Science in Society Archive

The ‘Deadly Dangers of Saturated Fat’ & the ‘Superlative Safety of Statins’

Part 1

Although these myths were thoroughly discredited recently, it is important to know how they originated and why they have persisted despite lack of proof and abundant evidence to the contrary Dr Paul J Rosch

The twin myths of the deadly dangers of saturated fat and the superlative safety of statins were thoroughly discredited recently (see [1, 2] Low Fat and Low Saturated Fat Diet Bad for Health and Statins for the Healthy are Harmful, SiS 66). Nevertheless, it is important to know how they originated and why they have persisted despite abundant evidence to the contrary.

Irrelevant animal experiments and false conclusions

It began with some irrelevant animal experiments and false conclusions. The presence of cholesterol in blood as well as atherosclerotic plaque had been known since 1850. In 1910, Adolf Windaus, a German physician and chemist, who later received a Nobel Prize for Chemistry, reported that atheroma in human aortas contained 6 times more free cholesterol than healthy arteries, and over 20 times more cholesterol ester [3].  A few years later Nikolai Anitschkow showed that feeding rabbits purified cholesterol obtained from egg yolks for two or three months produced lipid laden lesions in the aorta and other arteries [4].  However, there was little clinical interest in these observations as coronary heart disease was uncommon at the time.

That changed in 1950 when John Gofman, who had been impressed with Anitschkow’s experiments repeated them and replicated his results.  He was convinced that serum cholesterol and/or its dietary sources contributed to coronary atherosclerosis but knew this was not a direct effect as the cholesterol molecule was too large to pass through the arterial wall.  Little was known about how cholesterol was transported to different body sites to make vitamin D, testosterone, estrogen and other steroid hormones and Gofman was uniquely qualified to investigate this. Prior to receiving his medical degree in 1946, he obtained a Ph.D. in physics at Berkeley, where he studied under Nobel Laureates Ernest O. Lawrence and Glenn T. Seaborg.  Lawrence was awarded the 1939 Physics Nobel Prize for inventing the cyclotron, a device that accelerates charged particles.  Seaborg received the 1951 Chemistry Nobel Prize for using the cyclotron to discover uranium, plutonium, neptunium and other new elements and their isotopes, especially as uranium-235 was required to make the atomic bombs that ended the war with Japan.

Gofman learned of a new analytic ultracentrifugation device that had been developed in Sweden, and because of his superb background in physics and chemistry, immediately saw how it could be used to study cholesterol transport. He obtained one for his laboratory and found that the hypercholesteremic serum samples of his cholesterol-fed rabbits could be separated into two distinct compartments based on their density. The layer at the top of the serum sample was designated low-density lipoprotein cholesterol (LDL) and the deposit at the bottom of the test tube was called high-density lipoprotein cholesterol (HDL) [5].  As LDL appeared to be particularly proatherogenic, he proposed that it promoted the rapid progression of coronary disease in humans and later developed an atherogenic index based on lipoprotein values and ratios [6].   This stimulated myriad investigations, including the research of Michael S. Brown and Joseph L. Goldstein [7], who received the 1985 Nobel Prize in Physiology or Medicine “for their discoveries concerning the regulation of cholesterol metabolism' that led to the development of statins [8].  Gofman believed that avoiding animal fats and cholesterol would help prevent coronary disease, as indicated in his Introduction to The Low Fat, Low Cholesterol Diet: What To Eat And How To Prepare It, a 1951 book co-authored by his pediatrician wife, Dr Helen Gofman and others at Berkeley [9].

False association between animal fats, cholesterol and heart disease

Anitschkow also got a big boost from Ancel Keys, who chaired the 1951 conference of the UN’s Foodand Agriculture Organization in Rome. He asked the audience aboutdiet as it related to the heart attack epidemic in middle-aged men that was sweeping across the US.  Prior to 1920, less than 10 percent of all US deaths were due to heart disease,but by 1950, this had escalated toover 30 %. A University of Naples professor told him there was no such problem in his or nearby cities, which Keys personally verified.  The only exception he found was asmall class of wealthy people who dined on meat daily. The general public had meat once or twice a week and mostly ate pasta, fruits and vegetables. He also found that except for the meat eaters, the average cholesterol levels were low, and concluded that there was an association between a high fat diet, elevated serum cholesterol and coronary heart disease rates, just as Anitschkow proposed. Within a few years, Keys identified six countries where there were similar findings [10], and subsequently embarked on his extensive Seven Countries study in healthy middle-aged men that appeared to confirm these cause-effect relationships [11].

