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Skeletal buffer function and symptomatic magnesium deficiency.

W F Langley, D J Mann

    Medical Hypotheses
    |January 1, 1991
    PubMed
    Summary
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    Magnesium (Mg++) depletion can lead to neurological dysfunction. The parathyroid gland

    Area of Science:

    • Neurology
    • Endocrinology
    • Mineral Metabolism

    Background:

    • Magnesium (Mg++) depletion is a significant factor in neurological dysfunction and seizures.
    • The skeletal system, regulated by the parathyroid gland, plays a crucial role in buffering Mg++ levels.
    • Initial asymptomatic presentation can mask severe underlying issues until homeostatic mechanisms are activated.

    Purpose of the Study:

    • To investigate the hypothesis that parathyroid hyperactivity and Mg++ deficiency can trigger neurological symptoms.
    • To explore the ion transfer mechanisms between serum, cerebrospinal fluid, and bone during these conditions.
    • To propose analogous syndromes in clinical medicine based on veterinary observations.

    Main Methods:

    • Review of evidence supporting the proposed ion transfer hypothesis.

    Related Experiment Videos

  • Analysis of the interplay between serum ionic calcium (Ca++), parathyroid hormone (PTH) secretion, and Mg++ levels.
  • Examination of the role of the skeletal system as an ion buffer.

    • Main Results:

    • A rise in serum Ca++ in Mg++ deficient subjects inhibits PTH secretion.
    • This inhibition triggers the transfer of Ca++, Mg++, and other ions from extracellular fluid into bone.
    • Mg++ ions transfer from cerebrospinal fluid to blood and then to bone, potentially inducing neurological signs.

    Conclusions:

    • Parathyroid hyperactivity and Mg++ deficiency, coupled with elevated serum Ca++, can precipitate neurological symptoms.
    • The severity and duration of symptoms are linked to the extent of Ca++ and Mg++ depletion in bone and serum Ca++ levels.
    • Sympathetic stimulation may facilitate the symptom complex, with potential analogies in sodium (Na+) regulation.