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J Am Coll Cardiol, 2004; 44:1934-1935, doi:10.1016/j.jacc.2004.08.008 © 2004 by the American College of Cardiology Foundation |
Retired Medical Inspector of the Italian State Railways, CP 671, 60001-970 Fortaleza (CE), Brazil
(Email: baschetti{at}baydenet.com.br).
Nothing in biology makes sense except in the light of evolution.Theodosius Dobzhansky, 1973
Considering that humankind and its metabolic physiology are biological products of evolution, one might well ask why Weinberg's report (1) not only ignores the evolutionary arguments supporting the dietheart hypothesis, but also advances the evolutionarily untenable thesis that the low-fat, high-carbohydrate diet is responsible for the current epidemics of obesity, type II diabetes, and the metabolic syndrome.
Weinberg seems to forget that the low-fat, high-carbohydrate diet represents the diet "for which human beings are in essence genetically programmed" (2), because their metabolic physiology has been evolutionarily molded by a nutritional environment in which, for millions of years, that diet was practically the sole one available to our ancestors (3). For 99% of its evolution, humankind indeed lived mainly on fruits and vegetables, which consist essentially of carbohydrates, and consumed little fat, because game was very lean and cattle-breeding, chicken farming, butter, dairy products, margarines, and oils did not exist (2).
Weinberg fails to note that coronary heart disease and type II diabetes were virtually absent in some traditional populations that ate mainly carbohydrates and consumed two to three or even five times less fat than Westerners (2). As evidence that the dietheart hypothesis is correct, those populations, after their switch to Western diets, are currently facing epidemics of cardiovascular disease (2), type II diabetes (2,3), and obesity (3).
Weinberg also fails to note that in rural China, where dietary energy derives mostly from carbohydrates and the consumption of fat is less than one-half that of Americans, coronary artery disease mortality is 16.7-fold lower than that in the U.S. (3). As an additional support of the dietheart hypothesis, in urban China the proportion of cardiovascular disease deaths rose from 12.1% in 1957 to 35.8% in 1990 because of the greatly increased fat consumption, favored by the global availability of cheap vegetable oils (2).
Weinberg's critique of the dietheart hypothesis is based on the misleading results of dietary trials, most of which investigated the effects of diets that were called "low-fat" inappropriately. As a paradigmatic example, if we consider that diets exceeding 10% to 15% of energy as fat were virtually impossible in the low-fat nutritional environment that shaped our metabolic physiology (3), the expression "low fat" is inappropriate to define a diet providing 31% of energy as fat (4). The beneficial effects of an evolutionarily defined low-fat diet providing only 10% of energy as fat are unquestionable (5).
Weinberg argues that low-fat, high-carbohydrate diets are unhealthy because they decrease high-density lipoprotein (HDL) cholesterol and increase triglycerides. However, populations that consume mostly carbohydrates, despite having low HDL cholesterol, are virtually free from coronary heart disease (2). Moreover, the low-fat, high-carbohydrate diet, instead of increasing triglycerides, may actually reduce them, as long as sugar intake is kept low (5), to limit the harmful effectscaused by sugars consumed in solid forms or in solutions exceeding the physiologic limit imposed by evolution, namely 4.18 MJ/l (3).
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R. Baschetti Definition of low-fat diets. Arch Intern Med, July 10, 2006; 166(13): 1419 - 1420. [Full Text] [PDF] |
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