And from "The Cholesterol Myths" by Uffe Ravnskov, M.D., Ph.D.:
(10). But the Israeli study did not support the words of Diet and Health, because total cholesterol, not LDL-cholesterol, had the strongest relationship to risk of coronary disease.
The second paper claimed by the Diet and Health-authors was a 1977 report from the Framingham Study by Dr. Tavia Gordon and her colleagues (11). This study concerned HDL cholesterol, however. Only logistic regression coefficients (a statistical concept unknown to most doctors) for coronary disease on LDL-cholesterol were given, and one of the conclusions of the paper was that ”LDL-cholesterol ...is a marginal risk factor for people of these age groups” (men and women above 50 years). Some of the coefficients were indeed low. For women above the age of 70 it was negative, which means that women at that age ran a greater risk of having a heart attack if their LDL-cholesterol was low than if it was high. Thus, there was no support either from Gordon's paper.
Also, the third paper (12) concerned HDL-cholesterol only. No support again.
The fourth reference was to the National Cholesterol Education Program, which produced another large review without original data (13). One of its conclusions was that ”a large body of epidemiologic evidence supports a direct relationship between the level of serum total and LDL-cholesterol and the rate of CHD.” The large body of evidence was to be found in three references. The first one was another large review without original data, Optimal resources for primary prevention of atherosclerotic disease (14), with Dr. Kannel as the first author. I shall return to their review below.
The next reference was yet a large review (15), but nothing in that review was said about the connection between the LDL-level and the incidence of coronary heart disease.
The last reference was an analysis of various lipoproteins as risk factors in the Honolulu Heart Study (16). The conclusion of that paper was that ”both measures of LDL-cholesterol were related to CHD prevalence, but neither appeared to be superior to total cholesterol”.
Before I discuss Kannel's review I shall mention another conclusion in the National Cholesterol Education Program: ”The issue of whether lowering LDL-cholesterol levels by dietary and drug interventions can reduce the incidence of CHD has been addressed in more than a dozen randomized clinical trials”. This is a most misleading statement because at that time, in 1988, only four randomized trials including LDL-cholesterol analysis had previously been published (17), and only in one of them the number of heart attacks was lowered significantly.
Let me now return to the review by Kannel and colleagues, the one used as evidence by the authors of The Cholesterol Education Program, which in turn was used as evidence by the authors of Diet and Health. Almost nothing was written about LDL-cholesterol in Kannel's review except for the following (page 164A): ”Longitudinal studies within populations show a consistent rise in the risk of CHD in relation to serum total cholesterol and LDL-cholesterol at least until late middle-age”.
A little more cautious conclusion than in Diet and Health, it may seem, but even for this prudent statement the evidence was weak. References to six studies were given. In two of them LDL-cholesterol was not analysed or mentioned at all (18); in two reports LDL-cholesterol was only correlated to the prevalence of heart disease (19); in one report two tables was aimed at the subject (tables 8 and 9) and showed that the predictive power of LDL-cholesterol was statistically nonsignificant (20); in one study LDL-cholesterol was predictive for heart disease, but only for men between 35 and 49 and for women between 40 and 44 (21).
In conclusion, the ”large body of evidence” was cooked down to one single study, which showed a predictive value for LDL-cholesterol but for a few age groups only. LDL-cholesterol is neither centrally nor causally important, it has not the strongest and most consistent relationship to risk of CHD, it has not a direct relationship to the rate of CHD, and it has not been studied in more than a dozen randomized trials.
But how then has the idea of the bad cholesterol emerged? As mentioned in the National Cholesterol Education Program, there are two main reasons. First, there was the discovery of a defective LDL-receptor in familial hypercholesterolemia and its consequence, the extremely high level of LDL-cholesterol in the blood of individuals with this disease. The discoverers, Nobel prize winners Michael Brown and Joseph Goldstein, suggested that the high LDL-cholesterol was the direct cause of the vascular changes seen in such individuals and also suggested that a similar mechanism was operating in the rest of us (22). Second, feeding experiments in animals raised the animals' LDL-cholesterol and produced vascular changes that have been called atherosclerosis by the experimentators.
