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Stress Reactions in Magnesium Deficiency.

Mildred Seelig

Stress hormones (catecholamines and corticosteroids), that evoke responses allowing for increased survival in life-threatening situations, can increase the risk of cardiac damage, as severe as sudden cardiac death when magnesium (Mg) deficiency exists. The stress hormones mediate release and utilization of substrates for production of energy and for improved voluntary and cardiac muscle performance, and mobilize tissue minerals: both Mg and calcium (Ca). The resultant (transitory) increase of serum Mg protects against arrhythmias and intravascular
coagulation in the short-term. However, if the serum Mg reach levels that exceed the renal threshold, it is excreted. Additionally, free fatty acids - released through the lipolytic effect of catecholamines - inactivate Mg in serum and tissues. Both responses intensify Mg deficiency. The stress hormone elevation of serum Ca, once the kidneys have restored Mg to the low limit of the normal range after the stress-induced rise, can result in a high enough Ca/Mg ratio to increase
risks of both intravascular coagulation and arrhythmia. A vicious cycle can ensue, as high Ca/Mg ratios stimulate additional catecholamine secretion by the adrenal medulla and by secretory granules at nerve endings and in the myocardium. Conversely, high Mg/Ca ratios suppress
catecholamine release. Low Mg also increases output of mineralocorticoids, which in turn directly enhance urinary excretion of Mg and intensify cardiopathogenicity of both Mg deficiency and catecholamine excess. Furthermore, low arterial tissue Mg can lead to
coronary arterial constriction - directly and through humoral vasopressors. Reduced myocardial Mg increases vulnerability to cardiac damage, that can result in chronic disease. Genetic differences in Mg homeostasis may be responsible for differences in susceptibility to pathologic reactions to stress. Mg deficiency and stress mutually enhance one another

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