Volume 6, Issue 1, 2003
Compared to other cultural groups, the risk of coronary artery disease in this population is amplified by two to twenty fold. For this reason, elevated total homocysteine levels, known as hyperhomocysteinemia, have been discovered to be atherogenic. In a causal, dose-related mechanism, homocysteine increases thrombotic activity and causes oxidative damage to the endothelium. Although there are both nutritional and genetic causes of hyperhomocysteinemia, studies have concluded that amongst Asian Indians deficiencies in folate and cobalamin are the primary factors. Although native Indians have an insufficient intake of folic acid and cobalamin, migrant Asian Indians are deficient only in cobalamin. The principal cause of folic acid and cobalamin deficiency is the vegetarian diet consumed by a large proportion of Indians, but it is also due to cooking methods, malabsorption, gastrointestinal disorders, and intestinal bacterial composition. The need to decrease the rising incidence of coronary artery disease offers a significant reason for the issues of folic acid fortification and multivitamin therapy to take priority in the Indian public health agenda.
The United States Department of Agriculture Food Guide Pyramid was released in 1992, and has subsequently become the most widely used and recognized nutritional guide in this country. Analysis of the Pyramid's development, however, suggests that industry lobbying and a desire to simplify the message resulted in recommendations that failed to reflect current nutrition science. While large-scale studies have yet to elucidate the precise relationships between diet and disease, diet does appear to play a role in both risk for and prevention of several chronic diseases. Studies show beneficial effects of a diet low in red meat and refined grains, and high in unsaturated fats, whole grains, vegetables, and fruits. Shifting responsibility for nutrition policy from the USDA to an agency with fewer ties to the food industry might permit more objective guidelines. New agricultural and industry policies will also be needed to align food supply with recommended consumption.
The disturbing trends in increasing numbers of overweight and obese Americans tend not to reflect a lack of effort on the part of the American public to control their weight, but rather a failure to make the attempt in a scientifically sound and effective manner. It may be the frustration associated with this trend that accounts for the popularity of high-fat, low-carbohydrate diets, pushed in books and in the popular media. This paper reviews the physiological basis for these diets, as compared to the low-fat, high-carbohydrate diet recommended by conventional scientific wisdom, with particular attention paid to the effects of these diets on fat-free mass. Fat-free mass, or total body mass minus fat mass, is an important indicator of resting metabolic rate. It is therefore important to the future success of the diet to conserve relative to fat mass when losing weight. In a survey of reliable, peer-reviewed sources, referenced specifically below, it was found that initial weight loss and changes in body composition are independent of the macronutrient sources consumed, but that a negative energy balance is the fundamental key to weight and fat loss. In addition, associated with low-carbohydrate diets are serious health concerns, such as the long-term effects of these diets on cholesterol, blood pressure, bones and kidneys.
Ephedrine is a sympathomimetic, which stimulates the sympathetic nervous system and increases the rate and strength of heart contractions. Presently, it is an immensely popular ingredient in dietary supplements (over three billion servings a year in 1999) known for its ability to decrease body weight and body fat. However the side effects of the ephedra alkaloids have not gone without notice. Annals of Internal Medicine in March 2003 found that 64% of all the adverse reactions such as stroke, seizure and myocardial infarction reported to poison control centers around the country that deal with the herbal supplements had to do with ephedra. This staggering number as well as some high profile deaths temporally linked to the use of ephedrine supplements has added to the controversy calling for a ban of the supplements. Studies into the cardiovascular effects of ephedrine ingestion (< 60 mg) have shown mixed results. Because ephedra is an herb, only if the FDA proves a clear danger to public health can it curb sales. Therefore the controversy lingers, calling for a universal standard of proper dosage and proper labeling so that more evidence can be gathered to determine the safety of the popular supplement.
Grape seed proanthocyanidin extract (GSPE) is a popular dietary supplement that has been shown to have a wide variety of beneficial actions. First brought into public consciousness as one of the key active components of red wine, proanthocyanidins are bioavailable in plasma and have potent antioxidant activity. Their free radical scavenging properties are greater than popular antioxidants such as vitamins C and E, and GSPE shows a superior ability to protect cells against lipid peroxidation and DNA fragmentation. GSPE also exhibits cardioprotective effects by preserving myocardial function after ischemia and reperfusion, and reduces total cholesterol levels in combination with the anti-aging supplement chromium polynicotinate through a synergistic effect. GSPE has been shown to inhibit the growth of cancer cells, while encouraging growth in normal human cells and protecting normal human cells against the toxicity of chemotherapeutic agents. Proposed mechanisms for GSPE's activity towards cancer cells include GSPE-modulated upregulation of bcl-Xs and JNK genes leading to apoptosis, as well as downregulation of bcl-Xl expression and mitogenic signaling to promote cell growth. Toxicity and mutation studies have demonstrated the safety of GSPE, supporting the use of GSPE as a health supplement.
Recent reports have suggested that soy may adversely affect the thyroid gland, increasing goiter formation and thyroid cancer risk (5). Isoflavones in soy inhibit the enzyme thyroid peroxidase (TPO) and thus negatively affect thyroid hormone synthesis in vitro (7). However, studies in rats have found that some additional, unidentified components in soy protein may be needed besides the isoflavones to exert anti-thyroid actions in vivo. Soy protein has been found to induce goitrogenesis in rats, but only in those that are iodine-deficient (10). Therefore, susceptibility to soy-induced goiters may not be substantial unless some other goitrogenic risk factor, such as iodine deficiency, is also present. Studies have also found that iodine-deficient diets containing 30% soy protein can induce thyroid carcinoma in rats (13). In contrast, however, retrospective human studies such as the Bay Area Thyroid Cancer Study found soy to reduce thyroid cancer incidence (14,15). Hence, more research is needed, particularly in the form of prospective human clinical trials, to clarify the relationship between soy and the thyroid. At present, it would be wise for consumers to abstain from excessive soy protein consumption and consume only moderate levels of soy before more research is done.
Recent evidence supports the hypothesis that tea does, in fact protect against cardiovascular disease. Some of the latest data by Hodgson et al, suggests that dietary flavonoids in tea significantly improves endothelium-dependent and endothelium-independent flow-mediated vasodilation (2.3%; P=.008 & 4.2%; P=.03 respectively). Similar results were obtained in a study by Duffy et al, where it was found that short- and long-term tea consumption significantly improved endothelium dependent flow-mediated vasodilation (P<.001). Such improvement in endothelial function is a likely mechanism by which tea exerts its protective effects. Geleijnse et al found that drinking at least 375 mL of tea per day reduced the risk of having a heart attack (RR: 0.57; 95%CI: 0.33, 0.98) compared to not drinking tea. However, previous studies failed to show that tea was preventive of heart attack. In another study, Mukamal et al found that moderate and heavy tea drinkers had lower mortality after heart attack (hazard ratio: 0.69; 95% CI: 0.53, 0.89 & hazard ratio: 0.61; 95% CI 0.42, 0.86 respectively). These studies have several limitations, however, that must be addressed in further research to clearly determine whether tea might help prevent cardiovascular disease and how it might exert such effects.