The biology of obesity

First in Series on Obesity Topic:

The cornerstone of any dietary treatment of obesity is reduction of energy intake, and sustainment of a lower energy intake to prevent weight regain. Camilla Verdich, PhD, and colleagues discuss the role of fat, carbohydrates and protein on body weight

By the year 2000, being overweight or obese was more common than being normal weight among the adult population in many European countries and the US.1 Although fat intake is one of the potential obesity-promoting factors that has gained more attention in obesity research, the role of fat intake in the development of obesity is still controversial, and the findings are not consistent.2 In animal models, changing from a low-fat diet to a high-fat diet leads to an increase in body fat and an increase in the inter-individual and inter-strain variation in body fat, suggesting a genetic susceptibility to becoming obese on a high-fat diet.3,4

Cross-sectional studies have indicated positive associations between dietary fat energy per cent and body weight, but such studies cannot distinguish between the possible effects of obesity on fat intake, vice versa, or common effects on both obesity and fat intake of an underlying third factor.

There are some paradoxical observations regarding the relationship between reported fat intake and obesity that raise the suspicion that there is no simple relation between the two. In the US and in many European countries, fat intake has decreased during the last decade, whereas the prevalence of obesity has increased. This may be interpreted as an indication that reducing dietary fat may not lead to a concomitant reduction in obesity. However, increased under-reporting of fat intake may bias these observations,5 and subgroups of the population may have increased their fat intake and become obese, whereas others may have reduced their fat intake.

In line with the findings from animal models, a high habitual fat energy percentage has been shown to be associated with a high mean body mass index, as compared to low-fat consumers.6 Another common feature between animal and human studies is that between-subject variation is higher in high-fat consumers, and that some individuals appear to be protected from developing obesity even when consuming a high-fat diet.6

Camilla Verdich, PhD, and TIA Sorensen, PhD, are at Copenhagen University Hospital, Denmark. Karine Clement, Fabienne Foufelle, PhD, and P Ferre are with INSERM, France, the French National Institute for Health and Medical Research. Excerpted from Functional Foods, Ageing and Degenerative Disease, C Remacle and B Reusens, editors. ISBN 0-8493-2538-2. Published by Woodhead Publishing Ltd, England. http://www.woodheadpublishing.com/

References
1. Strauss RS, Pollack HA. Epidemic increase in childhood overweight, 1986-98. JAMA 2001; 286(22):2845-8.
2. Lissner L, Heitmann BL. Dietary fat and obesity: evidence from epidemiology. Eur J Clin Nutr 1995; 49(2):79-90.
3. West DB, et al. Dietary obesity in the mouse: interaction of strain with diet composition. Am J Physiol 1995; 268(3):R658-R665.
4. Salmon DM, Flatt JP. Effect of dietary fat content on the incidence of obesity among ad libitum fed mice. In J Obes 1985; 9(6):443-9.
5. Heitmann BL, et al. Do we eat less fat, or just report so? Int J Obes Relat Metab Disord 2000; 24(4):435-42.
6. Macdiarmid J, et al. High and low fat consumers, their macronutrient intake and body mass index: further analysis of the National Diet and Nutrition Survey of British Adults. Eur J Clin Nutr 1996; 50(8):505-12.

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