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    Cholesterol Myths by Uffe Ravnskov MD PhD: References


    Posted by .(JavaScript must be enabled to view this email address)
    Wednesday, November 12, 2014 9:30 am Email this article

    These are the references for the book
    The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease
    by Uffe Ravnskov, MD, PhD.

    [1] Olsson B. Hur upplevs deltagande i riskfak?tor? screning? Allmän Medicin 11, 144-147, 1990.

    [2] Keys A. Atherosclerosis: A problem in newer public health. Journal of Mount Sinai Hospital New York 20, 118-139, 1953.

    [3] Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodolo?gic note. The New York State Journal of Medicine 57, 2343-2354, 1957.

    Although Yerushalmy and Hilleboe were very critical of Keys’s ideas and his use of statistics, these authors were cited by Stamler as a support for the diet-heart idea. (Levy RI, Rifkind BM, Dennis BH, Ernst ND.(edit): Nutrition, Lipids, and Coronary Heart Disease. A Global View. Raven Press 1979, p. 32)

    [4] Kircher T, Nelson J, Burdo H. The autopsy as a measure of accuracy of the death certificate. The New England Journal of Medicine 313, 1263-1269, 1985.

    Carter JR. The problematic death certificate. The New England Journal of Medicine 313, 1285-1286, 1985.

    [5] Lundberg GD, Voigt GE. Reliability of a presumptive diagnosis in sudden unexpected deaths in adults. Journal of the American Medical Association 242, 2328-2330, 1979.

    [6] Zarling EJ, Sexton H, Milnor P. Failure to diagnose acute myocardial infarction. JAMA 250, 1177-1181, 1983.

    [7] Reid DD, Rose GA. Assessing the comparability of mortality statistics. British Medical Journal 2, 1437-1439, 1964.

    [8] Wolf, S. The Artery and the Process of Atherosclerosis (2). Plenum Press, New York 1972, tabell 2, p 31.

    [9] Keys, A. Coronary heart disease in seven countries. Circula?tion 41, suppl. 1, 1-211, 1970.

    [10] Masironi R. Dietary factors and coronary heart disease. Bulletin of the World Health Organization 42, 103-114, 1970.

    [11] Syt?kowski PA, Kannel, WB, D’Agostino RB: Changes in risk factors and the decline in mortality from cardiovascular disease. The Framingham Heart Study. The New England Journal of Medicine 322, 1635-41, 1990.

    [12] a. Oshima K. Statistical trend in the incidence of cerebrovas?cular accidents and coronary heart disease in Japan. In: Schettler G, Goto Y, Hata Y, Klose G (edit). International symposium on athero?sclerosis IV. Springer-Verlag, Berlin 1977.

    b. Kimura N. Changing patterns of coronary heart disease, stroke, and nutrient intake in Japan. Preventive Medicine 12, 222-227, 1983.

    c. Ueshima H, Tatara K, Asakura S. Declining mortality from ischemic heart disease and changes in coronary risk factors in Japan, 1956-1980. American Journal of Epidemiology 125, 62-72, 1987. The authors thought that the decreasing mortality was due to better treatment of high blood pressure, but it has never been shown that lowering the blood pressure has any effect on coronary heart disease; only stroke is prevented.

    [13] Guberan E. Surprising decline of cardiovascular mortality in Switzerland: 1951-1976. Journal of Epidemiology and Community Health 33, 114-120, 1979.

    [14] Mann’s descriptions of the Masai tribe is found in the following papers:

    a. Mann GV, Shaffer RD, Sandstead HH. Cardiovas?cular disease in the Masai. Journal of Atherosclerosis Research 4,289-312, 1964.

    b. Mann GV, Shaffer RD, Rich A. Physical fitness and immunity to heart-disease in Masai. The Lancet 2, 1308-1310, 1965.

    c. Mann GV, Shaffer R. Cholesteremia in pregnant Masai women. JAMA 197, 123-125, 1966.

    d. Mann GV, and others. Atherosclerosis in the Masai. American Journal of Epidemiology 95, 26-37, 1972.

    [15] Shaper AG. Cardiovas?cular studies in the Samburu tribe of northern Kenya. American Heart Journal 63, 437-442, 1962.

    Camel herdsmen in Somalia who live almost entirely on camel’s milk also have very low cholesterol values: Lapic?cirella V, and others. Enquete clinique, biologique et cardiogra?phique parmi les tribus nomades de la Somalie qui se nourissent seulement de lait. Bulletin of the World Health Organization 1962;27:681-97.

    [16] Biss K, Taylor CB and others. The Masai’s protection against atherosclero¬sis. Pathol Microbiol 35, 198-204, 1970.

    Ho K-J, Taylor CB and others. The Masai of East Africa: Some unique biologi¬cal characteristics. Arch Pathol 91, 387-410, 1971

    Biss K, Taylor CB and others: Some unique biologic characteristics of the Masai of East Africa. NEJM 284, 694-699, 1971.

    Biss K, Taylor CB and others. Atherosclerosis and lipid metabolism in the Masai of East Africa. African J Med Sci 2, 249-257, 1971

    [17] Taylor knew how to decide whether their cholesterol metabolism was inherited or not. In the US he studied a 24-year-old Masai student and found that his cholesterol was as low as that of his comrades back in Kenya, a finding he claimed was a proof of his idea. But to use a determination from only one individual as a scientific proof is appalling bearing in mind the great variations of blood cholesterol between different human beings.

    [18] Day J, and others. Anthropo?me?tric, physiological and biochemical differences between urban and rural Maasai. Atheroscle?ro?sis 23, 357-361, 1976

    [19] Keys A. Coronary heart disease - the global picture. Atherosclerosis 22, 149-192, 1975.

    [20] Charters AD, Arya BP. Incidence of ischaemic heart-disease among indians in Kenya. The Lancet 1, 288-289, 1960.

    [21] Malhotra SL, Epidemiology of ischaemic heart disease in India with special reference to causation. British Heart Journal 29, 895-905, 1967.

    [22] Zukel WJ, and others. A short-term community study of the epidemiology of coronary heart disease. American Journal of Public Health 49, 1630-1639, 1959.

    [23] Finegan A, and others. Diet and coronary heart disease: dietary analysis on 100 male patients. American Journal of Clinical Nutrition 21, 143-148, 1968.

    [24] Kushi LH, and others. Diet and 20-year mortality from coronary heart disease. The Ireland-Boston diet-heart study. The New England Journal of Medicine 312, 811-818, 1985.

    [25] Gordon T, and others. Diet and its relation to coronary heart disease and death in three populations. Circulation 63, 500-515, 1981.

    [26] McGee DL, and others. Ten-year incidence of coronary heart disease in the Honolulu heart program. Relationship to nutrient intake. American Journal of Epidemiology 119, 667-676, 1984.

    [27] Ravnskov U. The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. Journal of Clinical Epidemiology 51, 443-460, 1998.

