![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Center for Human Nutrition, University of Colorado Health Sciences Center, Denver, CO 80262
3To whom correspondence and reprint requests should be addressed.
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONThe role of dietary...SUMMARYREFERENCES |
|---|
KEY WORDS: • body weight regulation • energy balance
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONThe role of dietary...SUMMARYREFERENCES |
|---|
), and the prevalence is increasing
in most countries around the world (WHO 1998
). Although
genetics appear to play a major role in the regulation of body weight
(Bouchard and Tremblay 1997
), the rapid increase in the
prevalence of obesity in the U.S. over the past two decades suggests
that environmental factors are promoting, or at least favoring obesity
in susceptible individuals. These factors must be identified to
initiate successful public health efforts to prevent obesity and its
associated health risks.
The human body has some ability to regulate energy in that energy
intake
(EI)4
can be adjusted to energy expenditure (EE) and vice versa. The fact
that body weight is maintained at a relatively constant level in most
people over many years suggests that this must be the case. Studies of
over- and underfeeding show that EE is altered to compensate for and to
oppose changes in energy balance (EBAL)
(Horton et al. 1995
, Roberts et al. 1996
). However, these changes are not sufficient to completely
counter the effects on EI, and a change in body mass results. When the
over- or underfeeding stops, subjects tend to return to their initial
body weights, usually by adjusting EI, again suggesting that some
regulation occurs. The rapid increase in the prevalence of obesity
suggests that environmental factors are exerting constant pressure to
increase EI and decrease EE, and that the strength of these factors is
overriding the strength of our defense mechanisms (Fig. 1
).
|
). In this paper, we review evidence for the role of
dietary fat in regulating energy balance and promoting the development
of obesity. |
The role of dietary fat in regulating energy balance |
|---|
|
TOPABSTRACTINTRODUCTIONThe role of dietary...SUMMARYREFERENCES |
|---|
Diets that contain 30% or more of energy from fat reliably produce
obesity in rats, mice, dogs and primates as a result of increased EI
and efficiency of energy storage (Hill et al. 1989
,
Sclafani 1989
, West and York 1998
).
Alternatively, obesity is rare in animals fed a low fat (LF) diet
(<20%), even when animals are maintained in small cages that limit
physical activity. Although there are strains and some animals within
strains that resist becoming obese when fed HF diets
(Pagliassotti et al. 1997
), the chances of becoming
obese increase with increasing dietary fat (Salmon and Flatt 1985
). Dietary obesity can be reversed by switching rodents
from a HF to a LF diet, but the extent to which this occurs depends on
the extent and duration of the dietary obesity (Hill et al. 1989
).
Laboratory studies in human subjects.
Several groups have studied the effect of diet composition on
short-term (
2 wk) energy regulation in humans in which the
outcome was a surrogate for development of obesity, such as change in
EI or in energy or fat balance (Lissner et al. 1987
,
Stubbs et al. 1995
, Thomas et al. 1992
).
The advantage of these studies is the precision with which the
composition of the diet can be manipulated, the self-selection of
foods, and the use of measured rather than self-reported intake.
Limitations include the need for subjects to consume required foods and
differences in palatability and energy density between diets.
Nonetheless, results are remarkably consistent with almost every study,
showing higher total EI (~200 to 700–800 kcal/d) when consuming a HF
diet (>40% of total energy). Subjects may consume more with
consumption of HF diets because of the higher energy density
(Stubbs et al. 1995
), palatability (Schiffman et al. 1998
) or other behavioral or metabolic differences
(Reed et al. 1992
). However, most of these studies
compared diets containing 40% or more energy from fat to those
containing 20% or less. In human subjects, we have very little
information about the effects of dietary fat intake between 20 and 40%
on energy intake.
The mechanisms by which excess dietary fat leads to positive
EBAL have been investigated in a number of
paradigms. Dietary-induced thermogenesis (DIT) is lower when HF
diets are consumed, compared with LF diets (Flatt et al. 1985
). However, at an intake of 2000 kcal/d, the difference in
DIT between a 20 and a 40% fat diet (assuming protein is constant)
would be very small (~24 kcal/d). A more important factor is the
efficiency with which excess dietary fat is stored. A greater
proportion of excess energy is stored during fat overfeeding
(~90–95%) compared with an equivalent amount of carbohydrate
overfeeding (~75–85%) (Horton et al. 1995
).
Carbohydrate overfeeding produced progressive increases in carbohydrate
oxidation and total EE, whereas fat overfeeding had minimal effects of
fat oxidation and total EE. Although these differences may not persist
during extended overfeeding, repeated bouts of HF overfeeding could
lead to an accumulation of more excess energy than would repeated bouts
of carbohydrate overfeeding. This scenario probably occurs in most
individuals on a day-to-day basis.