Strong support for Anitschkow also came from the Framingham study, which had been initiated by the National Heart Institute in 1948 to identify factors thatcontributed to heart disease [12]. Residents of this small manufacturing town near Boston were periodically investigated for anything that might conceivably influence the development of coronary heart disease, including blood levels of sugar, cholesterol and other chemicals, fat consumption, smoking, degree of obesity, physical activity and exercise habits. Their 6-year follow-up analysis of over 4 000 healthy men and women aged 31-65 found that serum cholesterol measured at the start was significantly higher among those who experienced coronary events during this period. The Framingham study went on to identify other modifiable risk factors such as smoking, hypertension, obesity, diabetes and lack of exercise, which had additive effects.  Nevertheless, the major culprit was elevated cholesterol from dietary fat. This was reinforced by the 1977 McGovern Senate Committee on Nutrition report that advised avoiding saturated fats to lower cholesterol levels and prevent heart disease [13].

Official government policy established on cholesterol as the culprit

This became official government policy with the establishment of the National Cholesterol Education Program in 1985, and is ongoing.  September has been designated National Cholesterol Education Month, during which everyone is urged to have their cholesterol and lipoprotein levels measured.  That’s not surprising as the role of cholesterol and LDL now seemed to be indisputable. In a 1958 editorial, Dr. William Dock, a renowned cardiologist and Chairman of the Department of Pathology at Stanford University Medical School, wrote [14]: “Thus the early work of Anitschkow bears comparison with that of Harvey on the circulation and of Lavoisier on the respiratory exchange of oxygen and carbon dioxide.” Dock also compared the significance of Anitschkow’s research to Koch’s discovery of the tubercle bacillus. And a more recent ranking of “Cardiology's Ten Greatest 20th Century Discoveries” [15] listed the top three as 1) The Electrocardiogram, 2) Preventive Cardiology and the Framingham Study, and 3) The “Lipid Hypotheses” and Atherosclerosis.

How could we have been so wrong for so long?

Note that the last author used the term “Lipid Hypotheses” to include both the saturated fat diet-heart disease theory as well as the belief that elevated cholesterol was the cause of coronary atherosclerosis. But neither of these hypotheses has ever been proven. With respect to Antischkow's monumental discovery, rabbits are herbivorous and cholesterol is a foreign substance they cannot utilize or metabolize.  In addition, although serum cholesterols were often over 1 ooo mg/L (26mmol/L), the lipid deposits in arteries consisted mainly of macrophage derived foam cells rather than the fibrous and atheromatous plaques found in patients with symptomatic coronary atherosclerosis [16]. More importantly these findings could not be reproduced when the experiments were repeated in rats, dogs and other meat eaters, so they should not be extrapolated to people.

As noted in [1], although Keys had data on 22 countries, he cherry picked the seven that best supported his theory. When all the countries were included, there was no fatty diet-heart disease link [17], and had he selected Israel, Sweden, Germany and France, he would have concluded that the more saturated fat and cholesterol consumed, the lower the incidence of coronary heart disease. Despite that, Keys was featured on the cover of Time magazine, and his claim that saturated fats in the diet clogged arteries and caused heart disease was now supported by so many prestigious organizations and authorities that it was viewed as gospel. It was severely criticized by others, such as Russell Smith, a psychologist with a strong background in mathematics and physiology. He meticulously reviewed over 2 000 studies on the links between dietary fat, cholesterol and heart disease and came to this conclusion [18]:

“The word “landmark” has often been used to describe Ancel Keys Seven Countries Study, commonly cited as proof that the American diet is atherogenic. The dietary assessment methodology was highly inconsistent across cohorts and thoroughly suspect. In addition, careful examination of the death rates and associations between diet and death rates reveal a massive set of inconsistencies and contradictions. . . . It is almost inconceivable that the Seven Countries study was performed with such scientific abandon. It is also dumbfounding how the NHLBI/AHA alliance ignored such sloppiness in their many “rave reviews” of the study. . . . . In summary, the diet-CHD relationship reported for the Seven Countries study cannot be taken seriously by the objective and critical scientist.”