    [28] National Research Council. Diet and health. Implica?tions for reducing chronic disease risk. Washington D.C. 1989, National Academy Press. The citation is found on page 193.

    [29] Gotto AM, LaRosa JC, Hunninghake D, and others. The cholesterol facts. A summary of the evidence relating dietary fats, serum cholesterol, and coronary heart disease. A joint statement by the American Heart Association and the National Heart, Lung, and Blood Institute. Circulation 81, 1721-33, 1990. The citation is found on page 1725.

    [30] Kannel WB. The role of cholesterol in coronary atherogenesis. Medical Clinics of North America 58, 363-379, 1974.

    [31] Stamler J, Wentworth D, Neaton JD. Is relationship between serum cholesterol and risk of premature death from coronary heart death disease continuous and graded? JAMA 256, 2823-2828, 1986.

    [32] To be statistically correct deciles are not defined in this way, but as all diet-heart papers have used this definition I have done it also to avoid confusion.

    [33] Kannel WB, Castelli WP, Gordon T. Cholesterol in the prediction of atherosclerotic disease. Annals of Internal Medicine 90, 85-91, 1979.

    [34] Anderson KM, Castelli WP, Levy D. Cholesterol and mortality. 30 years of follow-up from the FraminghamStudy. JAMA 257, 2176-2180, 1987.

    [35] Simons LA and coworkers. Risk factors for coronary heart disease in the prospective Dubbo study of Australian elderly. Atherosclerosis 117, 107-118, 1995.

    [36] Zimetbaum P and others. Arteriosclerosis 12, 416-423, 1992

    [37] Krumholz HM and coworkers. Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years. JAMA 272, 1335-1340, 1994.

    [38] Gotto AM, LaRosa JC, Hunninghake D, and others. The cholesterol facts. A summary of the evidence relating dietary fats, serum cholesterol, and coronary heart disease. A joint statement by the American Heart Association and the National Heart, Lung, and Blood Institute. Circulation 81, 1721-33, 1990.

    [39] Castelli WP and others. Cardiovascular risk factors in the elderly. American Journal of Cardiology 63, 12H-19H, 1989.

    [40] Claude Lenfant, the director of NHLBI recently answered a critical paper by the journalist Thomas Moore by claiming that, according to the Framingham study, high blood cholesterol was a risk factor for old people of both sexes. (The Atlantic, jan. 1990, p. 8).

    [41] Oliver MF. The optimum serum cholesterol. The Lancet 2, 655, 1982.

    [42] Jacobs D, and others. Report of the conference on low blood cholesterol: Circulation 86, 1046-60, 1992

    [43]Forette B, Tortrat D, Wolmark Y. Cholesterol as risk factor for mortality in elderly women. The Lancet 1, 868-870, 1989. Ironically, in my practice it is usually old women who are worrying about their cholesterol level.

    [44] Dagenais GR, and others. Total and coronary heart disease mortality in relation to major risk factors - Quebec cardiovascular study. Canadian Journal of Cardiology 6, 59-65, 1990.

    [45] Shanoff HM, Little JA, Csima A. Studies of male survivors of myocardial infarction: XII. Relation of serum lipids and lipoproteins to survival over a 10-year period. Canadian Medical Association Journal 103, 927-931, 1970

    [46] a: Gertler MM et al. American Journal of the Medical Sciences 247, 145-155, 1964; b: Frank CW, Weinblatt E, Shapiro S. Circulation 47, 509-517, 1973; c: Mulcahy R, et al. British Heart Journal 37, 158-165, 1975; d: Schatzkin A et al. American Journal of Epidemiology 120, 888-899, 1984; e: Khaw KT, Barrett-Connor E. Journal of Cardiopulmonary Rehabilitation 6, 474-480, 1986; f: Olsson G, Rehnqvist N. Cardiology 74, 457-464, 1987

    [47] Carlson LA, Böttiger LE, Åhfeldt P-E. Risk factors for myocardial infarction in the Stockholm prospec?tive study. Acta Medica Scandinavica 206, 351-360, 1979.

    [48] Böttiger LE, Carlson LA. Risk factors for death for males and females. Acta Medica Scandinavica 211, 437-442, 1982.

    [49] Beaglehole R, and others. Cholesterol and mortality in New Zealand Maoris. British Medical Journal 1, 85-287, 1980.

    [50] Shestov DB and coworkers. Increased risk of coronary heart disease death in men with low total and low-density-lipoprotein cholesterol in the Russian Lipid Research Clinics prevalence follow-up study. Circulation 88, 846-853, 1993

    [51] Craig WE, Palomaki GE, Haddow JE. Cigarette smoking and serum lipid and lipoprotein concentrations: an analysis of published data. British Medical Journal 298, 784-788, 1989. This is a meta-analysis of 54 studies of lipid levels in smokers and non-smokers. Total cholesterol was 3 percent, VLDL 10.4 percent, LDL 1.7 percent and triglycerides 9.1 percent higher among smokers, and HDL 5.7 percent lower than among non-smokers. Interestingly, the authors thought that part of the explanation for the risk of smoking is its effects on the blood lipids; they did not consider the possibility that the changes of the blood levels may be secondary.

    [52] Dattilo AM, Kris-Etherton PM. Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis. American Journal of Clinical Nutrition 56, 320-328, 1992.

    [53] Assmann G, Schulte H. The prospective cardiovascular Münster study: prevalence and prognostic significance of hyperlipidemia in men with systemic hypertension. American Journal of Cardiology 59, 9G-17G, 1987.

    [54]Dimsdale JE, Herd A. Variability of plasma lipids in response to emotional arousal. Psychosomatic Medicine 44, 413-430, 1982. Rosenman RH. Relationships of neurogenic and psychological factors to the regulation and variability of serum lipids. Stress Medicine 9, 133-140, 1993.

    [55] Even the Nobel Award winners Joseph Goldstein and Michael Brown have looked at Keys’s illustrations only and mention only the great difference between Finland and Japan. (Brown MS, Goldstein JL. How LDL-receptors influence cholesterol and atherosclerosis. Scientific American 251, 52-60, 1984)

    [56] Keys A, and others. Lessons from serum cholesterol studies in Japan, Hawaii and Los Angeles. Annals of Internal Medicine 48, 83-94, 1958.

    [57] Worth RM, and others. Epidemiologic studies of coronary heart disease and stroke in Japanese men living in Japan, Hawaii and California: mortality. American Journal of Epidemiology 102, 481-490, 1975.

    [58]a: Marmot MG, Syme SL. Acculturation and coronary heart disease in Japanese-americans. American Journal of Epidemio?logy 104, 225-247, 1976. b: Marmot MG, and others. Epidemiologic studies of coronary heart disease and stroke in Japanese men living in Japan, Hawaii and California: Prevalence of coronary and hyperten?sive heart disease and associated risk factors. American Journal of Epidemiology 102, 514-525, 1975.

