Long-term magnesium supplementation improves glucocorticoid metabolism 105 5 enzyme activity of intracellular 11β-HSDs and A-ring reductases can be quantified from 24-h urine concentrations of cortisol, cortisone, and their metabolites. This approach provides important insight into the intracellular regulation of glucocorticoids. A potential limitation of our study is that we were not able to define effects of oral magnesium supplementation on the 11β-HSD type 1 activity. The 11β-HSD type 1 activity can only be inferred from the THFs/THE ratio when the cortisol/cortisone ratios is unchanged 14. In the current study, the cortisol/cortisone ratio was changed after the treatment period in the magnesium group, which may imply an effect on wholebody 11β-HSD activity, rather than an effect on the specific 11β-HSD type 1 activity. Second, licorice-derivatives, such as glycyrrhizic acid, inhibit the enzymatic activity of 11β-HSD type 2. Whether the intake of licorice has influenced our results, is not entirely clear, because no data on licorice intake were available. However, participants were requested not to change their dietary intake pattern during the study. Results from the food frequency questionnaires showed indeed that dietary intake (macro and micronutrient intake) did not change during the study, suggesting that it is unlikely that licorice intake affected our results 2. Furthermore, we could not differentiate whether the effect on glucocorticoid metabolism was due to supplementation of magnesium or due to potential effects of citrate. However, in our future study, we will address effects of different magnesium supplements (magnesium citrate, magnesium oxide and magnesium sulphate) on cardiovascular risk markers, including arterial stiffness and blood pressure 38. Finally, as the post-hoc analyses we performed are exploratory and hypothesis-generating, the current findings should be interpreted with caution. To conclude, we observed a beneficial effect of oral magnesium supplementation towards a lower 24-h urinary cortisol excretion together with an increased activity of 11β-HSD type 2. Our findings may indicate improved glucocorticoid metabolism induced by oral magnesium supplementation, suggesting a potential mechanism by which increased dietary magnesium intake lowers CVD risk. Our results provide a basis to further investigate effects of oral magnesium supplementation on CVD risk and underlying mechanisms. Conflict of interest The authors declare no conflicts of interest.
RkJQdWJsaXNoZXIy MTk4NDMw