iThyroid.com

Title

Magnesium metabolism in hyperthyroidism.

Author

Disashi T; Iwaoka T; Inoue J; Naomi S; Fujimoto Y; Umeda T; Tomita K

Address

Third Department of Internal Medicine, Kumamoto University School of Medicine, Japan.

Source

Endocr J, 43(4):397-402 1996 Aug

Abstract

Changes in magnesium metabolism, along with those in sodium, were investigated in 17 patients with Graves' disease (14 females and 3 males, mean +/- SD, 44.8 +/- 12.2 years) and their relationship to plasma levels of thyroid hormones were assessed before and after treatment. Each patient was studied in hyperthyroid state and euthyroid state after treatment. Each patient was studied in hyperthyroid state and euthyroid state after treatment with methimazole. Treatment with methimazole increased the magnesium concentration both in erythrocytes (2.00 +/- 0.18 vs. 2.08 +/- 0.24 mmol/l cells, P < 0.05) and in serum (0.72 +/- 0.12 vs. 0.84 +/- 0.11 mmol/l, P < 0.001) but both urinary output and fractional excretion of magnesium decreased significantly (P < 0.05 and P < 0.001, respectively). The erythrocyte sodium concentration decreased with treatment (10.7 +/- 2.6 vs. 8.1 +/- 1.1 mmol/l cells, P < 0.001) but the serum sodium remained unchanged (140.9 +/- 1.9 vs. 140.9 +/- 2.1 mmol/l, NS). Urinary excretion of sodium also decreased with treatment (P < 0.05), but only changes in indices of magnesium metabolism (decrease in renal fractional excretion, rise in serum level) correlated significantly with those of the thyroid functions with treatment. These observations clearly indicate that in Graves' disease, the magnitude of magnesium metabolism alteration is closely related to the extent of the increase in thyroid hormones in plasma.

Title

Effects of dietary magnesium on sodium-potassium pump action in the heart of rats.

Author

Fischer PW; Giroux A

Address

Nutrition Research Division, Health and Welfare Canada, Ottawa, Ontario.

Source

J Nutr, 117(12):2091-5 1987 Dec

Abstract

Sprague-Dawley rats were fed a basal AIN-76 diet containing 80, 200, 350, 500 or 650 mg of magnesium per kilogram of diet for 6 wk. Ventricular slices, as well as microsomal fractions, were prepared from the hearts and were used to determine sodium-potassium pump activity. Sodium-potassium pump activity was assessed in the microsomal membranes by determining the ouabain-inhibitable Na+, K+-ATPase activity and [3H]ouabain binding, and in the ventricular slices, by determining ouabain-sensitive 86Rb uptake under K+-free conditions. The ATPase activity increased with increasing dietary magnesium, so that in the hearts of those animals that were fed 500 and 650 mg of magnesium/kg diet, it was significantly greater than the activity in the hearts of the animals fed 80 and 200 mg/kg diet. Similarly, 86Rb uptake by heart slices from rats fed 500 and 650 mg of magnesium/kg diet was significantly greater than the uptake by heart slices from animals fed 80 and 200 mg/kg diet. [3H]Ouabain binding did not change with increasing dietary magnesium. Thus, magnesium deficiency appears to have no effect on the number of sodium-potassium pump sites, but does decrease the activity of the pump. It is suggested that this leads to an increase in intracellular Na+, resulting in a change in the membrane potential, and may contribute to the arrhythmias associated with magnesium deficiency.

The following study suggests that boron is essential for proper magnesium metabolism. Also, this study may shed light on why fructose increases the severity of a copper deficiency--it causes adverse effects when magnesium is low.

Magnes Res 2000 Mar;13(1):19-27

Magnesium deficiency in the rat: effects of fructose, boron and copper.