    [59] Conference of the health effects of blood lipids: optimal distributions for populations. Workshop report: Epidemiologi?cal section. Preven?tive Medi?cine 8, 609-766, 1979.

    [60] Kannel WB, Doyle JT, Ostfeld AM, et al. Optimal resources for primary prevention of atherosclerotic diseases. Atherosclerosis study group. Circulation 1984;70:157A-205A. The quotation is found on page 164A.

    [61] National Research Council. Diet and health. Implications for reducing chronic disease risk. Washington D.C. 1989, National Academy Press. The quotation is found on page 166.

    [62] Ekelund L-G, and others. Physical fitness as a predictor of cardiovascular mortality in asymptomatic North American men. The Lipid Research Clinics mortality follow-up study. The New England Journal of Medicine 319, 1379-84, 1988.

    [63] Thompson PD, and others. High density lipoprotein metabolism in endurance athletes and sedentary men. Circulation 84, 140-152, 1991.

    [64] Pocock SJ and others. High density lipoprotein cholesterol is not a major risk factor for ischaemic heart disease in British men. British Medical Journal 292, 515-519, 1986.

    [65] Gordon DJ and others. High-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies.

    [66] Pocock SJ, Shaper AG, Phillips AN. Concentrations of high density lipoprotein cholesterol, triglycerides, and total cholesterol in ischaemic heart disease. British Medical Journal 298, 998-1002, 1989. Circulation 79, 8-15, 1989.

    [67] Keys A. and others. HDL serum cholesterol and 24-year mortality of men in Finland. International Journal of Epidemiology 13, 428-435, 1984.

    [68] Fumeron F. and others. Lowering of HDL2-cholesterol and lipoprotein AI particle levels by increasing the ratio of polyunsaturated to saturated fatty acids. American Journal of Clinical Nutrition 53, 655-659, 1991.

    [69]

    [70] Medalie JH and others. Five-year myocardial infarction incidence-II. Association of single variables to age and birthplace. Journal of Chronic Diseases 26, 329-349, 1973.

    [71] Gordon T. and others. High density lipoprotein as a protective factor against coronary heart disease The American Journal of Medicine 62, 707-714, 1977.

    [72] 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 57, 538-545, 1987.

    [73] 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 148, 36-69, 1988.

    [74] Kannel WB and others. Optimal resources for primary preven?tion of atherosclerotic diseases. Atheroscle?rosis study group. Circulation 70, A157A-205A, 1984.

    [75] Grundy SM. Cholesterol and coronary heart disease: a new era. JAMA 256, 2849-2858, 1986

    [76] Hulley SB, Rhoads GG. The plasma lipoproteins as risk factors: comparison of electrophoretic and ultracentrifuga?tion results. Metabolism 31, 773-777, 1982.

    [77] The Multiple Risk Factor Interven?tion Trial (MR.FIT ), the Newcastle trial, the Lipid Research Clinic’s trial, and the Helsinki Heart Study. For references to these studies, see chapter 7.

    [78] a: Yaari and others. The Lancet 1981;1:1011-1015.; b. Keys A: Seven Countries. Harvard University Press 1980.

    [79] a. Rhoads GG, Gulbrandsen CL, Kagan A. Serum lipoproteins and coronary heart disease in a population study of Hawaii Japanese men. The New England Journal of Medicine 294, 293-298, 1976. b. The Pooling Project Research Group. Journal of Chronic Diseases 31, 201-306, 1978

    [80] Conference on the health effects of blood lipids: optimal distributions for populations. Preventive Medicine 8, 612-, 1979; table 8 and 9.

    [81] Kannel WB, Castelli WP, Gordon T. Cholesterol in the prediction of atherosclerotic disease. New perspectives based on the Framingham study. Annals of Internal Medicine 90, 85-91, 1979

    [82] Ravnskov U.Quotatin bias in reviews of the diet-heart idea. J Clin Epidemiol 48, 713-719, 1995.

    [83] Scientific Steering Committee on behalf of the Simon Broome Register Group. Risk of fatal coronary heart disease in familial hyper-cholesterolaemia. British Medical Journal 303, 893-896, 1991

    [84] Sijbrands EJG and others. Mortality over two centuries in large pedigree with familial hypercholesterolaemia: family tree mortality study. British Medical Journal 322, 1019-1023, 2001

    [85] Keys A, and others. Lessons from serum cholesterol studies in Japan, Hawaii and Los Angeles. Annals of Internal Medicine 48, 83-94, 1958.

    [86] a) Shaper AG. Cardiovascular studies in the Samburu tribe of northern Kenya. American Heart Journal 63, 437-442, 1962.

    b) Shaper AG, and others. Serum lipids in three nomadic tribes of northern Kenya. American Journal of Clinical Nutrition 13, 135-146, 1963.

    [87] Lapiccirella V., and others. Enquête clinique, biologique et cardiographique parmi les tribus nomades de la Somalie qui se nourissent seulement de lait. Bulletin of the World Health Organization 27, 681-697, 1962.

    [88] Prior IA, and others. Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau Island studies. American Journal of Clinical Nutrition 34, 1552-1561, 1981.

    [89] Stanhope JM, Sampson VM, Prior IAM. The Tokelau Island migrant study: serum lipid concentrations in two environments. Journal of Chronic Disease 34, 45-55, 1980.

    [90] Ramsay LE, Yeo WW, Jackson PR. Dietary reduction of serum cholesterol concentration: time to think again. British Medical Journal 303, 953-957, 1991

    [91] According to a personal communication from George Mann who was the director of this part of the Framingham study. George Mann left the project after three years before all data had been gathered.

    [92] Nichols AB, and others. Daily nutritional intake and serum lipid levels. The Tecumseh study. American Journal of Clinical Nutrition 29, 1384-1392, 1976.

    [93] Weidman WH, and others. Nutrient intake and serum cholesterol level in normal children 6 to 16 years of age. Pediatrics 61, 354-359, 1978.

    [94] Frank GC, Berenson GS, Webber LS. Dietary studies and the relationship of diet to cardiovascular disease risk factor variables in 10-year-old children - the Bogalusa heart study. The American Journal of Clinical Nutrition 31, 328-340, 1978

    [95] Morris JN, and others. Diet and plasma cholesterol in 99 bank men. British Medical Journal 1, 571-576, 1963.

    [96] Kroneld R, and others. Hälsobeteende och riskfak?torer för hjärt- och kärlsjukdomar i östra och sydvästra Finland. Suomen Lääkärilehti 45, 735-739, 1990.

