In January, 2009, The American Journal of Medicine published a 62-page supplement (vol. 122, number 1A) entitled “Management of Atherosclerosis: A Practical Guide in 2008.”
I scanned it with attention to the Diet-Heart Hypothesis: the idea that dietary factors – such as saturated fat, total fat, cholesterol – cause or aggravate atherosclerosis. Atherosclerosis is colloquially referred to as “hardening of the arteries,” and is a major cause of heart attacks, strokes, and peripheral arterial disease.
One section, “The Pathology of Atherosclerosis: Plaque Development and Plaque Responses to Medical Treatment” is written by William Insull, M.D., who is with the Lipid Research Clinic at Baylor College of Medicine. Here are selected quotes, and my comments in brackets:
Several risk factors may intensify or provoke atherosclerosis through their effects on low-density lipoprotein (LDL) particles and inflammation. These risk factors most frequently include hypertension, tobacco smoking, diabetes mellitus, obesity, and genetic predispositon; the molecular details of how they work are not yet known.
[No mention of diet.]
Early fatty streak development [thought to be a precursor to atherosclerosis] begins in childhood and adolescence. . . . The initial step occurs when LDL particles leave the blood and enter the arterial intima, where, if LDL levels are increased, they accumulate.
[Not entirely clear whether he’s referring to increase LDL in the bloodstream or inside the intima cells – I suspect inside the cells.]
All of these changes may be significantly influenced by risk factors, notably the stress of local hemodynamics and blood flow patterns, hypertension, tobacco smoking, and diabetes, as well as genetically determined arterial susceptibility or resistance to atherosclerosis. The mechanism of these risk factors in influencing atherosclerosis are the target of intensive investigation by molecular pathology, along with proteomics and genomics, conducted to determine the exact molecular biological prosesses involved in their development.
[Again, no mention of diet.]
Dr. Insull does include a table on page S11 that mentions therapeutic reduction of atherogenic plasma lipoproteins by diet, exercise, statins, and other lipid-lowering therapies, but there is no further mention of diet in his article.
Another section, “”Sick Fat,” metabolic Disease, and Atherosclerosis,” is by Harold E. Bays, M.D., of the Louisville (KY) Metabolic and Atherosclerosis Research Center. Selected quotes:
Most major CHD [coronary heart disease] risk factors are modifiable; these include metabolic disorders such as type 2 diabetes mellitus, hypertension, and dyslipidemia.
[No mention of diet.]
His Table 2, “Major risk factors for future atherosclerotic coronary heart disease events” includes history of atherosclerosis, type 2 diabetes, high blood pressure, dyslipidemia, cigarette smoking, adiposopathy, age 45 or older (men), age 55 or older (women), and family history of CHD.
[No mention of diet.]
Among hunter-gatherer populations who follow their indigenous lifestyles, CHD is a rarity. This is in large measure due to a striking reduction in major CHD risk factors, such as markedly reduced [blood] cholesterol levels, in these populations.
[No mention of dietary cholesterol and saturated fats in this context.]
High blood pressure increases CHD risk. Large-scale observational data show a doubling of mortality from ischemic heart disease and stroke for every 20 mm Hg increase in systolic blood pressure or 10 mm Hg increase in diastolic blood pressure.
[Off topic, but a “fun fact,” at least to a doctor.]
As most primary care clinicians are acutely aware, one of the most basic interventions for treating and/or preventing the most common diseases found in medical practice, including CHD, is encouraging patients to adopt favorable nutritional and lifestyle habits.
[No additional text clarifies his “favorable nutritional . . . habits.”]
A later section, “Prevention and Treatment of Atherosclrosis: A Practitioner’s Guide for 2008,” is by Sandra J. Lewis, M.D., with the Oregon Health and Science University in Portland.
Dr. Lewis reiterates the aforementioned major risk factors for atherosclerosis, adding physical inactivity, and not mentioning diet as a major risk factor. She recommends inquiring about eating habits, and encourages “healthy eating.” A quote:
Therapeutic lifestlye changes constitute first-line therapy for reducing LDL cholesterol levels in persons at risk for atherosclerotic CV [cardiovascular] events. All persons, regardless of their short- or long-term risks, should be counseled to adopt positive changes, including a low-cholesterol diet, increased physical activity, and cessation of smoking. Diets should include limits for saturated fats, polyunsaturated fats, monounsatrauted fats, total fat, carbohydrates, and protein. Total cholesterol ineake should be kept to under 200 mg/day.
These recommendations seem to emanate from the 2001 report of the National Cholesterol Education Program, Adult Treatment Panel III. Note: they refer to treatment of people with higher-than-optimal LDL cholesterol levels, not to the general population.
I began questioning the validity of the Diet-Heart Hypothesis in 2009. This monograph seemed like the perfect place for a review of it.
The overall tone of the monograph is very much in favor of statin drugs for reducing the morbidity and mortality of atherosclerosis, particularly in the coronary arteries. Statins are powerful LDL cholesterol-lowering agents. But that proves nothing one way or the other about the Diet-Heart Hypothesis.
Little in this 62-page monograph supports the diet-heart hypothesis and the idea that everyone needs to limit intake of saturated fat, total fats, or cholesterol.