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PubMed2002

The central role of magnesium deficiency in Tourette's syndrome: causal relationships between magnesium deficiency, altered biochemical pathways and symptoms relating to Tourette's syndrome and several reported comorbid conditions.

Prior studies have suggested a common etiology involved in Tourette's syndrome and several comorbid conditions and symptomatology. Reportedly, current medications used in Tourette's syndrome have intolerable side-effects or are ineffective for many patients. After thoroughly researching the literature, I hypothesize that magnesium deficiency may be the central precipitating event and common pathway for the subsequent biochemical effects on substance P, kynurenine, NMDA receptors, and vitamin B6 that may result in the symptomatology of Tourette's syndrome and several reported comorbid conditions. These comorbid conditions and symptomatology include allergy, asthma, autism, attention deficit hyperactivity disorder, obsessive compulsive disorder, coprolalia, copropraxia, anxiety, depression, restless leg syndrome, migraine, self-injurious behavior, autoimmunity, rage, bruxism, seizure, heart arrhythmia, heightened sensitivity to sensory stimuli, and an exaggerated startle response. Common possible environmental and genetic factors are discussed, as well as biochemical mechanisms. Clinical studies to determine the medical efficacy for a comprehensive magnesium treatment option for Tourette's syndrome need to be conducted to make this relatively safe, low side-effect treatment option available to doctors and their patients.

Humans↗
PubMed1993

Audiogenic seizures in magnesium-deficient mice: effects of magnesium pyrrolidone-2-carboxylate, magnesium acetyltaurinate, magnesium chloride and vitamin B-6.

Magnesium deficiency in mice causes and increases audiogenic seizures. This effect was reversed by oral administration of magnesium acetyltaurinate (ATaMg), magnesium pyrrolidone-2-carboxylate (PCMH), MgCl2. When treatment was discontinued, audiogenic seizures recurred only in the groups treated with PCMH or MgCl2. Following intraperitoneal administration of AtaMg, the mice were protected against audiogenic seizures after 4 h and this protection persisted for up to 72 h after the treatment. With the other magnesium salts (PCMH and MgCl2) maximum protection occurred by 6 h after the injection, but after that time the number of seizures increased sharply. Intraperitoneal taurine alone only reduced the severity of the audiogenic seizures. The length of treatment needed to inhibit audiogenic seizures was reduced by treatment with a combination of vitamin B-6 (a magnesium fixing agent) and PCMH or MgCl2. However this combination of vitamin B-6 and magnesium salts did not prevent the recurrence of audiogenic seizures, which was only achieved by ATaMg. The results suggest that audiogenic seizures in magnesium-deficient mice form a model of magnesium depletion. This depletion is completely inhibited by the combination of an inhibitory neurotransmitter (taurine) and magnesium, in the form of magnesium acetyltaurinate.

Acoustic Stimulation↗
PubMed1995

Systemic magnesium deficiency disclosed by magnesium loading test in patients with essential hypertension.

The present study was designed to determine whether magnesium (Mg) deficiency is present in patients with essential hypertension. We measured the retention of an intravenously administered Mg load (0.2 mmol/kg MgSO4 over 4 h), and serum and erythrocyte Mg concentrations in 17 inpatients with essential hypertension and in 15 normotensive controls. There was no significant difference between the two groups in erythrocyte Mg concentration (normotensives vs., hypertensives: 2.0 +/- 0.5 vs. 2.1 +/- 0.4 mmol/l cells), serum Mg concentration (normotensives vs. hypertensive: 2.1 +/- 0.2 vs. 2.1 +/- 0.2 mg/dl), or in urinary Mg excretion (normotensives vs. hypertensives: 65.8 +/- 25.5 vs. 73.7 +/- 26.7 mg/day). However, Mg retention was significantly higher in hypertensives than in normotensives (normotensives vs. hypertensives: 31.8 +/- 12.1 vs. 41.9 +/- 13.3%). These results suggest that a systemic Mg deficiency, which is undectectable by serum or erythrocyte Mg determination, may exist in patients with essential hypertension.

Adult↗
PubMed1980

Effect of parathyroid hormone on renal calcium and magnesium reabsorption in magnesium deficient rats.

