Formal Medical Studies by Researchers, Universities and Hospitals concerning Magnesium from Around the World
The Benefits of sufficient Magnesium, curative effects of Magnesium supplementing, and dangers of Magnesium deficiency has been established by formal medical studies across the globe. Studies and results listed below include from the USA, France, German, Japan, Great Britain, South Africa, Netherlands, Denmark, Hungary and Switzerland. (Start by scrolling down the page to spot topics of interest to you...)
Magnesium and carbohydrate metabolism
<THERAPIE (France), 1994, 49/1 (1-7)
<>The interrelationships between magnesium and carbohydrate metabolism have regained considerable interest over the last few years. Insulin secretion requires magnesium: magnesium deficiency results in impaired insulin secretion while magnesium replacement restores insulin secretion. Furthermore, experimental magnesium deficiency reduces the tissues sensitivity to insulin. Sub clinical magnesium deficiency is common in diabetes. It results from both insufficient magnesium intakes and increase magnesium losses, particularly in the urine. In type 2, or non-insulin-dependent, diabetes mellitus, magnesium deficiency seems to be associated with insulin resistance. Furthermore, it may participate in the pathogenesis of diabetes complications and may contribute to the increased risk of sudden death associated with diabetes. Some studies suggest that magnesium deficiency may play a role in spontaneous abortion of diabetic women, in fetal malformations and in the pathogenesis of neonatal hypocalcemia of the infants of diabetic mothers. Administration of magnesium salts to patients with type 2 diabetes tend to reduce insulin resistance. Long-term studies are needed before recommending systematic magnesium supplementation to type 2 diabetic patients with subclinical magnesium deficiency. Disorders of magnesium metabolism
Endocrinology and Metabolism Clinics of North America (USA), 1995, 24/3
<>Magnesium depletion is more common than previously thought. It seems to be especially prevalent in patients with diabetes mellitus. It is usually caused by losses from the kidney or gastrointestinal tract. A patient with magnesium depletion may present with neuromuscular symptoms, hypokalemia, hypocalcemia, or cardiovascular complication. Physicians should maintain a high index of suspicion for magnesium depletion in patients at high risk and should implement therapy early.
<>Evidence suggests that magnesium deficiency may play an important role in cardiovascular disease. In this study, we evaluated the effects of a magnesium infusion and dietary-induced isolated magnesium deficiency on the production of thromboxane and on angiotensin II-mediated aldosterone synthesis in normal human subjects. Because insulin resistance may be associated with altered blood pressure, we also measured insulin sensitivity using an intravenous glucose tolerance test with minimal model analysis in six subjects. The magnesium infusion reduced urinary thromboxane concentration and angiotensin II-induced plasma aldosterone levels. The low magnesium diet reduced both serum magnesium and intracellular free magnesium in red blood cells as determined by nuclear magnetic resonance (186plus or minus10 (SEM) to 127plus or minus9 mM, p<0.01). Urinary thromboxane concentration measured by radioimmunoassay increased after magnesium deficiency. Similarly, angiotensin II-induced plasma aldosterone concentration increased after magnesium deficiency. Analysis showed that all subjects studied had a decrease in insulin sensitivity after magnesium deficiency (3.69plus or minus0.6 to 2.75plus or minus0.5 min- 1 per microunit per milliliterx10-4, p<0.03). We conclude that dietary- induced magnesium deficiency 1) increases thromboxane urinary concentration and 2) enhances angiotensin-induced aldosterone synthesis. These effects are associated with a decrease in insulin action, suggesting that magnesium deficiency may be a common factor associated with insulin resistance and vascular disease.
DIABETOLOGIA (Germany, Federal Republic of), 1990, 33/9 (511-514)
<>Magnesium is an important ion in all living cells being a cofactor of many enzymes, especially those utilising high energy phosphate bounds. The relationship between insulin and magnesium has been recently studied. In particular it has been shown that magnesium plays the role of a second messenger for insulin action; on the other hand, insulin itself has been demonstrated to be an important regulatory factor of intracellular magnesium accumulation. Conditions associated with insulin resistance, such as hypertension or aging, are also associated with low intracellular magnesium contents. In diabetes mellitus, it is suggested that low intracellular magnesium levels result from both increased urinary losses and insulin resistance. The extent to which such a low intracellular magnesium content contributes to the development of macro- and microangiopathy remains to be established. A reduced intracellular magnesium content migth contribute to the impaired insulin response and action which occurs in Type 2 (non-insulin-dependent) diabetes mellitus. Chronic magnesium supplementation can contribute to an improvement in both islet Beta-cell response and insulin action in non-insulin-dependent diabetes subjects.