George Mann, the highly respected Professor of Medicine and Chemistry at Vanderbilt and a co-director of the Framingham study at the time, was even more vitriolic [19]:

“Saturated fat and cholesterol in the diet are not the cause of coronary heart disease. That myth is the greatest scientific deception of this century, perhaps of any century. The diet-heart hypothesis has been repeatedly shown to be wrong, and yet, for complicated reasons of pride, profit and prejudice, the hypothesis continues to be exploited by scientists, fund-raising enterprises, food companies and even governmental agencies. The public is being deceived by the greatest health scam of the century.”

“The greatest health scam of the century”

Observational studies can show a statistical correlation but not causation. Keys repeatedly tried several times to demonstrate significant changes in serum cholesterol by altering dietary fat intake with no success [20]. Decades later, he wrote [21]: “Dietary cholesterol has an important effect on the cholesterol level in the blood of chickens and rabbits, but many controlled experiments have shown that dietary cholesterol has a limited effect in humans.

He was even more emphatic in a subsequent Internet magazine interview [22]: “There’s no connection whatsoever between cholesterol in food and cholesterol in blood. And we’ve known that all along. Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit.”  However, by this time, most of the country was on a low fat or Prudent Diet that not only restricted saturated fat, but also increased polyunsaturated liquid vegetable fats such as corn oil.

The first report on the Prudent Diet was from the Joliffe Anti-Coronary Club in Manhattan, which had as controls a group of healthy middle-aged men who followed their usual diet of lots of eggs, butter, cheese and red meat. The Prudent Diet cohort strictly avoided these and substituted a special margarine rich in polyunsaturated fats for butter. After four years, although serum cholesterol was reduced in those following the Prudent Diet, eight had died from a myocardial infarction, compared to none in the control group [23].

Numerous other attempts to reduce coronary disease by limiting saturated fat intake also failed and several observational studies similarly found that saturated fat restriction was associated with increased risk of coronary heart disease deaths [24-28]. As Sylvan L Weinberg, a past president of the American College of Cardiology, warned in a subsequent editorial [29]:

“The low-fat–high-carbohydrate diet, promulgated vigorously by the National Cholesterol Education Program, National Institutes of Health, and American Heart Association since the Lipid Research Clinics-Primary Prevention Program in 1984, and earlier by the U.S. Department of Agriculture food pyramid, may well have played an unintended role in the current epidemics of obesity, lipid abnormalities, type II diabetes, and metabolic syndromes. This diet can no longer be defended by appeal to the authority of prestigious medical organizations or by rejecting clinical experience and a growing medical literature suggesting that the much-maligned low-carbohydrate–high-protein diet may have a salutary effect on the epidemics in question.”

The Framingham study, which established cholesterol as the most important risk factor for coronary heart disease, was never able to prove this or to show that saturated fat increased serum cholesterol or coronary disease. During the early 1950s, detailed information on dietary habits had been obtained on a thousand participants.  A follow-up analysis in 1971 found no connection between diet andserum cholesterol and the authors concluded [30]: “These findings suggest a cautionary note with respect to hypotheses relating diet to serum cholesterol levels. There is a considerable range of serum cholesterol levels within the Framingham Study Group. Something explains this inter-individual variation, but it is not diet.” The senior author William Kannel was then Director of the Framingham study, and this report was never published for obvious reasons.  However, over two decades later, William Castelli, who succeeded Kannel as Director, wrote [31]:

In Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people’s serum cholesterol...we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories weighed the least and were the most physically active.”  And a 30-year follow-up revealed that [32] 'For each 1 mg/dl drop of cholesterol there was an 11 % increase in coronary and total mortality.”

Saturated fat-heart disease hypothesis thoroughly discredited

The Tecumseh Community Health Study, which utilized data on the composition of over

2 700 foods, found that cholesterol and triglyceride levels were unrelated to quality, quantity, or proportions of fat, carbohydrate, or protein consumed [33]. Participants who ate the least cholesterol also had the highest blood cholesterol levels.

