What does research say causes atherosclerosis?

Atherosclerosis, according to the American Heart Association (AHA), is the name given to the “…fatty deposits that clog arteries” (2017, para. 1). “These buildups are called plaque” and “they’re made up of cholesterol, fatty substances, cellular waste products, calcium and fibrin (a clotting material in the blood)” (AHA, 2017, para. 1).

According to Benjamin and Roberts (2013):

Studying atherosclerosis at necropsy (death) or after endarterectomy (surgical removal of fat from the arterial lining to open the vein) has convinced Roberts that the only real long-term therapy for the western world’s number one disease is prevention. Although the Framingham investigators and others have convinced most physicians and the lay public that atherosclerosis is a multifactorial disease, Roberts is convinced that the disease has a single cause, namely cholesterol, and that the other so-called atherosclerotic risk factors are only contributory at most. As shown in figure 1, most of the risk factors do not in themselves cause atherosclerosis (p. 124-125)


Figure 1. Roberts and Benjamin (2013). Atherosclerotic Risk Factors. Retrieved October 3, 2016.

According to Roberts (2010):

The view that atherosclerosis is a multifactorial disease has muddled the waters in my view. This is not to say that cigarette smoking, increased blood pressure, diabetes mellitus or obesity, and inactivity are not harmful— of course they are— but if serum LDL cholesterol is 60 mg/dl or serum total cholesterol is 150 mg/dl, there is no evidence (with extremely rare exceptions) in my view that these other risk factors cause atherosclerosis (p. 1364).

McDougall’s Moments: Atherosclerosis

According to Castelli (2001), the director of the Framingham heart study, during the first 50 years of Framingham heart study only 5 individuals developed coronary artery disease with a cholesterol level less than 150 mg/dl (p. 16F). Therefore keeping cholesterol under 150mg/dl is essential in preventing heart disease. According to Kannel, Castelli, and Gordon (1979), “prospective data at Framingham and elsewhere have shown conclusively that risk of coronary heart disease in persons younger than age 50 is strikingly related to the serum total cholesterol level” (p. 85). Roberts (2010) believes “the only way to produce atherosclerosis experimentally is by feeding high-cholesterol and/or high-saturated fat diets to herbivores” (p. 1364).

Only animal products contain cholesterol, and animal products also contain saturated fat and trans fat, while whole plant-based foods contain little to no saturated fat, except for tropical oils like coconut and palm oils, palm kernel oils which contain large amounts of saturated fat (United States Department of Health and Human Services and the United States Department of Agriculture (DHH and USDA, 2015, p. 90, 92). Therefore, to reduce or eliminate the risk of developing cardiovascular disease, or having future complications, complete avoidance of animal-based foods as well as plant-based vegetable oils and tropical oils like coconut and palm kernel oils should be followed to greatly reduce the risk of increasing LDL cholesterol levels. The Institute of Medicine (2002), recognizes that there is no safe level of consumption of “saturated fat, cholesterol, or trans fatty acids, as increased risk exists at levels above zero” (para. 8).

According to Benjamin and Roberts (2013) “Studying atherosclerosis… has convinced Roberts that the only real long-term therapy for the Western World’s number one disease is prevention” (p. 124).

According to Benjamin and Roberts (2013), the number one cause of atherosclerosis is cholesterol. The four arguments he uses to back his claims are as follows: 1. Atherosclerosis can be demonstrated in herbivorous animals such as monkeys and rabbits by feeding them cholesterol and saturated fat, if the animal is carnivorous such as a dog or cat the results cannot be reproduced. Even blowing smoke in a rabbit’s face for its entire life does not produce atherosclerosis. 2. The plaque that narrows arteries contains cholesterol. 3. Societies with high cholesterol levels have higher rates of heart attacks, while those with low levels of cholesterol experience lower rates. 4. When cholesterol levels diminish, with the use of drugs, so do atherosclerotic events. He explains that while humans consider themselves carnivores our features and characteristics resemble that of herbivores (p. 124).

The characteristics are detailed below:


Table 1. Roberts and Benjamin (2013). The differences between carnivores and herbivores. Retrieved October 3, 2016.

Milton Mills, MD: Are Humans Designed to Eat Meat

How can Roberts claim that consuming cholesterol and saturated fat, found in animal products, increases the risk of atherosclerosis?

William Clifford Roberts has been the editor in chief of the American Journal of Cardiology since 1982 (Roberts & Frye, 2007, p. 269). According to Roberts & Frye (2007):

From July 1964 until March 1993 he [William Clifford Roberts] headed the pathology section or branch of the national heart, lung, and blood institute. He has published just over 1400 articles, authored or edited 24 books… Since March 1993, he has been executive director of the Baylor Heart and Vascular Institute of Baylor university medical center in Dallas Texas… He has been the editor in chief of The American Journal of Cardiology since 1982 (25 years) (p. 269).

Roberts (1992) states that of the following independent risk factors:

Male sex, family history of premature coronary events, cigarette smoking (> 10/day), systemic hypertension, diabetes mellitus and severe obesity (>30% overweight) should be viewed as cholesterol-dependent atherosclerotic risk factors and not in themselves as atherogenic. There is no doubt that atherosclerotic events are more common in people with these risk factors, but only in those populations with an average serum total cholesterol level above 3.9 mmol/l. (p. S5)

Roberts believes that being male, having a family history of premature coronary events, cigarette smoking, systemic hypertension, diabetes mellitus and severe obesity do not cause atherosclerosis (“fatty deposits that can clog arteries” [AHA, 2017, para. 1]), but increased cholesterol levels do cause atherosclerosis.

Roberts (1992) and the National Cholesterol Education Program (NCEP, 2002) have both concluded that populations that have low total cholesterol levels <150 mg/dL (or LDL cholesterol <100 mg/dL) throughout their life do not experience or have a near-absence of CHD (p. 552; p. 3164). According to Kannel, Castelli, Gordon, and McNamara (1971), risk of each particular clinical manifestation of coronary heart disease (including angina, myocardial infarction, and sudden death) proved proportional to the antecedent serum cholesterol level in men of all ages studied (p. 3). Meaning as total serum cholesterol increases so does the risk of coronary heart disease.

Kannel, Castelli, Gordon, & McNamara (1971) also recognized that there was nothing to suggest that some particular level was “critical.” Hence, it does not appear logical to examine the relation of cholesterol to risk of coronary heart disease in terms of “hypercholesterolemia” but rather in terms of the actual concentration of cholesterol in the plasma (p. 4). Total cholesterol, or the total serum cholesterol, proved to be more accurate when determining heart attack risk more than any other blood cholesterol marker.

It should be noted that the United States Department of Health and Human Services and the United States Department of Agriculture (HHS and USDA, 2015) recognize that humans have no need for dietary cholesterol and that the body produces all it needs (p. 32). Therefore, any excess cholesterol from dietary sources may be harmful to humans.


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