The clinical and public health impact of the metabolic syndrome (MetS) has increased substantially in recent years. MetS is defined by a constellation of cardiovascular disease risk factors including: insulin resistance, elevated blood pressure, impaired glucose tolerance, central obesity, and atherogenic dyslipidemia as well as impaired clotting, increased inflammatory burden, and oxidative stress. Recently, there has been burgeoning experimental, clinical, and epidemiological data that provides strong evidence that dietary magnesium intake and supplementation are inversely associated with the risk for MetS and its components. In this review, we describe and discuss the myriad of integrated physiological mechanisms through which magnesium deficiency and the resultant altered magnesium status may lead to the development of the MetS and each of its components.