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Magnesium plays important roles in boosting mitochondrial efficiency, one of the major components of Boost MitoHealth. Despite its critical role in energy production, a vast majority of the US population is deficient in this essential mineral. Mag deficiency is implicated in the development of cardiovascular diseases including hypertension, heart failure, ventricular arrhythmias, and type 2 diabetes.

Many enzymatic reactions involved in mitochondrial energy production are dependent on magnesium ions. Thus, 30- 45% of the cellular Mag is found in mitochondrial. Mag is transported from the cytoplasm into mitochondria via a system including magnesium-selective transporter (MRS2) expressed in the mitochondrial inner membrane Disruption of this gene affected Mg levels in cells, which in turn adversely affected energy production, mitochondrial morphology and made the cells vulnerable to cellular stress.

In diabetics, Mg improved mitochondrial ATP production and decreased ROS and calcium overload. In this model, Mag supplementation reduced oxidative stress, improved ATP production, and importantly, prevented cardiac diastolic dysfunction.

Established is that ageing is associated with impaired mitochondrial functions. Thus, in an experimental mouse model of premature ageing, dietary Mag supplementation improved mitochondrial functions (improved ETC activity, ATP synthesis, and MMP).

Treatment of vascular smooth muscle cells from these aged mice with mag-enriched medium improved mitochondrial function, i.e., increased ATP production and antioxidant capacity. Importantly, Mag supplementation increased lifespan, and reduced the calcification of vascular smooth muscle, a common condition associated with ageing.

Fortunately, mag is enriched in many food sources…green leafy vegetables (e.g., spinach), cereals, vanilla yogurt, seeds, soybeans, halibut, and beverages such as tea, cocoa, and coffee.

Dietary recommendations are 400 – 420 mg for men and 310 – 310 mg for women. The higher levels are recommended for older people.



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