The images are licensed under a Creative Commons Attribution 3.0 Unported License, unless otherwise noted. When you take thyroid, it energizes your cells to make ATP, and it happens that ATP binds magnesium, so you don’t really take up magnesium into the cell very efficiently unless you have adequate thyroid. The use of calcium supplementation for the management of primary postmenopausal osteoporosis (PPMO) has increased significantly in the past few years. Serum ionized magnesium and calcium in women after menopause: inverse relation of estrogen with ionized magnesium.
To study the serum concentrations of the sex steroid hormones and free divalent cations Mg2+ and Ca2+ in healthy women at or past menopause and to compare them with the serum concentrations of healthy, cycling women of child-bearing age at different stages of the menstrual cycle. Serum levels of the sex steroids (estrogen, progesterone, and testosterone) and of Ca2+ and Mg2+ were measured in menopausal and postmenopausal women, and in healthy, cycling women at five different stages of the menstrual cycle. The Mg2+ and total Mg levels of the postmenopausal women were inversely related to the serum level of estrogen and were similar to the levels present during the early follicular phase of healthy women of child-bearing age. Serum levels of Mg2+ and total Mg were inversely correlated with the estrogen concentration in menopausal women.
Magnesium deficiency enhances oxidative stress and collagen synthesis in vivo in the aorta of rats. Magnesium deficiency has been shown to produce vascular lesions in experimental animals, but the underlying mechanisms of vascular injury are not clear. Magnesium deficiency-related changes in lipid peroxidation and collagen metabolism in vivo in rat heart. Magnesium deficiency is known to produce a cardiomyopathy, characterised by myocardial necrosis and fibrosis.
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Effect on the mineral density of calcaneous bone in postmenopausal women on hormonal therapy. The Ca2+ level was unrelated to the sex steroid hormones present, but it was increased compared with that of younger women in both the follicular phase and the luteal phase.
Serum levels of Ca2+ were significantly elevated in menopausal women compared with younger women, but the ratio of Ca2+ to Mg2+, a measure of cardiovascular problems, was not elevated in the postmenopausal women. It has been reported that in rodents, magnesium deficiency enhances circulating levels of factors that promote free radical generation and are mitogenic. As part of the ongoing investigations in this laboratory to establish the biochemical correlates of these histological changes, the present study probed the extent of lipid peroxidation and alterations in collagen metabolism in the heart in rats fed a magnesium-deficient diet for 28, 60 or 80 days. Elemental magnesium burns with a bright, white flame and a temperature of more than 3000 K. Controlled studies showed no significant effect of calcium intake on mineral density of trabecular bone and a slight effect on cortical bone. Magnesium concentration in skeletal and cardiac muscle was similar for hyperthyroid and control rats, but magnesium concentration in these same tissues of hypothyroid rats was decreased. In pursuance of these observations, the present study tested the hypothesis that magnesium deficiency may enhance oxidative stress and trigger an accelerated growth response in vivo in the aorta of rats. While lipid peroxidation was measured by the thiobarbituric acid reaction, collagen turnover rates and fibroblast proliferation were assessed using [3H]-proline and [3H]-thymidine, respectively. Since PPMO is predominantly due to demineralization of trabecular bone, there is no justification for calcium megadosing in postmenopausal women.


Magnesium distribution and retention in rat tissues is altered considerably, depending on the functional status of thyroid gland. Oxidative stress was evaluated in terms of levels of thiobarbituric acid-reactive substances in the serum and aorta and activity of superoxide dismutase and catalase in the aorta; fractional rates of collagen synthesis were assessed using [3H]-proline. Tissue levels of magnesium and calcium were determined by atomic absorption spectrophotometry.
Soft tissue calcification is a serious risk factor during calcium megadosing under certain conditions. Serum and tissue levels of magnesium and calcium were determined by atomic absorption spectrophotometry.
A 39% increase in the cardiac tissue level of thiobarbituric acid reactive substances was observed on day 60 of deficiency (p the present study provides evidence of increased lipid peroxidation and net deposition of collagen in the myocardium in response to dietary deficiency of magnesium.
A total dietary program emphasizing magnesium instead of calcium for the management of PPMO takes into account the available data on the effects of magnesium, life-style and dietary habits on bone integrity and PPMO. The present study demonstrated for the first time that magnesium deficiency significantly (P These findings suggest that magnesium deficiency may trigger a wound healing response, involving oxidative injury and growth stimulation, in the vascular system. These changes were, however, not directly related to alterations in the tissue levels of Mg. When this dietary program was tested on 19 postmenopausal women on hormonal replacement therapy who were compared to 7 control postmenopausal women, a significant increase in mineral bone density of the calcaneous bone (BMD) was observed within one year.
It is suggested that the increase in cardiac collagen synthesis and fibroplasia associated with Mg deficiency may represent reparative fibrogenesis, upon oxidative damage to the cardiac muscle, and is mediated by a mechanism independent of changes in cardiac tissue levels of Mg. Fifteen of the 19 women had had BMD below the spine fracture threshold before treatment; within one year, only 7 of them still had BMD values below that threshold.



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