The World Health Organization’s Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) epidemiologic project was undoubtedly the largest study ever designed to explore the relationship between risk factors and cardiovascular disease.  It began in 1971 as a collaborative effort involving 32 centers in 21 countries that monitored approximately 10 million men and women aged 25-64 for ten years. It thoroughly discredited the saturated fat–heart disease hypothesis. All the countries in the top eight for saturated fat consumption had lower death rates for heart disease than all of the eight countries that consumed the least fat. The French consumed three times as much saturated fat as the Azerbaijani but had one-eighth the rate of heart disease deaths. Heart disease mortality in Finland was four times greater than in Switzerland, even though saturated fat consumption was similar [34].

Although such epidemiologic studies cannot prove or disprove causal relationships, no large scale interventional trial has ever demonstrated that restricting saturated fat reduces the risk of coronary disease [35, 36]. This was true even when combined with reducing other risk factors like hypertension and cigarettes as evidenced by the $115 million Multiple Risk Factor Intervention Trial (MRFIT). This involved 28 medical centers and 250 researchers who screened 361 662 men and deliberately chose those who were at the highest risk in order to increase the power of the test.

Compared to matched controls, cholesterol intake was cut by 42 %, saturated fat consumption by 28 %, total calories by 21 %, and there was a significant reduction in hypertension and cigarette smoking after 8 years. Although there was a modest fall in serum cholesterol, there was no effect on coronary heart disease and the disappointing conclusion was [37]: “The overall results do not show a beneficial effect on Coronary Heart Disease or total mortality from this multifactor intervention.

The Women's Health Initiative (WHI) study was established by NIH in 1991 to address the most common causes of death, disability and impaired quality of life in postmenopausal women. This 15-year $625 million project involved 161 808 healthy postmenopausal women followed at 40 clinical centers that included three interventional clinical trials; Hormone Therapy, Calcium/Vitamin D supplementation and Dietary Modification. The Dietary Modification component evaluated the effect of a low-fat and high fruit, vegetable and grain diet on the prevention of CHD, breast and colorectal cancers. Study participants followed either their usual eating habits or the dietary regimen noted above. The results indicated that despite some reduction in cardiovascular risk factors such as blood lipids and diastolic blood pressure, there was no significant reduction in the risk of coronary heart disease or stroke in the cohort that restricted fat and increased fruit, vegetables and grain [38, 39].

As William James, the father of modern psychology noted, “There is nothing so absurd that it cannot be believed as truth if repeated often enough.” Although many more articles could be cited, most people still believe that saturated fatcauses heart attacks. Other reasons for this will be explored in Part 2, whichwill haveafocus on statin safety and efficacy, why figures don’t lie but liars can figure, why measuring cholesterol is a waste of time and money, and what really causes heart disease; so stay tuned!


Dr Paul J Rosch

The author is Chairman of the Board of The American Institute of Stress, Clinical Professor of Medicine and Psychiatry at New York Medical College, and Honorary Vice President of the International Stress Management Association and Chairman of its US branch. He has held numerous important posts including the 1998-99 President of The Pavlovian Society, an organization of distinguished international scientists devoted to integrating basic and clinical research, President of the New York State Society of Internal Medicine, Chairman of the International Foundation for Biopsychosocial Development and Human Health, Expert Consultant on Stress to the United States Center for Disease Control, President, Westchester Diabetes Association, and President, Yonkers Academy of Medicine. He has received many honors, including the Outstanding Physician’s Award of the New York State Medical Society, Man of the Year Award with a Congressional Citation, the Schering Award, and the International Distinguished Service Award of the American Rural Health Association.  In 1985, he received an award from the American Society for Contemporary Medicine and Surgery for 'contributions to our understanding of stress, health, and disease'. The Russian Academy of Medical Sciences bestowed the I.M. Sechenov Memorial Medal on him in 1993 and he is one of the few foreign members ever elected to full Fellowship in this prestigious organization.  He was also the recipient of the 2001 annual Innovation Award of The International Society for the Study of Subtle Energies and Energy Medicine.