These arguments are weak, however. If LDL-cholesterol were the devil himself LDL-cholesterol would clearly be a better predictor than total cholesterol, because the latter include also the ”good” HDL-cholesterol. And experiments on animals can only be suggestive and cannot prove anything about human diseases. Besides, the vascular findings in laboratory animals do not look like human atherosclerosis at all, and it is impossible to induce a heart attack in animals by diet alone (23). And finally, findings pertaining to people with a rare genetic error in cholesterol metabolism are not necessarily valid for the rest of us (24).
Thus, the experimentors claim support from unsupportive epidemiological and clinical studies, and the epidemiologists and the clinicians claim support from inconclusive experimental evidence. The victims of this miscarriage of justice are an innocent and useful molecular construction in our blood, producers and manufacturers of animal fat all over the world, and millions of healthy people who are frightened and badgered into eating a tedious and flavorless diet that is said to lower their bad cholesterol.
Read also:
Ravnskov U. High cholesterol may protect against infections and atherosclerosis recently published in Quarterly Journal of Medicine (2003;96:927-34).
10. Medalie JH and others. Five-year myocardial infarction incidence-II. Association of single variables to age and birthplace. Journal of Chronic Diseases 1973;26:325-349.
11. Gordon T. and others. High density lipoprotein as a protective factor against coronary heart disease. American Journal of Medicine 1977;62:707-714.
12. Watkins LO and others. Racial differences in high-density lipoprotein cholesterol and coronary heart disease incidence in the usual-care group of the multiple risk factor intervention trial. American Journal of Cardiology 1987;57:538-545.
13. The Expert Panel. Report of the National Cholesterol Education Program expert panel on detection, evaluation, and treatment of high blood cholesterol in adults. Archives of Internal Medicine 1988;148:36-69.
14. Kannel WB and others. Optimal resources for primary prevention of atherosclerotic diseases. Atherosclerosis study group. Circulation 1984;70:157A-205A.
15. Grundy SM. Cholesterol and coronary heart disease: a new era. JAMA 1986;256:2849-2858.
16. Hulley SB, Rhoads GG. The plasma lipoproteins as risk factors: comparison of electrophoretic and ultracentrifugation results. Metabolism 1982;31:773-777.
17. The Multiple Risk Factor Intervention Trial (MR.FIT), the Newcastle trial, the Lipid Research Clinic's trial, and the Helsinki Heart Study.
18. Yaari S and others. Associations of serum high density lipoprotein and total cholesterol with total, cardiovascular, and cancer mortality in a 7-year prospective study of 10000 men. The Lancet 1981;1:1011-1015.
- Ancel Keys. Seven Countries. A multivariate analysis of death and coronary heart disease. Harvard University Press 1980.
19. Rhoads GG, Gulbrandsen CL, Kagan A. Serum lipoproteins and coronary heart disease in a population study of Hawaii Japanese men. New England Journal of Medicine 1976;294:293 298.
- The Pooling Project Research Group. Relationship of blood pressure, serum cholesterol, smoking habit, relative weight and ECG abnormalities to incidence of major coronary events: final report of the pooling project. Journal of Chronic Diseases 1978;31:201-306.
20. Conference on the health effects of blood lipids: Optimal distributions for populations. Workshop report: Epidemiological section. Preventive Medicine 1979;8:612. No LDL data were presented in that report either.
21. Kannel WB, Castelli WP, Gordon T. Cholesterol in the prediction of atherosclerotic disease. New perspectives based on the Framingham study. Annals of Internal Medicine 1979;90:85 91.
22. Brown MS, Goldstein JL. How LDL receptors influence cholesterol and atherosclerosis. Scientific American 1984;251:52-60.
23. For more details, read the papers by William Stehbens
24. Ravnskov U. An elevated serum cholesterol is secondary, not causal, in coronary heart disease. Medical Hypotheses 1991;36:238-41.
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