Kenney MA, McCoy JH

School of Human Environmental Sciences, University of Arkansas, Fayetteville 72701, USA. kenney@comp.uark.edu

Magnesium (Mg) participates in many biochemical reactions which involve a variety of other nutrients. To elucidate some nutrient interactions, fructose (FR) and starch (ST) were compared as carbohydrate sources, and boron (B) and copper (Cu) were added to low-Mg diets for young male rats. Lack of Mg always caused characteristic deficiency symptoms. FR resembled Mg deficiency in effects on body, liver, and kidney weights and on plasma cholesterol level, but did not affect serum Mg or calcium (Ca). FR effects apparently were not mediated by changes in plasma Mg and Ca concentrations and were not prevented by adding Cu. B appeared to lessen effects of a low-Mg diet on body growth, serum cholesterol, and ash concentration in bone, but exacerbated deficiency symptoms, without affecting the concentration of Mg or Ca in serum. Results suggest that increased FR intake and marginal B might adversely affect individuals whose Mg status is suboptimal.

In the following study we see that nearly half of patients complaining of chronic fatigue symptoms and fibromyalgia (companion diseases to hypothyroidism) have magnesium deficiencies.

Magnes Res 1997 Dec;10(4):329-37

Magnesium deficit in a sample of the Belgian population presenting with chronic fatigue.

Moorkens G, Manuel y Keenoy B, Vertommen J, Meludu S, Noe M, De Leeuw I

Department of Internal Medicine, University Hospital, Antwerp, Belgium.

97 patients (25 per cent males, ages ranging from 14 to 73 years, median 38 years) with complaints of chronic fatigue (chronic fatigue syndrome, fibromyalgia or/and spasmophilia) have been enrolled in a prospective study to evaluate the Mg status and the dietary intake of Mg. An IV loading test (performed following the Ryzen protocol) showed a Mg deficit in 44 patients. After Mg supplementation in 24 patients, the loading test showed a significant decrease (p = 0.0018) in Mg retention. Mean values of serum Mg, red blood cell Mg and magnesuria showed no significant difference between patients with or without Mg deficiency. No association was found between Mg deficiency, CFS or FM. However serum Mg level was significantly lower in the patients with spasmophilia than in the other patients.

PMID: 9513929, UI: 98175116

 

The following study also shows that fibromyalgia is associated with magnesium deficiency.  Very importantly it also indicates that magnesium deficiency may be a consequence of thiamine (vitamin B-1) deficiency and that selenium status is slightly correlated with magnesium levels.  This shows that there is some interdependence of selenium and magnesium and that thiamine may be critical for magnesium metabolism and possibly selenium metabolism.

 

Magnes Res 1994 Dec;7(3-4):285-8

Selenium and magnesium status in fibromyalgia.

Eisinger J, Plantamura A, Marie PA, Ayavou T

Centre Hospitalier de Toulon, France.

Muscle pain has been associated with magnesium (Mg) and selenium (Se) deficiency: magnesium and selenium status were investigated in fibromyalgia (FM). Erythrocyte (E), leucocyte (L) and serum (S) magnesium, serum selenium and zinc, and vitamin B1, B2, A or E status were assessed in 22 patients with fibromyalgia and in 23 age-matched healthy controls. LMg is significantly increased (P < 0.05) and EMg slightly decreased in fibromyalgia. These magnesium abnormalities are associated with previously-reported impairment of thiamin metabolism. Antioxidant status (as well as plasma malondialdehyde) is unchanged in fibromyalgia and serum selenium levels, slightly but not significantly correlated with serum magnesium, is normal.

PMID: 7786692, UI: 95306266

 

The following study indicates that riboflavin (vitamin B-2) is not involved in magnesium metabolism. 

 

Magnes Res 1993 Jun;6(2):165-6

Absence of correlation between magnesium and riboflavin status.

Eisinger J, Clairet D, Brue F, Ayavou T

Department of Rheumatic Diseases, Centre Hospitalier, Toulon, France.

Erythrocyte magnesium and glutathione reductase activity coefficient (EGR-AC), reflecting vitamin B-2 status, were assessed in 11 athletes, 20 patients with fibromyalgia, 18 patients with hypothyroidism, and 13 controls. No correlation was demonstrated between erythrocyte magnesium and EGR-AC.

PMID: 8274362, UI: 94100069