Dr Rosch has served as Editor-in-Chief of Stress Medicine, Associate Editor of The International Journal of Emergency Mental Health, and International Journal of Stress Management, and on the Editorial Board of many publications including the Journal of Human Stress, International Journal of Psychosomatics, Cardiovascular Reviews and Reports, Comprehensive Therapy, Journal of Human Behavior, and Health Inform; Essential Information on Alternative Health Care.   He has organized and presided over the annual International Congress on Stress since 1988 (For further information visit www. stress.org)

Dr Rosch authors the Wellsprings of Health section of Creative Living and Health and Stress, the monthly Newsletter of the American Institute of Stress.  He is co-author of The Doctors Guide to Instant Stress Relief, Magnet Therapy, DeStress, Weigh Less, senior editor of Bioelectromagnetic Medicine and editor of Bioelectromagnetic and Subtle Energy Medicine.  He has appeared on numerous national and international television programs such as The Today Show, Good Morning America, 60 Minutes, Nova, CBS, NBC, PBS, BBC and CBC network presentations.  His editorials and comments have been published in every major medical journal including the New England Journal of Medicine, Annals of Internal Medicine, Journal of The American Medical Association, British Medical Journal and The Lancet.   He has been interviewed and widely quoted in Time, Fortune, Newsweek, The Reader’s Digest, The Wall Street Journal, New York Times, USA Today, The Washington Post, The London Times, and numerous other publications here and abroad. The annual Paul J. Rosch Award was established by the Brazil branch of The International Stress Management Association, he is a member of the International Advisory Committee School of Psychology and Social Science, Universidad de Flores in Buenos Aires, and an International Institute of Stress Medicine is being established in his honor in Mexico (Instituto Internacional de Medicine del Estrés Dr. Paul J. Rosch).

Article first published 24/06/15



References

  1. Ho MW. Low fat and low saturated fat diet bad for health (posted 13/04/2015). Science in Society 66 2015.
  2. Ho MW. Statins for the healthy are harmful (posted 15/04/2015). Science in Society 66  2015.
  3. Windhaus A. Uber der Gehalt normaler und atheromatöser Aorten an Cholesterol und Cholesterinester. Zeitschrift Physiol Chemie 1910, 67, 174-6.
  4. Anitschkow N, Chatalov S. Über experimentelle Cholesterinsteatose und ihre Bedeutung für die Entstehung einiger pathologischer Prozesse. Zentralbl Allg Pathol 1913,  24,1–9. [On experimental cholesterin steatosis and its significance in the origin of some pathological processes. Reprinted in Arteriosclerosis 1983,3, 178–82] 
  5. Gofman JW, Lindgren F, Elliott H, Mantz W, Hewitt J, Herring V. The role of lipids and lipoproteins in atherosclerosis. Science 1950, 111,166-71.
  6. Gofman JW. Serum lipoproteins and the evaluation of atherosclerosis. Ann N Y Acad Sci 1956, 64, 590-5.
  7. Goldstein JL, Brown MS. Familial hypercholesterolemia: identification of a defect in the regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity associated with overproduction of cholesterol. Proc Natl Acad Sci USA 1973, 70, 2804-8.
  8. Brown MS and Goldstein JL. The Nobel Prize in Physiology or Medicine, 1985, http://www.nobelprize.org/nobel_prizes/medicine/laureates/1985/press.html
  9. Dobbin EV, Gofman HF, Jones HC, Lyon L, Young C-B. The Low Fat, Low Cholesterol Diet: What To Eat And How To Prepare It. Doubleday & Company, Inc., Garden City, New York, 1951.
  10. Keys A. Atherosclerosis: A problem in newer public health. J Mount Sinai Hosp NY 1953, 20,118-39.
  11. Keys A. Coronary heart disease in seven countries. I. The study program and objectives. Circulation 1970, 41, 1–8.
  12. Kannel WB, Dawber TR, Kagan A et al. Factors of risk in the development of coronary heart disease--six-year follow-up experience. The Framingham Study. Ann Intern Med 1961, 55, 33-50.
  13. U.S. Senate Select Committee on Nutrition and Human Needs. Dietary Goals for the United States, 2nd ed. Washington, DC, U.S. Government Printing Office, 1977.
  14. Dock W. Research in arteriosclerosis; the first fifty years. Ann Intern Med 1958;49:699–705.
  15. Mehta NJ, Khan IA. Cardiology’s 10 Greatest Discoveries of the 20th Century. Texas Heart Inst J 2002, 29,164-71.
  16. Kolodgie FD, Katocs Jr AS, Largis EE, Wrenn SM et al. Hypercholesterolemia in the Rabbit Induced by Feeding Graded Amounts of Low-Level Cholesterol. Arteriosclerosis, Thrombosis, and Vascular Biology 1996, 16, 1454-64.
  17. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodologic note. NY State J Med 1957, 57, 2343-54.
  18. Smith RL. Diet, Blood cholesterol and coronary heart disease: A critical review of the literature. Santa Monica, CA. Vector Enterprises Inc 1991, 4-47-4-49.
  19. Mann GV. Diet-heart: end of an era. N Engl J Med 1977, 297, 644-50.
  20. Keys A, Anderson JT, Mickelsen O, Adelson SF, Fidanza F. Diet and serum cholesterol in man: lack of effect of dietary cholesterol. J Nutr 1956, 59, 39-56.
  21. Keys A. Normal plasma cholesterol in a man who eats 25 eggs a day. N Engl J Med 1991, 325, 584.
  22. Keys A. 'Interview with Ancel Keys' Eating Light Magazine, 1997. 


