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Results for “Magnesium Deficiency”

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PubMed1990

Magnesium-deficient diet aggravates anaphylactic shock and promotes cardiac myolysis in guinea pigs.

Actively sensitized guinea pigs were rendered Mg(2+)-deficient for 2-3 weeks and then subjected to immune stress. No differences could be seen between treated and control groups prior to immune challenge. 1-2 h after antigen challenge, 95% of the Mg(2+)-deficient animals were observed to be anaphylactic, i.e. apathetic, dyspneic, and they had a rapid pulse rate. Only 4% of the control animals showed signs of anaphylaxis. Serum magnesium concentration, [Mg2+], fell from 1.32 +/- 0.07 mM in control guinea pigs to 0.56 +/- 0.04 mM in those fed an Mg(2+)-deficient diet. Cardiomyolysis (CM) developed in 19% of the anaphylactic animals and in 3% of the controls. We conclude that Mg(2+)-deficient animals continue to function, provided conditions are normal, but they are unable to withstand stress. The heart, however, appears to be better equipped to defend itself against Mg2+ deficiency and low serum [Mg2+], a supposition supported by the fact that heart [Mg2+] is not significantly reduced in hypomagnesemic guinea pigs (0.864 +/- 0.021 microgram/mg dry weight in control, and 0.834 +/- 0.062 microgram/mg dry weight in magnesium-deficient animals). The data indicate that hypomagnesemia heightens the intensity of the immune response, thereby exacerbating both anaphylactic shock (AS) and CM. A normal serum [Mg2+] would thus seem essential for protection against immune stress.

Anaphylaxis↗
PubMed1993

Effects of a magnesium-deficient diet on sleep organization in rats.

The influence of magnesium, one of the most important cations in the vertebrate body, on the sleep-wakefulness cycle and ECoG patterns in chronically implanted rats recorded during the light period over a 6-hour period was investigated. Two groups of rats were studied. Group 1 (6 rats): after a control period of 2 weeks, the rats were maintained for 9 weeks on a Mg(2+)-deficient diet. Group 2 (5 rats): after a control period of 2 weeks, the rats were maintained for 7 weeks on a Mg(2+)-deficient diet followed by 4 weeks on a normal diet (recovery period: weeks 8-11). Mg(2+)-deficient diet for 9 weeks induced sleep and ECoG time-dependent alterations. After 6-7 weeks on a Mg(2+)-deficient diet (n = 11) sleep analysis showed a significant increase of wakefulness (+50%) at the expense of slow wave sleep (-24%) but paradoxical sleep was not significantly modified. After 9 weeks of a Mg2+ deficient diet, sleep was disorganized: light sleep and polyspikes occurred indicating an increase in neuronal excitability. When Mg2+ was reintroduced in food and water, sleep organization and ECoG recordings were restored to their original patterns. Our findings which are in line with previous clinical and pharmacological observations provide conclusive arguments for the neuroprotective effect of magnesium ions in neurologic disorders and epileptiform activity. Mg2+ deficiency induces ECoG alterations in the rat which bear some similarities with those seen in neurogenic spasmophilic syndromes in man.

Animals↗
PubMed2006

Vitamin D insufficiency and the blunted PTH response in established osteoporosis: the role of magnesium deficiency.

