Less saturated fat is better for the heart. That goes without saying. Or does it? When researchers at the Harvard School of Public Health examined the associations between dietary macronutrients—fats and carbohydrates—and the progression of coronary atherosclerosis among postmenopausal women, the results were quite surprising.
Heart catherization (quantitative coronary angiography) was performed at baseline and after a mean follow-up of 3.1 years in 235 postmenopausal women with established coronary heart disease (CHD). The subjects’ usual dietary intake was assessed at baseline. The women’s mean total-fat intake was 25% of total calories.
In multivariate analyses, Mozaffarian and colleagues found that a higher saturated- fat intake was associated with a smaller decline in mean minimal coronary diameter and less progression of coronary stenosis during follow-up. For women in the lowest quartile for saturated-fat intake, the decline in diameter was 0.22 millimeters (mm). For women in the second quartile, the decline was 0.10 mm. For those in the third quartile, it was 0.07 mm. And women in the fourth quartile showed no decline. This inverse association was more pronounced among women with lower monounsaturated fat and higher carbohydrate intakes and, possibly, with lower total-fat intake.
In contrast, carbohydrate intake was positively associated with progression of atherosclerosis, particularly when the food’s glycemic index (GI) was high. Polyunsaturated fat was positively associated with progression when this fat replaced other fats, but not when it replaced carbohydrate or protein. Monounsaturated and total-fat intakes were not associated with progression.
The investigators concluded that in postmenopausal women with relatively low total-fat intake, “a greater saturated- fat intake is associated with less progression of coronary atherosclerosis, whereas carbohydrate intake is associated with a greater progression.”
This is the first study to evaluate the associations between dietary macronutrients and atherosclerotic progression in women. The nutrient associations uncovered here were independent of a variety of other risk factors, including age, diabetes, smoking, body mass index, physical activity, prior myocardial infarction or PTCA (percutaneous transluminal coronary angioplasty), and other dietary habits.
Nonetheless, these results do not encourage a return to diets high in saturated fat, because such diets clearly raise total cholesterol and LDL (bad) cholesterol and therefore increase the risk of cardiovascular disease in both men and women. The findings do, however, reinforce previous research findings that high carbohydrate intakes, especially of high-GI foods, increase triglycerides and decrease HDL (good) cholesterol more dramatically than high intakes of saturated fat. This lipid response may have more dire cardiovascular health consequences over time than a diet that is low in total fat and rich in saturated fat. This is an important point for fitness professionals to understand when making dietary recommendations.
In an insightful follow-up editorial titled “Saturated Fat Prevents Coronary Artery Disease? An American Paradox” (in the same issue of the American Journal of Clinical Nutrition), lipid experts Robert Knopp, MD, and Barbara Retzlaff, RD, MPH, of the University of Washington, Seattle, elaborated on this apparent paradox. They particularly addressed the different blood lipid responses to dietary-fat intake between men and women. Following are several relevant points that Knopp and Retzlaff made with respect to the issue of saturated-fat and carbohydrate intakes and the role of triglycerides in CHD risk among women.
The diet described in the Mozaffarian study was low in fat, averaging 25% of total calories. The subjects were women with CHD who had characteristics consistent with the metabolic syndrome (i.e., abdominal fat gain, elevated blood pressure, high triglycerides, low HDL cholesterol). Two-thirds of these women were taking sex hormones. These points must be taken into account when interpreting the study. Notably, the effects of high-carbohydrate intakes on triglycerides and HDL cholesterol concentrations appear to have been exaggerated by the interactions of the female sex of the subjects, the exogenous sex hormones and the metabolic syndrome.
The effects of a low-fat, high-carbohydrate diet versus a higher-fat, lower-carbohydrate diet differ for the two main types of hyperlipidemia: simple hypercholesterolemia (elevated cholesterol) and combined hyperlipidemia (elevated levels of both cholesterol and triglycerides). In men with simple hypercholesterolemia, a diet with less than 25% fat and greater than 60% carbohydrate was associated with a sustained 40% increase in triglycerides, a 3.5% decrease in HDL cholesterol, and no further decrease in LDL cholesterol in comparison with higher fat intakes (Knopp et al. 1997). In persons with combined hyperlipidemia, a low-fat diet caused no worsening of triglycerides or HDL cholesterol, but a 2-year diet consisting of greater than 40% fat and less than 45% carbohydrate was associated with lower triglycerides in subjects at a stable weight (Retzlaff et al. 1995). In the subjects of Mozaffarian’s study, a greater saturated-fat intake paralleled a total-fat intake ranging from 18% of energy in the first quartile to 32% in the fourth quartile (the fourth being the highest fat intake). Modest favorable trends in triglycerides and HDL cholesterol concentrations were observed with higher fat intakes.
Triglycerides and HDL cholesterol are stronger predictors of CHD in women, whereas the LDL cholesterol concentration is a stronger predictor in men (Knopp et al. 1994). Because healthy women secrete and remove triglycerides (especially very low density lipid particles) at twice the rate that men do, conditions impairing lipo-protein removal would be expected to exaggerate the hyperlipidemic response in women compared with men. This sex difference is seen in the development of diabetes. The development of insulin resistance and obesity is associated with a greater lipoprotein increase in women than in men. The exaggerated decreases in HDL cholesterol concentrations observed with the consumption of a low-fat diet in women but not men appear to be another facet of this effect.
Knopp and Retzlaff concluded that the study by Mozaffarian and colleagues draws attention to the different effects of diet on lipoprotein physiology and cardiovascular disease risk. These effects include the paradox that a high-fat, high-saturated fat diet is associated with diminished CHD progression in women with the metabolic syndrome, a condition that is epidemic in the United States. This paradox presents a challenge to researchers to differentiate the effects of dietary fat on lipoproteins and cardiovascular disease risk in men and women, on the different lipid disorders and on the metabolic syndrome.