  23. Christakis G, Rinzler SH, Archer M, Kraus A. Effect of the Anti-Coronary Club program on coronary heart disease. Risk-factor status. JAMA 1966, 198(6), 597-604.
  24. Renaud S, deLorgeril M. Wine, alcohol, platelets and the French Paradox for coronary heart disease, Lancet 1992,  339(8808), 1523-6.
  25. Willcox DC, Willcox BJ, Todoriki H, Suzuki M. The Okinawan Diet: Health implications of a low-calorie, nutrient-dense, antioxidant-rich dietary pattern low in glycemic load. J Am Coll Nutr 2009, 28 Suppl, 500S-16S.
  26. Wolf S, Bruhn G. Rose. Further data on the incidence of myocardial infarction in Roseto and neighboring Pennsylvania communities revisited. Transactions of the American Climatological Association 1973, 85, 100-112.
  27. McCann MB, Clancy RE, Gore I, Stoudt HW et al. Nutritional and epidemiologic factors related to heart disease. World Rev Nutr Dietet 1970, 12, 1-42.
  28. Malhotra, S L. Serum lipids, dietary factors and ischemic heart fisease. Am J Clin Nutr 1967. 20, 462-74.
  29. Weinberg SL. The diet–heart hypothesis: a critique.  J Am Coll Cardiol 2004, 43(5), 731-3.
  30. Kannel, W. B. and Gordon, T.: The Framingham Study. Diet and Regulation of Serum Cholesterol. Section 24, Dept. of Health, Education and Welfare. Washington, D. C., 1971.
  31. Castelli W. Concerning the Possibility of a Nut. . . Arch Int Med 1992, 152(7), 1371-2.
  32. Anderson KM, Castelli WP, Levy D. Cholesterol and mortality. 30 years of follow-up from the Framingham study. JAMA 1987, 257, 2176-80.
  33. Nichols AB, Ravenscroft C, Lamphear DE, Ostrander LD. Independence of serum lipid levels and dietary habits. The Tecumseh Study. JAMA 1976, 236(17), 1948-53.
  34. Stewart AW, Kuulasmaa K, Beaglehole R, for the WHO MONICA Project. Ecological analysis of the association between mortality and major risk factors of cardiovascular disease. The World Health Organization MONICA Project. Intern J Epidemiol 1994, 23, 505-16.
  35. Reiser R. Saturated fat in the diet and serum cholesterol concentration: a critical examination of the literature. Am J Clin Nutr 1973, 26, 524-55.
  36. Ravnskov U. Cholesterol lowering trials in coronary heart disease: frequency of citation and outcome. BMJ 1992, 305, 15-9.
  37. Multiple Risk Factor Intervention Trial Research Group. Multiple risk factor intervention trial: risk factor changes and mortality results. JAMA 1982, 248, 1465-77.
  38. Howard BV, Van Horn L, Hsia J, et al. Low-fat dietary pattern and risk of cardiovascular disease: the Women's Health Initiative Randomized Controlled Dietary Modification Trial. JAMA 2006, 295, 655-66.
  39. Howard BV, Curb JD, Eaton CB, et al. Low-fat dietary pattern and lipoprotein risk factors: the Women's Health Initiative Dietary Modification Trial. Am J Clin Nutr 2010, 91, 86074.

