Objective-Moderate consumption of beer is associated with lower cardiovascular (CV) risk. To explore the underlying mechanisms we studied the acute effects of the constituents of beer (alcohol and antioxidants), on established predictors of CV risk: endothelial function, aortic stiffness, pressure wave reflections and aortic pressure.Research Methods & Proceedures-In a randomized, single -blind, cross -over study 17 healthy, non-smoking, volunteers (28.5±5.2 years and 24.4±2.5 BMI) consumed in 3 separate days, at least one week apart: a) 400 ml of beer & 400 ml water, b) 800 ml of dealcoholized beer (same amount of polyphenols), and c) 67 ml of vodka & 733 ml water (same amount of alcohol). Each time aortic stiffness (pulse wave velocity, pressure wave reflections (Aix), aortic and brachial pressure (Sphygmocor device) and endothelial function (brachial flow mediated dilatation) were assessed at fast and 1 and 2 hours postprandial.Results-Aortic stiffness was significantly and similarly reduced by all 3 interventions. However, endothelial function was significantly improved only after beer consumption (average of 1.33%, CI 0.15-2.53). Although wave reflections were significantly reduced by all 3 interventions (average of beer: 9.1%, dealcoholized beer: 2.8%, vodka 8.5%, all CI within limits of significance), the reduction was higher after beer consumption compared todealcoholized beer (p=0.018). Pulse pressure amplification (i.e. brachial/aortic) was increased by all 3 test drinks.Corresponding author: Kalliopi Karatzi PhD, Department of Nutrition and Dietetics, Harokopio University, Athens, Greece. 8 Mykonou str., Voula, 16673, Athens, Greece. Tel/Fax: + 30 210 8950786, pkaratzi@hua.gr. The authors declare that they have no conflict of interest. HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptConclusions-Beer improves acutely parameters of arterial function and structure, in healthy non-smokers. This benefit seems to be mediated by the additive or synergistic effects of alcohol and anti-oxidants and merits further investigation.

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The antioxidant activity (AA) of fruits and vegetables has been thoroughly investigated but less is known about the AA of dietary supplements (DS). We therefore assessed the AA of three to five DS each from pomegranate, milk thistle, green tea, grapes, goji, and acai using four widely used standard methods. The secondary objective was to determine the effects of in vitro digestion on their AA. The AA of the DS prior to digestion ranked as follows: pomegranate > resveratrol > green tea > grape seed > milk thistle and very low in goji and acai with significant group variability in AA. The AA after in vitro simulated digestion of the mouth, stomach, and small intestine compared to undigested supplement was decreased for green tea and grape seed but increased for pomegranate, resveratrol, milk thistle, goji, and acai to various extents. Although polyphenols provide the major antioxidant potency of the tested supplements, our observations indicate that digestion may alter antioxidant properties depending in part on the variations in polyphenol content.

Peripheral artery disease (PAD) is a serious but relatively underdiagnosed and undertreated clinical condition associated with a marked reduction in functional capacity and a heightened risk of morbidity and mortality. The pathophysiology of lower extremity PAD is complex, and extends beyond the atherosclerotic arterial occlusion and subsequent mismatch between oxygen demand and delivery to skeletal muscle mitochondria. In this review, we evaluate and summarize the available evidence implicating mitochondria in the metabolic myopathy that accompanies PAD. Following a short discussion of the available in vivo and in vitro methodologies to quantitate indices of muscle mitochondrial function, we review the current evidence implicating skeletal muscle mitochondrial dysfunction in the pathophysiology of PAD myopathy, while attempting to highlight questions that remain unanswered. Given the rising prevalence of PAD, the detriment in quality of life for patients, and the associated significant healthcare resource utilization, new alternate therapies that ameliorate lower limb symptoms and the functional impairment associated with PAD are needed. A clear understanding of the role of mitochondria in the pathophysiology of PAD may contribute to the development of novel therapeutic interventions.