Hypomagnesemia and Cardiovascular Risk in Type 2 Diabetes

Hypomagnesemia is 10-fold more common in individuals with type 2 diabetes (T2D) than in the healthy population. Factors that are involved in this high prevalence are low Mg(2+) intake, gut microbiome composition, medication use, and presumably genetics. Hypomagnesemia is associated with insulin resistance, which subsequently increases the risk to develop T2D or deteriorates glycemic control in existing diabetes. Mg(2+) supplementation decreases T2D-associated features like dyslipidemia and inflammation, which are important risk factors for cardiovascular disease (CVD). Epidemiological studies have shown an inverse association between serum Mg(2+) and the risk of developing heart failure (HF), atrial fibrillation (AF), and microvascular disease in T2D. The potential protective effect of Mg(2+) on HF and AF may be explained by reduced oxidative stress, fibrosis, and electrical remodeling in the heart. In microvascular disease, Mg(2+) reduces the detrimental effects of hyperglycemia and improves endothelial dysfunction; however, clinical studies assessing the effect of long-term Mg(2+) supplementation on CVD incidents are lacking, and gaps remain on how Mg(2+) may reduce CVD risk in T2D. Despite the high prevalence of hypomagnesemia in people with T2D, routine screening of Mg(2+) deficiency to provide Mg(2+) supplementation when needed is not implemented in clinical care as sufficient clinical evidence is lacking. In conclusion, hypomagnesemia is common in people with T2D and is involved both as cause, probably through molecular mechanisms leading to insulin resistance, and as consequence and is prospectively associated with development of HF, AF, and microvascular complications. Whether long-term supplementation of Mg(2+) is beneficial, however, remains to be determined.