Magnesium is very demanding for all human ,because of anthropologic
effects of primary nutritional deficiency of magnesium occur infrequently in infants (11) but are even less common in adults unless a relatively low magnesium intake is accompanied by prolonged diarrhoea or excessive urinary magnesium losses (12). Susceptibility to the effects of magnesium deficiency rises when demands for magnesium increase markedly with the resumption of tissue growth during rehabilitation from general malnutrition (6, 13). Studies have shown that a decline in urinary magnesium excretion during protein-energy malnutrition (PEM) is accompanied by a reduced intestinal absorption of magnesium. The catch-up growth associated with recovery from PEM is achieved only if magnesium supply is increased substantially (6, 14).
Most of the early pathologic consequences of magnesium depletion are neurologic or neuromuscular defects (12, 15), some of which probably reflect the influence of the element on potassium flux within tissues. Thus, a decline in magnesium status produces anorexia, nausea, muscular weakness, lethargy, staggering, and, if deficiency is prolonged, weight loss. Progressively increasing with the severity and duration of depletion are manifestations of hyperirritability, hyperexcitability, muscular spasms, and tetany, leading ultimately to convulsions. An increased susceptibility to audiogenic shock is common in experimental animals. Cardiac arrhythmia and pulmonary oedema frequently have fatal consequences (12). It has been suggested that a sub-optimal magnesium status may be a factor in the aetiology of coronary heart disease and hypertension but additional evidence is needed (16). therefore magnesium is very crucial ,Why?
Magnesium serves as a cofactor in more than 300 enzymatic reactions, such as those responsible for regulating blood pressure, glycaemic control and lipid peroxidation. Magnesium activates adenosine triphosphatase (ATPase), which is essential for cell membrane functioning and is also the energy source of the Na+–K+ pump. In rat models, magnesium deficiency has been shown to decrease the activity of the Na+–K+ pump, leading to an increase in intracellular sodium, which alters the membrane potential. In studying the sodium kinetic and membrane potential in the aorta of magnesium-deficient rats, Madden et al also showed that magnesium deficiency caused the membrane potential to be less polarised as a result of intracellular sodium accumulation, suggesting Na+–K+pump inhibition. This change in membrane potential has been hypothesised as a potential mechanism for causing arrhythmias. Magnesium is also known to be a cofactor important for the functioning of the enzymes in cardiac mitochondria. Additionally, magnesium has been demonstrated to modulate the potassium-proton exchange. Cation selectivity in sodium and potassium exchange for protons is highly dependent on magnesium. Thus, magnesium also protects against potassium loss. Intracellular magnesium deficiency may also cause an increase in intracellular sodium and calcium, which predisposes to arterial vasospasm, increased catecholamine release, increased fatty acids and lipids, as well as intravascular hypercoagulability. Furthermore, magnesium deficiency has been shown to play a role in inflammation in the rat model. Weglicki et al showed that during progression of magnesium deficiency, there is an increase in the serum levels of inflammatory cytokines interleukin-1, interluein-6 and tumour necrosis factor after 3 weeks of magnesium-deficiency diet. Magnesium deficiency also leads to an exaggerated response to immune stress and oxidative stress through activation of neuroendocrinological pathways. This inflammatory response predisposes to proatherogenic changes in lipoprotein metabolism, endothelial dysfunction, thrombosis and hypertension, contributing to the pathogenesis of metabolic syndrome as well as cardiovascular diseases.
See https://openheart.bmj.com/content/5/2/e000775
Magnesium critically stabilizes enzymes, including many ATP-generating reactions. Thus, ATP metabolism, muscle contraction and relaxation, normal neurological function, release of neurotransmitters etc. are magnesium dependent. Magnesium also contributes to the regulation of vascular tone, heart rhythm, platelet-activated thrombosis and bone formation.
Article Magnesium Basics
Magnesium is critical and copfactor for
1-diabetics
2-heart disease
3-hypertension
4-renal disease
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Article Magnesium and Human Health: Perspectives and Research Directions
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