Epidemiologic studies.
Most, but not all cross-sectional studies show a modest positive
relationship between dietary fat intake and one or more indices of
obesity (Lissner and Heitmmann 1995
). There are major
limitations to these studies, including reliance on self-reported
EI, adjustments for potential confounders, the inability of diet
surveys to capture variability in dietary fat intake and the fact that
group comparisons do not always characterize obesity in a population
with accuracy. In the Diet and Nutrition Survey of British Adults, for
example, the mean body mass index was similar in habitual LF (<35%)
and HF (>45%) consumers, although the distribution was skewed to the
right in the latter group (Blundell and Macdiarmid 1997
).
Clinical trials.
We identified 12 prospective, randomized-control trials (RCT) in 13
cohorts that compared a LF diet with a usual or control diet, and EI
was measured (Table 1
). Eight of these studies were 
1 y in duration. These studies produced
reductions in self-reported dietary fat intake of 2.8–18% with
concomitant decreases in EI of 40–570 kcal/d (Bloemberg et al. 1991
, Boyar et al. 1988
, Boyd et al. 1990
, Buzzard et al. 1990
, Gatenby et al. 1997
, Kasim et al. 1993
, Lee-Han et al. 1988
, Pritchard et al. 1996
, Sheppard et al. 1991
, Simon et al. 1997
, Stefanick et al. 1998
, Weststrate et al. 1998
). Reducing
intake of dietary fat also appears to be effective in reducing body
weight. A recent review (Bray and Popkin 1998) found 28
intervention studies where subjects were asked to reduce dietary fat
without energy restriction. There was an average weight loss of 1.6
g/day for each 1% reduction in dietary fat. A recent meta-analysis
indicated that in 15 of 16 identified studies, reducing dietary fat led
to a greater, yet modest decrease in body weight (2.5 kg, 95%
confidence interval = 1.5–3.5 kg, P < 0.0001)
compared with the control groups (Astrup et al., unpublished
data). There were significant positive correlations between the
reduction in dietary fat and amount of weight loss (r
= 0.37) and between initial body weight and weight loss
(r = 0.52). This latter result suggests that the
greatest effect of a LF diet on weight loss might be seen in overweight
subjects. However, none of these studies were specifically designed to
assess the effects of a reduction in dietary fat on either body weight
or EI, and few studies examined the effects in overweight or obese
individuals.
|
has been used as
evidence that LF diets are not effective in producing weight loss
(Willett 1998
). Hypercholsteremic, moderately overweight
men were assigned to one of four dietary conditions (22, 25, 26, and
27% fat). Because all groups lost an equivalent amount of body weight
(2–3 kg), Willett (1998)
has argued that decreasing
dietary fat does not contribute to weight loss. This is an unconvincing
argument. First, the range of differences in dietary fat across groups
was small. Second, it may be that the reduction to 27% accounted for
the majority of the weight loss effects and that further reductions
provided minimal additional benefit. There may exist a threshold of
dietary fat below which the changes of overeating are small and above
which they are high. At present, it is not known if such a threshold
exists or whether it is the same in all populations. Low fat diets and the prevention of weight regain.
Additional support for the role of LF diets in regulating body weight
comes from studies of formerly obese individuals, a group considered to
be at high risk for weight regain. After weight loss induced by an
energy-restricted diet, weight regain at 2 y was less in
subjects assigned to an ad libitum LF diet (5.4 kg) than those
consuming a fixed energy intake diet (11.3 kg) (Toubro and Astrup 1997
). Subjects in the National Weight Control Registry,
a database of over 2000 individuals successfully maintaining a weight
loss of at least 30 pounds for at least 1 y, report eating a diet
low in fat (24%) and participating in very high levels of physical
activity (Klem et al. 1997
).
|
SUMMARY |
|---|
|
TOPABSTRACTINTRODUCTIONThe role of dietary...SUMMARYREFERENCES |
|---|
Exactly why HF diets promote excess EI is not clearly understood,
although energy density appears to be an important factor
(Poppitt and Prentice 1996
, Roberts et al. 1998
). Nonetheless, reducing dietary fat is still a desired
outcome, although a better understanding of energy density may lead to
additional ways to modify the diet to prevent obesity. Whether
manipulations in energy density, palatability and variety of snack
foods play a role in reducing ad libitum intake of dietary fat requires
more investigation.
