Abstract

We hypothesized that curcumin would improve resistance and conduit artery endothelial function and large elastic artery stiffness in healthy middle-aged and older adults. Thirty-nine healthy men and postmenopausal women (45-74 yrs) were randomized to 12 weeks of curcumin (2000 mg/day Longvida®; n=20) or placebo (n=19) supplementation. Forearm blood flow response to acetylcholine infusions (FBFACh; resistance artery endothelial function) increased 37% following curcumin supplementation (107±13 vs. 84±11 AUC at baseline, P=0.03), but not placebo (P=0.2). Curcumin treatment augmented the acute reduction in FBFACh induced by the nitric oxide synthase inhibitor NG monomethyl-L-arginine (L-NMMA; P=0.03), and reduced the acute increase in FBFACh to the antioxidant vitamin C (P=0.02), whereas placebo had no effect (both P>0.6). Similarly, brachial artery flow-mediated dilation (conduit artery endothelial function) increased 36% in the curcumin group (5.7±0.4 vs. 4.4±0.4% at baseline, P=0.001), with no change in placebo (P=0.1). Neither curcumin nor placebo influenced large elastic artery stiffness (aortic pulse wave velocity or carotid artery compliance) or circulating biomarkers of oxidative stress and inflammation (all P>0.1). In healthy middle-aged and older adults, 12 weeks of curcumin supplementation improves resistance artery endothelial function by increasing vascular nitric oxide bioavailability and reducing oxidative stress, while also improving conduit artery endothelial function.

Highlights

  • Cardiovascular diseases (CVD) are the primary cause of death in developed societies [1, 2]

  • Improvement in resistance artery endothelial function is mediated by increases in nitric oxide bioavailability and reductions in vascular oxidative stress

  • Our findings provide evidence for curcumin supplementation as a promising nutraceutical-based treatment for improving nitric oxide-mediated vascular endothelial function and oxidative stress

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Summary

Introduction

Cardiovascular diseases (CVD) are the primary cause of death in developed societies [1, 2]. Advancing age is the major risk factor for CVD, with a ~70% prevalence of CVD in men and women over 60 years of age [1, 3] This increase in CVD risk with aging is due primarily to adverse changes to arteries, in particular, the development of vascular endothelial dysfunction and increased stiffness of large elastic arteries [4]. Both resistance artery (microvascular) and conduit artery (macrovascular) endothelial function, as measured by endothelium-dependent dilation (EDD), decline with advancing age [5,6,7,8,9,10,11] and each is independently predictive of future risk of cardiovascular events and mortality [12,13,14,15]. Decreased nitric oxide bioavailability with age is in part driven by the presence of oxidative stress, an increase in reactive oxygen species relative to antioxidant defenses, and chronic low-grade inflammation [8, 20,21,22]

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