    [97] Kahn HA, and others. Serum cholesterol: Its distribution and association with dietary and other variables in a survey of 10,000 men. Israel Journal of the Medical Sciences 5, 1117-1127, 1969. Stamler’s group performed a similar study on 1900 middle-aged men. This study is impossible for anyone but statisticians to evaluate, since absolute figures were absent. The relationship between the diet and heart mortality after the age of 19 was also studied, but again without giving any figures. Dietary saturated fat did not show any relationship with heart mortality, the authors admitted, but as their results were seen “within the context of the total literature,” they supported the diet-heart idea. (She?kelle RB., and others. Diet, serum cholesterol, and death from coronary heart disease. The Western Electric Study. The New England Journal of Medicine 304, 65-70, 1981)

    [98] Balogh M, Kahn HA, Medalie JH. Random repeat 24-hour dietary recalls. American Journal of Clinical Nutrition 24, 304-310, 1971.

    [99] Hopkins PN. Effects on dietary cholesterol on serum cholesterol: a meta-analysis and review. Am J Epidemiol 123, 221-234, 1986.

    [100] Katan MB and others. Am J Epidemiol 123, 221-234, 1986

    [101] Keys A. : A problem in newer public health. Journal of the Mount

    Sinai Hospital New York 20, 118-139, 1953.

    [102] Landé KE, Sperry WM. Human in relation to the cholesterol content of the blood serum. Archives of Pathology 22, 301-312, 1936.

    [103]Epstein FH, Ostrander LD. Detection of individual susceptibility toward coronary disease. Progress of Cardiovascular Diseases 13, 324-342, 1971. An association between cholesterol concentration and coronary was also recognized among individuals without the extreme manifestations of typical hyper?lipidemia or hypercholesterolemia, the authors wrote, a statement in conflict with the data of the paper and their own conclusions.

    [104] Paterson JC, Armstrong R, Armstrong EC. Serum lipid levels and the severity of coronary and cerebral in adequately nourished men, 60 to 69 years of age. Circulation 27, 229-236, 1963.

    [105] Mathur KS, and others. Serum cholesterol and in man. Circulation 23, 847-852, 1961.

    [106]Marek Z, Jaegermann K, Ciba T. and levels of serum cholesterol in postmortem investigations. American Heart Journal 63, 768-774, 1962.

    [107]Méndez J, Tejada C. Relationship between serum lipids and aortic atherosclerotic lesions in sudden accidental deaths in Guatemala City. American Journal of Clinical Nutrition 20, 1113-1117, 1967

    [108]Cabin HS, Roberts WC. Relation of serum total cholesterol and triglyceride levels to the amount and extent of coronary arterial narrowing by atherosclerotic plaque in coronary heart disease. American Journal of Medicine 73, 227-234, 1982.

    [109]Feinleib M, and others. The relation of antemortem characteristics to cardiovascular findings at necropsy. The Framingham study. 34, 145-157, 1979.

    [110]Okumiya N, and others. Coronary and antecedent risk factors: Pathologic and epidemiologic study in Hisayama, Japan. American Journal of Cardiology 56, 62-66, 1985.

    [111]Hatano S, Matsuzaki T. in relation to personal attributes of a Japanese population in homes for the aged. Int. Symp. of IV. Edit.: Schettler G, Goto Y, Hata Y, Klose G. Springer-Verlag N.Y. 1977, p 116-120.

    [112]Solberg LA, and others. Stenoses in the coronary arteries. The Oslo study. Laboratory Investigation 53, 648-655, 1985.Unsystematic relationships, selected autopsy studies and low correlation coefficients were also found in the following papers:

    Rhoads GG, and others. Coronary risk factors and autopsy findings in Japanese-American men. Laboratory Investigation 38, 304-311, 1978

    Reed DM, and others. Serum lipids and lipoproteins as predictors of atherosclerosis. An autopsy study. Atherosclerosis 9, 560-564, 1989.

    [113] Pearson TA. Coronary arteriography in the study of the epidemiology of coronary artery disease. Epidemiol. Rev. 6, 140-166, 1984. In his review Pearson mentions a number of angiographic studies which he claimed had found a relationship between blood cholesterol levels and degrees of. But three of them found no relationship; one of these is reference number 14 (see the text), the other two are: Nitter-Hauge S, Enge I. Relation between blood lipid levels and angiogra?phically evaluated obstructions in coronary arte?ries. British Heart Journal 35, 791-795, 1973 and Barboriak JJ, and others. Coronary artery occlusion and blood lipids. American Heart Journal 87, 716-721, 1974. An unsupportive study was ignored by Pearson: Fuster V, and others. Arteriogra?phic patterns early in the onset of the coronary syndromes. British Heart Journal 37, 1250-1255, 1975.

    [114] Cramér K, Paulin S, Werkö L. Coronary angiographic findings in correlation with age, body weight, blood pressure, serum lipids, and smoking habits. Circulation 33, 888-900, 1966.

    [115] Gore I, Hirst AE, Koseki Y. Comparison of aortic in the United States, Japan, and Guatemala. American Journal of Clinical Nutrition 7,50-54, 1959

    [116] Resch JA, Okabe N, Kimoto K. Cerebral. Geriatrics November 1969, 111-132.

    [117] Lindsay S, Chaikoff IL. Naturally occurring arteriosclerosis in animals: a comparison with experimentally induced lesions. In Sandler M, Bourne GH. (ed) Atherosclerosis and its origin. Academic Press, New York 1963, p 349-437.

    Detweiler DK, Ratcliffe HL, Luginbühl H. The significance of naturally occurring coronary and cerebral arterial disease in animals. Annals of the New York Academy of Science 149, 868881, 1968.

    [118] Vastesaeger MM. The contribution of comparative atherosclerosis to the understanding of human atherosclerosis. Journal of Atherosclerosis Research 8, 377-380, 1968.

    Stout C, Groover ME. Spontaneous versus experimental atherosclerosis. Annals of the New York Academy of Science 162,89-98, 1969.

    Stout LC, Bohorquez MS. Significance of intimal arterial changes in non-human vertebrates. Medical Clinics of North America 58, 245-255, 1974.

    Stehbens WE. An appraisal of cholesterol feedings in experimental atherogenesis. Progress of Cardiovascular Research 29, 107-128, 1986.

    Stehbens WE. Vascular complications in experimental atherosclerosis. Progress of Cardiovascular Research 29, 221-237, 1986.

    [119] Taylor CB, Manalo-Estrella P, Southworth J. Atherosclerosis in rhesus monkeys. II. Arterial lesions associated with hypercholesterolemia induced by dietary fat and cholesterol. Archives of Pathology 74, 16-34, 1962

    [120] Taylor CB, Patton DE, Cox GE. Atherosclerosis in rhesus monkeys. VI. Fatal myocardial infarction in a monkey fed fat and cholesterol. Archives of Pathology 76, 404-412, 1963.

    [121] Kramsch DM, and others. Reduction of coronary atherosclerosis by moderate conditioning exercise in monkeys on an atherogenic diet. The New England Journal of Medicine 305, 14831489

    [122] Cornfield J, Mitchell S. Selected risk factors in coronary disease. Archives of Environmental Health 19, 382-394, 1969.

