Dietary Modification and CVD Prevention
Authors: Cheryl A. M. Anderson, Lawrence J. Appel
Journal: JAMA (2006)

CARDIOVASCULAR DISEASE (CVD) IS THE LEADING cause of mortality in women in the United States and throughout most of the world. The contemporary approach to prevention of CVD includes lifestyle modification for all adults and medical therapy for those with CVD risk factors (hypertension, hypercholesterolemia, or diabetes). The report in this issue of JAMA by Howard et al from the Women’s Health Initiative (WHI) is timely, given recent major initiatives that focus on CVD prevention in women. In 1991, the National Institutes of Health launched the WHI research program, a series of major clinical trials and large observational studies that addressed the most common causes of death and disability in postmenopausal women—CVD, cancer, and osteoporosis. The WHI research program involved extraordinary commitment and effort on the part of numerous investigators and staff members and more than 100 000 participants. Their efforts already have and will continue to advance the health of postmenopausal women. One of the WHI studies, the WHI Dietary Modification Trial, was a randomized controlled trial that tested whether a behavioral intervention designed to lower total intake of dietary fat and increase intakes of fruits, vegetables, and grains would decrease the risk of breast and colorectal cancer. Cardiovascular disease was a prespecified secondary outcome. As noted by the authors, the WHI Dietary Modification Trial was not optimally designed to test hypotheses related to CVD; however, they reasoned that reducing total fat intake could have collateral benefits by lowering intake of saturated fat and trans fatty acids and thereby decrease the risk of CVD. The WHI Dietary Modification Trial enrolled 48 835 women (mean age, 62.3 years)—20% of whom were nonwhite. Women assigned to the active intervention attended group sessions designed to promote behavioral changes that would reduce dietary intake of total fat to 20% of energy, increase intakes of fruits/vegetables to at least 5 servings/d, and increase grain intake to at least 6 servings/d. The intervention intensity was moderate—18 sessions during the first 12 months and 4 times per year thereafter. As in most behavioral intervention trials, mean achieved dietary levels fell short of goal. In the active intervention group, total fat intake decreased from 37.8% to 28.8% of energy, while mean servings per day of fruits and vegetables increased from 3.6 to 4.9. Mean servings per day of grains were essentially unchanged, ie, approximately 4.5 at baseline and follow-up. Concomitantly, there were reductions in intake of saturated fat (12.7% to 9.5% of energy), trans fatty acid (2.8% to 1.6% of energy), polyunsaturated fat (7.8% to 6.1% of energy), and monounsaturated fat (14.4% to 10.8% of energy). On average, the comparison group made few dietary changes. As a result, differences in CVD risk factors between the intervention and comparison groups were minimal—eg, at year 3, there were net reductions of 3.55 mg/dL in levels of low-density lipoprotein cholesterol and less than 1 mm Hg in blood pressure. The main CVD findings are that the intervention had no effect on risk of coronary heart disease, stroke, and total CVD. Hazard ratios for each of the major CVD outcomes were close to 1. In women without CVD at baseline, there were trends toward decreased CVD risk. Paradoxically, among the 3.4% of women with prior CVD, the intervention was associated with a slightly increased risk of CVD. This latter finding could have occurred by chance alone, given the large number of statistical tests. A thorough exposition of the data in this subset of women should be conducted and published before any conclusion is drawn. The first question one might ask is why was there a null finding in this study? As is commonplace in lifestyle intervention trials, the study population was healthier than anticipated. Specifically, fewer CVD events occurred than were expected. In addition, the intervention had minimal effect on the major, diet-related CVD risk factors. Its impact on blood pressure was small because the intervention did not implement dietary modifications that lower blood pressure—eg, reduced salt intake, increased potassium intake, the DASH (Dietary Approach to Stop Hypertension) diet, and weight loss. The intervention reduced intakes of fats that increase risk of CVD (saturated fat and trans fatty acids) but also of those that might be protective (polyunsaturated fats and monounsaturated fats). Most participants were overweight or obese (mean body mass index, 29.1), but the intervention did not address weight, the primary risk factor for diabetes. Over the