There is an immediate need for research aimed at achieving population reductions in dietary fat intake. However, a food supply that is high in fat is not the only factor promoting obesity in the U.S. Although not the focus of this review, it is clear from the literature that declining levels of physical activity are also contributing to the obesity epidemic. In a physically active society, our food supply might not produce high levels of obesity. We should expand our public health efforts to reduce dietary fat intake and increase physical activity.
We must move beyond the debate about the role of high fat diets in producing obesity. The message to the public should be to advocate consumption of a low fat diet, with <30% of calories coming from fat. Although we lack definitive data to suggest that this level is appropriate for the entire population, the available data suggest that this level of fat intake should greatly reduce the likelihood of overeating in most individuals.
|
FOOTNOTES |
|---|
2 Supported by National Institutes of Health Grants DK42549 and DK48520.
4 Abbreviations used: DIT, dietary-induced thermogenesis; EBAL, energy balance; EE, energy expenditure; EI, energy intake; HF, high fat; LF, low fat; RCT, randomized control trial.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONThe role of dietary...SUMMARYREFERENCES |
|---|
1.
Bloemberg B. P., Kromhout D., Goddijn H. E., Jansen A., Obermann-de Boer G. L. The impact of the Guidelines for a Healthy Diet of The Netherlands Nutrition Council on total and high density lipoprotein cholesterol in hypercholesterolemic free-living men. Am. J. Epidemiol. 1991;134:39-48
2.
Blundell J. E., Macdiarmid J. I. Passive overconsumption. Fat intake and short-term energy balance. Ann. N.Y. Acad. Sci. 1997;827:392-407
3. Bouchard C., Tremblay A. Genetic influences on the response of body fat and fat distribution to positive and negative energy balances in human identical twins. J. Nutr. 1997;127(suppl. 5):943S-947S
4. Boyar A. P., Rose D. P., et al Response to a diet low in total fat in women with postmenopausal breast cancer: a pilot study. Nutr. Cancer 1988;11:93-99[Medline]
5.
Boyd N. F., Cousins M., et al Quantitative changes in dietary fat intake and serum cholesterol in women: results from a randomized, controlled trial. Am J Clin Nutr 1990;52:470-476
6. Buzzard I. M., Asp E. H., et al Diet intervention methods to reduce fat intake: nutrient and food group composition of self-selected low-fat diets. J. Am. Diet. Assoc. 1990;90:42-50, 53[Medline]
7. Flatt J. P., Ravussin E., et al Effects of dietary fat on postprandial substrate oxidation and on carbohydrate and fat balances. J. Clin. Investig. 1985;76:1019-1024
8. Flegal K. M., Carroll M. D., et al Overweight and obesity in the United States: prevalence and trends, 1960–1994. Int. J. Obes. 1998;22:39-47[Medline]
9.
Gatenby S. J., Aaron J. I., et al Extended use of foods modified in fat and sugar content: nutritional implications in a free-living female population. Am. J. Clin. Nutr. 1997;65:1867-1873
10. Hill J. O., Dorton J., et al Reversal of dietary obesity is influenced by its duration and severity. Int. J. Obes. 1989;13:711-722[Medline]
11.
Horton T. J., Drougas H., et al Fat and carbohydrate overfeeding in humans: different effects on energy storage. Am. J. Clin. Nutr. 1995;62:19-29
12. Insull W., Jr, Henderson M. M., Prentice P. L., Thompson D. J., Clifford C., Goldman S., Gorbach S., Moskowitz M., Thompson R., Woods M. Results of a randomized feasibility study of a low-fat diet. Arch. Int. Med. 1990;150:421-427[Abstract]
13.
Kasim S. E., Martino S., et al Dietary and anthropometric determinants of plasma lipoproteins during a long-term low-fat diet in healthy women. Am. J. Clin. Nutr. 1993;57:146-153
14.
Klem M. L., Wing R. R., et al A descriptive study of individuals successful at long-term maintenance of substantial weight loss. Am. J. Clin. Nutr. 1997;66:239-246
15. Knopp R. H., Walden C. E., et al Long-term cholesterol-lowering effects of 4 fat-restricted diets in hypercholesterolemic and combined hyperlipidemic men. The Dietary Alternatives Study. J. Am. Med. Assoc. 1997;278:1509-1515[Abstract]
16.
Lee-Han H., Cousins M., et al Compliance in a randomized clinical trial of dietary fat reduction in patients with breast dysplasia. Am. J. Clin. Nutr. 1988;48:575-586
17. Lissner L., Heitmann B. L. Dietary fat and obesity: evidence from epidemiology. Eur. J. Clin. Nutr. 1995;49:79-90[Medline]
18.
