my investigation of the weston a. price foundation & it's attack on the conventional wisdom that "saturated fats & cholesterol are bad and people should consume as little as possible" led me to the talk page of the wikipedia article on "saturated fat" (the article has serious NPOV problems), where I found this fascinating several paragraphs. the author is apparently anonymous.
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The scientific picture is unclear. Much of the early research into possible links between dietary fat consumption and cardiovascular disease involved young- and middle-aged American men. For this group, there is a positive corrleation between serum LDL levels and cardiovascular morbidity and mortality. For elderly men, the correlation is actually negative, i.e., those with lower LDL levels tend to have higher cardiovascular morbidity and mortality. For women, there is no correlation. In some studies outside the U.S., the correlations seen in American males don't hold up. Since nondietary factors such as stress can affect both serum cholesterol levels and susceptibility to cardiovascular disease, a cause-and-effect relationship between saturated fat consumption and disease outcomes isn't easily established.
The effect of saturated fat consumption on LDL cholesterol levels has been studied extensively, with mixed results. It seems that a rise in serum LDL can be reliably produced in some specific test subjects by feeding them increased amounts of specific saturated fatty acid sources (e.g., coconut oil, which is high in lauric and myristic acids). The broad picture points in the direction of a link, but when the numerous studies are evaluated comparatively, generalizations are hard to make.
Some observational evidence, most notably Willett's Nurses Health Study at Harvard, supports the theory that saturated fat is atherogenic, though it appears to be much less so than trans fat. Arriving at such conclusions requires adjusting for a number of lifestyle-related confounders such as smoking, exercise habits, and vegetable consumption, leaving the disease implication of trans fat quite clear-cut but that of saturated fat much less so.
No dietary intervention (feeding) trial has ever produced a decrease in cardiovascular disease outcomes through dietary reduction of saturated fat and, thereby, reduction of serum LDL levels. The Lyon trial, which compared an artificially-constructed Mediterranean-type diet (intervention group) against a lowfat diet (control group), is sometimes cited in this regard, as it called for, among other things, replacing butter with olive oil. The experiment was terminated early by its ethics committee due to much higher mortality in the control group than in the intervention group. Two factors make it incorrect to conclude that a reduction in saturated fat was responsible for the improvement in outcomes. First, average serum LDL levels remained virtually identical between the two groups throughout the course of the experiment. Second, due to culinary considerations, the intervention group was supplied free of charge with a specially-formulated margarine as an alternative to olive oil. The margarine was made with a low-erucic acid rapeseed oil (similar to canola oil) in an attempt to mimic olive oil's high content of monounsaturated fat. Some researchers believe that the experimental outcome may have been primarily the result of introducing a substantial source of the essential omega-3 fat alpha-linolenic acid (ALA), in which Western diets are typically deficient and in which rapeseed oil is rich.
The notion of ALA's importance was bolstered by a study published in October, 2006 in the Journal of the American College of Cardiology. It found that walnuts, a rich source of ALA, reduce the typical postprandial rise in inflammatory markers that normally follows consumption of a meal high in saturated fat. This suggests that saturated fat may be dangerous primarily when consumed in a diet deficient in ALA.
Cardiovascular events have been reduced in clinical studies of LDL-lowering statin drugs, but this is now widely considered to be at least in part due to these drugs' antiinflammatory properties. Notably, at least one study has produced favorable outcomes with a statin chemically modified to make it incapable of lowering LDL.
Finally, within the past three years or so, advanced imaging techniques have made it possible to directly study the growth of arterial lesions over time. While this mode of investigation is still in its infancy, one such study has already implicated polyunsaturates in the growth of arterial plaque and cleared saturates and monounsaturates.
In short, while it is true that saturated fat is widely characterized as "artery-clogging" by health authorities and in the popular press, the scientific picture is unresolved. If saturated fat is ultimately given a clean bill of health, this will be the most embarassing dietary advice reversal in the history of medicine, so it seems likely that a mountain of contradictory evidence will have to accumulate before the medical community budges.
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posted by 83.95.117.36 13:04, 23 April 2007 (UTC)
