The effects of oral potassium and magnesium supplementation on blood pressure and the serum lipid level in humans

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The aim of this study is to examine the effects of oral magnesium (Mg) supplementation on blood pressure (BP) and related factors, such as urinary catecholamine, and the lipid metabolism. In the first study (13 healthy young subjects), a double-blind, crossover study was performed (Study-I) while the second study consisted of 30 elderly subjects (Study-II). In study I, the subjects consumed a control-diet (Ca : 500, Mg 250mg/day) with oral supplementation of a placebo (P-period), and the oral supplementation of Mg-hydroxide (Mg : 393-471mg/day) with the control diet (Mg-period) for 10 days, respectively. The urinary Mg excretion significantly increased during the Mg-period, while the systolic and diastolic BP did not change between the p- and Mg-periods. The urinary norepinephrine excretion (UNE) decreased 12% during the Mg-period compared to the P-period, whereas the other related variables did not change during Mg supplementation. In addition, the UNE and BP during the Mg-period sign … More ificantly decreased in the subjects whose 24-hurinary Mg excretion increased to twice that in the P-period. The LCAT also significantly increased during the Mg-period, but the HDL-cholesterol, total-cholesterol and triglyceride all remained unchanged. In studyII, the systolic and diastolic BP significantly decreased during the Mg-period, but not in the P-period. The plasma aldosterone concentration and hematocrit significantly increased in the Mg-period compared to the control period. There was also a significant positive correlation between the %-change from the control to the Mg-period of the UNE and that of the diastolic BP.However, the urinary K excretion positively correlated with the UNE.A statistically significant increase in the LCAT, HDL-cholesterol and apo-AI was observed after Mg supplementation. These results therefore suggest that Mg supplementation may both lower the BP through natriuresis and the suppression of UNE release, and improve the lipid levels through the activatation of LCAT in humans. Less