be argued that this is simply a desirable and
inevitable consequence of a low-fat diet and thus should not be
WILLETT 559S
TABLE 2
Randomized trial of a low-fat diet in 72 women1
Baseline 12 mo Difference
Dietary fat (% of energy)
Low-fat diet 36.3 17.6 —
Control 35.6 33.8 —
Weight (kg)
Low-fat diet 66.8 63.4 23.4
Control 72.7 71.9 20.8
Percentage of body
weight (%)
Low-fat diet 31.8 30.3 21.5
Control 35.1 34.3 20.8
Waist-to-hip ratio
Low-fat diet 0.74 0.73 20.01
Control 0.77 0.76 20.01
HDL cholesterol (mmol/L)
Low-fat diet 1.56 1.44 20.12
Control 1.47 1.56 +0.09
1 From reference 39.
FIGURE 3. Changes in fat and energy intake and body weight over
1 y (37).
controlled for in the study design. However, low energy density
is not an inevitable characteristic of low-fat diets; as many of the
low-fat foods presently being promoted in our commercial food
supply are based on sugar or highly refined carbohydrates and
often have energy values similar to those of their high-fat counterparts.
On the other hand, in the Mediterranean tradition, abundant
amounts of vegetables are consumed along with whole
grains and olive oil, thus providing a high-fat, high-fiber, and
high-volume diet. Because there is not an inevitable relation
between the percentage of fat and the energy density of diets, it
is important to distinguish between these effects in the design of
studies to assess the effect of the percentage of energy from fat
on body weight. Whether the energy density of the diet has an
important effect on long-term body fat is, of course, an important
question in itself, and short-term studies suggest that this may be
the case (17, 20, 35, 49–51). However, the contrasts between
short- and long-term studies of dietary fat indicate the need for
long-term studies of energy density and body weight before any
conclusions can be drawn. Also, it is possible that in highly
sedentary populations with low energy demands, the energy density
may need to be extremely low to have any important effect.
Subtle aspects of the diets being compared could potentially
confound randomized trials of dietary fat composition and body
weight. Studies in animals fed cafeteria-style diets suggest that
palatability, flavor, and texture may influence over- or undereating
(52). More subtle aspects of palatability may be difficult to
control in any particular circumstance, but at least an attempt to
do so should be made so as not to artificially favor one group or
another. The relative palatability of the diets may be specific to
the study population.
Finally, the possibility exists that individuals vary in their
genetic susceptibility so that some will gain weight with high-fat
diets and others will not. A recent study suggests that a family
history of obesity might be an indicator of susceptibility to
weight gain with high-fat diets (53). Although it is possible that
susceptible individuals exist, the lack of any substantial overall
effect of fat reduction on body weight in the long-term randomized
trials suggests that the susceptible subgroup is not large or
that other persons are susceptible to weight gain with high-carbohydrate
diets.
The fact that studies of dietary fat fail to explain the prevalence
and increase in excess body fat in our population indicates
the need to consider alternative causes. Abundant evidence
clearly supports a central role of physical activity in the regulation
of body fat. Numerous cross-sectional studies indicate an
equilibrium between physical activity and body fatness, and
intervention studies show that increased physical activity at least
stabilizes body weight and may lead to modest reductions (54).
It has been noted that the magnitude of physical activity in these
intervention studies was small in relation to the levels of activity
typical of nonindustrialized countries, so the full potential effect
of higher activity levels has not been adequately addressed in
such investigations (54).
The characteristics and availability of food and the social context
of food consumption are also likely to have important effects
on body fatness, but these are difficult to study in free-living populations.
The food industry has invested greatly in research on texture,
color, sweetness, saltiness, and flavor of food, as well as on
its packaging and promotion, all of which has been designed to
enhance consumption. It seems highly unlikely that these efforts
have not contributed to overweight, although these contributions
are difficult to quantify. A national character that values quantity
and abundance over quality and presentation may further aggravate
the situation. Finally, the almost ubiquitous presence of food
in our life and the convenience with which it is eaten is likely to
contribute further to overconsumption, but again quantification of
such subjective factors is probably impossible.
CONCLUSIONS
In short-term studies, a modest reduction in body weight is
typically seen in individuals assigned to diets with a lower percentage
of energy from fat. However, compensatory mechanisms
appear to operate such that in the longer term, fat consumption
within the range of 18–40% of energy appears to have little if
any effect on body fatness. The nature of these compensatory
mechanisms is presently unknown. The possibility that individuals
vary in their susceptibility to high-fat or high-carbohydrate
diets deserves further examination. Nevertheless, diets high in
fat are not the primary cause of the high prevalence of excess
body fat in our society, nor are reductions in dietary fat a solution.
Other means will be needed to reduce substantially the
prevalence of obesity; enhancement of physical activity appears
to be the most effective physiologic alternative.
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560S IS DIETARY FAT A DETERMINANT OF BODY FAT?
TABLE 3
Twelve-week weight change in 35 women consuming 5000 kJ diets1
Percentage of Baseline Change in
energy from fat weight weight
kg
10% 95.0 24.5
20% 88.2 26.8
30% 101.4 26.9
40% 85.0 26.8
1 From reference 44.
FIGURE 4. Fat and energy restriction and weight change over 18 mo
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WILLETT 561S
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APPENDIX A
In the meta-analysis by Mensink and Katan (42), the change
in serum HDL (mg/dL) = 0.47 (carbohydrate ฎ saturated fat) +
0.34 (carbohydrate ฎ monounsaturated fat) + 0.28 (carbohydrate
ฎ polyunsaturated fat), where substitutions of fat for carbohydrate
are in percentage of energy. A value of 0.4 was used
as an approximate weighted average representing a typical mix
of dietary fats and assuming the proportions were not substantially
changed. If a more substantial weight loss occurs, a correction
could be made for this, ideally by using the data on
changes in weight and HDL concentrations internal to the study.
562S IS DIETARY FAT A DETERMINANT OF BODY FAT?
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