Tubular magnesium reabsorption was investigated by recollection micropuncture and in vivo microperfusion techniques in acutely thyroparathyroidectomized rats made magnesium deficient by dietary deprivation. Henle's loop which normally reclaims the major portion of filtered magnesium was examined by elevation of intraluminal magnesium concentration. The transport capacity in these conditions was significantly lower in magnesium deficient rats (41%) compared to normal animals (71%) at comparable magnesium delivery rates. Acute infusion of MgCl2 further depressed loop magnesium reabsorption independent of intraluminal magnesium delivery. Parathyroid hormone did not alter magnesium transport capacity in magnesium deficient rats but resulted in enhanced transport in acutely hypermagnesemic deficient rats. Calcium reabsorption followed a similar qualitative pattern as magnesium with respect to loop function and urinary excretion. These results are consistent with a depressed transport capacity for magnesium in the loop of Henle of magnesium deficient rats which is independent of intraluminal magnesium delivery and circulating parathyroid hormone level.

Absorption↗
PubMed1995

Inhibition of mouse-killing behaviour in magnesium-deficient rats: effect of pharmacological doses of magnesium pidolate, magnesium aspartate, magnesium lactate, magnesium gluconate and magnesium chloride.

Magnesium deprivation induced interspecific aggressive behaviour (muricidal behaviour) in rats undoubtedly attributable to magnesium deficiency since magnesium chloride, by correcting magnesium deficiency, suppressed it. Inhibition of magnesium deficiency-induced behaviour by various magnesium salts should enable the classification of the therapeutic effects of these salts. Consequently we compared the effects of various magnesium salts used therapeutically on the inhibition of the acute muricidal behaviour induced by magnesium deficiency. All the magnesium salts used (chloride, pidolate, aspartate, gluconate, lactate) suppressed the muricidal behaviour. There was no significant difference in the duration of the treatment needed to inhibit this comportment for each of the salts studied. In contrast, significant differences appeared, concerning the different phases of muricidal behaviour. Magnesium pidolate significantly increased the attack latency (P < 0.05). By repeating the muricidal assays, we showed that magnesium pidolate treated rats had a muricidal behaviour rate which was lower than that of the other magnesium salt-treated rat groups. Consequently, it can be assumed that all the magnesium salts used had an acute anti-muricidal, perhaps anti-stress, effect and that magnesium pidolate presented, on this experimental model the greatest efficacy.

Aggression↗
PubMed1996

Muscle cramps and magnesium deficiency: case reports.

Magnesium deficiency is more common than is believed. This article discusses florid magnesium deficiency in two patients and the results of treatment. While neither case was difficult to diagnose, the severity of symptoms was unusual. Magnesium deficiency should always be included in the differential diagnosis of patients who present with persistent or severe muscle pain.

Adolescent↗
PubMed1990

Effects of potassium or potassium/magnesium supplementation on potassium content of body tissues and fluids in furosemide-treated rats on magnesium-deficient or magnesium-sufficient diet.

Persistent Mg2+ deficiency may interfere with restoration of normal tissue K+ levels. This study examined: a) the effects of chronic furosemide treatment on K+ of sartorius, aorta and ventricle of rats fed Mg2(+)-deficient (100 ppm) or Mg2(+)-sufficient (400 ppm) diet and deionized water; b) whether normal tissue K+ is restored by oral K+ or K+/Mg2+ supplementation with continued furosemide therapy. Levels of Mg2+ were also measured. Furosemide (20 mg/kg i.p.) decreased K+ in sartorius, aorta and ventricle by 5.5, 4.3 and 19.9 microEq/gm (p less than .05), respectively, in rats fed 100 ppm Mg2+ diet. Furosemide did not alter K+ levels in rats fed 400 ppm Mg2+ diet. K+ supplementation (1 mEq/kg for 7 days) restored K+ to normal in sartorius but the addition of Mg2+ supplementation was necessary to restore K+ levels to normal in ventricle and aorta. These data indicate that furosemide can decrease tissue K+ in rats on a Mg2(+)-deficient diet. This decrease can be reversed during diuretic administration by K+ supplementation in sartorius, or K+ plus Mg2+ supplementation in ventricle and aorta.

