“The toxic effects of excessive intracellular calcium (decreased respiration and increased excitation) are opposed by magnesium. Both thyroid and progesterone improve magnesium retention. Estrogen dominance is often associated with magnesium deficiency, which can be an important factor in osteoporosis (Abraham and Grewal, 1990; Muneyyirci-Delale, et al., 1999).” -Ray Peat, PhD
“Instead of taking dietary supplements, it is far safer in general to use real foods, and to exclude foods which are poor in nutrients. For example, magnesium is typically deficient in hypothyroidism, and the safest way to get it is by using orange juice and meats, and by using epsom salts baths.” -Ray Peat, PhD
J Reprod Med. 1990 May;35(5):503-7.
A total dietary program emphasizing magnesium instead of calcium. Effect on the mineral density of calcaneous bone in postmenopausal women on hormonal therapy.
Abraham GE, Grewal H.
The use of calcium supplementation for the management of primary postmenopausal osteoporosis (PPMO) has increased significantly in the past few years. A review of the published data does not support calcium megadosing during postmenopause. Controlled studies showed no significant effect of calcium intake on mineral density of trabecular bone and a slight effect on cortical bone. Since PPMO is predominantly due to demineralization of trabecular bone, there is no justification for calcium megadosing in postmenopausal women. Soft tissue calcification is a serious risk factor during calcium megadosing under certain conditions. 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. 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. 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.
Fertil Steril. 1999 May;71(5):869-72.
Serum ionized magnesium and calcium in women after menopause: inverse relation of estrogen with ionized magnesium.
Muneyyirci-Delale O, Nacharaju VL, Dalloul M, Altura BM, Altura BT.
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.
Controlled clinical study.
An academic medical center.
Women of varying age and duration of menopause, and healthy, cycling women.
MAIN OUTCOME MEASURE(S):
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. 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 Mg2+ and total Mg were inversely correlated with the estrogen concentration in menopausal women. 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.
Magnesium retention compromised in hypothyroidism.
Quotes by Ray Peat, PhD:
“In hypothyroidism, the brain exciting hormones adrenaline, estrogen, and cortisol are usually elevated, and the nerve-muscle relaxant magnesium is low.”
“Low-thyroid cells are unable to retain magnesium efficiently, and a magnesium deficiency prevents muscle relaxation, wasting energy. Adequate sodium prevents urinary magnesium loss.”
“Magnesium, which is protective against excitatory damage and is a calcium antagonist, tends to be retained in proportion to the activity of thyroid hormone.”
“Magnesium, retained in the cell largely under the influence of ATP and thyroid, is our basic “calcium blocker,” or calcium antagonist.”
Am J Vet Res. 1978 Jan;39(1):159-61.
Effect of thyroid state on magnesium concentration of rat tissues.
The effect of alteration of thyroid status by thiouracil (0.1% concentration in drinking water for 60 days) or exogenous thyroxine (25 mg/dg of body weight administered SC from days 30 to 60) on magnesium content of rat tissues following exogenous magnesium was evaluated. Treatment of rats with magnesium solution (25 mg of magnesium sulfate/dg of body weight) resulted in increased magnesium concentration in most tissues of hypothyroid and hyperthyroid rats, with the mesenchymal-derived tissues (aorta, trachea, and ear cartilage) exhibiting the greatest increases (respectively, 154, 130, and 133% of control group values for hypothyroid rats, and 115, 108, and 107% of control group values for the hyperthyroid group). 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. Magnesium distribution and retention in rat tissues is altered considerably, depending on the functional status of thyroid gland.
Consequences of magnesium deficiency.
Int J Biochem Cell Biol. 1997 Nov;29(11):1273-8.
Magnesium deficiency enhances oxidative stress and collagen synthesis in vivo in the aorta of rats.
Shivakumar K, Kumar BP.
Magnesium deficiency has been shown to produce vascular lesions in experimental animals, but the underlying mechanisms of vascular injury are not clear. It has been reported that in rodents, magnesium deficiency enhances circulating levels of factors that promote free radical generation and are mitogenic. 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. 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. Serum and tissue levels of magnesium and calcium were determined by atomic absorption spectrophotometry. The present study demonstrated for the first time that magnesium deficiency significantly (P < 0.001) increases levels of thiobarbituric acid-reactive substances in the aorta of rats. Other changes in the aorta of animals on the Mg-deficient diet included a significant reduction (54%, P < 0.001) in the activity of superoxide dismutase and catalase (37%, P < 0.01) and a 19% increase in net fractional rates of collagen synthesis (P < 0.05). While serum magnesium was significantly reduced in these animals (P < 0.001), aortic tissue levels of magnesium in these animals remained unaltered throughout the duration of the study, suggesting the existence of other control mechanisms, apart from reduced tissue levels of magnesium, mediating the observed effects. These findings suggest that magnesium deficiency may trigger a wound healing response, involving oxidative injury and growth stimulation, in the vascular system.
Int J Biochem Cell Biol. 1997 Jan;29(1):129-34.
Magnesium deficiency-related changes in lipid peroxidation and collagen metabolism in vivo in rat heart.
Kumar BP, Shivakumar K, Kartha CC.
Magnesium deficiency is known to produce a cardiomyopathy, characterised by myocardial necrosis and fibrosis. 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. 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. 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 < 0.001). A marked drop in collagen deposition rate (59%, p < 0.001%) on day 28 but a significant rise in fractional synthesis rate (12%, p < 0.001) and collagen deposition rate (24%, p < 0.001) on day 60 were observed. A fibroproliferative response in the heart was evident on day 80 but not at earlier time-points. Thus, the present study provides evidence of increased lipid peroxidation and net deposition of collagen in the myocardium in response to dietary deficiency of magnesium. These changes were, however, not directly related to alterations in the tissue levels of Mg. 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.