Got something to say about this page? Comment

Comment on this article

Comments may be published. All comments are moderated. Name and email details are required.

Name:
Email address:
Your comments:
Anti spam question:
How many legs does a spider have?

There are 5 comments on this article so far. Add your comment above.

dhinds Comment left 25th June 2015 06:06:56
This long article addresses a serious cause of mortality but arrives at no conclusion, other than the unsubstantiated idea that dietary content has no effect on blood cholesterol levels. Evaluated from a perspective of semantics, the article is perverse, and not up to the standards I have come to expect from i-sis. Hopefully, the sequel will present concepts with far more substance.

dhinds Comment left 27th June 2015 06:06:08
While I found fault with the article and consider the credits presented by the author to be excessive, the following url links to a more credible perspective. http://www.stress.org/stress-alzheimers-and-memory-loss/ I hope the sequel contains less hype.

Todd Millions Comment left 27th June 2015 20:08:46
Your Radiation this week-At Veterans Today ,is reporting counts per minute(partial)approaching 1000 for two recording/detector stations in the US-one of them not very far from me.As normal background was in the 10 count per minute range in pre-atomic bomb/water boiler times- having bogus studies blaming this ALL on smoking,Diet and bad genes is very useful too those profiting from the extinction of us all.

Carina Comment left 7th October 2015 10:10:52
So sad to see that you've fallen for the LCHF and meat and dairy industry propaganda, when so many of your other science articles are well researched and bring up valid points that mainstream media don't. No, humans do not need any more cholesterol than the body is able to produce by itself, because we are definitely not carnivores. We are herbivores with the ability to be omnivores if necessary but not with long lasting good health benefits unless meat intake is very low. The reason LCHF adherants see improvements in their health in the beginning is not because they omit carbs, and eat a lot of meat and saturated fats (which has never been a big part of human diets, until very recently), but because they omit SIMPLE carbs. They end up thinking that the meat and saturated fat must be good for them when it's actually going to ruin their health in the long run. (Unless they eat a lot of complex carbs and very little meat and dairy.) We should be happy that the meat and dairy industries have not been able to shut up scientists that have found these foods to be harmful. Maybe thanks to the drug companies (for once) we have seen research that oppose the meat industry, although statins are a horrible solution to the problem. That I completely agree with. No drugs, less meat eating and more complex carbs is the only sensible solution.

George Henderson Comment left 23rd December 2015 07:07:11
We can certainly find human diets that are high in saturated fat with low risk of atherosclerosis, such as the diets of Pacific Islanders getting mot of their energy from coconuts, and we can find well-studied populations where a high intake of fat, most of which comes from animal sources, is associated with a greatly reduced risk of heart disease; for example, men have the most heart attacks in any population, and the men in this population who eat most fat (mostly from dairy and meat) have the lowest mortality from heart disease. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2005.01520.x/pdf Whereas the women in that population, who get more MUFA from vegetable oils (liquid margarine) and less from meat than the men, have higher cancer mortality with higher fat intake, and no protection from CHD. In this meta-analysis we find that saturated fat is not correlated with heart disease, but that higher intake of a trans fat found in dairy and beef fat is associated with a greatly reduced incidence of diabetes. http://www.bmj.com/content/351/bmj.h3978 The article is about saturated fat and cholesterol, not about meat. Meat avoidance is all very well for some, but it is a fringe activity requiring a robust physical and mental constitution, much like mountain climbing, and, like mountain climbing, should not be recommended for the whole population.

Recommended Reading

search | sitemap | contact
© 1999 - 2017 i-sis.org.uk