    [123] Report of a research committee to the medical research council. Controlled trial of soya-bean oil in myocardial infarction. The Lancet 2, 693-700, 1968.

    [124] Leren P. The effect of plasma cholesterol lowering diet in male survivors of myocardial infarction. Acta Medica Scandinavica Suppl. 466, 1966.

    [125] Dayton S, and others. A controlled clinical trial of a diet high in unsaturated fat in preventing complications of atherosclerosis. Circulation 40, suppl. II, 1-63, 1969.

    [126] The Coronary Drug Project Research Group. The coronary drug project. Design, methods, and baseline results. Circulation 47, suppl. 1, 1-50, 1973.

    [127] Ibid. Initial findings leading to modifications of its research protocol. JAMA 214, 1303-1313, 1970.

    [128] Ibid. Findings leading to discontinuation of the 2.5-mg/day estrogen group. JAMA 226, 652-657, 1973.

    [129] Ibid. Findings leading to further modifications of its protocol with respect to dextrothyroxine. JAMA 220, 996-1008, 1972.

    [130] Ibid. Clofibrate and niacin in coronary heart disease. JAMA 231, 360-381, 1975.

    [131] 10.2 percent non-lethal heart attacks in the nicotinic acid group against 13.8 percent in the control group. Information about the number of suspect heart attacks was absent. This is not unimportant because the diagnosis “heart attack” is often doubtful; a more critical approach may have been used unintentionally in the nicotinic acid group. Information about both certain and suspect cases of thrombosis and stroke was given, however.

    [132] Canner PL, and others. Fifteen year mortality in coronary drug project patients: long-term benefit with niacin. Journal of the American College of Cardiology 8, 1245-1255, 1986.

    [133] Dorr AE and others. Colestipol hydrochloride in hypercholesterolemic patients-effect on serum cholesterol and mortality. Journal of Chronic Disease 31, 5-14, 1978.

    [134] The primary results from the WHO trial are found in British Heart Journal 40, 1069-1118, 1978, the follow-up results in Lancet 2, 379-385, 1980.

    [135] Salonen JT, Puska P, Mustaniemi H. British Medical Journal 2, 1178-1183, 1979.

    [136] Salonen JT. Primary prevention of sudden coronary death: a community-based program in North Karelia, Finland. Annals of the New York Academy of Science 382, 423-437, 1982.

    Tuomilehto J, and others. Decline in cardiovascular mortality in North Karelia and other parts of Finland. British Medical Journal 293, 1068-1071, 1986

    [137] Salonen JT. Did the North Karelia project reduce coronary mortality? The Lancet 2, 269, 1987.

    [138] Oliver MF. North Karelia project. Lancet 2, 518, 1987.

    [139] Hufvud?stadsbladet 23. juni 1988. The public in Finland does not yet know that the North Karelia project failed.

    [140] Hjermann I, Byre KV, Holme I, Leren P. Effect of diet and smoking intervention on the incidence of coronary heart disease. Report from the Oslo study group of a randomized trial in healthy men. The Lancet 1981;2:?1303-10.

    [141] The weight loss in the treatment group is easily overlooked because body weight was not given in kilogrammes but in relative body weight (body weight divided by the square of body height).

    [142] Kannel WB. New perspectives on cardiovascular risk factors. American Heart Journal 114, 213-219, 1987

    [143] Increased mortality after lipid-lowering diets was seen in the following experiments: a: Rose GA, and others. Corn oil in the treatment of ischemic heart disease. British Medical Journal 1, 1531-1533, 1965. b: Woodhill JM, and others. Low fat, low cholesterol diet in secondary prevention of coronary heart disease. Adv. Exp. Med. Biol. 109, 317-330, 1978.

    No difference was found in these experiments:

    Research Committee to the Medical Research Council:Low-fat diet in myocardial infarction: A controlled trial. The Lancet 2, 501-504, 1965

    Research Committee to the Medical Research Council: Controlled trial of soya-bean oil in myocardial infarction. The Lancet 2, 693-700, 1968

    Research Committee of the Scottish Society of Physicians: Ischaemic Heart Disease: a secondary prevention trial using clofibrate. British Medical Journal 4, 775-784, 1971.

    [144]The coronary primary prevention trial: design and implementation. Journal of Chronic Disease 32, 609-631, 1979.

    [145] The results from the first seven years of MR.FIT were published in JAMA 248, 1465-1477, 1982, and in American Journal of Cardiology 58, 1-13, 1986.

    [146] The pilot study was published in Circulation 37, suppl. I, 1-428, 1968; figures of the diet and blood cholesterol in The multiple risk factor intervention trial (MRFIT). IV. Intervention on blood lipids. Preventive Medicine 10, 443-475, 1981; table IX,1 and table XII,e

    [147] JAMA 248, 1465-1477, 1982)

    [148] Mortality rates after 10.5 years for participants in the multiple risk factor intervention trial. JAMA 263, 1795-1801, 1990

    [149] Journal of the American Dietetic Association 86, 744-758, 1986

    [150] The Lipid Research Clinic’s coronary primary prevention trial results. 1. Reduction in incidence of coronary heart disease. JAMA 251, 351-64, 1984.

    [151] The coronary primary prevention trial: design and implementa?tion. Journal of Chronic Disease 32, 609-631, 1979. Criticism of the change of the statistical demands were published in JAMA 253, 3091, 1985 together with the response from the trial directors.

    [152] JAMA 253, 3091, 1985.

    [153] The Atlantic, January 1990; page 10

    [154] British Medical Journal 301, 815, 1990.

    [155] Miettinen TA, and others. Multifactorial primary prevention of cardiovascular diseases in middle-aged men. JAMA 254, 2097-2102, 1985.

    [156] Frick MH, and 18 coworkers. Helsinki heart study: Primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia. The New England Journal of Medicine 317, 1237-1245, 1987.

    [157] Frick MH, and others. Efficacy of gemfibrozil in dyslipaemic subjects with suspected heart disease. An ancillary study in the Helsinki heart study frame population. Annals of Medicine 25, 41-45, 1993.

    [158] Koivisto P, Miettinen TA. Long-term effects of ileal bypass on lipoproteins in patients with familial hypercholesterole?mia. Circulation 70, 290-296, 1984.

    [159] Buchwald H. and others. Effect of partial ileal bypass surgery on mortality and morbidity from coronary heart disease in patients with hyper?cholesterolemia. Report of the program on the surgical control of the hyperlipidemias (POSCH). The New England Journal of Medicine 323, 946-955,1990.

    [160] Brensike JF, and 14 others. Effects of therapy with cholesty?ramine on progression of coronary atherosclerosis: results of the NHLBI type II coronary intervention study. Circulation 69, 313-324, 1984.

