Tag Archives: cholesterol

Science In Support of the Mediterranean Diet

Atherosclerosis is the formal term for “hardening of the arteries.”  Who cares how hard they are, as long as the arteries deliver blood to our organs, right?

Atherosclerosis in the arteries that supply blood to the heart – essentially a hollow muscle that pumps blood – is called coronary heart disease disease (CHD) or coronary artery disease (CAD).

LDL cholesterol is the “bad cholesterol” that is associated with atherosclerosis.  Generally, the higher the LDL, the worse the atherosclerotic complications: plaque build-up leads to poor circulation to vital organs, arterial blood clots, even death of tissue due to blocked arteries.  Oxidation of LDL cholesterol facilitates atherosclerosis.

People at high risk for coronary heart disease include type 2 diabetics, smokers, people with high blood pressure or cholesterol abnormalities, and people with a family history of coronary heart disease.  Advanced age is another strong risk factor.

The ongoing PREDIMED Study is designed to test the the effects of the traditional Mediterranean diet in primary prevention of coronary heart disease in a high risk population.  9000 study participants will be assigned to one of three diets:  1) low-fat, 2) Mediterranean plus extra olive oil, or 3) Mediterranean plus extra nuts.  The Mediterranean diet is moderate in percentage of calories derived from fat, and the main source of fat is olive oil.  Virgin olive oil has a particularly high content of antioxidant phenolic compounds.  Nuts are also a rich source of antioxidant phytochemicals.  These antioxidants can prevent the harmful transmogrification of plain LDL into oxidized LDL.

A group of 372 early study enrollees were randomly assigned to one of the three diet groups.  In both of the Mediterranean diet groups, researchers found reduced oxidized LDL, reduced blood pressures, lower total cholesterol, and lower total-HDL cholesterol ratios, more than in the low-fat diet group.

These observed changes would tend to reduce the incidence and severity of atherosclerotic complications.  When PREDIMED is completed, we’ll know whether the traditional Mediterranean diet, compared with a low-fat diet, is better at preventing death and disease from coronary heart disease.  That’s where the rubber meets the road.

Steve Parker, M.D.


Montserrat, Fito, et al.  Effect of a Traditional Mediterranean Diet on Lipoprotein Oxidation: A Randomized Controlled Trial.  Archives of Internal Medicine, 167 (2007): 1,195-1,203.

Prevencion con Dieta Mediterranea Study (PREDIMED)  http://www.predimed.org

Do Eggs Cause Heart Attacks and Premature Death?

At the beginning of my 30-year medical career, egg consumption was condemned as a cause of heart attacks.  Heart attacks can kill.  How did eggs kill?  It was thought to be related to the cholesterol content – 200 mg per egg – leading to higher serum cholesterol levels, which clogged arteries (atherosclerosis), leading to heart attacks.

Fifteen years ago the pendulum began to swing the other direction: Egg consumption didn’t seem to matter much, if at all.

The evidence is usually collected in observational, epidemiologic studies of large groups of people.  The groups are analyzed in terms of overall health, food intake (e.g., how many eggs per week), healthy lifestyle factors, etc.  Egg consumption of the group is broken down, for example, into those who never eat eggs, eat 1-4  eggs per week, eat 5-10 per week, or over 10 eggs weekly.  A group is followed and re-analyzed over 10-20 years and rates various diseases and causes of death are recorded.  Researchers don’t follow just 25 people like this over time.  You need thousands of participants to find statistically significant differences.

The debate about eggs was re-opened (although never really closed) by the publication in April, 2008, of an article in The American Journal of Clinical Nutrition.  Scientists of the Physicians’ Health Study suggest that consumption of seven or more eggs weekly is associated with significantly increased risk, over 20 years, of all-cause mortality.  Interestingly, this level of consumption did not cause heart attacks or strokes.  Study participants, by the way, were 21,327 Harvard-educated male physicians.  5,169 deaths occurred during 20 years of follow-up.  If you’re not a Harvard-educated male physician, the study results may not apply to you.

When physicians with diabetes  – type 2’s mostly, I assume –  were analyzed separately, consumption of even less than seven eggs per week was associated with higher all-cause mortality.

Several other observational studies looking at this same issue have found no association between egg consumption and cardiovascular disease, heart attacks, and all-cause mortality.

Bottom line?  If you worry about egg consumption, limit to 7 or less per week.  If you have type 2 diabetes, consider limiting to 4 or less per week.

I wouldn’t be surprised if a study were published next week saying “eat as many eggs as you want; they don’t have adverse health effects.”

Remember, all the cholesterol is in the yolk.  Try making an omelet using the whites only.  But in our lifetimes you’ll never see an observational study looking at egg white consumption and mortality rates.

I’m still not convinced egg consumption is worth losing sleep over.  “More studies are needed…”

Steve Parker, M.D.References:

Djousse, L. and Gaziano, J. M.  Egg consumption in relation to cardiovascular disease and mortality: the Physicians’ Health Study.  American Journal of Clinical Nutrition, 87 (2008): 964-969.

Dawber, T.R, et al.  Eggs, serum cholesterol, and coronary heart disease.  American Journal of Clinical Nutrition, 36 (1982): 617-625.

Nakamura, Y., et al.  Egg consumption, serum cholestrol, and cause-specific and all-cause mortality: the National Integrated Project for Prospective Observation of Non-communicable Disease and Its Trends in the Aged, 1980.  American Journal of Clinical Nutrition, 80 (2004): 58-63.

Time to Abandon the Diet-Heart Hypothesis?

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.

My Comments

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.

Steve Parker, M.D.