The skinny on fat and heart disease

Townsend Letter for Doctors and Patients, June, 2006 by Alan R. Gaby

An eight-year study published in the Journal of the American Medical Association (2006;295:655-666), the results of which were circulated extensively in the media, concluded that reducing total fat intake and increasing intakes of vegetables, fruits, and grains did not significantly reduce the risk of coronary heart disease, stroke, or cardiovascular disease in postmenopausal women. The study was roundly criticized by some, embraced by the it-doesn't-matter-what-you-eat crowd, and ignored by many who are tired of the seemingly constant barrage of contradictory messages about nutrition emanating from the scientific community. In actuality, the study seems like a multimillion-dollar waste of money that added little to our understanding about diet and cardiovascular disease.

Some 48,835 postmenopausal women (aged 50-79 years), enrolled in the Women's Health Initiative Dietary Intervention Trial, were randomly assigned to an intervention group or a control group. The intervention group received intensive behavior modification designed to reduce total fat intake to 20% of calories, to increase intakes of vegetables and fruits to a total of five servings per day, and to consume at least six servings of grains per day. The participants completed food-frequency questionnaires at baseline, after one year, and periodically thereafter. During a mean follow-up period of 8.1 years, there were no significant differences between the intervention and control groups in the incidence of coronary heart disease, stroke, or cardiovascular disease.

One of the most important weaknesses of the study was that the participants appeared to be engaging in mass fibbing regarding what they were eating. According to the food-frequency questionnaires, the mean energy intake of the women in the intervention group decreased from baseline to year one by 290 kcal/day and from baseline to year six by 358 kcal/day. With that degree of calorie restriction, this group of overweight women (mean baseline weight, 169 pounds) should have lost enormous amounts of weight. However, their mean body weight fell by only 2.5 pounds after six years, suggesting that energy intake was greater than was being reported. Consequently, fat intake was also probably higher than claimed, and the report of a modest increase in vegetable and fruit consumption may not have been reliable either.

Even according to the questionable data from the food-frequency questionnaires, the women never reached the target goal of reducing fat intake to 20% of energy. The mean fat intake in the intervention group was reported as 24.3% of energy at year one and 28.8% of energy at year six. It is noteworthy that women who reported consuming the lowest amounts of saturated fat and trans fatty acids and the highest amounts of fruits and vegetables experienced statistically significant reductions in heart disease incidence, with risk reductions of 18% for low saturated fat intake, 19% for low trans fatty acid intake, and 12% for high vegetable and fruit intake. Those observations suggest that dietary modifications do, in fact, influence the risk of heart disease.

I have never been much of a believer in the idea that total fat intake is a major determinant of heart disease risk. The first heart attack ever reported in the medical literature was less than 100 years ago, and some people were consuming high-fat diets long before that. In addition, there are certain populations around the world that consume high-fat diets and have a low incidence of heart disease. Most of the epidemiological studies that found an association between fat intake and heart disease were confounded by the fact that there is a strong correlation between fat consumption and refined-sugar intake. The physiological effects of high sugar consumption (increased platelet aggregation, increased triglyceride levels, lower HDL-cholesterol levels, increased blood pressure) suggest that refined sugar is more important than fat as a cause of heart disease.

Some individuals are more sensitive than others to increases in dietary fat intake. However, other people run into problems when they eat too much protein or too many carbohydrates. While a high-fat diet may cause hypertriglyceridemia or hypercholesterolemia, high-protein intake can promote hyperhomocysteinemia, and high-carbohydrate intake (even complex carbohydrates) worsens insulin resistance in a subset of the population. The optimal balance of macronutrients probably varies from person to person, but there is no obvious reason to indict fat as the "bad" macronutrient.

The effects that the different macronutrients have on metabolism and health depend in part on micronutrient status. For example, in rats fed a high-fat diet, the development of atherosclerosis can be prevented by increasing the magnesium content of the diet. If higher fat intake does increase heart disease risk in Western societies, that effect might be due to an impaired capacity to metabolize fat, resulting in part from the low content of magnesium and other nutrients in refined and processed food. Similarly, whether or not a high-protein diet will raise homocysteine levels depends on our intake of folic acid, vitamin B6, vitamin B12, betaine, and choline; and whether a high-carbohydrate diet will promote insulin resistance depends in part on the chromium, magnesium, and B-vitamin content of the diet.