After decades of epidemiologic and clinical research, the influence of overall diet on health and disease, particularly coronary heart disease (CHD), has become widely accepted. 1 The pioneering ecological and metabolic studies of Keys and colleagues placed the focus on fat types, showing that populations consuming more saturated fatty acids (SFA) had higher blood cholesterol levels and associated higher rates of coronary heart disease (CHD), 2 while individuals fed SFA had increased blood cholesterol levels, as opposed to the effects of monounsaturated (MUFA) or polyunsaturated fatty acids (PUFA). Cholesterol changes derived from switching fatty acid species in the diet were found to be predictable with specific equations. 3-5 Subsequent epidemiologic studies confirmed that elevated serum cholesterol was a strong independent risk factor for CHD. This led to the formulation of the diet-heart hypothesis, whereby high intake of saturated fats leads to elevated cholesterol levels, which in turn promote atherosclerosis, coronary artery occlusion, and subsequent ischemic events. 6 Though the diet-heart hypothesis shaped dietary guidelines towards reduction of all dietary fat, with a concomitant increase in carbohydrates, it proved futile in reducing the incidence of cardiovascular disease (CVD) in women. 7 However, no randomized controlled trial (RCT) of a low-fat diet for effects on CVD events has been conducted in men. In the last three decades, the decreasing fat consumption as percentage of energy in the US population has done little to slow the increasing rates of obesity and type 2 diabetes mellitus (T2DM). 8 It is now widely recognized that higher-fat diets can be beneficial if healthy fats are consumed, while high-carbohydrate diets (particularly those with high glycemic load) might be contributing to CHD 9-12 and other negative health outcomes. 12,13 As reviewed here, healthy, plant-based unsaturated fats are major components of widely consumed edible seeds, such as tree nuts and peanuts.
Among seeds, nuts are particularly rich in vitamin E compounds, mainly α-tocopherol, a well-known antioxidant that, together with vitamin C, carotenoids, and selenium, contributes to the body’s defense against reactive oxygen species. α-Tocopherol, the biologically most active and most frequently studied form of vitamin E, is a lipid-soluble molecule transported in blood in lipoprotein fractions that acts as a peroxyl radical scavenger in lipid environments, preventing lipid peroxidation in lipoproteins and membranes. By reducing LDL oxidation or other mechanisms, vitamin E also displays anti-inflammatory properties, inhibits platelet aggregation, and enhances NO bioavailability. 123 This helps explain the beneficial health effects of lifelong high intake of vitamin E. Thus, a large meta-analysis of 15 cohort studies reported that vitamin E intake was associated with a reduced CHD risk, with RR=0.76 (95% CI, 0.63-0.89) for the top tertile compared with the bottom tertile of intake. 124 However, large-scale RCTs have shown an unexpected lack of efficacy for different doses of supplemental vitamin E or other antioxidants against CVD. 125 A likely reason for the discrepancy between prospective studies and RCTs is that the latter usually enrolled patients with prior CHD or at high risk of CVD; established atherosclerotic damage is unlikely to regress with antioxidant treatment. Likewise, there is no evidence from RCTs that vitamin E helps prevent or manage T2DM. 121 Hence, the use of vitamin E or other antioxidant vitamin supplements for CVD prevention is discouraged, while the recommendation stands for a healthy diet, rich in food sources of antioxidant nutrients such as fruits and vegetables, including seeds. 22
Conflict of Interest Disclosures: Dr. Ros and Dr. Hu have received grants from the California Walnut Commission, Sacramento, CA, and Dr. Ros is a non-paid member of its Scientific Advisory Committee.
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Date and time: Fri, 14 Jan 2022 12:13:43 GMT