Chapter 7 166 In a post-hoc analysis of a previous RCT, we have shown that magnesium citrate supplementation has a beneficial effect towards a lower 24-urinary cortisol excretion together with an increased activity of 11β-HSD type 2, which may provide a proof of concept that dietary magnesium intake influences glucocorticoid metabolism, consistent with results of earlier preclinical studies. In contrast with the main finding of the prior trial, in our multi-arm RCT, we found that arterial stiffness and blood pressure were unchanged after magnesium supplementation for 24-wk. In a nonprespecified subgroup analysis, we observed a significant effect of magnesium sulfate supplementation towards decreased arterial stiffness in individuals with prevalent increased arterial stiffness at baseline. This effect size is comparable with the previous observed effects size where magnesium citrate was supplemented. Although we could not confirm the previously observed effect in subjects of the general population, our subgroup analysis suggests that it is feasible to further investigate potential effects of magnesium supplementation on arterial stiffness in a population with increased arterial stiffness. Further, this study showed that bioavailability was higher after magnesium citrate supplementation compared to magnesium oxide and magnesium sulfate supplementation, as evident by 24-h urinary magnesium excretion. Although more RCTs are warranted to confirm our finding, magnesium supplementation might be a promising (adjunct) treatment to reduce cardiovascular risk in a population with severe arterial stiffness, such as T2D and CKD patients. Finally, our study showed that 450 mg magnesium per day can be safely supplemented in the general population with normal renal function. Our findings therefore set the stage for future trials with higherdose magnesium supplementation in higher-risk populations.
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