Lissner L., Levitsky D. A., et al Dietary fat and the regulation of energy intake in human subjects. Am. J. Clin. Nutr. 1987;46:886-892
19.
Pagliassotti M. J., Gayles E. C., et al Fat and energy balance. Ann. N.Y. Acad. Sci. 1997;827:431-448
20. Poppitt S. D., Prentice A. M. Energy density and its role in the control of food intake: evidence from metabolic and community studies. Appetite 1996;26:153-174[Medline]
21. Pritchard J. E., Nowson C. A., et al Bone loss accompanying diet-induced or exercise-induced weight loss: a randomised controlled study. Int. J. Obes. Relat Metab. Disord. 1996;20:513-520[Medline]
22. Reed D. R., Friedman M. I., et al Experience with a macronutrient source influences subsequent macronutrient selection. Appetite 1992;18:223-232[Medline]
23. Roberts S. B., Fuss P., et al Effects of age on energy expenditure and substrate oxidation during experimental overfeeding in healthy men. J Gerontol. A Biol. Sci. Med. Sci. 1996;51:B148-B157[Abstract]
24. Roberts S. B., Pi-Sunyer F. X., et al Physiology of fat replacement and fat reduction: effects of dietary fat and fat substitutes on energy regulation. Nutr. Rev. 1998;56:S29-S41discussion S41–S49
25. Salmon D. M., Flatt J. P. Effect of dietary fat content on the incidence of obesity among ad libitum fed mice. Int. J. Obes. 1985;9:443-449[Medline]
26. Schiffman S. S., Graham B. G., et al Orosensory perception of dietary fat. Curr. Dir. Psychol. Sci. 1998;7:137-143
27. Sclafani A. Dietary-induced overeating. Ann. N.Y. Acad Sci. 1989;575:281-289[Medline]
28.
Sheppard L., Kristal A. R., et al Weight loss in women participating in a randomized trial of low-fat diets. Am. J. Clin. Nutr. 1991;54:821-828
29. Simon M. S., Heilbrun L. K., et al A randomized trial of a low-fat dietary intervention in women at high risk for breast cancer. Nutr. Cancer 1997;27:136-142[Medline]
30.
Stefanick M. L., Mackey S., et al Effects of diet and exercise in men and postmenopausal women with low levels of HDL cholesterol and high levels of LDL cholesterol [see comments]. N. Engl. J. Med. 1998;339:12-20
31.
Stubbs R. J., Harbron C. G., et al Covert manipulation of dietary fat and energy density: effect on substrate flux and food intake in men eating ad libitum. Am. J. Clin. Nutr. 1995;62:316-329
32.
Thomas C. D., Peters J. C., et al Nutrient balance and energy expenditure during ad libitum feeding of high-fat and high-carbohydrate diets in humans. Am. J. Clin Nutr. 1992;55:934-942
33.
Toubro S., Astrup A. Randomised comparison of diets for maintaining obese subjects’ weight after major weight loss: ad lib, low fat, high carbohydrate diet v fixed energy intake. Br. Med. J. 1997;314:29-34
34. West D. B., York B. Dietary fat, genetic predisposition, and obesity: lessons from animal models. Am. J. Clin. Nutr. 1998;67(suppl. 3):505S-512S[Abstract]
35. Weststrate J. A., van het Hof K. H., et al A comparison of the effect of free access to reduced fat products or their full fat equivalents on food intake, body weight, blood lipids and fat-soluble antioxidants levels and haemostasis variables. Eur. J. Clin. Nutr. 1998;52:389-395[Medline]
36. Willett W. C. Dietary fat and obesity: an unconvincing relation. Am. J. Clin. Nutr. 1998;68:1149-1150[Medline]
37. World Health Organization Obesity: Preventing and Managing the Global Epidemic 1998 World Health Organization Geneva, Switzerland.
This article has been cited by other articles:
|
|
 |
|
  H. Zhang, X. Chen, J. Aravindakshan, and M. R. Sairam Changes in Adiponectin and Inflammatory Genes in Response to Hormonal Imbalances in Female Mice and Exacerbation of Depot Selective Visceral Adiposity by High-Fat Diet: Implications for Insulin Resistance Endocrinology, December 1, 2007; 148(12): 5667 - 5679. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Morens, M. Keijzer, K. de Vries, A. Scheurink, and G. van Dijk Effects of high-fat diets with different carbohydrate-to-protein ratios on energy homeostasis in rats with impaired brain melanocortin receptor activity Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2005; 289(1): R156 - R163. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
