Relations of Dietary Magnesium Intake to Biomarkers of Inflammation and Endothelial Dysfunction in an Ethnically Diverse Cohort of Postmenopausal Women

OBJECTIVE Although magnesium may favorably affect metabolic outcomes, few studies have investigated the role of magnesium intake in systemic inflammation and endothelial dysfunction in humans. RESEARCH DESIGN AND METHODS Among 3,713 postmenopausal women aged 50-79 years in the Women's Health Initiative Observational Study and free of cardiovascular disease, cancer, and diabetes at baseline, we measured plasma concentrations of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), turnor necrosis factor-alpha receptor 2 (TNF-alpha-R2), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), and E-selectin. Magnesium intake was assessed using a semiquantitative food frequency questionnaire. RESULTS After adjustment for age, ethnicity, clinical center, time of blood draw, smoking, alcohol, physical activity, energy intake, BMI, and diabetes status, magnesium intake was inversely associated with hs-CRP (P for linear trend = 0.003), IL-6 (P < 0.0001), TNF-alpha-R2 (P = 0.0006), and sVCAM-1 (P = 0.06). Similar findings remained after further adjustment for dietary fiber, fruit, vegetables, folate, and saturated and trans fat intake. Multivariable-adjusted geometric means across increasing quintiles of magnesium intake were 3.08, 2.63, 2.31, 2.53, and 2.16 mg/l for hs-CRP (P = 0.005); 2.91, 2.63, 2.45, 2.27, and 2.26 pg/ml for IL-6 (P = 0.0005); and 707, 681, 673, 671, and 656 ng/ml for sVCAM-1 (P = 0.04). An increase of 100 mg/day magnesium was inversely associated with hs-CRP (-0.23 mg/l +/- 0.07; P = 0.002), IL-6 (-0.14 +/- 0.05 pg/ml; P = 0.004), TNF-alpha-R2 (-0.04 +/- 0.02 pg/ml; P = 0.06), and sVCAM-1 (-0.04 +/- 0.02 ng/ml; P = 0.07). No significant ethnic differences were observed. CONCLUSIONS High magnesium intake is associated with lower concentrations of certain markers of systemic inflammation and endothelial dysfunction in postmenopausal women.