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Hypomagnesemia, which may be difficult to diagnose, can complicate diabetes mellitus or a variety of cardiovascular diseases. In some patients, an infused multielectrolyte preparation is often the best solution.
Four patients with gastrointestinal disorders, and one patient with chronic alcoholism presented with both hypocalcemia and hypomagnesemia. Pharmacological doses of either ergocalciferol or dihydrotachysterol did not correct the hypocalcemia except in one patient who had a minimal rise in serum calcium. Parathormone levels were high in three patients and exogenous parathormone given to the fourth subject failed to elicit a rise in serum calcium, implying impairment of the calcemic response to parathormone. Magnesium repletion simultaneously corrected the hypomagnesemia and hypocalcemia. Balance data suggested that the rise in serum calcium was in part, at least, due to increased mobilization of minerals from bone. While the mechanism remains speculative, it appears that magnesium facilitates the release of calcium from bone in the presence of adequate amounts of vitamin D and parathormone.
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A link between Mg deficiency and sudden death is suggested by a substantial number of studies published over the past three decades. Data come from epidemiologic, autopsy, clinical, and animal studies. They suggest that: (1) Sudden death is common in areas where community water supplies are Mg-deficient. (2) Myocardial Mg content is low in people who die of sudden death. (3) Cardiac arrhythmias and coronary artery vasospasm can be caused by Mg deficiency and (4) Intravenous Mg reduces the risk of arrhythmia and death immediately after acute myocardial infarction. Because of these data, Mg supplementation has been proposed as a possible method of reducing the risk of sudden death. Suggested ways of supplementing Mg include public education to change dietary habits, addition of Mg to community water supplies, fortification of foods, and oral supplementation. Despite the substantial number of studies linking Mg deficiency with sudden death, no prospective studies have yet investigated whether large-scale Mg supplementation is useful for the primary prevention of sudden death.
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The effect of thalidomide on circulating cytokines and myocardial lesion formation was investigated in Mg-deficient rats. After two weeks on a Mg-deficient diet, rats show an increase in circulating levels of tumor necrosis factor-alpha and interleukin 1. Thalidomide (1 mg/day) caused a complete inhibition of the increase in circulating tumor necrosis factor-alpha levels, without having an effect on interleukin 1. However, a marked increase in cardiomyopathic lesion formation was observed in Mg-deficient animals treated with thalidomide; possible mechanisms for thalidomide's enhancement of myocardial injury are discussed.
We examined the effect of reducing ambient and intracellular free Mg ion ([Mg]i) concentrations on insulin action in epididymal adipocytes from male Sprague-Dawley rats in terms of (1) cellular transport of nonmetabolizable 2-deoxyglucose, (2) [U-14C]glucose oxidation to CO2, and (3) D-[3H]glucose incorporation into triglycerides. There were no significant differences in basal or insulin-stimulated transport of 2-deoxyglucose between adipocytes cultured in physiologic (1.24 mmol) or low (0.16 mmol) Mg for up to 24 hours. In contrast, insulin-stimulated but not basal [U-14C]glucose oxidation to CO2 was significantly reduced in adipocytes cultured in low versus physiologic Mg (P < .05 to .01). Similarly, there were no differences in basal glucose incorporation into triglycerides between cells cultured in low or physiologic Mg media for up to 24 hours. However, long-term (24-hour) but not short-term (2-hour) exposure of cells to low Mg was associated with a significant 30% reduction in insulin-stimulated D-[3H]glucose incorporation into triglycerides. When adipocytes incubated in low Mg were reincubated in high Mg (1.24 or 5 mmol) for 30 minutes, normal insulin-stimulated D-[3H]glucose incorporation into triglycerides was restored. Incubation of adipocytes in low Mg (0.16 mmol) for 24 hours resulted in a significant decrease in [Mg]i (264 +/- 89 v 437 +/- 125 micromol/cell [mean +/- SEM]) as compared with cells incubated in physiologic Mg (1.24 mmol; P < .01). These data support a role for intracellular Mg deficiency in the development of insulin resistance and suggest that the effect occurs at a site(s) distal to glucose entry into the cell. The effect of Mg deficiency on insulin action appears to be reversible.
Calcium absorption was measured by 47Ca disappearance from ligated duodenal loops and 47Ca uptake by tibiae in chicks fed diets containing one of four levels of Mg for two weeks. The diets, otherwise identical, contained 88 (group 1), 150 (group 2), 200 (group 3) and 1000 (group 4) ppm Mg. There were no statistically significant differences in 47Ca absorption. Mucosal CaBP and intestinal alkaline phosphatase were slightly, but not significantly, elevated in the Mg depleted chicks in groups 1 and 2 compared to groups 3 and 4. Microscopic examination of the tibiae showed marked alterations in morphology in chicks fed the 88 ppm Mg diet. The thickness of the epiphyseal plate was reduced, and the morphologic signs of osteolysis and chondrolysis, normally observed in the metaphysis, appeared to be absent. The mid-diaphysis was thickened and showed marked reduction in both osteoblast and osteocytie activity. Blood calcium levels were significantly reduced in the Mg deficient chicks. It was concluded that Mg depletion in chicks altered Ca homeostasis primarily by changing bone structure and function.
