Mg deficit causes neuromuscular manifestations, including positive Chvostek and Trousseau signs, muscular fasciculations, tremor, tetany, nausea, and vomiting. The pathogenesis of the neuromus-cular irritability is complex, and it implicates the central and peripheral nervous system, the neuromuscular junction, and muscle cells.
Mg deficit perturbs Ca homeostasis and hypocal-cemia is a common manifestation of severe Mg deficit. Impaired release of parathyroid hormone (PTH) and skeletal end organ resistance to PTH appear to be the major factors implicated, probably by a decrease in adenylcyclase activity.
Perturbations in the action and/or metabolism of vitamin D may also occur in Mg deficit. Because Mg plays a key role in skeletal metabolism, Mg deficit may be a possible risk factor for osteoporosis. However, epidemiologic studies relating Mg intake to bone mass or rate of bone loss have been conflicting, and further investigation is necessary to clarify the role of Mg in bone metabolism and osteoporosis.
Hypokalemia is frequently encountered in Mg deficit. This is due to an inhibition of Na,K-ATPase activity that impairs K and Na transport in and out of the cell and to stimulation of renin and aldoster-one secretion that increases K urinary excretion.
There is increasing evidence that Mg deficiency may be involved in the development of various pathologies. Mg deficit is frequent in diabetes and can be a factor in insulin resistance. It can modify insulin sensitivity, probably by influencing intracel-lular signaling and processing. Mg deficit has also been implicated in the development or progression of micro- and macroangiopathy and neuropathy.
Mg deficit appears to act as a cardiovascular risk factor. Experimental, clinical, and epidemiological evidence points to an important role of Mg in blood pressure regulation. Mg deficit can lead to cardiac arrhythmias and to increased sensitivity to cardiac glucosides. Mg deficit may also play a role in the development of atherosclerosis. In experimental animal models, dietary Mg deficiency results in dyslipidemia, increased sensitivity to oxidative stress, and a marked proinflammatory effect, thus accelerating atherogenosis. Macrophages and poly-nuclear neutrophils are activated and synthesize a variety of biological substances, some of which are powerful inducers of inflammatory events (cytokines, free radicals, and eicosanoids). The effect of Mg depletion or Mg supplementation may result in the ability of Mg to modulate intracellular calcium. Pharmacological doses of Mg may reduce morbidity and mortality in the period following infarction. The beneficial effect of Mg may result from calcium-antagonist action, decreased platelet aggregation, and decreased free radical damage.
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