Jerry Stamler on the Tierney-Taube Critique of Epidemiology and ‘Diet-Heart’

To: The Editor, Science Times

The Tierney piece “Diet and Fat…” (Science Times, Oct. 9, 2007) was long on viewpoint, assertion, and allegation, short on scientific facts. Permit me to set down key facts:

1. Animal Experimentation: For 100 years, laboratory investigators have induced atherosclerosis (hardening of the arteries), including severe atherosclerosis, the lesion causing most heart attacks and many strokes, by feeding diets “enriched” with cholesterol (e.g., from egg) and fat to mammalian and avian species, herbivorous/carnivorous/omnivorous including non-human primates (monkeys, baboons). No evidence exists for the notion that the human species – unlike others – is immune to the adverse long-term effects of such diets on arteries; extensive evidence exists to the contrary (summarized below).
2. Clinical investigation: Since the 1920s, when first generation cardiologists learned how to diagnose non-fatal myocardial infarction (MI) (heart attack), evidence has accumulated that MI victims have high blood cholesterol, high blood pressure, diabetes, obesity and are smokers more frequently than expected by chance: the earlier in life the MI, the more likely these adverse findings; MI victims rarely have favorable levels of all these risk factors.
3. Metabolic ward studies: In the post- WW II decades, multiple controlled experiments in metabolic wards demonstrated that several dietary changes sizably reduced average blood cholesterol levels, particularly decreased intake of saturated fat, cholesterol, and trans fat; increased intake of polyunsaturated fat and water—soluble fiber; weight loss. Among many investigators accomplishing these studies, two outstanding research groups made particular contributions – Ancel Keys and colleagues (University of Minnesota), Mark Hegsted and colleagues (Harvard University) – both disparaged without cause by Tierney.
4. Biochemical and pharmaceutical research: Konrad Bloch was appropriately awarded a Nobel Prize for his years-long meticulous research on the multiple biochemical steps involved in liver synthesis of cholesterol, starting from the small acetate molecule. This work, including identification of the rate-limiting (slowing) step and the enzyme catalyzing it, became the basis for pharmaceutical development of the statins, drugs that markedly lower blood cholesterol by blocking its synthesis at the rate-limiting step.
5. Clinical trials: Multiple large-scale long-term tests – double-blind randomized controlled trials – demonstrated that sustained high-order (30-40+%) reduction of blood cholesterol to favorable (well under 200mg/dl) levels slowed, stopped, reversed atherosclerosis in coronary and other arteries, prevented first an recurrent heart attacks, and prolonged life. These data dramatically confirmed prior evidence on efficacy of long term serum cholesterol falls (e.g., with diet, and the drugs cholestyramine and nicotinic acid). Other clinical trials had earlier demonstrated that sustained blood pressure reduction by modern drugs effectively prevented heart attacks and strokes and prolonged life of people with high blood pressure. Correspondingly, multiple trials showed that improved eating patterns (epitomized by the DASH diet) sizably reduced adverse blood pressure levels in prehypertensive and hypertensive adults. These diets – emphasizing higher intakes of fruits, vegetables, whole grains, beans, seeds/nuts, low fat and fat free dairy products, fish/shellfish, and lower intakes of red meats, fats (total and saturated), eggs, sweets, salt – also lower blood cholesterol.
6. Epidemiologic research: From the late 19th century on, multiple population studies have yielded concordant findings: Across populations, the higher the population average dietary saturated fat and cholesterol intake, the higher the population average serum cholesterol and the higher the coronary heart disease (CHD) rate, a 3-way relationship that has been unequivocally established; these relations are consistent in repeated studies (including for 22 countries, Tierney to the contrary not withstanding); with increase over the post-WW II decades in population average intake of these fats in many countries, CHD rates increased; with decreased intake in other countries, CHD rates declined. In the U.S. sizable declines in population average intake of saturated fat/cholesterol (also in total fat) from the 1960s to the 1990s led to declines in average blood cholesterol from about 240mg/dl to about 200mg/dl (despite the obesity epidemic), achieving a national health goal (all too little heralded). As shown repeatedly in studies of migrants, conspicuously in Japanese Americans compared to Japanese in Japan, and as indicated by the evidence just cited on short-term population trends, the driving forces behind the marked cross population differences in coronary rates are lifestyle differences (not differences in population genetics), and consequent differences in population average levels of key established major CHD risk factors, especially blood cholesterol.

