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Letters to the Editor |
VA Medical Center, Geriatric Division, Department of Medicine, 79 Middleville Road, Northport, NY 11768-2290, E-mail: shingshing.yeh{at}med.va.gov
Weill Medical College, Cornell University, New York Presbyterian Hospital 520 E 70th St, Starr 341, New York, NY 10021
Dear Sir:
We thank Caddell for pointing out the important role of magnesium deficiency in cachexia. Although the focus of our review was on the cytokines themselves, we agree that there are numerous factors to be considered in geriatric cachexia (1). Inadequate food intake, reduced absorption, cytokine production, and medications can all affect the nutritional status of the elderly. Thiazide diuretics and loop diuretics are among the most common medications taken by the elderly and they clearly can cause a loss of magnesium. This loss may be overlooked because of apparently normal serum magnesium concentrations. However, when skeletal muscle biopsies are performed, subnormal magnesium and potassium concentrations are found (2). Insufficient dietary supplies of magnesium may inhibit protein synthesis by decreasing serum insulin-like growth factor I (2). Therefore, minerals like magnesium and vitamins are important supplements in the treatment of cachexia.
We agree that magnesium deficiency may exacerbate the elevation of inflammatory cytokines caused by other etiologies. Furthermore, magnesium deficiency may decrease endogenous antioxidant capacity and diminish host defenses. Magnesium deficiency may play an essential role in cellular reactions and in immunoinflammatory processes (3). Magnesium deficiency can also affect mineral homeostasis, induce membrane damage, increase lipid peroxidation, and increase cytokine concentrations, thus reducing immunocompetence (4). Weglicki et al (5–7) found that dramatic elevations in interleukin 6, interleukin 1, and tumor necrosis factor 
may promote cardiac lesions in magnesium-deficient rodents. This activation of immune cells probably occurs early in magnesium deficiency because magnesium-deficient rats that received magnesium-replacement therapy before endotoxin challenge had significantly lower tumor necrosis factor production than controls (3). It was also noted that vitamin E supplements can prevent the occurrence of myocardium reperfusion injury, possibly through the restoration of endogenous antioxidant defenses in the hypomagnesemic state (7).
Stress and chronic inflammation, under conditions of mineral or antioxidant deficiency, probably further stimulate the secretion of catecholamines and cortisol, which then stimulate the release of cytokines. As we emphasized in our review, cytokines rarely act alone because they stimulate a variety of cell types to produce and secrete a cascade of other cytokines (1). All of these interactions point to the complex roles of cytokines in causing cachexia (1). The effects of magnesium supplementation, the use of antioxidants, as well as the use of cytokine inhibitors in the treatment of geriatric cachexia require further study.
REFERENCES
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