Sabaté J., G.E. Fraser, 1994. Nuts: a new protective food against coronary heart disease. Current Opinion in Lipidology. 5:11-16.
Recent epidemiological findings indicate that frequent nut consumption offers protection from fatal and non-fatal coronary heart disease events. Although human nutrition studies seem to indicate that nut consumption lowers total and LDL cholesterol, the unique nutrient composition of nuts invites speculation on other mechanisms of protection.
Fraser, G.E., 1994. Diet and coronary heart disease: beyond dietary fats and low-density-lipoprotein cholesterol. Am J Clin Nutr. 59(suppl):1117S-23S.
Traditionally, the effects of diet on coronary heart disease have been attributed to the effects of medium-chain fatty acids, soluble fiber, and dietary cholesterol on serum low-density-lipoprotein (LDL) cholesterol concentrations. We review evidence here that many other dietary substances may affect risk, often via mechanisms not involving LDL-cholesterol concentrations directly. Such substances include phytosterols, tocotrienols, arginine, and antioxidant vitamins. The effects of diet on high-density-lipoprotein-cholesterol concentrations, triglycerides (fasting and postprandial), oxidized LDL particles, prostaglandins, and endothelium-derived relaxing factor are described. Finally, an illustration of some epidemiologic associations between diet and coronary disease events is made from the Adventist Health Study data.
Abbey, M., M. Noakes, G.B. Belling, P.J. Nestel, 1994. Partial replacement of saturated fatty acids with almonds or walnuts lowers total plasma cholesterol and low-density-lipoprotein cholesterol. Am J Clin Nutr. 59:995-9.
Sixteen normolipidemic male volunteers aged 41 +/- 9 y (mean +/- SD) consumed a diet providing 36% of energy as fat (92 g fat/d) for 9 wk. A daily supplement of nuts (providing half of the total fat intake) was provided against a common background diet. In the first 3-wk period the background diet was supplemented with raw peanuts (50 g/d), coconut cubes (40 g/d), and a coconut confectionary bar (50 g/d), designed to provide 47 g fat with a ratio of polyunsaturated to monounsaturated to saturated fatty acids (P:M:S) to match the Australian diet (reference diet). During the following 3 wk the background diet was supplemented with monounsaturated fatty acid-rich raw almonds (84 g/d), equivalent to 46 g fat, and during the final 3-wk period the background diet was supplemented with polyunsaturated fatty acid-rich walnuts (68 g/d), equivalent to 46 g fat. Compared with the reference diet there were significant reductions in total and LDL cholesterol, 7% and 10%, respectively, after supplementation with almonds, and 5% and 9%, respectively, after supplementation with walnuts.
Sabaté, J., 1993. Does nut consumption protect against ischaemic heart disease? Eur J of Clin Nutr. 47(suppl.1):S71-5.
Results of an epidemiological study conducted among California Adventists provides strong evidence that frequent nut consumption has a protective effect on both fatal and non-fatal ischaemic heart disease. It’s plausible, due to the unique composition of nuts, that nuts favorably affect heart disease risk factors and interfere with the process of atherogenesis. Results of human nutritional studies, with varying degrees of methodological rigor all seem to indicate that eating nuts lowers serum cholesterol and favorably modifies the lipoprotein profile.
Klevay, L.M., 1993. Copper in nuts may lower heart disease risk. Arch Intern Med. 153: 401-2.
In this commentary on the Seventh-Day Adventist study, the author discuses the fact that nuts are relatively high in copper and that this may provide protection against a variety of disorders related to atherosclerosis. Copper deficiency is the only nutritional insult that has been shown to produce abnormal electrocardiograms, glucose intolerance, hypercholesterolemia, hypertension, hyperuricemia, injury by free radicals and thrombosis in animals. More than 31 men and women have responded to diets low in copper with potentially harmful changes in glucose tolerance, blood pressure, blood lipids and electrocardiograms. Copper in these daily diets ranged from 0.65 to 1.02 mg amounts. Eating an ounce of nuts can add approximately 0.37 mg of copper to daily intakes.
Cooke, J.P., P. Tsao, A. Singer, B.Y. Wang, J. Kosck, H. Drexler, 1993. Anti-atherogenic effect of nuts: is the answer NO? Arch Intern Med. 153:896, 899, 902.
In a commentary regarding the Seventh Day Adventist study, the authors highlight the fact that frequent nut consumption reduced the risk of experiencing fatal or nonfatal heart attacks by 50%. A possible explanation for the protective effect may be that nuts are high in arginine, a basic amino acid that is a precursor to nitric oxide (NO). The latter is known to inhibit plaque formation, or atherogenesis, which can lead to heart attacks. Studies have shown that people with hypercholesterolemia have reduced activity of NO. Adding arginine-rich nuts to the diet may help increase NO activity and thereby reduce the risk of heart attacks.
Singh, R.B., S.S. Rastogi, R.Verma, L. Bolaki, R. Singh, 1992. An Indian experiment with nutritional modulation in acute myocardial infarction. Am J Cardiol. 69:879-85.
In a randomized, single-blind intervention trial, 406 patients 24 to 48 hours after acute myocardial infarction (AMI) were assigned to either diet A (204 patients, group A) or B (202 patients, group B) for 6 weeks. At entry to the study, mean age, male sex, risk factors, complications, possible and definite AMI, and drug therapy were comparable between the 2 groups. Dietary adherence to intervention and control diets was checked by questionnaire, and drug therapy by tablet count. Group A received significantly lower calories, a higher percentage of calories from complex carbohydrates, vegetable/fish proteins, polyunsaturated fatty acids, and a higher polyunsaturated/saturated fat ratio diet than did group B (higher total calories and saturated fatty acids). Group A also received less dietary cholesterol, salt and caffeine, and higher soluble dietary fiber, vitamins and minerals than did group B. After 6 weeks, group A had a significant decrease in mean serum total (-20.5 vs -8.6 mg/dl) and low-density lipoprotein (-16.6 vs -6.4 mg/dl) cholesterols, and triglycerides (-15.5 vs -7.6 mg/dl), with no decrease in high-density lipoprotein cholesterol (-1.5 vs -1.3 mg/dl) compared with the initial levels and changes in group B. Group A also had a greater decrease in mean body weight (3.4 vs 1.3 kg) than that of group B.