There is a growing body of evidence that suggests high fat intake may specifically contribute to overeating and obesity, more so than other dietary energy sources like carbohydrates. Although fat is energy dense, it appears to have a weak effect on satiety (3). In contrast to the carbohydrates, fat oxidation seems to be is largely unrelated to fat intake, and dietary fats are more efficiently used and more readily converted to body fat (3). In fact, recent evidence suggests that carbohydrates may not make a significant contribution to body fat in humans under normal feeding conditions in humans (3). Finally, there is longitudinal data that point to a causal relationship between fat intake and weight gain over time in certain individuals (3).
Official recommendations are based on the evidence that reduced fat, particularly saturated fat, leads to a reduction in serum cholesterol, a known risk factor for coronary heart disease. Some investigators have also postulated that a reduction in fat intake may decrease mortality from breast, colon, and prostate cancers (4-6). Browner and colleagues have estimated that if the population were to follow the current dietary recommendations for fat intake, coronary heart disease mortality rates could decrease as much as 20% depending on age (7). Based on their assumptions of the relationship between fat intake and heart disease and cancer, they have also estimated that 42,000 of the 2.3 million adult deaths oc- g curring in the U.S. each year could be deferred (7). j
The general consensus is that both the quantity and type of dietary fat are t?
important in preventing certain chronic diseases such as coronary heart disease.
The Eskimos, for example, ingest mainly a high fat diet of fish, and experience ^
less coronary heart disease and thrombosis than persons eating the high fat diets that contain mostly saturated fats (9). The major mechanism would seem to be the effects of the fats on the proportion of serum cholesterol associated with the high-density lipoproteins (HDL) as compared with the serum cholesterol associated with the low-density lipoproteins (LDL). That is, the diets that have a higher proportion of polyunsaturated fats, such as those diets that contain fish and certain vegetable sources or the monounsaturated (e.g. olive oil) fats, tend to reduce the
Food Product Fat Mimetics
risk from CHD. Conversely, diets rich in saturated fats increase the ratio of LDL-cholesterol to HDL-cholesterol increasing the risk of a coronary heart disease incident (9,10). However, it is not quite as simple as it seems because different saturated fats and dietary sources of saturated fat have different influences on the level of LDL-cholesterol (11). For example, dairy products which are high in myristic acid (14:0) appear to increase levels of LDL-cholesterol whereas beef fat, containing palmitic (16:0) and stearic (18:0) acids, do so to a lesser extent and cocoa butter, with a high proportion of stearic acid, increases LDL-choles-terol only slightly. This would strongly indicate that other dietary constituents are interacting and playing a vital role in this process.
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