Carbohydrate Restriction and
Cardiovascular Risk
Jocelyne G. Karam, MD, Fiby Nessim, MD,
Samy I. McFarlane, MD, MPH, and Richard D. Feinman, PhD
Corresponding author
Richard D. Feinman, PhD
Department of Biochemistry, State University of New York
Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, NY
11203, USA.
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 generalizations,
emphasizing changes in lipid markers.
