Carbohydrate restriction and cardiovascular risk

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Corresponding author Richard D. Feinman, PhD Department of Biochemistry, State University of New York Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, NY 11203, USA. E-mail: [email protected] Current Cardiovascular Risk Reports 2008, 2:88–94 Current Medicine Group LLC ISSN 1932-9520 Copyright © 2008 by Current Medicine Group LLC

Originally developed as a strategy for weight loss, diets based on restriction of carbohydrates were traditionally of concern because of the assumed increased cardiovascular risk if the carbohydrates were replaced with fat. It now appears that such diets are associated with an improvement in markers of cardiovascular risk, even with higher saturated fat intake and even in the absence of weight loss. Various evidence supports this paradigm shift: 1) carbohydrate restriction improves markers of atherogenic dyslipidemia (triglycerides, high-density lipoprotein cholesterol, apolipoprotein B–apolipoprotein A-1 ratio) and reduces the more atherogenic small, dense low-density lipoprotein cholesterol; 2) high amounts of dietary carbohydrates increase de novo fatty acid synthesis and plasma triglycerides; and 3) large, long-term studies of traditional dietary fat reduction continue to fail to demonstrate the predicted improvement in cardiovascular disease risk. Cardiovascular disease is the leading cause of morbidity and mortality in the Western world. It seems appropriate to consider carbohydrate reduction as a useful, if not the preferred, alternative to low-fat diets, which have met with limited success.

Introduction Recent studies suggest a substantial reversal of our understanding of the role of dietary carbohydrate restriction in cardiovascular (CV) risk. Long established as a strategy for weight loss, low-carbohydrate diets are traditionally not recommended because of the concern that the carbohydrates will be replaced with fat, with assumed deleterious effects on CV risk. It is now clear,

however, that replacement of dietary carbohydrates with fat generally leads to improvement in atherogenic dyslipidemia (raised triglycerides, low high-density lipoprotein [HDL] cholesterol, and small low-density lipoprotein [LDL] particles), even with higher saturated fat (SF) and even under conditions in which no weight loss occurs [1••,2,3]. The underlying basis of these effects is reduction of the elevated levels of insulin that follow carbohydrate ingestion. Insulin inhibits lipolysis, activates lipoprotein lipase, and stimulates de novo fatty acid synthesis. These responses bias metabolism toward fat accretion, toward elevation of triglycerides and reduction in HDL, and away from oxidation. Insulin per se might be described as atherogenic [4]. Continued high insulin stimulation effects a negative feedback system that manifests as insulin resistance and, under conditions of nutrient excess, hyperinsulinemia may lead to obesity. Obesity and the insulin-resistant state further exacerbate the effects of high carbohydrates on CV risk. We describe recent reports that support these generalizat