Dietary fat and body fat: is there a relationship?

Abstract

Excess body fat accounts for approximately 30 to 40% of coronary heart disease, many cancers of several types, most cases of adult onset diabetes, and a substantial proportion of cases of disabling osteoarthritis. Diet and lifestyle factors are the primary reasons for the high rates of overweight among individuals in the United States; migrating populations from countries with minimal adiposity who come to the United States typically gain substantial weight. For example, Japanese men living in San Francisco had a threefold higher prevalence of obesity compared with those in Japan. In addition, the major secular increases in adiposity within populations, including the general U.S. population, cannot be explained by genetic factors. Dietary fat is often held responsible for these high rates of adiposity. Indeed, a primary justification for recommendations to reduce dietary fat is an expected reduction in obesity. Several reasons exist to support the hypothesis that a high percentage of energy from fat in the diet may lead to greater body fat: (1) dietary fat is the most energy-dense macronutrient in the diet, (2) fats give flavor and palatability to foods, which could increase their consumption, and (3) fat produces a lower thermogenic effect than carbohydrate and thus may be utilized more efficiently. Finally, Flatt has suggested that carbohydrate intake, but not fat intake, is regulated; therefore, individuals on a high-fat diet will tend to consume more total energy to gain the same amount of carbohydrate as those on the low-fat diet. For these reasons, it is reasonable to examine whether the fat composition of the diet has an important relationship to body fat. The prevalence of overweight in affluent countries with high-fat intakes tends to be higher than in poorer regions of the world with low-fat diets. However, this relationship is seriously confounded by differences in the availability of food and level of physical activity between rich and poor countries. Among European countries, where economic differences are less stark, no association was observed between the national percentage of energy from fat and median body mass index (BMI) for men, and for women the relation was inverse. It is notable that, as fat intake has declined as a percent of energy over the last 25 years in the United States, the prevalence of obesity has dramatically increased. Cross-sectional studies between dietary fat and body fatness within populations have been inconsistent. Unfortunately, such studies are prone to artifactual associations because both avoidance of dietary fat and caloric restraint in avoiding overweight have become strongly linked with general health consciousness in recent years. Because of the serious potential for confounding that is extremely difficult to control, both cross-sectional and prospective observational studies are likely to be particularly unhelpful in determining the causal relationship between the fat composition of diets and body fat. Randomized trials are clearly the most desirable way to determine the effects of dietary fat on body fat, but surprisingly few long-term studies have been designed to address this issue. In short-term randomized trials, lasting from a few weeks to 6 months, modest weight losses (,1–2 kg) are typically seen when 10 to 15% of energy from fat is replaced by carbohydrate. Because these effects are small and potentially transient, only long-term studies can determine the efficacy of fat reduction as a method of weight control. In the few long-term randomized trials of the effect of fat reduction on body weight that have been conducted to date, weight reduction was usually not the primary outcome. Those lasting 1 year or more are summarized in Figure 1. In general, only small differences in weight (1–2 kg) were seen, and weight losses on low-fat diets were not cumulative over time. In the study of Kasim et al., fat intake among overweight women was reduced to 17.6% of energy at 1 year, therefore providing a major contrast in diets. The difference in weight change between intervention and control groups was somewhat greater than in the other studies (2.6 kg); however, lean Address correspondence and reprint requests to Dr. Walter C. Willett, Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA. This paper was delivered at the October 23–25, 1997 conference “The Determination, Treatment, and Prevention of Obesity,” which was sponsored by the Institute of Nutrition, University of North Carolina at Chapel Hill; Department of Nutrition, School of Public Health and School of Medicine, University of North Carolina at Chapel Hill; and School of Medicine, East Carolina University, in cooperation with the North American Association for the Study of Obesity, the National Institutes of Health, the American Cancer Society, and Eli Lilly & Company. Received November 6, 1997; accepted April 16, 1998.