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American Journal of Clinical Nutrition, Vol. 72, No. 1, 204-205, July 2000
© 2000 American Society for Clinical Nutrition

Letter to the Editor

Reply to R Sichieri

George A Bray and Barry M Popkin

Pennington Biomedical Research Center 6400 Perkins Road Baton Rouge, LA 70808-4124 E-mail: brayga{at}mhs.pbrc.edu

Dear Sir:

The continuing discussion of the relation between body fat and obesity is of value for the perspectives it raises. Sichieri argues that in Brazil the increasing prevalence of obesity has not been accompanied by an increase in fat consumption.

As we have pointed out, fat is only one component of the energy that is eaten and it is an imbalance between total energy intake and energy expenditure that ultimately leads to obesity. However, fat is a particularly important nutrient for several reasons. First, it does not stimulate its own oxidation. Second, it is more energy dense than the other nutrients and energy density has been implicated in control of energy intake. Third, stores of fat are >100 times the daily intake of fat and the storage depot provides an enormous reservoir for continued accumulation of energy. In animals fed high-fat diets, obesity is an expected event, although some strains resist this dietary change. It is unlikely that humans differ from other animals and escape this biological inevitability, although given the same access to high-fat diets not all individuals become obese. Finally, it is likely that there is an interaction between the level of activity and the risk of developing obesity when eating a high-fat diet. Such a relation would tie the changes in energy expenditure to the effects modulating energy intake. Several studies showed that obese individuals have impaired handling of fat that tends to lead to recrudescence of obesity.

The data presented by Sichieri in the accompanying letter need to be juxtaposed with data published in 1990 by the World Health Organization on the relation between fat intake and the prevalence of obesity in Brazil (1). What is missing in Sichieri's data set is the relation of fat intake in Brazil to the development of obesity. The data from the World Health Organization report are reproduced here because they are not widely known (Figure 1Go). Shown in the figure is that as the fat content of the Brazilian diet increased, body mass index in Brazil also increased (1).



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  		FIGURE 1.. Household diet and adiposity in Brazil according to dietary staples (adapted from reference 1).

 
In reanalyzing the data we published earlier, we found that the effect of a lower-fat diet on weight loss differed between overweight persons and normal-weight persons (2; Figure 2Go). Astrup et al (3) found a similar difference in the response to a low-fat diet between normal-weight and overweight subjects. This newer analysis incorporated an additional 7 studies (4–10). Thus, we continue to believe that dietary fat is an important contributor to the development of obesity in populations with increasing fat intake and that dietary fat contributes to the development and maintenance of obesity in genetically predisposed persons eating high-fat diets (11).



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  		FIGURE 2.. The effect of a reduction in the percentage of energy from fat on grams of weight lost per day. From reference 2.

 

REFERENCES

  1. World Health Organization. Consultation for the first global analysis of diet in relation to chronic diseases. World Health Organ Tech Rep Ser 1990;797.
  2. Richards MK, Paeratakul S, Bray GA, Popkin BM. Current theories regarding the influence of diet and the control of obesity. In: Wilson T, Temple N, eds. Frontiers in preventive nutrition. Totowa, NJ: Humana Press (in press).
  3. Astrup A, Ryan L, Grunwald GK, et al. The role of dietary fat in body fatness: evidence from a preliminary meta-analysis of ad libitum low-fat dietary intervention studies. Br J Nutr (in press).
  4. Baer JT. Improved plasma cholesterol levels in men after a nutrition education program at the worksite. J Am Diet Assoc 1993;93:658–63.[Medline]
  5. Weststrate JA, van het Hof KH, van den Berg 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 antioxidant levels and haemostasis variables. Eur J Clin Nutr 1998;52:389–95.[Medline]
  6. Stefanick ML, Mackey S, Sheehan M, Ellsworth N, Haskell WL, Wood PD. Effects of diet and exercise in men and postmenopausal women with low levels of HDL cholesterol and high levels of LDL cholesterol. N Engl J Med 1998;339:12–20.[Abstract/Free Full Text]
  7. Thuesen L, Henriksen LB, Engby B. One-year experience with a low-fat, low-cholesterol diet in patients with coronary heart disease. Am J Clin Nutr 1986;44:212–9.[Abstract/Free Full Text]
  8. Knopp RH, Walden CE, Retzlaff BM, et al. Long-term cholesterol-lowering effects of 4 fat-restricted diets in hypercholesterolemic and combined hyperlipidemic men: The Dietary Alternatives Study. JAMA 1997;278:1509–15.[Abstract/Free Full Text]
  9. Simon MS, Heilbrun LK, Boomer A, et al. A randomized trial of a low-fat dietary intervention in women at high risk for breast cancer. Nutr Cancer 1997;27:136–42.[Medline]
  10. Pritchard JE, Nowson CA, Wark JD. Bone loss accompanying diet-induced or exercised-induced weight loss: a randomized controlled study. Int J Obes Relat Metab Disord 1996;20:513–20.[Medline]
  11. Bray GA, Popkin BM. Dietary fat does affect obesity! Am J Clin Nutr 1998;68:1157–73.



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