Conclusion

We have reviewed several dietary components that have been implicated in the pathogenesis of cardiovascular disease. The contribution of most nutrients appears to revolve around their ability to influence the serum lipid profile - total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, and the various apoproteins.

There is a need to look beyond serum lipids, however. Besides influencing a specific set of measurable laboratory parameters, nutrients must impact the pathogenesis of disease through biochemical and molecular alterations at the cellular level. This milieu of biochemical reactions and interactions is ultimately the most consequential to the dietary pathogenesis, prevention, and therapy of cardiovascular disease. We will doubtless continue to receive information about the important benefits of “nutrient A” on “function B,” and physicians, scientists, patients, and the public will try to make sense of these assertions.

Yet one must remember that nutrients are but small components of the whole chemical “package” that makes up a particular food or group of foods. Other properties of additional components in food may work synergistically or antagonistically, or act as innocent bystanders in cardiovascular disease chemo-protection and pathogenesis. It is unlikely that in years to come a single nutrient - will be uncovered as “the cause” of CAD. More likely, further investigation will describe the subtle interactions of various dietary components with an individual’s genome, in concert with other cardiovascular risk factors, such as tobacco use, diabetes mellitus, hypertension, hypoestrogene-mia, stress, and obesity. Researchers probably will demonstrate that it is not just one or two nutrients or dietary factors that are critical, but the diet as a whole.

Consider an 88-year-old, generally healthy man who had a verified consumption of 20 to 30 whole eggs per day (Kern 1991). Despite this incredibly high daily cholesterol intake (12,953 micromoles), his total cholesterol was only 5.18 mmol per liter (200 mg per deciliter), and his LDL-cholesterol was 3.68 mmol per liter (142 mg per deciliter). It appears that he had compensated for his dietary excess by excreting excess cholesterol bound in bile acids in his stool. Thus, how an individual utilizes the diet biochemically may be as important as the diet itself.

We are not yet in a position to predict which people will do well with high cholesterol intake and which will not. In the meantime, it is prudent to follow the recent dietary guidelines of the National Research Council, which stress a diet containing 15 to 20 percent of calories from protein, 25 to 30 percent of calories from dietary fat, and the remaining calories from complex carbohydrates, such as whole grains, vegetables, and fruits.

These guidelines were put forward as death rates from CAD were falling, and there is no shortage of advocacy groups ready and willing to take credit for this reduction. But it is most probably the result of many lifestyle changes, among them declining use of tobacco (at least in the United States, when considered for all members of the population combined); better emergency medical services; improved inhospital treatments; and, of course, dietary modifications. As noted, change in diet has a particular appeal as an explanation because it is the only one of these factors that daily affects each and every member of society. And, as the new millennium dawns, it would seem that dietary intervention to prevent CAD has proved to be a successful means of secondary prevention for those people who have already incurred a cardiac event, even if the utility of such intervention as a means of primary prevention, applied to entire populations, remains controversial.

We should also bear in mind that the debate over diet and heart disease is being conducted in a very public arena, and an arena in which diet and heart disease are only one aspect of a more general tension over questions focusing on personal risk and responsibility. In the case of heart disease, these questions have stirred a broad-based popular reaction. No longer are discussions of diet and the heart confined to the pages of medical journals, but they can now be found in practically every issue of widely circulating newspapers and magazines. One good example is an extensive and detailed analysis questioning the overall importance of cholesterol in heart disease - indeed, dismissing “The Cholesterol Myth” - in the Atlantic Magazine (Moore 1989a). In the same year that this essay appeared, it was also published in expanded form as a book (Moore 1989b).

Public skepticism about the importance of diet in heart disease is also apparent in cartoons. One, in the New Yorker magazine (January 16, 1989: 39), shows a man starting to eat a huge oatmeal muffin. The caption reads:“Wellness update:Thirty-year-old man starting on the twenty-five-thousand-pound oat-bran muffin he must consume over forty years in order to reduce significantly his risk of death from high cholesterol.”

This and countless other less-than-reverent cartoons constitute widespread cultural markers that express a number of popular reactions to the diet-heart hypothesis. First, they ventilate frustration at the gospel of eating for one’s heart (or for health in general). And given a culture in which the average person is daily bombarded with images of food, with much of the easiest food to acquire and consume that which is likely to be least beneficial for preventing heart disease, this frustration is understandable. Such cartoons also reflect a general lack of conviction that altered diets will “work” against heart disease - a skepticism that primary prevention trials have thus far failed to address convincingly. At a lay level, most people know (or have heard of) someone who has lived to a ripe old age while engaging in near-constant dietary indiscretions, whereas someone who ate “right” and stayed fit may have suffered an early death. Epidemiologists might discount the relevance of such anecdotes, but they can have a major impact on popular perceptions of risk and disease, especially when the behavior that is being advocated may be neither easy nor (seemingly) pleasurable.

The popular reaction against dietary constraints also raises fundamental questions of personal versus public responsibility. If someone has CAD, whose fault is it? The choices people make about what to eat are limited by the cultural world in which they live, so to what extent is the larger society to be held responsible? And, if one is personally accountable for what foods are consumed, then should a “healthy lifestyle” make a difference in terms of how much one pays for health or life insurance?

Finally, what is the disease here? Is it CAD, or is it high cholesterol? We should not lose sight of the fact that blood lipids are merely surrogates for what is most important - the disability and death that come from CAD and CVD. Keeping track of these differences is important. First, it can help to maintain focus on the ultimate goals of therapy and not allow us to become sidetracked by that which is easier to effect. Second, it will prevent the labeling of a large percentage of the population as “diseased” simply because of a high lipid profile. The answers to the questions raised in this chapter are unlikely to come purely from the accumulation of more and more data, because the prevention controversies are also fueled by “hidden ideological, structural, and professional fac-tors”(Aronowitz 1994).

Melissa H. Olken Joel D. Howell

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