Dietary Fats and Heart Disease
Not long after dietary cholesterol was proposed as a cause of heart disease, Dr Ancel Keys found that dietary fats raised cholesterol. That increased the pressure on doctors and led to another intervention: Cut out fats, particularly saturated animal fats an tropical oils! But we've been eating these fats for the whole of our existence as a species on this planet; heart disease was very rare before the 1920s. So is the evidence against fats as strong as is claimed?
The dietary fats hypothesis
The 'lipid hypothesis' as it is called began with a study published by Dr Ancel Keys in 1953(See the story here). Ancel Keys suggested that a fatty diet might play a part as a cause of CHD.[1] Using data from just 6 countries, Keys compared the death rates from CHD and the amounts of fats eaten in those countries to demonstrate, he said, that heart disease mortality was related to fat intake.
And so the 'lipid hypothesis' (lipid is a word that encompasses fats, waxes and sterols) was born. However, at that time, data from another 16 countries were available. If they are added the picture is a lot less clear. For example, Finland has 7 times as many deaths as France, but Finns eat less fat; and Mexico has the lowest number of deaths, yet Mexicans have 3 times the fat consumption of Japan. These are three of the countries Keys didn't use.
Despite its faults, some of which didn't become apparent until later, Keys had what looked like a plausible hypothesis to explain the high levels of heart disease in some countries.
Now, anyone can have a hypothesis. What you have to do then is prove it. In medicine, the usual way is to select two groups of people, as identical for sex, age, and lifestyle as possible. One group, called the intervention group, tries the new diet, drug or whatever, while the other, called the control group, carries on as normal. After a suitable time, the two groups are compared and differences noted.
Keys' 'fatty diet-causes-heart disease' hypothesis was persuasive, but was it true? To test it, many large-scale, long-term, human intervention studies were set up in many parts of the world. These involved hundreds of thousands of subjects and hundreds of doctors and scientists and cost billions of dollars in an attempt to prove that a fatty diet caused heart disease. What they found was the opposite of what they expected.
The Anti-Coronary Club Project, launched in 1957 compared two groups of New York businessmen 49 to 59 years old. One group followed a 'Prudent Diet' which replaced butter with corn oil and margarine, eggs with cold cereal and skim milk, and beef with chicken and fish. A control group ate eggs for breakfast and meat three times per day.[2]
The report noted that the cholesterol levels of those on the Prudent Diet were significantly lower than the control group eating eggs and meat — but there were eight deaths from heart disease among the Prudent Dieters and no deaths from heart disease in the control group.
After the Framingham researchers foujnd thast dietary cholesterol didn't increase blood cholesterol, they studied intakes of saturated fats but again found no relation with blood cholesterol; there was still no relation when they studied total calorie intake. The researchers then considered the possibility that something was masking the effects of diet, but no other factor made the slightest difference. After 22 years of intense expert study and analysis, the researchers concluded: 'There is, in short, no suggestion of any relation between diet and the subsequent development of CHD in the study group.'[3] That was in 1970, and no finding since has changed that view.
The other studies also showed little convincing correlation between either the amount of fat eaten and heart disease or the type of fat eaten and heart disease but there were a handful of exceptions. These supportive trials are cited far more often than the much larger number of unsupportive ones.[4]
One that did seem to support the 'healthy' recommendations was a Finnish trial involving 1,222 men published in 1985.[5] Men in the intervention group were seen regularly and advised about diet, physical activity and smoking. Those with high blood pressure or high cholesterol levels were treated with drugs. The men in this group did as they were advised and, as a result, the 'predicted risks' for CHD were halved during the trial. It was hailed as a great success because 'The program markedly improved the risk factor status'.
In other words, they succeeded in changing their subjects' diets, and so on. In December 1991, the results of a 15-year follow-up to that trial were published.[6] During this period the intervention group had continued to be instructed on diet, smoking and exercise and treated for high blood pressure and cholesterol when present. Were they healthier? Did they live longer?