    [161] Levy RI. and 14 others. The influence of changes in lipid values induced by cholestyramine and diet on progression of coronary artery disease: results of the NHLBI type II coronary intervention study. Circulation 69, 325-337, 1984.

    [162] Blankenhorn DH, and others. Beneficial effects of combined colestipol-niacin therapy on coronary atherosclerosis and coronary venous bypass grafts. JAMA 257, 3233-3240, 1987.

    [163] Roberts L. Study bolsters case against cholesterol. Science 237, 28-29, 1987. An ironic description of the marketing of the CLAS trial.

    [164]Brown G and others. Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B. The New England Journal of Medicine 323:1289-98, 1990.

    [165]Brown G and others. Reflex constriction of significant coronary stenosis as a mechanism contributing to ischemic left ventricular dysfunction during isometric exercise. Circulation 70:18-24, 1984

    [166] Glagov S and others. Compensatory enlargement of human atherosclerotic coronary arteries. The New England Journal of Medicine 316:1371-1375, 1987.

    [167] Bemis CE, and others. Progression of coronary artery disease. A clinical arte?riogra?phic study. Circula?tion 47, 455-464, 1973.

    [168] Kimbiris D, and others. Devolutionary pattern of coronary atherosclerosis in patients with angina pectoris. Coronary arteriographic studies. American Journal of Cardiology 33, 7-11, 1974.

    [169] Shub C, and others. The unpredictable progression of symptomatic coronary artery disease. Mayo Clinic Proceedings 56, 155-160, 1981.

    [170] a: McLaughlin PR, and others. Long-term angiographic assessment of the influence of coronary risk factors on native coronary circulation and saphenous vein aorto?coronary grafts. American Heart Journal 93, 327-333, 1977.

    b: Marchandise B, and others. Angiographic evaluation of the natural history of normal coronary arteries and mild coronary atherosclerosis. American Journal of Cardiology 41, 216-220, 1978.

    c:. Kramer JR, and others. Progression and regression of coronary atherosclerosis: relation to risk factors. American Heart Journal 105, 134-144, 1983.

    [171] Waters D, Craven TE, Lespérance J. Prognostic significance of progression of coronary atherosclerosis. Circulation 87, 1067-1075, 1993

    [172] Ravnskov U. Cholesterol lowering trials in coronary heart disease: frequency of citation and outcome. British Medical Journal 305, 15-19, 1992

    [173] British Medical Journal, 305, 420-422, and 717, 1992

    [174] Stampfer MJ, and others. Postmenopausal estrogen therapy and cardiovascular disease. Ten-year follow-up from the nur?ses’ health study. The New England Journal of Medicine 325, 756-62, 1991.

    [175] Davey Smith G, Song F, Sheldon TA. Cholesterol lowering and mortality: the importance of considering initial level of risk. British Medical Journal 306, 1367-1373, 1993.

    [176] International Task Force for Prevention of Coronary Heart Disease. Prevention of coronary heart disease: Scientific background and new clinical guidelines. Nutrition, Metabolism and Cardiovascular Diseases 2, 113-156, 1992. Recall that the citation is from a paper written before the statin trials were published.

    [177] de Lorgeril M and others. Lancet 343, 1454-1459, 1994.

    [178] Lancet. 354, 447-55, 1999.

    [179] Scandinavian Simvastatin Survival Study Group. Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 344, 1383-9, 1994.

    [180] MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomized placebo-controlled trial. Lancet 360:7-22, 2002.

    [181] Sacks FM and others. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. N Engl J Med 335, 1001-9, 1996.

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    [186] The following studies did not find that a high cholesterol is a risk factor for a new heart attack:

    a. Gertler MM and others. Am J Med Sci 247, 145-55, 1964.

    b. Shanoff HM and others. Can Med Ass J 103, 927-31, 1970.

    c. Frank CW and others. Circulation 47, 509-17, 1973.

    d. Mulcahy R and others. Br Heart J 37, 158-65, 1975.

    e. Schatzkin A et al. Am J Epidemiol 129, 888-899, 1984.

    f. Khaw KT, Barrett-Connor E. J Cardiopulm Rehab 6, 474-80, 1986.

    g. Olsson G, Rehnqvist N. Cardiology 74, 457-64, 1987.

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    Vaughan CJ and others. Statins do more than just lower cholesterol? Lancet 348, 1079-82, 1996.

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    (b) Corsini A and others. New insights into the pharmacodynamic and pharmacokinetic properties of statins. Pharmacol Ther 84, 413-28, 1999.

    [193] Hidaka Y and others. Inhibition of cultured vascular smooth muscle cell migration by simvastatin (MK-733). Atherosclerosis 95, 87-94, 1992.

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    Schrör K. Platelet reactivity and arachidonic acid metabolism in type II hyperlipoproteinaemia and its modification by cholesterol-lowering agents. Eicosanoids 3, 67-73, 1990.

    Davi G. and others. Increased thromboxane biosynthesis in type IIa hypercholesterolemia. Circulation 85, 1792-8, 1992.

    [195] Meiser BM and others. Simvastatin decreases accelerated graft vessel disease after heart transplantation in an animal model. Transpl Proc 25, 2077-9, 1993.

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    [199] Phillips PS and others. Ann Intern Med 137, 581-585, 1990

    [200] Sinzinger H, O’Grady J. Professional athletes suffering from familial hypercholesterolaemia rarely tolerate statin treatment because of muscular problems. Br J Clin Pharmacol 57: 525-8, 2004.

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    [202] Langsjoen PH, Langsjoen AM. The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications. Biofactors 18, 101-11, 2003.

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    Schuit AJ and others. Low serum cholesterol and death due to accidents, violence, or suicide. Lancet 1993;341:827.

    Gallerani M and others. Serum cholesterol concentration in parasuicide. BMJ 310, 1632-6, 1995.

    Vevera J and others. Cholesteol concentrations in violent and non-violent women suicide attempters. Eur Psych 18, 23-7, 2003.

    Marcinko D. and others. Progr Neuro-Psychopharm Biol Psych 32, 193-196, 2007.

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    [211] King DS and others. Cognitive impairment associated with atorvastatin and simvastatin. Pharmacotherapy 23, 1663-7, 2003

    [212] Wagstaff LR, Mitton MW, Arvik BM, Doraiswamy PM. Statin-associated memory loss: analysis of 60 case reports and review of the literature. Pharmacotherapy. 23, 871-80, 2003

    [213] Henderson VW and others. Serum lipids and memory in a population based cohort of middle age women. J Neurol Neurosurg Psych 74, 1530-4, 2003.

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    [215] http://www.bmj.com/cgi/eletters/322/7293/1019#17446

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    [218] Kenis I and others. Simvastatin has deleterious effects on human first trimester placental explants. Hum Reprod. 20, 2866-72, 2005

    [219] Newman TB, Hulley SB. Carcinogenicity of lipid-lowering drugs. JAMA 275, 55-60, 1996

    [220] Ravnskov U, McCully KS, Rosch PJ. The statin-low cholesterol-cancer conundrum. Quarterly Journal of Medicine 105, 383-338, 2012.