INTRODUCTION: Vitamin D insufficiency is common, however within individuals, not all manifest the biochemical effects of PTH excess. This further extends to patients with established osteoporosis. The mechanism underlying the blunted PTH response is unclear but may be related to magnesium (Mg) deficiency. The aims of this study were to compare in patients with established osteoporosis and differing degrees of vitamin D and PTH status : (1) the presence of Mg deficiency using the standard Mg loading test (2) evaluate the effects of Mg loading on the calcium-PTH endocrine axis (3) determine the effects of oral, short term Mg supplementation on the calcium-PTH endocrine axis and bone turnover. METHODS: 30 patients (10 women in 3 groups) were evaluated prospectively measuring calcium, PTH, Mg retention (Mg loading test), dietary nutrient intake (calcium, vitamin D, Mg) and bone turnover markers (serum CTX & P1CP). Multivariate analysis controlling for potential confounding baseline variable was undertaken for the measured outcomes. RESULTS: All subjects, within the low vitamin D and low PTH group following the magnesium loading test had evidence of Mg depletion [mean(SD) retention 70.3%(12.5)] and showed an increase in calcium 0.06(0.01) mmol/l [95% CI 0.03, 0.09, p=0.007], together with a rise in PTH 13.3 ng/l (4.5) [95% CI 3.2, 23.4, p=0.016] compared to baseline. Following oral supplementation bone turnover increased: CTX 0.16 (0.06) mcg/l [95%CI 0.01, 0.32 p=0.047]; P1CP 13.1 (5.7) mcg/l [95% CI 0.29, 26.6 p=0.049]. In subjects with a low vitamin D and raised PTH mean retention was 55.9%(14.8) and in the vitamin replete group 36.1%(14.4), with little change in both acute markers of calcium homeostasis and bone turnover markers following both the loading test and oral supplementation. CONCLUSIONS: This study confirms that in patients with established osteoporosis, there is also a distinct group with a low vitamin D and a blunted PTH level and that Mg deficiency (as measured by the Mg loading test) is an important contributing factor.

Aged↗
PubMed1986

Magnesium-deficient hairless rat: spleen cells mitogenic responses and variations in hormonal status.

Hairless rats with dermatosis induced with a poor magnesium diet were previously shown to bear biochemical and immunological abnormalities. It was therefore felt of interest to investigate the spleen cells proliferative responses from these rats, both in the rash and the remission phases, when testosterone and parathormone plasma levels were also determined. Results showed that proliferative responses to mitogens and PTH levels were inversely related to the intensity of the dermatosis, whereas testosterone levels were more or less decreased. The role of 1.25 dihydroxyvitamin D3 in these modifications is questionable.

Animals↗
PubMed2002

Magnesium deficiency: effect on bone and mineral metabolism in the mouse.

Insufficient dietary magnesium (Mg) intake has been associated in humans with low bone mass. Mg deficiency in the rat has suggested bone loss is due to increased bone resorption and/or inadequate bone formation during remodeling. The purpose of this study was to assess the effect of a low Mg diet on bone and mineral metabolism in the young and mature BALB/c mouse and explore the hypothesis that inflammatory cytokines may contribute to Mg deficiency-induced osteoporosis. Using an artificial diet, we induced targeted Mg depletion (0.002% Mg) with all other nutrients maintained at the normal level. In all Mg-depleted mice, hypomagnesemia developed and skeletal Mg content fell significantly. The serum Ca in Mg-deficient mice was higher than in control mice; however, serum PTH levels were not significantly different. Osteoprotegerin (OPG) in dosages that inhibit osteoclastic bone resorption did not prevent hypercalcemia in Mg-deficient animals. No significant difference in serum Ca was observed between groups when dietary Ca was reduced by 50%, suggesting that a compensatory increase in intestinal absorption might account for the hypercalcemia. Growth plate width decreased 33% in young Mg-deficient animals and chondrocyte columns decreased in number and length, suggesting that Mg deficiency reduced bone growth. Trabecular bone volume in the metaphysis of the tibia in these animals was decreased and osteoclast number was increased by 135%. Osteoblast number was significantly reduced. Immunohistochemistry revealed that substance P increased 230% and 200% in megakaryocytes and lymphocytes, respectively, after 1 day of Mg depletion. IL-1 increased by 140% in osteoclasts by day 3 and TNF alpha increased in osteoclasts by 120% and 500% in megakaryocytes on day 12. This study demonstrates a profound effect of Mg depletion on bone characterized by impaired bone growth, decreased osteoblast number, increased osteoclast number in young animals, and loss of trabecular bone with stimulation of cytokine activity in bone.

Animals↗