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Well, lab mice are not humans, and they are fed in a controlled manner whereas humans can pony over to the kitchen and engorge themselves in snack foods, but resveratrol-fed animals exhibited far less arterial plaque (-52%) than animals given a statin drug (-40%).  Furthermore, resveratrol equaled the reduction of circulating cholesterol as a statin drug (-19%). Since statin drugs do not prevent mortal heart attacks, but resveratrol pills do (at least in the animal lab), one wonders if it’s time to abandon Lipitor.  — Bill Sardi, Resveratrolnews.com

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J Nutr Biochem. 2013 Jan 18. pii: S0955-2863(12)00298-7. doi: 10.1016/j.jnutbio.2012.11.009. [Epub ahead of print]

Resveratrol protects against atherosclerosis, but does not add to the antiatherogenic effect of atorvastatin, in APOE*3-Leiden.CETP mice.

Berbée JF, Wong MC, Wang Y, van der Hoorn JW, Khedoe PP, van Klinken JB, Mol IM, Hiemstra PS, Tsikas D, Romijn JA, Havekes LM, Princen HM, Rensen PC.

Source

Department of General Internal Medicine, Endocrinology and Metabolic Diseases, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, the Netherlands; Department of Experimental Immunohematology, Sanquin Research Amsterdam, Amsterdam, the Netherlands. Electronic address: J.F.P.Berbee@lumc.nl.

Abstract

Resveratrol is a major constituent of traditional Asian medicinal herbs and red wine and is suggested to be a potential antiatherosclerotic drug due to its proposed hypolipidemic, anti-inflammatory and antioxidative properties. The aim of this study was to evaluate whether resveratrol protects against atherosclerosis development in APOE*3-Leiden.CETP (E3L.CETP) mice and adds to the antiatherogenic effect of mild statin treatment, currently the most widely used antiatherogenic therapy. E3L.CETP mice were fed a cholesterol-rich diet without (control) or with resveratrol (0.01% w/w), atorvastatin (0.0027% w/w) or both for 14 weeks. During the study plasma lipid, inflammatory and oxidative stress parameters were determined. Resveratrol reduced atherosclerotic lesion area (-52%) in the aortic root, comparable to atorvastatin (-40%) and the combination of both drugs (-47%). The collagen/macrophage ratio in the atherosclerotic lesion, a marker of plaque stability, was increased by resveratrol (+108%), atorvastatin (+124%) and the combination (+154%). Resveratrol decreased plasma cholesterol levels (-19%) comparable to atorvastatin (-19%) and the combination (-22%), which was completely confined to (very)low-density lipoprotein cholesterol levels in all groups. Post hoc analyses showed that the antiatherogenic effect of atorvastatin could be explained by cholesterol lowering, while the antiatherosclerotic effect of resveratrol could be attributed to factors additional to cholesterol lowering. Markers of inflammation and oxidative stress were not different, but resveratrol improved macrophage function. We conclude that resveratrol potently reduces atherosclerosis development and induces a more stable lesion phenotype in E3L.CETP mice. However, under the experimental conditions tested, resveratrol does not add to the antiatherogenic effect of atorvastatin.

Copyright © 2012 Elsevier Inc. All rights reserved.

PMID:23337345