The parkinsonism-dementia complex (PDC) and amyotrophic lateral sclerosis (ALS) were the fatal neurological diseases, showing very high incidence during 1950-1970 and dramatic decrease after 1970 on Guam. Through the research, the present author insisted that; (1) NFTs in Guam ALS patients are merely a background feature widely dispersed in the population, (2) Guam ALS and PDC are basically different diseases, and (3) Guam ALS occurs initially as classic ALS. As pathogeneses of the diseases, intake of low calcium (Ca) and magnesium (Mg) and high aluminum water and of some plant excitatory neurotoxin has been speculated. To elucidate the pathogenesis, the author performed an experiment exposing rats to low Ca and/or Mg intake for two generations, so as to follow the actual way of human living on the island, since several generations live continuously in the same environment. The study indicates that continuous low Mg intake for two generations induces exclusive loss of dopaminergic neurons in in rats, and may support the Mg hypothesis in the pathogenesis of PDC of Guam.
Sudden death losses occurred in 4-month-old beef calves with clinical signs of muscular dysfunction, including tetanic spasms. Gross lesions were not diagnostic. Microscopic lesions consisted of deposition of calcium salts in the elastic fibers of the arteries in the heart, lungs, and spleen and in the trabeculae of the spleen. Focal areas of interstitial nephritis were characterized by infiltration of lymphocytes and plasma cells. Samples of hay and silage that the cattle were consuming were low in magnesium. Calves with spasms responded to magnesium salts given intravenously, and losses ceased after a magnesium-containing supplement was fed free choice to the calves and cows.
Experimental Mg2+ deficiency was induced in a group of rats by feeding them a Mg2+-deficient diet for 23 days. They were pair-fed to compare with a control group of rats fed a Mg2+-sufficient diet. In the Mg2+-deficient group the plasma total cholesterol and triglyceride levels were increased while HDL-cholesterol was decreased. In the Mg2+-deficient group the plasma level of thiobarbituric acid reacting substances (TBARS) used as a measure for lipid peroxidation was increased. The increase was attributed to the increased cytosolic Ca2+ in Mg2+-deficiency which can cause: 1) increase of hydro and endoperoxide levels as a consequence of the increase of arachidonic acid release and eicosanoid synthesis in Mg2+-deficiency, and 2) inhibition of the mitochondrial respiratory activity and activation of Ca2+-dependent proteases which may activate the conversion of xanthine dehydrogenase to xanthine oxidase which generates active O2 species. In the Mg2+-deficient group, the fatty acid composition of the liver microsomes indicated a slower rate of conversion of linoleic acid to arachidonic acid which was consistent with the decrease of delta 6 desaturase activity in liver microsomes of Mg2+-deficient rats as measured in vitro. The decrease of delta 6 desaturase activity was attributed to the lower concentration of actual enzyme molecules as a result of the decreased rate of protein synthesis in Mg2+-deficiency. The possible effects of the increased catecholamine release in Mg2+-deficiency are discussed.
Mg deficiency was produced in rats by feeding a Mg-free diet. Ten days of dietary Mg depletion led to an increase in active duodenal Ca absorption in sham-operated animals, but this increase was abolished by thyroparathyroidectomy (TPTX). In addition, TPTX reduced Ca absorption in control aminals fed a Mg-containing diet. More prolonged Mg deficiency was produced by feeding sham-operated animals the Mg-free diet for 19 days. This condition resulted in more marked hypomagnesemia and a depression of Ca transport rates to the level observed in the TPTX groups. These results are consistent with the concept that adaptation of duodenal Ca transport in response to Mg deficiency occurs through an increase in parathyroid hormone (PTH) secretion; however, direct blood PTH measurements will be required to prove this point.
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Increased white blood cell counts or leukocytosis have been observed primarily in young rats fed diets extremely low in Mg (< 60 ppm) and high in phosphorus (0.5 % P). We investigated the influence that acute and moderate Mg deficiencies have on blood leukocytes at high and low dietary phosphorus levels. For four weeks, male Sprague-Dawley rats (initially 7 weeks old) were fed diets containing 30, 60, 120, 208, or 850 ppm Mg and either 0.3 % or 0.5 % dietary phosphorus. Total leukocytes were increased in rats fed 30 ppm Mg (p < 0.0001), and the leukocyte subpopulation counts of lymphocytes, neutrophils, monocytes and eosinophils increased significantly only in the rats fed 30 ppm Mg (p < 0.0001). B-cells decreased significantly as a percentage of lymphocytes (p < 0.0093) as dietary Mg decreased. As total counts in blood, B-cells, CD4 and CD8 cells were significantly increased in the rats consuming the 30 ppm Mg diet. Dietary phosphorus only had an effect in combination with the lowest dietary Mg. These results demonstrate a threshold effect for increased leukocytes during a Mg deficiency of four weeks. A Mg deficiency of a longer duration may show different results.