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    [222] Shepherd J and others. Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial. Lancet 360, 1623-30, 2002.

    [223] Iwata H and others. Use of hydroxy-methyl-glutaryl coenzume A reductase inhibitors is associated with risk of lymphoid malignancies. Cancer Science 97, 133-8, 2006.

    [224] Shepherd J and others. Effect of lowering LDL cholesterol substantially below currently recommended levels in patients with coronary heart disease and diabetes: the Treating to New Targets (TNT) study. Diabetes Care. 2006;29:1220-6.

    [225]Bradford RH and others. Expanded clinical evaluation of lovastatin (EXCEL) study results. Arch Intern Med 151, 43-9, 1991.

    [226] Executive Summary of the third report of the National Cholesterol Education Program (NCEP)expert panel on detection,evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III). JAMA 285, 2486-97, 2001.

    [227] Hecht HS, Superko HR. Electron beam tomography and National Cholesterol Education Program guidelines in asymptomatic women. J Am Coll Cardiol 37, 1506-11, 2001

    [228] Grundy SM and others. Coordinating Committee of the National Cholesterol Education Program. A summary of implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Arterioscler Thromb Vasc Bio 24, 1329-30, 2004

    [229] Nissen SE and others. Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial. JAMA 291, 1071-80, 2004.

    [230] Cannon CP and others. Comparison of intensive and moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med 350, 1495-504, 2004.

    [231] LaRosa JC and others for the Treating to New Targets (TNT) Investigators. Intensive Lipid Lowering with atorvastatin in Patients with Stable Coronary Disease. N Engl J Med 352, 1425-35, 2005.

    [232] Ravnskov U, Rosch PJ, Sutter MC. Intensive lipid lowering with atorvastatin in coronary disease. N Engl J Med 353, 94, 2005.

    [233] Pedersen TR and others. Incremental Decrease in End Points Through Aggressive Lipid Lowering (IDEAL) Study Group. High-dose atorvastatin vs usual-dose simvastatin for secondary prevention after myocardial infarction: the IDEAL study: a randomized controlled trial. JAMA 94, 2437-45, 2005.

    [234] Ravnskov U, Rosch PJ, Sutter MC. High-dose statins and the IDEAL study. JAMA 295, 2476, 2006.

    [235] Pedersen TJ and others. In reply. Same as ref. 114, page 2478

    [236] Smith R. The Trouble With Medical Journals. The Royal Society of Medical Press 2006.

    [237] Scott HD and others. Rhode Islands physicians’ recognition and reporting of adverse drug reactions. Rh I Med J 70, 311-6, 1987.

    [238] Jackevicius CA and others. Adherence with statin therapy in elderly patients with and without acute coronary syndromes. JAMA 288, 462-7, 2002.

    [239] Schalk BWM and others. Lower levels of serum albumin and total cholesterol and future decline in functional performance in older persons: the Longitudinal Aging Study Amsterdam. Age and Ageing 33, 266-72, 2004.

    [240] de Lau LML and others. Serum cholesterol levels and the risk of Parkinson’s disease. Am J Epidemiol 164, 998-1002, 2006.

    [241] Mielke MM and others, High total cholesterol levels in late life associated with a reduced risk of dementia. Neurology.64, 1689-95, 2005.

    [242] Elias PK and others. Serum cholesterol and cognitive performance in the Framingham Heart Study. Psychosom Med 67, 24-30, 2005

    [243] Li G. Serum cholesterol and risk of Alzheimer disease. Neurology 65, 1045-50, 2005.

    [244] Muldoon MF and others. Effects of Lovastatin on cognitive function and psychological well-being. Am J Med 108, 538-47, 2000.

    [245]http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3upd04_disclose.htm

    [246] Stemmermann GN, and others. J Nat Cancer Inst 67, 1179-1182, 1981.

    Morris DL, and others. Cancer 52, 1754-1759, 1983.

    Sherwin RW, and others. JAMA 257, 943-948, 1987

    Isles CG, and others. BMJ 298, 920-924, 1989

    Winawer SJ, and others. JAMA 263, 2083-2085, 1990

    Cowan LD, and others. Am J Epidemiol 131, 468-482, 1990).

    [247] Feinleib M. y. Preventive Medicine 11, 360-367, 1982

    [248] In many studies the risk of developing cancer with a low blood cholesterol level was just as great as the risk of developing coronary heart disease with a high one.

    [249]McHugh MI and others. Immunosuppression with polyunsaturated fatty acids in renal transplantation. Transplantation 24, 263-267, 1977

    [250] Pinckney ER. The potential toxicity of excessive polyunsaturates. Do not let the patient harm himself Am Heart J. 1973;85:723-6.

    [251] Alexander JC and others. Journal of Toxicology and Environmental Health 21, 295-309, 1987

    [252] Richie J and others. Edema and hemolytic anemia in premature infants. New England Journalof Medicine 279, 1185-1190, 1968

    [253] Dam H, Söndergaard E. The encephalomalacia produ?cing effect of arachidonic and linoleic acids. Zeitschrift für Ernäh?rungswissenschaft 2, 217-222, 1962.

    [254] Editorial. Atherosclerosis and auto-oxidation of cholesterol. The Lancet 1, 964-965, 1980.

    Steinberg D, and others. Beyond cholesterol. Modifica?tions of low-density lipopro?tein that increase its atheroge?nicity. The New England Journal of Medicine 320, 915-924, 1989.

    [255] Watanabe-rabbits have the same hereditary metabolic defect as individuals with familial hypercholester?olemia and develops very high blood cholesterol levels on their usual vegetarian diet.

    [256] Carew TE, Schwenke DC, Steinberg D. Antiatherogenic effect of probucol unrelated to its hypocholes?terolemic effect. Proceedings of the National Academy of Science USA 84, 7725-7729, 1987. Blood cholesterol of the control rabbits was lowered with another cholesterol-lowering drug lovastatin which has no antioxidant effect. But it was the number of fatty streaks which decreased, not the degree of atherosclerosis.

    [257] Clubb FJ, and others. Effect of dietary omega-3 fatty acid on serum lipids, plasma function and athero?sclero?sis in Watanabe heritable hyper?lipidemic rabbits. Atherosclerosis 9, 529-537, 1989. Cholesterol in the blood is present mainly as cholesteryl esters, which are compounds of chole?sterol and fatty acids.