Animals↗
PubMed1980

Light microscopic and ultrastructural changes of the exocrine pancreas in magnesium deficient rats.

In magnesium deficient rats with a clinical picture of protein malnutrition, pancreatic changes typical of protein malnutrition were expected. However, in rats fed for four weeks on a low magnesium diet (protein content 25%), light and electron microscopic studies revealed that the acinar cells of the pancreas were packed with zymogen granules, suggesting a disturbance in the discharge (rather than in the production) of the pancreatic enzymes. The mitochondria and the lumina of the RER were swollen. The nuclei had an irregular outline, the chromatin was aggregated into irregular granules and the nucleolemma of the nucleolus was fibrillar. It was suggested that the disturbance in the release of pancreatic enzymes might cause a maldigestion of the dietary protein, which eventually would lead to the condition of protein malnutrition in the magnesium deficient rats. The disturbance of exocytosis in the pancreas of magnesium deficient rats might be due to the preferential use of all the available magnesium for protein (enzymes) synthesis so that there were no magnesium ions left for the energy dependent discharge of the zymogen granules.

Animals↗
PubMed1999

[Magnesium excretion in urine is not a marker of magnesium deficiency. Reliability of an oral magnesium administration test].

BACKGROUND: Serum magnesium analysis does not reflect body content of magnesium. So substitution is based on empirical maneuvers. PATIENTS AND METHOD: In a study on 44 patients urinary magnesium excretion was analyzed before and after oral magnesium substitution (40 mval). The provable hypothesis was the estimation that patients in magnesium deficiency under chronical diuretic treatment (n = 11) would have a lower magnesium excretion than patients of the control group (n = 10). Further analysis was done with patients after orthotopic cardiac transplantation (n = 12) and those suffering from coronary heart disease (n = 11). RESULT: After oral administration of magnesium in all 4 groups there was a rise in blood levels, only significant in the patient group under chronic diuretic treatment. Urinary magnesium excretion, however, showed no significant differences. Patients after cardiac transplantation had the lowest rise in urinary magnesium excretion. CONCLUSION: There was no clear differentiation by means of this oral magnesium substitution test. Magnesium excretion even after oral substitution is of no value to analyze magnesium deficiency.

Administration, Oral↗
PubMed1992

[Heart rate disorders in potassium and magnesium deficiency].

Potassium and magnesium deficiencies are common in patients with heart disease. These are often coexistent and pathophysiologically related. Potassium deficiency cannot be treated without correction of concomitant magnesium deficiency. Correlations between serum levels and body stores are very poor for both ions. Therefore diagnosis and treatment of these conditions based on serum levels alone are erroneous. There is some evidence that it is primarily the intracellular depletion of these ions which is arrhythmogenic. Magnesium infusion has been proved effective in treatment of torsade de pointes ventricular tachycardia and arrhythmias induced by digoxin-intoxication, and is recommended in these conditions. Whether it is effective in other forms of arrhythmia is not yet elucidated.

Action Potentials↗
PubMed1996

Reversible model of magnesium depletion induced by systemic kainic acid injection in magnesium-deficient rats: I--Comparative study of various magnesium salts.

We developed three models of reversible magnesium depletion in rats resulting from the combined effects of kainic (KA) acid with magnesium deficiency, in order to compare the effects of various common magnesium salts (pidolate, aspartate, lactate, gluconate and chloride) and of magnesium acetyl taurinate (MgATa), administered daily (14 mg Mg2+, PO) for ten days. First, the immediate effects (wet dog shakes, clonic convulsions and death 1 h after injection) and late effects (fall from hole board between the second and tenth days post injection) of kainic acid at three different doses (3.6 and 11 mg/kg) were studied in magnesium deficient rats (50 ppm for 40 days) and in non-deficient rats (1700 ppm). The results showed that the effects of kainic acid were enhanced in magnesium deficient rats. Secondly, after ten days of physiological then pharmacological doses of magnesium, used as chronical supplementation, we showed that kainic acid administration combined with magnesium deficiency led to magnesium depletion of increasing severity depending on the dose of kainic acid. The observed magnesium depletions were weak at a dose of 3 mg/kg KA, moderate at a dose of 6 mg/kg and severe at a dose of 11 mg/kg. These depletions were more or less reversible, and this enabled the classification of the therapeutic effects of these salts on Mg depletion. Among common salts, magnesium pidolate presented the greatest efficacy but none of them fully prevented depletion. In contrast, MgATa was efficient on all the aspects of depletion, when administered preventively both chronically or acutely or as a single curative injection. Consequently the results we obtained in the present study, on a new model of magnesium depletion, showed the greatest efficacy of magnesium acetyl taurinate we demonstrated yet on other models of reversible magnesium depletion.

