We recently proposed that the
biological markers improved by
carbohydrate restriction were precisely those that define the
metabolic syndrome (MetS), and that the common thread was regulation of
insulin as a control
element. We specifically tested the idea with a 12-week study comparing two hypocaloric diets (approximately 1,500 kcal): a
carbohydrate-restricted diet (CRD) (%
carbohydrate:fat:
protein = 12:59:28) and a
low-fat diet (LFD) (56:24:20) in 40 subjects with atherogenic
dyslipidemia. Both interventions led to improvements in several metabolic markers, but subjects following the CRD had consistently reduced
glucose (-12%) and
insulin (-50%) concentrations,
insulin sensitivity (-55%),
weight loss (-10%), decreased adiposity (-14%), and more favorable
triacylglycerol (TAG) (-51%), HDL-C (13%) and total
cholesterol/HDL-C ratio (-14%) responses. In addition to these markers for MetS, the CRD subjects showed more favorable responses to alternative indicators of cardiovascular risk: postprandial
lipemia (-47%), the
Apo B/
Apo A-1 ratio (-16%), and
LDL particle distribution. Despite a threefold higher intake of dietary saturated fat during the CRD,
saturated fatty acids in TAG and
cholesteryl ester were significantly decreased, as was
palmitoleic acid (16:1n-7), an endogenous marker of lipogenesis, compared to subjects consuming the LFD. Serum
retinol binding protein 4 has been linked to
insulin-resistant states, and only the CRD decreased this marker (-20%). The findings provide support for unifying the disparate markers of MetS and for the proposed intimate connection with
dietary carbohydrate. The results support the use of
dietary carbohydrate restriction as an effective approach to improve features of MetS and cardiovascular risk.