Studies were made on the diabetic state and the pathogenesis of myocardial disorders in KK mice with the following results: (1) KK mice showed glucose intolerance, hyperinsulinemia and hyperlipidemia; (2) their electrocardiograms (ECGs) showed a marked left-axis deviation of the QRS vector; (3) they showed epicardial calcification and myocardial disorders; (4) the Ca content of their myocardiums was much higher, and the Mg contents in the erythrocytes and myocardiums were much lower than those of control mice; (5) the addition of Mg to the drinking water of KK mice normalized these changes, and suppressed their myocardial disorders, but did not normalize their ECG changes. These results suggested that Mg deficiency plays an important role in the development of myocardial disorders in KK mice.
Mice were fed diets containing 960 mg (control), 100 mg (moderately Mg deficient) and 30 mg (severely Mg deficient) of Mg/kg. After 20 days, mice were inoculated with Babesia hylomysci (from Dr. Wery, Anvers, Belgium). Significant increases in RBC Mg levels were observed following infection. All the control and moderately deficient mice died from infection, whereas the severely Mg-deficient diet protected mice against infection, as shown by a decrease in parasitaemia and mortality. The decrease in RBC Mg, modifications in membrane properties and increased oxidant stress are possible explanations for the protective effect of severe Mg deficiency. When mice were maintained for 2 months after inoculation on a severely Mg-deficient diet and were then switched to a control diet, all survived and had low parasitaemias. After 1 month, these mice were rechallenged with B. hylomysci and 89% survived.
Previous studies have provided evidence that Mg deficiency affects lipid metabolism. The present experiments were designed to assess whether the hypertriglyceridemia associated with Mg deficiency was related to alterations in post-heparin lipase activity (PHLA). Mg-deficient and control diets were pair-fed to weanling Wistar rats for eight days and plasma lipoproteins were separated into various density classes by sequential preparative ultracentrifugation. Triglycerides were significantly increased in chylomicrons and in the very low density lipoprotein, low density lipoprotein and high density lipoprotein (HDL) fractions. Cholesterol and phospholipid levels were significantly lower in the HDL fraction. PHLA in deficient rat was substantially lower than in control rats. The inverse correlation between plasma triglyceride concentration and PHLA strongly suggests that hypertriglyceridemia is the result of defective lipolysis of plasma triglycerides in Mg-deficient rats. Further examination of the PHLA was carried out by salt-mediated inhibition of lipoprotein lipase (LPL) and by heparin sepharose affinity chromatography and purified rat LPL antiserum. The results indicate that hepatic lipase is significantly decreased in Mg-deficient rats but the low PHLA is due mainly to a decline in LPL. However, total LPL activity, that is, both the intracellular and the extracellular pools of LPL in adipose tissue, heart and diaphragm, were unaffected by Mg deficiency. The results suggest that the decrease of LPL activity in the plasma of Mg-deficient rats may be due to a selective decrease in the heparin-releasable pool of enzyme.
Hypercalcemia, rather than hypocalcemia, has been observed in conjunction with severe magnesium (Mg) depletion in rat, in contrast to the development of hypocalcemia in Mg deficiency in various animal models. In the present study, a possible involvement of parathyroid hormone (PTH) in the development of hypercalcemia in rat was studied by using a newly-developed sensitive and specific radioimmunoassay system for the determination of rat PTH. In normal rat model, hypercalcemia occurred in association with a decrease of serum phosphate levels in Mg deficiency. However, serum PTH levels were not suppressed despite the occurrence of hypercalcemia, suggesting PTH as an important factor for the development of hypercalcemia. Of interest, in 5/6-nephrectomized uremic model, hypocalcemia, rather than hypercalcemia, was observed in Mg-deficient rats. Serum PTH levels seemed to be higher, but not statistically significant probably due to a small number of rats. However, infusion study clearly demonstrated that PTH secretion was significantly increased in Mg-deficient uremic rats compared with Mg-replete counterparts. The reason for an increase of serum PTH responses might be explained by Mg depletion itself in addition to a fall in serum Ca levels, because infusion study revealed that the magnitude of the stimulation of PTH secretion was increased in Mg deficiency despite the similar degrees of changes in serum Ca levels and that the set point for the suppression of PTH secretion by Ca might be altered in Mg deficiency. Taken these data together, it was strongly suggested that Mg depletion might enhance PTH secretion in rat.