Assessing magnesium (Mg) status is difficult as most Mg is deposited in the cells and bones. Mg deficiency can only result through poor dietary intake or chronic alcoholism, as otherwise the body has its own mechanism of conserving Mg by limiting urinary excretion. Though Mg does not directly interplay with the pathophysiology of hypertension, it plays a role in the active transport of Ca and K across cell membranes. Both Ca and K affect BP. Furthermore, Mg also is involved in the production of prostaglandin E1, which is a vasodilator and thus lowers BP. Severe Mg deficiency can lead to hypocalcemia and hypokalemia, thus raising BP.

A meta-analysis of 22 studies with 1173 normotensive and hypertensive adults provided evidence that Mg supplementation for 3-24 weeks decreases systolic BP by 3-4 mm Hg and diastolic BP by 2-3 mm Hg (Kass et al. 2012). Another systematic review and meta-analysis of prospective studies showed that increased serum Mg lowered the risk of CVD (DelGobbo et al. 2013).

Mg is abundant in the body. Due to an increase in the consumption of processed foods, most people do not have enough Mg in their diets. Mg is found in varying amounts in drinking water and is also found naturally in green leafy vegetables such as spinach, legumes, nuts, seeds, and fortified cereals and whole grains.

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