African Americans have the highest overall mortality rate and the highest out-of-hospital coronary death rates of any ethnic group in the United States, particularly at younger ages. Recent guidelines from the National Cholesterol Education Program (NCEP): Expert Panel on the Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATPIII) indicate that lowering of LDL become the primary target in reducing coronary heart disease (CHD). Mounting evidence indicate that elevated LDL cholesterol is a major risk factor in developing CHD, and that the hypercholesterolemia tends to cluster with other cardiovascular risk factors.

This clinical cluster, commonly known as metabolic syndrome, has been defined by the ATPIII as: 1) abdominal obesity (waist circumference >102 cm in men and >88 cm in women), 2)  >150 mg/dL, 3) HDL <40 mg/dL in men and <50 mg/dL in women, 4) fasting glucose >110 mg/dL, 5) hypertension (systolic blood pressure [SBP] >130 mmHg or diastolic blood pressure [DBP] >85 mmHg. The prevalence of metabolic syndrome, as estimated 10 years ago from the noninstitutionized U.S. population, was 22.8% (men) and 22.6% (women). Major findings in the third National Health and Nutrition Examination Survey (NHANES III, 1988-1994) indicate that metabolic syndrome was present in 4.6%, 22.4%, and 59.6% of normal-weight, overweight, and obese U.S. adults.

George Washington Carver, who postulated 70 years ago numerous health benefits from soybeans, peanuts, and sweet potatoes, may have suggested that the increased LDL, especially in high-risk minorities, may well be helped with the soybean foods. Soybeans contain high-quality protein (as assessed by the FDA’s “Protein Digestibility Corrected Amino Acid Score”), soluble fiber, the “good” unsaturated fat, and several classes of anticarcinogens (protease inhibitors, phytosterols, saponins, and isoflavones). The isoflavones are heterocyclic phenols structurally similar to the estrogenic steroids—frequently termed phytoestrogens because of their abili­ty to exert estrogen-like effects. Major isoflavones include genistein, daidzein, and glycetin. These compounds are usually identified in mg/g of soy protein. Isoflavones, which are excellent antioxidants, have more affinity for the estrogen receptor beta (ERB) than the estrogen receptor alpha (ERA). This helps to explain their selective tissue effects.

To reduce one risk factor for CHD within metabolic syndrome (i.e., increased LDL cholesterol), the cholesterol-lowering properties of soy foods should be further investigated in populations at high risk for metabolic syndrome. The ATPIII specifically recommends a mul-tifaceted approach that emphasizes low-saturated fat diets combined with plant stanols/sterols (2 g/day) and increased viscous (soluble) fiber (10-25 g/day), weight reduction, and increased physical activity. canada drugs online

Table 1. Early Clinical

SourceHodges, RE, et al. Am J Clin Nutr. 1967;20:198-208. Study PopulationSix male Iowa prison inmates had a 14-day metabolic baseline period prior to study.
Goldberg AP, et al. Atherosclerosis. 1982;43:355-368. Twelve type-IIA hypercholesterolemia and four normals stabilized on NIH low-fat diet x six weeks.
Fumagalli R, et al. Atherosclerosis. 1982;43:341 -353. Seven type-ll Italian hyperlipoproteinemic subjects studied as inpatients.
Kolb S. & Sailer D. Nutr Report Internot. 1984;30:719-724. Fourteen German inpatients (11 type-IIA and three type-IIB) had 10 females and four males.
Venillo A, et al. Atherosclerosis. 1985;54:321-331. Italian outpatients (45 type-IIA and 21 type-IIB enrolled for four-month study.
Shorey RL, et al. Am Diet Assoc. 1985;85:1461-1465. Twenty-two male and nine female outpatients with mild hypercholesterolemia were studied.

The medical educational objectives are first to educate physicians as to the cholesterol-lowering properties of soybean foods and to provide a chronologic review of published mechanisms of action. The first suggestion that soy protein lowered serum came from six Iowa male prison inmates in 1967 with an ensuing lapse of 15 years before meaningful human trials were again reported (Table 1).