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The Official Newsletter of
updated January 3, 2013

Is the Lipid Theory Dead?

by Ron Brown, Ph.D., author of The Body Fat Guide 

"Ron Brown is a certified fitness trainer who doesn't have an inch of flab on his body. He'll tell you what you can do to become fit and trim too." 
Washington DC


THE FOLLOWING is an excerpt from my Ph.D. dissertation on plant-based diets.

Lipid hypothesis. Cardiovascular disease research has been dominated for almost half a century by the lipid hypothesis, even though most study findings contradict rather than support the hypothesis (Ravnskov, 2008). The first postulate of the lipid hypothesis is that a high saturated fat intake elevates blood cholesterol levels, and the second postulate of the hypothesis is that elevated blood cholesterol levels lead to atherosclerosis and other cardiovascular diseases (Stanley , 2010). Carbohydrate-rich diets and diets low in total fat and saturated fat have been recommended in accordance with the lipid hypothesis, but several study findings indicated that total cholesterol or LDL cholesterol levels remained unchanged in participants even when saturated fat intakes exceeded the upper recommended level by three to seven times (Ravnskov, 208, p. 236). Few studies support the finding that high saturated-fat intake causes cardiovascular disease (Stanley , 2010). After 20 years of following participants, researchers of the Nurses’ Health Study could not demonstrate that a maximum 10% reduction in blood serum cholesterol levels from reduced saturated-fat intake was sufficient to lower coronary heart disease risk (Stanley, 2010, p. 39). 

Findings from the Women’s Health Initiative, a study that included dietary modification with a low-fat diet, contradicted previous recommendations by nutrition experts to follow a low-fat diet to prevent chronic disease (Ottoboni & Ottoboni, 2007). The Women’s Health Initiative was a randomized, controlled trial conducted on 48,835 postmenopausal women recruited between 1993 and 1998, and the study cost $700 million—the largest study of women’s health ever funded by the U.S. government (Ottoboni & Ottoboni, p. 10). Participants in the Women’s Health Initiative were followed over eight years with periodic clinic visits and food questionnaires, and were divided between an experimental low-fat group that maintained dietary fat intake levels that were approximately 10% to 8% lower than participants in the control group who did not make any dietary modifications (Ottoboni & Ottoboni, p. 10). Although significantly reduced low-density lipoprotein cholesterol levels were found in the experimental group, reduced LDL levels were not great enough to impact chronic disease incidence, and there were no changes in beneficial high-density lipoprotein cholesterol levels in either group (Ottoboni & Ottoboni). 

The Women’s Health Initiative project officer for the National Institutes of Health, Jacques Rossouw, responded to vigorous criticism directed at findings from the Women’s Health Initiative study: “The strength of the reaction has been commensurate with the strength of the dogma it overturned” (Ottoboni & Ottoboni, 2007, p. 11). Recounting the public low-fat craze that has occurred since the 1980s following health recommendations to avoid dietary saturated fat, Hu (2007) noted that not all dietary fat is bad. Much of the increased refined carbohydrate and starchy food consumption that the public used to replace dietary fat has increased adiposity (body fat) and increased coronary heart disease risk by elevating triglyceride levels (Hu, 2007). A diet high in vegetable fat and vegetable protein derived from nuts and other plant foods was found to be more healthful than a low-fat diet high in starchy and refined carbohydrate foods (Hu, 2007). The public’s concern about developing cardiovascular disease from eating vegetable fat in a plant-based diet is not supported by scientific research (Hu, 2007). In spite of research findings contradicting the lipid hypothesis, politicians and the food and pharmaceutical industries continue to promote and profit from the public’s belief in dietary recommendations based on the lipid hypothesis (Ottoboni & Ottoboni, 2007).  

A natural experiment was conducted to examine how coconut consumption, dietary cholesterol, and saturated fat intake affected serum cholesterol levels in people inhabiting the Polynesian atolls at Pukapuka and Tokelau islands (Prior, Davidson, Salmond, & Czochanska, 1981). Plant-based diets in both island populations were low in dietary cholesterol from consuming small amounts of fish, but were high in saturated fat from consuming coconuts which provided the main source of energy (Prior et al., 1981). Although Tokelauans consumed twice as much coconut and had serum cholesterol levels that were 15 mg/dl higher than Pukapukans, Prior et al. (1981) reported that “vascular disease is uncommon in both populations and there is no evidence of the high saturated fat intake having a harmful effect in these populations” (p. 1552). 