    [258] Recently, Scott Grundy, the main designer of the diet recommendations from the National Heart, Lung and Blood Institute, wrote that it is not a good idea to substitute fatty acids of animal origin with polyunsaturated fatty acids: high intakes…might not be entirely safe. Of special concern to Grundy is that high intakes of linoleic acid (the most prevalent polyunsaturated fatty acid) may promote cancer in human beings as it does in laboratory animals. Besides, he gave most of the arguments I presented in Chapter 8, and he concluded that intakes above 7% of total calories seemingly cannot be advocated with prudence. Grundy did not explain how he found the limit of just seven percent, and his warnings against polyunsaturated fat appeared in the middle of a large review article concerning something else, and nothing was mentioned about it in the summary of his paper. (Grundy SM. Multifactorial etiology of hypercholesterolemia. Implications for prevention of coronary heart disease. Circulation 86, 1619-1635, 1992)

    [259] A thorough review of the history, chemistry and biological effects of the trans fatty acids is found in Enig MG. Trans fatty acids in the food supply: a comprehensive report covering 60 years of research. Enig Associates, Inc., Silver Spring 1993.

    [260] Hanis T and others. Effects of dietary trans-fatty acids on reproductive performance of Wistar rats. British Journal of Nutrition 61, 519-529, 1989.

    [261] Teter BB, Sampugna J, Keeny M. Milk fat depression in C57Bl/6J mice consuming partially hydrogenated fat. Journal of Nutrition 120;818-824, 1990.

    [262] Koletzko B. Trans fatty acids may impair biosynthesis of long-chain polyunsaturates and growth in man. Acta Pædiatrica 81;302-306, 1992.

    [263] Atal S, and others. Comparison of body weight and adipose tissue in male C57BI/6J mice fed diets with and without trans fatty acids. Lipids 994;29;319-325.

    [264] Mensick RP and Katan MB. Effect of dietary trans fatty acids on high-density and low-density lipoprotein cholesterol levels in healthy subjects. The New England Journal of Medicine 323, 439-445, 1990

    [265] Consensus Conference: Lowering blood cholesterol to prevent heart disease. JAMA 253, 2080-2086, 1985. The description of the conference is mainly based on Thomas J. Moore. Heart Failure, Random House, New York, 1989. Moore’s book is a critical portrayal of the buildup to the cholesterol campaign. His views have been violently criticized by the diet-heart proponents. However, no one has questioned his description of the conference.

    [266] According to Moore, the communiqué had been written before the meeting.

    [267] Some of the many critical voices are listed here:

    Palumbo PJ. National cholesterol education program: does the emperor have any clothes? Mayo Clinic Proceedings 63, 88-90, 1988.

    Oliver MF. Consensus or nonsensus conferences on coronary heart disease. The Lancet 1, 1087-1089, 1985.

    Merz B. Low-fat diet may be imprudent for some, say opponents of population-based cholesterol control. JAMA 256, 2779-2780, 1986.

    Pinckney ER, Smith RL. Statistical analysis of lipid research clinic’s program. The Lancet 1, 503, 1987. Pinckney and Smith concluded that “the US government via the NHLBI has launched a nationwide program to alter the diet of Americans, based on a study (costing $150 million of public money) that had a faulty statistical analysis. What is more, the statistical defects were known to the trial’s organisers and to the journal that published the results.”

    Patel C. The lipid research clinic’s trial. The Lancet 1, 633-634, 1984. Patel has calculated that if the result of the LRC trial is transferred to England and Wales one of every 400 coronary deaths could be saved each year, amounting to the cost of about £140 million a year and of gastrointestinal side effects in more than 130 000 healthy individuals.

    Editorial. The Lancet 1, 333-334, 1988. The author stressed the fact that there is little correlation between dietary fat intake and cholesterol level; that no convincing dietary prevention study had been published; and that the increase in deaths from other causes in the drug trials “cannot be ignored simply because it did not form part of the hypothesis that these trials were designed to test.”

    [268] The full story about Kilmer McCully was published in New York Times on August 10, 1997. Go to http://www.thincs.org click, on “Members,” look for his name and click on “Interview.”

    [269] Enig MG. Trans fatty acids in the food supply: a comprehensive report covering 60 years of research. Enig Associates, Silver Spring, MD, 1993.

    Enig MG. Know Your Fats: The Complete Primer for Understanding the Nutrition of Fats, Oils, and Cholesterol. Bethesda Press, Silver Spring, MD, 2000.

    [270] Gurr MI. Prog Lipid Res 31, 195-243, 1992.

    [271] Mann GV. N Engl J Med 297, 644-50, 1977.

    Mann GV. Nutrition Today July/August, p. 12-14, 1985.

    [272] Pinckney ER and Pinckney C. The Cholesterol Controversy. Sherbourne Press, Los Angeles, 1973.

    [273] Reiser R. Am J Clin Nutr 26, 524-55, 1973.

    Reiser R. Am J Clin Nutr 40, 654-8, 1984.

    [274] Paul Rosch’s view on the cholesterol campaign is available in Health and Stress. The Newsletter of The American Institute of Stress, 1995, nr 1; 1998, nr 1; 1999, nr 8; 2001, nr 2,4,7.

    Read also:

    Rosch, PJ. Statins don’t work by lowering lipids. Electronic response in BMJ 17. Nov 2001.

    Rosch PJ. JAMA 286, 2001, 2400.

    [275] Friedman M, Rosenman RH, Byers SO. J Geron?t 10, 60-85, 1955.

    Rosenman RH. Homeostasis 34, 1-43, 1993.

    [276] Smith RL Diet, blood cholesterol and coronary heart disease: a critical review of the literature. Vector Enterprises. Vol. 1, 1989; Vol. 2, 1991.

    Smith RL. The Cholesterol Conspiracy. Warren H. Green, Inc. St. Louis, 1991. (c) Smith RL. Am Clin Lab November, p. 26-33, 1989.

    [277] Stehbens WE. Lancet 1, 606-11, 1987.

    Stehbens WE. Prog Cardiovasc Dis. 33, 119-36, 1990.

    [278] Werkö L. Am Heart J 91, 87-98, 1976.

    Werkö L. Prevention of heart attacks. Ann Clin Res 11, 71-9, 1979.

    Werkö L. Diet, lipids and heart attacks. Acta Med Scand 206, 435-9, 1979.

    Werkö L. Acta Med Scand 221, 323-33, 1987.

    Werkö L. J Intern Med 237, 507-18, 1995.

    ———

    Here are links to the other chapters in the book.

    ———

    This chapter is from the book
    The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease
    by Uffe Ravnskov, MD, PhD.

    Dr. Ravnskov has given me the permission to share this version of his book to help educate the world about the cholesterol campaign.

    Information about Uffe Ravnskov, MD, PhD is posted here.

    More information about Cholesterol Myths is posted on his website here.

    Dr. Ravnskov posted his book for free here.

    Several versions of the ebook can downloaded from Dropbox here or from SmashWords here.

    Uffe Ravnskov, MD, PhD is the founder of The International Network of Cholesterol Skeptics (THINCS.org) which can be found here.

    Articles on the same subject can be found here:


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