Effect of low-carbohydrate diets on cardiometabolic risk, insulin resistance, and metabolic syndrome

Purpose of review An obesity epidemic has resulted in increasing prevalence of insulin resistance, hyperinsulinemia, metabolic syndrome (MetS), and cardiovascular disease (CVD). The Diet-Heart Hypothesis posited that dietary fat is the culprit. Yet dietary fat reduction has contributed to the problem, not resolved it. The role of hyperinsulinemia, the genesis of its atherogenic dyslipidemia and systemic inflammation in CVD and its reversal is reviewed. Recent findings Overnutrition leads to weight gain and carbohydrate intolerance creating a vicious cycle of insulin resistance/hyperinsulinemia inhibiting fat utilization and encouraging fat storage leading to an atherogenic dyslipidemia characterized by hypertriglyceridemia, low HDL, and small dense LDL. The carbohydrate-insulin model better accounts for the pathogenesis of obesity, MetS, and ultimately type 2 diabetes (T2DM) and CVD. Ketogenic Diets reduce visceral obesity, increase insulin sensitivity, reverse the atherogenic dyslipidemia and the inflammatory biomarkers of overnutrition. Recent trials show very high adherence to ketogenic diet for up to 2 years in individuals with T2DM, reversing their metabolic, inflammatory and dysglycemic biomarkers as well as the 10-year estimated atherosclerotic risk. Diabetes reversal occurred in over 50% and complete remission in nearly 8%. Therapeutic carbohydrate-restricted can prevent or reverse the components of MetS and T2DM.