Concerns over dyslipidemia and cardiovascular disease four decades ago encouraged health professionals to recommend replacing dietary coconut oil with soybean oil, but concerns were based on misleading results from food industy studies that used hydrogenated coconut oil with modified oleic and linoleic fatty acids (Assunção, Ferreira, dos Santos, Cabral, & Florêncio, 2009). Assunção et al. (2009) supplemented either filtered coconut oil or soy bean oil into equivalent reduced-calorie diets given to separate groups of obese females who were instructed to exercise. Because much of the saturated fat in coconut oil is medium-chain fatty acids that are converted directly by the liver into energy and are less likely to be stored in adipose tissue, the coconut-oil group lost more abdominal fat than the soybean-oil group (Assunção et al, 2009). By the end of the diet the coconut-oil group also had healthier lipid serum profiles, including a raised HDL level and lowered LDL:HDL ratio, while the soybean-oil group had reverse results with a lowered HDL level, raised total cholesterol level, and a raised LDL:HDL ratio (Assunção et al., 2009).

Contradicting nutritional recommendations to promote low-fat versions of animal-based foods, or to substitute one animal-based food for another (e.g., substituting chicken or fish for red meat), Campbell and Campbell (2006) found that reducing animal-fat intake alone did not reduce chronic disease risk unless protein intake from animals was also reduced. In animal experiments, T. Colin Campbell demonstrated that a protein in cow milk, casein, was carcinogenic in amounts normally consumed by humans, and that cancer growth occurred when daily calories from total dietary animal-based protein increased above 10% (Campbell & Campbell, 2006). Cancer growth reversed when daily calories from dietary animal protein fell to no more than 10%, while protein from plant sources did not show any carcinogenic effect (Campbell & Campbell, 2006). 

T. Colin Campbell further investigated his laboratory findings in an epidemiological study conducted in China , in which disease prevalence was compared with the diet consumed by the population in various Chinese counties (Campbell & Campbell, 2006). Higher animal-protein intake was associated with increased cancer prevalence and other degenerative diseases in a Chinese-population sample (Campbell & Campbell, 2006). Total daily calories consumed from animal protein was 0.8% in rural China, in contrast to 10–11% in the United States (Campbell & Campbell, 2006). 

The belief that dietary fat and cholesterol cause chronic disease was traced to earlier investigations showing a strong positive correlation between animal-fat intake and diseases like breast cancer, although plant fat intake did not show the same correlation (Campbell & Campbell, 2006). Explaining that correlation does not indicate causation, Campbell and Campbell (2006) wrote, “We now know that the attention paid to fat and cholesterol was misguided. The possibility that no one wanted to consider was that fat and cholesterol were merely indicators of animal food intake” (p. 119). 

Addendum: A major study not referenced in my Ph.D. dissertation is a meta-analysis of epidemiological studies finding no association between saturated fat intake and cardiovascular disease (Siri-Tarino et al., 2010). Also, researchers confirm that oxidized cholesterol is associated with arterial plaque (See How Cooking Clogs Your Arteries).


Assunção, M. L., Ferreira, H. S., dos Santos, A. F., Cabral Jr., C. R., & Florêncio, T. M. M. T. (2009). Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity. Lipids, 44, 593–601. doi:10.1007/s11745-009-3306-6

Campbell, T. C., & Campbell, T. M., II (2006). The China study: Startling implications for diet, weight loss, and long-term health. Dallas, TX: BenBella.

Hu, F. B. (2007). Diet and cardiovascular disease prevention: The need for a paradigm shift. Journal of the American College of Cardiology, 50, 22–24. doi:10.1016/j.jacc.2007.04.027

Ottoboni, A., & Ottoboni, F. (2007). Low-fat diet and chronic disease prevention: The Women’s Health Initiative and its reception. Journal of American Physicians and Surgeons, 12, 10–13.

Prior, I. A., Davidson, F., Salmond, C. E., & Czochanska, Z. (1981). Cholesterol, coconuts, and diet on Polynesian atolls: A natural experiment: The Pukapuka and Tokelau Island studies. American Journal of Clinical Nutrition, 34, 1552–1561.

Siri-Tarin, P. W., Sun, Q., Hu, F. B., & Krauss, R. M. (2010). Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. American Journal of Clinical Nutrition, 91, 535–546.

Stanley, J. (2010). How good is the evidence for the lipid hypothesis? Lipid Technology, 22, 39–41. doi:10.1002/lite.200900076

Ravnskov, U. (2008). The fallacies of the lipid hypothesis. Scandinavian Cardiovascular Journal, 42, 236–239. doi:10.1080/14017430801983082 

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