Based on the volume of research, calcium is the most commonly associated mineral with bone formation, structure and health. But bone is a complex composite that contains a number of essential minerals. The skeleton can act as a reservoir for these minerals and release them to the blood under the control of hormones. This is important because if dietary levels fall, minerals are resorbed from bones to supply the plasma for important physiological functions, and this can has a detrimental effect on skeletal density. Recent research shows that increases in the blood pH, caused by diets high in animal protein and low in plant foods, can result in mineral resorption, as homeostatic mechanisms are put in place to neutralise acidic blood through release of mineral salts. While dietary intakes of calcium have been emphasised to women in recent decades, little attention has been paid to dietary intakes of magnesium.
Magnesium is an important component of bone, but evidence suggests that intakes in Western countries ate too low. Magnesium is an important cation in animals, but less than 1% is contained within the extracellular compartment. Around 95% of the intracellular magnesium is bound to negatively charged molecules such as ribosomes, membranes and ATP. Magnesium is required as a co-factor in around 300 enzymes, with a particularly well known role being in the ATP-magnesium complex that is required for catalytic activity in a number of reactions. Magnesium is also required for the function of ion channels. Around 50-60% of the total body pool is contained within bone, which can act as a store of magnesium during times of low intake. Intakes of magnesium have been shown to be below the recommended government intake in a number of studies, and deficiency can cause multiple symptoms due to the diverse physiological roles of the metal.
Animal models were used initially to understand magnesium deficiency, symptoms of which are neuromuscular hyperexcitability, possibly resulting from a concomitant hypocalcaemia. This hypocalcaemia is likely caused by a fall in circulating magnesium decreasing the binding of magnesium ions to the parathyroid receptor on parathyroid cells, which decreases parathyroid hormone release and causes hypocalcaemia. This is supported by evidence showing subjects with low magnesium status also have low levels of parathyroid hormone. The low levels of parathyroid hormone also decrease serum concentrations of 1,25-dihydroxyvitamin D, which in concert with parathyroid hormone, is a major regulator of skeletal bone turnover. Magnesium deficiency may therefore have detrimental effects on skeletal health and may have a profound influence on calcium homeostasis within the skeleton. In this respect, magnesium deficiency may be just as important as calcium deficiency in the skeletal problems associated with bone disorders, such as osteoporosis.
Epidemiological evidence links magnesium deficiency to osteoporosis, and some studies have found associations between dietary magnesium intakes and bone mineral density in post- and pre-menopausal women. Interestingly, magnesium supplementation of subjects with osteoporosis has not been extensively studied, although limited data suggests that increasing magnesium intake promote greater bone mineral density. Magnesium deficiency may lead to osteoporosis because magnesium causes new cell formation in bone (mitogenesis) and is also required to create small bone crystals, large crystals being associated with weaker bone structure. Magnesium therapy, may normalise parathyroid hormone, 1,25-dihydroxyvitamin D and allow correct structural formation of bone, normalising skeletal health. The role of magnesium in bone health has generally been ignored by the mainstream medical community, but nutritionists appear aware of the importance of optimal magnesium intakes in the diet, which are likely much higher than the recommended government intakes of less than 500mg/d.
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