NO!
Not only did those who continued to follow the carefully controlled, cholesterol-lowering diet have more deaths in total, they were more than twice as likely to die of heart disease as those who didn't — some success!
Dr Michael Oliver, Professor of Cardiology at Edinburgh University's Cardiovascular Research Unit, commenting on these results in the British Medical Journal, wrote that:
'This runs counter to the recommendations of many national and international advisory bodies which must now take the recent findings from Finland into consideration. Not to do so may be ethically unacceptable. . . . We must now face the fact that the evidence from large, well conducted trials gives little support to hopes that altering the lifestyle of the community at large, when started in middle age, will reduce cardiac deaths or total mortality.' [7]
If heart disease really did result from eating saturated fats — as we are told — it would be reasonable to expect to find more heart disease in the nineteenth century when the fats we ate were all from animal sources; and we could have expected a decrease in heart disease with the introduction of vegetable-based margarines and consequential reduction in intakes of butter and other animal fats in the early twentieth century. Yet the reverse is true.
Results of some early studies of fats and coronary thrombosis suggested that individual saturated fatty acids were likely to cause blood platelets to clump together and form clots (thromboses). But these studies were conducted in vitro (in glass dishes), a method now known to give entirely wrong results. For example, an in vitro study from 1962 reported that the saturated fatty acid, stearic acid, found widely in animal fats, considerably shortened the time needed for a clot to form whereas unsaturated fatty acids had almost no such effect.[8] In the model used, other saturated fatty acids commonly found in animal fats also increased clot formation. But contradictory results from other studies meant that results taken together were inconclusive. In 1996 a study looked at this whole vexed question by testing individual saturated fatty acids in vivo — in real, live people.[9] It showed the exact opposite of what had been observed in the laboratory studies: the saturated fats suspected of increasing the risk of a blood clot actually reduced the risk of clotting.
Another worry about saturated fats, that they might contribute to heart disease by adversely affecting blood cholesterol sub-fractions (HDL and LDL), has also been shown to be unwarranted. A study, presented at the Canadian Institute of Food Science and Technology's conference in June 2001 by Margaret French, of Canada's Department of Agricultural, Food and Nutritional Science, found that 112g (4 ounces) of beef eaten twice daily raised neither total nor LDL cholesterol any more than diets that were primarily of chicken, beans and pulses.[10] French also noted that saturated fats had benefits such as lowering stress hormone levels and improving blood flow.
CHD and saturated fat in Tokelau vs Pukapuka
Studies of human populations in a natural setting rarely allow us to compare like with like so that a single difference in diet can be studied. But two populations of Polynesians living on the Pacific atolls, Pukapuka and Tokelau, do provide such an opportunity. In 1981 the relative effects of their diets on cholesterol levels was studied.[11] Coconut is the chief source of energy for both groups; being over 90% saturated, coconut oil is the world's most saturated natural fat. The sole difference between the two populations is that Tokelauans obtain 63% of energy from coconut, compared with 34% among the Pukapukans. You won't be surprised to know that with almost twice the saturated fat intake, blood cholesterol levels are higher in Tokelauans. However, cardiovascular disease is equally uncommon in both populations.
Margarine causes more illness
With animal fats denigrated and the backing of the medical world, the vegetable oil and food processing industries who were the main beneficiaries of any research that found fault with traditional foods, began promoting cheap-to-produce vegetable margarines and cooking oils. These could now be sold at prices which rivalled the price of butter and animal fats. In 1983 a multi-year British study, the WHO European Collaborative Trial in the Multifactorial Prevention of Coronary Heart Disease (CHD), involving 18,210 men aged between 40 and 59, showed clearly that eating these was ill-advised.[12] Men who switched to 'healthy' margarines and vegetable oils had twice the death rate of those on an 'unhealthy' saturated fat diet, even though the men on the saturated fat diet also continued to smoke. Despite this, the authors perversely reported that 'There was no clear effect on hard CHD end-points (coronary deaths and myocardial infarction) or on all-causes mortality.'