Within Populations-Epidemiologic Studies of Individuals:

For individuals within populations (e.g., individual Americans in three large Chicago studies, the Framingham Study, the large MRFIT screen study, etc. etc.), the higher the person’s blood cholesterol, non-HDL-cholesterol, LDL-cholesterol, blood glucose, blood pressure, body mass, the greater the risk of coronary and cardiovascular disease; smoking compounds risk at any and all levels of these major established risk factors; effects are combinative; in a high percentage of American adults, two or more of these major risk factors are high, placing them at especially high risk. Dietary/exercise habits influence levels in individuals of the major metabolic risk factors. In the fewer studies with adequate research funding to study dietary habits of individuals in depth, dietary cholesterol/saturated fat relates significantly not only to blood cholesterol at baseline, but also to long-term coronary risk (e.g., 25-year follow-up data of the Chicago Western Electric Study). Given commonality of high cholesterol/saturated fat/calorie intake among middle-aged Americans, only a small percentage (less than 10%) have favorable levels of all five readily measured major risk factors – blood cholesterol/glucose/blood pressure/body mass and are not smokers. They are low risk; for them, likelihood of experiencing coronary disease in minimal – reduced 90% compared to all others. The disease ceases to be epidemic in its onslaught. Large Harvard population studies – of nurses, other health professionals – report similar favorable consequences of low risk, defined based on favorable levels of multiple dietary and physical activity traits, as well as non-smoking.

In summary, massive concordant evidence from multiple research disciplines has been accumulated over decades of research. This evidence is the foundation for the repeated judgment by independent expert research groups that adverse lifestyles, especially adverse eating patterns (including high intakes of cholesterol/saturated fat/trans fat/total fat), cause the coronary epidemic. The first such statement, in 1960, for the American Heart Association (AHA), prepared by a group of researchers under the chairmanship of senior scientist Dr. Irvine H. Page, issued after undergoing repeated review, noted the causative connection and drew the appropriate inference: by improving population lifestyles, first and foremost eating habits, it may be possible to prevent coronary disease. Since then, repeated AHA scientific statements – up to and including the most recent on a year or two ago – have refined and affirmed the etiologic inference and the public health recommendations; similarly from other expert groups, e.g., those periodically reviewing and up-dating the “Dietary Guidelines for Americans” for the U.S. Departments of Agriculture/Health and Human Services; the expert groups preparing concordant statements for the American Cancer Society, the American Diabetes Association, the World Health Organization, government public health departments in Great Britain/Scandinavian countries/Italy/etc. These groups worldwide have all been made up of independent scientists of their successive generations. Tierney’s viewpoint inferring that they have been incompetent biased is just not credible.

Americans – and people from other countries – have heard the recommendations and have to a degree acted on them (despite repeated efforts, mainly from special commercial interests, to counter them). For example, dietary fat composition and amounts are healthier today than in 1960, and (as noted) average serum cholesterol levels are down. Smoking rates are down. And, the bottom line, coronary death rates are down more than 50%, stroke death rates even more. The flank of the epidemic has been turned – but the epidemic has yet to be ended. And there are problems: witness the obesity epidemic, apparently still waxing. The discussion here is on matters of prime public health importance – this is no ivory tower scholastic matter. Given that fact, it must be said straight out: Tierney’s piece is non-science, fatally flawed; Science Times has a responsibility to do it right. (Jeremiah Stamler).