Skeletal buffer function and symptomatic magnesium deficiency

Abstract A major factor relating to the oversight of neurological dysfunction and seizures caused by magnesium (Mg++) depletion, involves the buffer functions of the skeletal system orchestrated primarily by the parathyroid. A Mg++ depleted subject may appear relatively asymptomatic until a short period after homeostatic responses go into effect. The result can be devastating if not recognized promptly and treated appropriately. This series of events can best be demonstrated in veterinary medicine but we propose that analogous syndromes occur in clinical medicine. Evidence is presented to support the hypothesis that in subjects with parathyroid hyperactivity and Mg++ deficiency, the stimulus of a rise in serum ionic calcium (Ca++), and the resultant inhibition of parathyroid hormone (PTH) secretion, trigger the transfer of Ca++, Mg++ and other ions from the extracellular space into the exchangeable bone compartment. More importantly, there is a transfer of Mg++ ions from the cerebrospinal fluid into the blood and ultimately into the bone compartment. If the gradient is large and the stimulus adequate, neurological signs and symptoms may be induced. The degree of Ca++ and Mg++ depletion of the peripheral bone and the amount and duration of Ca++ ion increase largely determine the duration and severity of symptoms. The symptom complex is facilitated by sympathetic stimulation. An analogous situation may exist with sodium (Na+).