Curcumin supplementation improves vascular endothelial function in healthy middle-aged and older adults by increasing nitric oxide bioavailability and reducing oxidative stress

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 (FBF_ACh; 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 FBF_ACh induced by the nitric oxide synthase inhibitor NG monomethyl-L-arginine (L-NMMA; P=0.03), and reduced the acute increase in FBF_ACh 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.

Keywords: aging; arterial stiffness; curcumin; endothelium-dependent dilation; inflammation; oxidative stress.

Figure 1

Participant progress through study.

Figure 2

Forearm blood flow (FBF) in response to increasing doses (left and middle) and area under the dose-response curve (AUC; right) to acetylcholine (FBF_ACh) at week 0 and after 12 weeks of placebo or curcumin supplementation. Data are mean ± SE; FAV, forearm volume; Group by time P=0.02, *P=0.03 vs. curcumin week 0.

Figure 3

Forearm blood flow (FBF) in response to increasing doses (left and middle) and area under the dose-response curve (AUC; right) to sodium nitroprusside (FBF_SNP) at week 0 and after 12 weeks of placebo or curcumin supplementation. Data are mean±SE; FAV, forearm volume; Group by time P=0.9.

Figure 4

Forearm blood flow (FBF) area under the dose-response curve (AUC) in response to acetylcholine (FBF_ACh) without (−) or with (+) NG monomethyl-L-arginine (L-NMMA; left) and nitric oxide-dependent dilation (right) at week 0 and after 12 weeks of placebo or curcumin supplementation. Data are mean±SE; *P<0.02 vs. corresponding group week FBF_ACh (left); Group by time P=0.04, *P=0.03 vs. curcumin week 0 (right).

Figure 5

Forearm blood flow (FBF) area under the dose-response curve (AUC) in response to acetylcholine (FBF_ACh) without (−) or with (+) vitamin C (vitC; left) and oxidative stress-mediated suppression of endothelium-dependent dilation (EDD; right) at week 0 and after 12 weeks of placebo or curcumin supplementation. Data are mean±SE; *P<0.05 vs. corresponding group week FBF_ACh (left); Group by time P=0.03, *P=0.02 vs. curcumin week 0 (right).

Figure 6

Brachial artery flow-mediated dilation (FMD) expressed as percent change at week 0 and after 4 and 12 weeks of placebo or curcumin supplementation. Data are mean±SE; Group by time P=0.001, *P=0.001 vs. curcumin week 0.

Figure 7

Brachial artery dilation to nitroglycerin expressed as percent change at week 0 and after 12 weeks of placebo or curcumin supplementation. Data are mean±SE; Group by time P=0.8.

Figure 8

Aortic pulse wave velocity (PWV; left) and carotid artery compliance (right) at week 0 and after 12 weeks of placebo or curcumin supplementation. Data are mean±SE; Data log transformed for statistical analysis; Both group by time P>0.2.