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indeed showed that supplementation of > 370 mg/day resulted in a more pronounced blood pressure-lowering effect. This lack of effect on blood pressure could be due to the total daily dose, which may have been too low to detect changes in blood pressure. Although blood pressure is a major determinant of arterial stiffness, we did not observe any change in blood pressure. Recently, we observed a significant reduction of arterial stiffness, measured by the PWV c–f, after 24 weeks of oral magnesium citrate supplementation (total daily dose of 350 mg) in the magnesium citrate group compared with the placebo group (8.3 m/s vs 9.1 m/s, respectively). The gold standard for quantifying arterial stiffness is the carotid–femoral pulse wave velocity (PWV c–f), a noninvasive method that measures the propagation of the forward pressure wave traveling along the aorta. Foods with relatively high magnesium contents include whole grains, leafy green vegetables, legumes and nuts.Īrterial stiffness is closely related to the extent of atherosclerosis, an independent cardiovascular risk factor, and predictive of future cardiovascular events and mortality. It is, therefore, not surprising that insufficient magnesium intake has been associated with a wide variety of metabolic disorders, such as insulin resistance, and common diseases that may result from metabolic deregulations, such as hypertension and ischemic heart disease. Magnesium is an essential mineral that acts as a cofactor in hundreds of enzymatic reactions in the human body. Retrospectively registered on 15 August 2018. As such, the study may contribute to the primary prevention of cardiovascular disease in slightly obese, but otherwise healthy, individuals. The present study is expected to provide evidence for the effects of different available magnesium formulations (organic and inorganic) on well-established cardiovascular risk markers, including arterial stiffness and blood pressure, as well as on the human gut microbiota.
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Measurements will be performed at baseline and at weeks 2, 12 and 24. Secondary outcomes are office blood pressure, measured by a continuous blood pressure monitoring device, and gut microbiota, measured in fecal samples. The primary outcome of the study is arterial stiffness measured by the carotid–femoral pulse wave velocity (PWV c–f), which is the gold standard for quantifying arterial stiffness. During a 24-week intervention, individuals will be randomized to receive: magnesium citrate magnesium oxide magnesium sulfate (total daily dose of magnesium for each active treatment 450 mg) or placebo. In this randomized, double-blind, placebo-controlled trial, a total of 162 healthy overweight and slightly obese men and women will be recruited. In addition, we aim to investigate possible underlying mechanisms, including changes in blood pressure and changes in gut microbiota diversity. Therefore, we aim to study the long-term effects of magnesium citrate, magnesium oxide and magnesium sulfate on arterial stiffness.
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It remained unclear whether the observed effect was due to magnesium or citrate, and whether other magnesium compounds may have similar effects. Recently, we showed that magnesium citrate supplementation results in a clinically relevant improvement of arterial stiffness. Arterial stiffness is closely related to the process of atherosclerosis, an independent cardiovascular risk factor, and predictive of future cardiovascular events and mortality.