They continued: 'However, there was a 36% reduction in the rate at which intervention subjects reported ill with other CHD (principally angina) during the study, and at the end fewer intervention men gave positive responses to a self-administered questionnaire on angina and chest pain.' So was there some benefit? Apparently not; the authors say: 'These apparent benefits were not substantiated by electrocardiographic evidence, suggesting that participation in a heart disease prevention campaign may bias reporting of symptoms.' Ultimately, they ignored their own findings and presented a politically correct conclusion, saying: 'The implication for public health policy in the U.K. is that a preventive programme such as we evaluated in this trial is probably effective. . . .'
Scientists at the Wynn Institute for Metabolic Research, London, UK, compared the fatty-acid composition of artery blockages. What they found was a high proportion of both omega-3 and omega-6 polyunsaturated fatty acids; what they did not find was saturated fatty acids. They suggested that 'current trends favouring increased intake of polyunsaturated fatty acids should be reconsidered.'[13]
Ten years later two further studies published simultaneously in the American Journal of Clinical Nutrition reinforced the findings that saturated fats actually protected against heart disease. The first found that a so-called 'healthy' carbohydrate-based diet increased the rate at which older women's arteries degenerated and that increasing intakes of saturated fat actually slowed down the progress of their atherosclerosis.[14] The second study found what its authors called a 'paradox' when they showed 'that a high-fat, high-saturated fat diet is associated with diminished coronary artery disease progression in women with the metabolic syndrome, a condition that is epidemic in the United States.'[15]
References
[1]. Keys A. Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp 1953; 20: 118.
[2]. Cristakis G. Effect of the Anti-Coronary Club Program on Coronary Heart Disease Risk-Factor Status. JAMA 1966; 198: 129-35.
[3]. Kannel WB, Gordon T. The Framingham Diet Study: diet and the regulations of serum cholesterol (Sect 24). Washington DC, Dept of Health, Education and Welfare, 1970.
[4]. Ravnskov U. Cholesterol lowering trials in coronary heart disease: frequency of citation and outcome. BMJ 1992; 305: 15-19.
[5]. Miettinen TA, Huttunen JK, Naukkarinen V, et al. Multifactorial primary prevention of cardiovascular diseases in middle-aged men. JAMA 1985; 254: 2097-2102.
[6]. Strandberg TE, Salomaa VV, Naukkarinen VA, et al. Long term mortality after 5-year multifactorial primary prevention of cardiovascular diseases in middle-aged men. JAMA 1991; 266: 1225-9.
[7]. Oliver MF. Doubts about preventing coronary heart disease. BMJ 1992; 304: 393-4.
[8]. Connor W. The acceleration of thrombus formation by certain fatty acids. J Clin Invest 1962: 41: 1199-205.
[9]. Tholstrup T, Andreasen K, Sanstrom B. Acute effect of high-fat meals rich in either stearic or myristic acid on hemostatic factors in healthy young men. Am J Clin Nutr 1996; 64: 168-76.
[10]. For further details, contact or see: http://www.meatingplace.com
[11]. Prior IA, Davidson F, Salmond CE, Czochanska Z. Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies. Am J Clin Nutr 1981; 34: 1552-61.
[12]. Rose G, Tunstall-Pedoe HD, Heller RF. UK heart disease prevention project: incidence and mortality results. Lancet 1983; 1: 1062-6.
[13]. Felton CV, Crook D, Davies MJ, Oliver MF. Dietary polyunsaturated fatty acids and composition of human aortic plaques. Lancet 1994; 344: 1195-6.
[14]. Mozaffarian D, Rimm EB, Herrington DM. Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. Am J Clin Nutr 2004; 80: 1175-84.
[15]. Knopp RH, Retzlaff BM. Saturated fat prevents coronary artery disease? An American paradox. Am J Clin Nutr 2004; 80: 1102-3.
