BACKGROUND: Experimental studies have linked hypomagnesemia with the development of vascular dysfunction, hypertension, and atherosclerosis. Prior clinical studies have yielded conflicting results but were limited by the use of self-reported magnesium intake or short follow-up periods. METHODS: We examined the relationship between serum magnesium concentration and incident hypertension, cardiovascular disease (CVD), and mortality in 3,531 middle-aged adult participants in the Framingham Heart Study offspring cohort. Analyses were performed using Cox proportional hazards regressions, adjusted for traditional CVD risk factors. RESULTS: Follow-up was 8 years for new-onset hypertension (551 events) and 20 years for CVD (554 events). There was no association between baseline serum magnesium and the development of hypertension (multivariable-adjusted hazards ratio per 0.15 mg/dL 1.03, 95% CI 0.92-1.15, P = .61), CVD (0.83, 95% CI 0.49-1.40, P = .49), or all-cause mortality (0.77, 95% CI 0.41-1.45, P = .42). Similar findings were observed in categorical analyses, in which serum magnesium was modeled in categories (<1.5, 1.5-2.2, >2.2 mg/dL) or in quartiles. CONCLUSIONS: In conclusion, data from this large, community-based cohort do not support the hypothesis that low serum magnesium is a risk factor for developing hypertension or CVD.
BACKGROUND: Experimental studies have linked hypomagnesemia with the development of vascular dysfunction, hypertension, and atherosclerosis. Prior clinical studies have yielded conflicting results but were limited by the use of self-reported magnesium intake or short follow-up periods. METHODS: We examined the relationship between serum magnesium concentration and incident hypertension, cardiovascular disease (CVD), and mortality in 3,531 middle-aged adult participants in the Framingham Heart Study offspring cohort. Analyses were performed using Cox proportional hazards regressions, adjusted for traditional CVD risk factors. RESULTS: Follow-up was 8 years for new-onset hypertension (551 events) and 20 years for CVD (554 events). There was no association between baseline serum magnesium and the development of hypertension (multivariable-adjusted hazards ratio per 0.15 mg/dL 1.03, 95% CI 0.92-1.15, P = .61), CVD (0.83, 95% CI 0.49-1.40, P = .49), or all-cause mortality (0.77, 95% CI 0.41-1.45, P = .42). Similar findings were observed in categorical analyses, in which serum magnesium was modeled in categories (<1.5, 1.5-2.2, >2.2 mg/dL) or in quartiles. CONCLUSIONS: In conclusion, data from this large, community-based cohort do not support the hypothesis that low serum magnesium is a risk factor for developing hypertension or CVD.
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