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%.

Summary 

Therapeutic carbohydrate-restricted can prevent or reverse the components of MetS and T2DM.

中文翻译：

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低碳水化合物饮食对心脏代谢风险，胰岛素抵抗和代谢综合征的影响

审查目的 

一个肥胖的流行已经导致胰岛素抵抗增加，高胰岛素血症，患病率代谢综合征（大都会）和心血管疾病（CVD）。饮食心脏假说认为，饮食脂肪是罪魁祸首。但是减少饮食中的脂肪导致了问题，但没有解决。综述了高胰岛素血症的作用，动脉粥样硬化血脂异常的发生，系统性炎症在CVD中的作用及其逆转。

最近的发现 

营养过剩导致体重增加和碳水化合物不耐受，造成胰岛素抵抗/高胰岛素血症的恶性循环，从而抑制脂肪利用并促进脂肪储存，导致动脉粥样硬化性血脂异常，其特征在于高甘油三酸酯血症，低HDL和低密度LDL。碳水化合物-胰岛素模型可以更好地说明肥胖，MetS以及最终导致2型糖尿病（T2DM）和CVD的发病机理。生酮饮食可减少内脏肥胖，增加胰岛素敏感性，逆转动脉粥样硬化血脂异常和营养过剩的炎症生物标志物。最近的试验表明，患有T2DM的个体在长达2年的时间内都非常坚持生酮饮食，从而逆转了其代谢，炎症和血糖异常的生物标志物以及10年估计的动脉粥样硬化风险。糖尿病逆转的发生率超过50％，完全缓解的发生率接近8％。

概要 

限制治疗性碳水化合物可以预防或逆转MetS和T2DM的成分。