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Study under review: Long-term magnesium supplementation improves arterial stiffness in overweight and obese adults: results of a randomized, double-blind, placebo-controlled intervention trial
Introduction
Magnesium is an essential mineral that is used by the body in over 300 biological processes. The best dietary sources of magnesium are seeds and nuts, green leafy vegetables, and whole grains, though it’s also found in smaller amounts in meat and dairy products, as well as in some fortified cereals. Medications like laxatives and chewable antacids also contain magnesium.
Low dietary magnesium has been linked to a number of health risks, including heart disease[1], stroke[2], and type 2 diabetes[3]. One very large meta-analysis[4] of 16 trials surveying a total of 300,000 participants found that for each 200 milligram per day increase in dietary magnesium, there was an associated 30% decrease in heart attacks. In the same analysis, only circulating magnesium levels (not dietary consumption) were correlated with overall cardiovascular disease (CVD) risk, which includes not only heart attacks, but also stroke, arrhythmia, and heart failure. For each 0.2 mmol/L increase in plasma magnesium concentrations, a 30% reduction in risk for CVD was observed.
Increased arterial stiffness, or the reduced ability of an artery to contract and expand as blood moves through it, is independently linked[5] to increased CVD risk. You might remember reading about pulse wave velocity (PWV, which is depicted in Figure 1) analysis in “Blueberries every day keeps high blood pressure at bay” (Study Deep Dives #6, April 2015). This is a non-invasive way to measure arterial stiffness. It involves placing pressure catheters at two points on the body and then measuring the time it takes for the “wave” of the heartbeat to travel between those two points. Traveling faster between those two points means the arteries the wave is traveling through are stiffer.

Most prior studies on the role of magnesium in CVD have used blood pressure[6], lipid profiles[7], and inflammatory markers[8] as surrogates for cardiovascular events. These studies have shown mixed or inconclusive results. Only one study has used PWV analysis as the surrogate (and secondary) endpoint. The study[9] was completed in healthy young men over an eight-week period, and no improvement was found in the magnesium group. This study attempted to evaluate a more relevant population for CVD, and used a much longer study duration of 24 weeks in order to assess the effects of magnesium on arterial stiffness as a marker for CVD risk, which may overcome the limitations of the previous study.
Magnesium is a mineral that is essential to hundreds of biological functions in the body. Low magnesium levels have been linked to a number of health risks, including cardiovascular disease. Prior trials have attempted to assess the role of magnesium supplementation in CVD by using blood pressure or other biological markers as endpoints, with mixed results. This study examined pulse wave velocity as a measure of arterial stiffness linked with CVD.
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