Administration, Oral↗
PubMed1995

Progressive magnesium deficiency increases mortality from endotoxin challenge: protective effects of acute magnesium replacement therapy.

OBJECTIVES: To study the effects of endotoxin on magnesium homeostasis; to determine if progressive magnesium deficiency alters outcome from endotoxin challenge; and to evaluate the efficacy of magnesium therapy in reducing endotoxin-induced mortality. DESIGN: Prospective, placebo-controlled, randomized, multiexperiment studies. SETTING: Research laboratory of a university hospital. SUBJECTS: Male Sprague Dawley rats (n = 299). INTERVENTIONS: Experiment 1 was designed to test if endotoxin alters magnesium homeostasis. Circulating total and ionized magnesium (estimated by ultrafilterable values) concentrations were determined in blood samples collected from animals after the randomized administration of placebo or 0.3, 3.0, or 30 mg/kg of endotoxin. A baseline blood sample was collected and then a second blood sample was obtained at 5, 15, 30, 60, 120, or 180 mins after endotoxin or placebo administration. In experiment 2, animals were randomized to receive magnesium-sufficient diets or magnesium-deficient diets for 6 wks. After 6 wks, the effects of the randomized administration of 3.0 mg/kg endotoxin or placebo were evaluated on mortality and analyte values (pH and blood gases, sodium, potassium, chloride, glucose, ionized calcium, hematocrit, total and ultrafilterable magnesium concentrations) in the three study groups (magnesium-sufficient, 3-wk magnesium-deficient, or 6-wk magnesium-deficient). In experiment 3, magnesium-deficient animals were randomized to receive 50 mmol/kg magnesium chloride or placebo, before or after the administration of 3.0 mg/kg of endotoxin. Baseline and 24-hr analyte determinations were performed and outcome was analyzed. MEASUREMENTS AND MAIN RESULTS: Experiment 1: Significant increases (p < .05) in circulating total magnesium concentrations were found in animals that received 30 mg/kg of endotoxin, at 120 mins (0.79 +/- 0.10 vs. 0.60 +/- 0.05 mmol/L), and 180 mins (0.74 +/- 0.04 vs. 0.56 +/- 0.04 mmol/L) compared with baseline values. Similarly, significant increases (p < .05) in ionized magnesium concentrations were observed 120 and 180 mins after 3.0 and 30 mg/kg of endotoxin compared with baseline values. Experiment 2: Magnesium deficiency was strongly (p < .02) associated with increased mortality from endotoxin challenge. Endotoxin administration (3.0 mg/kg) was lethal in 10 (43%) of 23 magnesium-sufficient animals, 15 (65%) of 23 3-wk magnesium-deficient animals, and 20 (83%) of 24 6-wk magnesium-deficient animals. Experiment 3: In magnesium-deficient animals, rats treated with magnesium replacement therapy had significantly increased survival from endotoxin administration (15 [52%] of 29 vs. five [17%] of 29, p < .01) compared with placebo-treated animals. CONCLUSIONS: a) Endotoxin challenge causes significant increases in circulating total and ionized magnesium concentrations. b) Progressive magnesium deficiency is strongly associated with increased lethality, and magnesium replacement therapy provides significant protection from endotoxin challenge. c) These experimental results support the concept that cellular injury is probably associated with increases in circulating magnesium concentrations. Furthermore, these experimental findings suggest that magnesium deficiency predisposes to worse outcome from endotoxin challenge, and that replacement therapy in the setting of magnesium deficiency may be warranted, especially in critically ill subjects.

Animals↗