Magnesium Deficiency in Alcoholism: Possible Contribution to Osteoporosis and Cardiovascular Disease in Alcoholics

Authors

  • Lisa Abbott,

    1. Department of Endocrinology, LAC+USC Medical Center, Los Angeles, California
    2. Orthopaedic Hospital/University of Southern California Bone Tissue Research Laboratories, Los Angeles, California
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  • Jerry Nadler,

    1. Department of Diabetes, Endocrinology, and Metabolism, City of Hope National Medical Center, Duarte, California.
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  • Robert K. Rude

    Corresponding author
    1. Department of Endocrinology, LAC+USC Medical Center, Los Angeles, California
    2. Orthopaedic Hospital/University of Southern California Bone Tissue Research Laboratories, Los Angeles, California
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  • This work was supported in part by the National Institutes of Health Grant HL-44404 and by the General Clinical Research Center Grant MOI-RR-43, and funds from the Orthopaedic Hospital.

Reprint requests: Robert K. Rude, M.D., LAC+USC Medical Center, 2025 Zonal Avenue, Unit I, Room 18415, Los Angeles, CA 90033.

Abstract

Magnesium (Mg) deficiency occurs frequently in chronic alcoholism and may contribute to the increased incidence of osteoporosis and cardiovascular disease seen in this population. Mg deficiency is primarily due to renal Mg-wasting and is exacerbated by dietary Mg deprivation, gastrointestinal losses with diarrhea or vomiting, as well as concomitant use of drugs such as diuretics and aminoglycosides. Osteoporosis is prevalent in the alcoholic population. Mg deficiency may contribute to increased bone loss by its effects on mineral homeostasis. In Mg depletion, there is often hypocalcemia due to impaired parathyroid hormone (PTH) secretion, as well as renal and skeletal resistance to PTH action. Serum concentrations of 1,25-vitamin D are also low. These changes are seen with even mild degrees of Mg deficiency and may contribute to the metabolic bone disease seen in chronic alcoholics. Hypomagnesemia in alcoholics may also contribute to increased cardiovascular disease by altering platelet function. Mg deficiency has been demonstrated to enhance platelet reactivity. In these studies, Mg was shown to inhibit platelet aggregation against various aggregation agents. Patients with Mg deficiency were shown to have increased platelet aggregation that was normalized with Mg therapy. The antiplatelet effect of Mg may be related to the finding that Mg inhibits the synthesis of thromboxane A2 and 12-hydroxyeicosatetraenoic acid, eicosanoids thought to be involved in platelet aggregation. Mg also inhibits the thrombin-induced Ca2+ influx in platelets, as well as stimulates synthesis of prostaglandin l2, the potent antiaggregatory eicosanoid. Therefore, Mg deficiency may increase platelet aggregation and cause increased hypertension and atherosclerotic cardiovascular disease in alcoholics.

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