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Because of the competing nature of calcium and magnesium, excessive calcium intake from foods or supplements can lead to a magnesium deficiency. The symptoms of magnesium deficiency are identical with many of the symptoms of thyroid disease, especially hyperthyroidism. People of Asian descent who get hyperthyroidism often become completely rigid and may be found lying in the streets this way. The condition is called hypokalemic periodic paralysis and is highly associated with hyperthyroidism. It's possible that the origin of the disease is not from low potassium (hypokalemia) but from low magnesium, which we know is a factor in hyperthyroidism.


The principal function of magnesium that is critical in thyroid disease is that it enables muscles to relax. With inadequate magnesium, the muscles cramp. When this happens to the heart muscles the heart does not go through a complete relaxation phase, and the next calcium-driven contraction begins before the relaxation is complete. This results in rapid heart beat and irregular heart rate known as arrhythmia.

Deficiency Effects and Symptoms:

According to the Nutrition Almanac, "Magnesium deficiency can easily occur because magnesium is refined out of many foods during processing. Cooking food removes the minerals; the oxalic acid in foods like spinach and phytic acid found in cereals bind magnesium in the body, as do unbalanced amounts of salts....A deficiency can occur in people with diabetes, those who use diuretics or digitalis preparations, the elderly, those with pancreatitis, chronic alcoholism, kwashiorkor, pregnancy, cirrhosis of the liver, arteriosclerosis or kidney malfunction, those on low-calorie or high-carbohydrate diets, and those who have severe malabsorption such as that caused  by chronic diarrhea or vomiting....Fluoride, high zinc levels, high levels of vitamin D, diuretics, and diarrhea will cause a deficiency of magnesium."

Also from N. A.: "Magnesium deficiency is thought to be closely related to coronary heart disease, including myocardial necrosis. An inadequate supply of this mineral may result in the formation of clots in the heart and brain and may contribute to calcium deposits in the kidneys blood vessels, and heart. Heart failure resulting from fibrillation and lesions in the small arteries is linked to a deficiency of magnesium, as is vasodilation, which is followed by hyperkinetic behavior and fatal convulsions."

"Symptoms of a deficiency may include gastrointestinal disorders, irregular heart rhythm, lack of coordination, muscle  twitch, tremors, weakness, apprehensiveness, personality changes, disorientation, confusion, depression, and irritability. A deficiency interferes with nerve and muscle impulses. Long-term deficiency can lead to tetany as in a calcium deficiency, alcoholic hallucinations, unusual face and eye movement, alopecia (baldness), swollen gums, and lesions of the gums."

Beneficial Effects:

N.A.: "Magnesium is vital in helping prevent heart attacks....After a heart attack, it has been found that supplementation provided a much higher survival rate and showed far less life-threatening dysrhythmias....It has also proved beneficial in the treatment of neuromuscular disorders, nervousness, tantrums, depression, sensitivity to noise, and hand tremor....Supplementing helps control dizziness, muscle weakness, twitching, heart disease, and high blood pressure,....reduce blood cholesterol and keep the arteries healthy....used for controlling convulsions in pregnant women, premature labor, and epileptic seizures."

Chocolate is a good source of magnesium and has a high magnesium to calcium ratio (about 4:1). Magnesium is low in hypers and the craving for chocolate may be driving my a need for magnesium. Unfortunately, chocolate may also be high in cadmium which is a probably negative factor for hyperT. Thus the craving for magnesium, if satisfied by eating chocolate, could exacerbate the symptoms of hyperT.

In this first study we see that magnesium is depleted in the  hyperthyroid state and treatment by Methimazole increases the magnesium content of both erythrocytes (red blood cells) and serum.  This emphasizes the need for magnesium supplementation in hyperthyroidism.

Magnesium metabolism in hyperthyroidism.
Disashi T; Iwaoka T; Inoue J; Naomi S; Fujimoto Y; Umeda T; Tomita K
Third Department of Internal Medicine, Kumamoto University School of Medicine, Japan.
Endocr J, 43(4):397-402 1996 Aug
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.

This second study examines the effect of magnesium on the sodium-potassium pump in the heart.  Magnesium deficiency is demonstrated to leave the number of pumps unaltered but to decrease the activity of the pumps.  This appears to result in an increase of sodium inside the cells with consequent arrhythmias in the heart.  This is evidence that supplementing magnesium can control rapid and irregular heartbeat experienced in hyperthyroidism.

Effects of dietary magnesium on sodium-potassium pump action in the heart of rats.
Fischer PW; Giroux A
Nutrition Research Division, Health and Welfare Canada, Ottawa, Ontario.
J Nutr, 117(12):2091-5 1987 Dec
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.

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

Subj: [hyperthyroidism] Re: InsomniaAnxiety

Date: 3/22/00 7:29:13 PM Pacific Standard Time

From: (Mary Ann Thomas)



Cire, You mention that you take 300mg of magnesium with 600mg of

calcium and there is a bit of talk surrounding whether or not these two

should be supplemented in a 2 to 1 ratio or 1 to 1 ratio. I think John

recommends something closer to a 1 to 1 ratio and I would like to share

my personal experience with calcium and magnesium supplementation.

I recently saw a Naturopath Physician who had me taking calcium and

magnesium in a ratio higher than two to one (I can't remember the exact

ratio right now). At this higher than recommended ratio I began having

trouble sleeping. Most nights I couldn't get to sleep and when I did I

would wake up a couple of hours later and be awake for several hours.

My back and neck also started giving me more problems than normal. I

had eye twitches and readily pulled muscles just from sleeping! My

thyroid grew to four times it's "normal" size.

When I finally reviewed my supplement list and discovered the imbalance

in the calcium and magnesium ratios I adjusted my ratio back to one to

one and all the above problems were alleviated including getting a full

nights sleep. I currently take 1200mg of magnesium to 600mg of calcium

and find that works about best for me. Perhaps you should consider

raising your magnesium.

Good Health to All!


Subj: [hyperthyroidism] Re: Insomnia/Anxiety

Date: 3/22/00 8:14:20 PM Pacific Standard Time

From: (Cire)



Mary, i think you're right. I mixed a teaspoon of Epsom salts in water and

drank it this afternoon. I noticed i started to yawn and feel better.

I took another dose at dinner time and once again it seemed like it helped.

I will be looking into taking more magnesium. I know the plants like it so

maybe there's a link here? Wouldn't it be something if it was as simple as

magnesium deficiency? Thanks to all for the support and insight, I really

appreciate it.