Top 10 dietary strategies for atherosclerotic cardiovascular risk reduction

Abstract

Poor dietary quality has surpassed all other mortality risk factors, accounting for 11 million deaths and half of CVD deaths globally. Implementation of current nutrition recommendations from the American Heart Association (AHA), American College of Cardiology (ACC) and the National Lipid Association (NLA) can markedly benefit the primary and secondary prevention of atherosclerotic cardiovascular disease (ASCVD). These include: 1) incorporate nutrition screening into medical visits; 2) refer patients to a registered dietitian nutritionist (RDN) for medical nutrition therapy, when appropriate, for prevention of ASCVD; 3) follow ACC/AHA Nutrition and Diet Recommendations for ASCVD prevention and management of overweight/obesity, type 2 diabetes and hypertension; 4) include NLA nutrition goals for optimizing low-density lipoprotein cholesterol (LDL-C) and non-high-density lipoprotein cholesterol (non-HDL-C) and reducing ASCVD risk; 5) utilize evidence-based heart-healthy eating patterns for improving cardiometabolic risk factors, dyslipidemia and ASCVD risk; 6) implement ACC/AHA/NLA nutrition and lifestyle recommendations for optimizing triglyceride levels; 7) understand the impact of saturated fats, trans fats, omega-3 and omega-6 polyunsaturated fats and monounsaturated fats on ASCVD risk; 8) limit excessive intake of dietary cholesterol for those with dyslipidemia, diabetes and at risk for heart failure; 9) include dietary adjuncts such as viscous fiber, plant sterols/stanols and probiotics; and 10) implement AHA/ACC and NLA physical activity recommendations for the optimization of lipids and prevention of ASCVD. Evidence on controversies pertaining to saturated fat, processed meat, red meat, intermittent fasting, low-carbohydrate/very-low-carbohydrate diets and caffeine are discussed.

Double Burden of Poverty and Cardiovascular Disease Risk among Low-Resource Communities in South Africa

“…It lowers LDL-C and glucose levels and, therefore, has a protective effect against CVD. [136] Lowering of cholesterol is achieved by the binding of fibre to bile acids, thereby escalating its excretion. This inhibits the production of cholesterol by the liver, resulting in lower blood cholesterol.…”

“…Saturated fatty acids (SFAs) and trans fatty acids (TFAs) have the greatest adverse effect on atherogenic cholesterol levels and are both associated with risk of CVD. [136,141] Increased SFA intakes increase LDL-C levels. [142] TFAs have a HDL-C lowering effect and also increase LDL-C levels and, therefore, increase the risk of CVD.…”

“…Although there has been controversy about SFA intake and CVD risk, sufficient evidence exists that high SFA intakes cause increased LDL-C level by downregulating LDL receptors. [136] PUFAs have a protective effect against CVD, specifically omega-6 PUFAs that significantly reduces total cholesterol and LDL-C levels as well as inflammatory markers. [145] High intakes of omega-3 PUFAs lowers the risk for myocardial infarction, CHD and CVD mortality and CVD events.…”

“…[145] High intakes of omega-3 PUFAs lowers the risk for myocardial infarction, CHD and CVD mortality and CVD events. [136] In addition, a diet rich in PUFA reduces the TC:HDL-C ratio and CHD incidence. [146] Linolenic acid (omega-3 fatty acid) and linoleic acid (omega-6 fatty acid) are essential fatty acids that cannot be physiologically produced and, therefore, need to be supplied by food sources.…”

Atherosclerosis Development and Aortic Contractility in Hypercholesterolemic Rabbits Supplemented with Two Different Flaxseed Varieties

“…Standard flaxseed varieties contain up to 55% alpha-linolenic acid (ALA), representing the richest plant source of omega-3 acids. ALA is considered one of the main cholesterol-lowering and anti-atherosclerotic ingredients [ 10 ] and was shown to suppress the production of proinflammatory interleukins and lower C-reactive protein and serum amyloid-A concentrations in human patients and experimental animals [ 11 ]. However, in contrast to those previous research, current studies found that ALA exhibited very low anti-inflammatory properties, although they could be more pronounced due to its metabolic conversion to very long-chain PUFAs [ 12 ].…”