<>The possibility that a magnesium deficiency might be the underlying cause of vasospastic angina (VA) and the efficacy of Mg administration in its treatment were studied. Subjects included 15 patients with VA and 18 healthy subjects as the control group. The erythrocyte Mg content was measured by atomic absorption, and serum Mg was measured by conventional chemical assay. The efficacy of Mg administration was studied in seven patients with VA. The results were as follows: (a) The mean erythrocyte Mg content was less in the group with frequent episodes of angina (1.59 plus or minus 0.11 mg/dl) than in the group without angina (2.11 plus or minus 0.38 mg/dl, p < 0.01) and in the control group (2.22 plus or minus 0.29 mg/dl, p < 0.01). There was no significant difference between the control group and patients of each group with respect to serum Mg. (b) Coronary arterial spasm was induced by ergonovine maleate in seven patients and was completely inhibited by the administration of Mg sulfate (40-80 mEq, hourly) in six of these patients; in the remaining patient neither obvious ST change nor chest pain occurred. Thus, it was concluded that the measurement of erythrocyte Mg content is useful to determine how easily vasospasm might occur in VA and that the administration of Mg might be developed as a new therapy for spasm associated with a low erythrocyte Mg content.
<>A 51-year-old man was diagnosed as having variant angina by documentation of typical ST elevation during anginal attack and also by showing coronary arterial spasm (#2 and #12) during hyperventilation on coronary arteriography. Large quantities of calcium blocking agents and nitrates could not improve his symptoms. Lack of intracellular magnesium was suspected from a daily excretion of urine magnesium (5.3 mEq) and magnesium tolerance test (56.7%). After hourly infusion of magnesium sulfate (80 mEq), coronary spasm could not be induced by ergonovine.
S. AFR. MED. J. (SOUTH AFRICA), 1983, 64/18 (697-698)
<>Magnesium deficiency may result from reduced dietary intake of the ion increased losses in sweat, urine or feces. Stress potentiates magnesium deficiency, and an increased incidence of sudden death associated with ischaemic heart disease is found in some areas in which soil and drinking water lack magnesium. Furthermore, it has been demonstrated experimentally that reduction of the plasma magnesium level is associated with arterial spasm. Careful studies are required to assess the clinical importance of magnesium and the benefits of magnesium supplementation in man.
<>Isolated coronary arteries from dogs were incubated in Krebs-Ringer bicarbonate solution and exposed to normal, high, and low concentrations of magnesium in the medium. Sudden withdrawal of magnesium from the medium increased whereas high concentrations of magnesium decreased the basal tension of the arteries. The absence of magnesium in the medium significantly potentiated the contractile responses of both small and large coronary arteries to norepinephrine, acetylcholine, serotonin, angiotensin, and potassium. These data support the hypothesis that magnesium deficiency, associated with sudden death ischemic heart disease, produces coronary arterial spasm.
<>Diabetes mellitus is the most common pathological state in which secondary magnesium deficiency occurs. Magnesium metabolism abnormalities vary according to the multiple clinical forms of diabetes: plasma magnesium is more often decreased than red blood cell magnesium. Plasma Mg levels are correlated mainly with the severity of the diabetic state, glucose disposal and endogenous insulin secretion. Various mechanisms are involved in the induction of Mg depletion in diabetes mellitus, i.e. insulin and epinephrine secretion, modifications of the vitamin D metabolism, decrease of blood P, vitamin B6 and taurine levels, increase of vitamin B5, C and glutathione turnover, treatment with high levels of insulin and biguanides. K depletion in diabetes mellitus is well known. Some of its mechanisms are concomitant to those of Mg depletion. But their hierarchic importance is not the same: i.e., insulin hyposecretion is more important versus K+ than versus Mg2+. Insulin increases the cellular inflow of K+ more than that of Mg2+ because there is more free K+ (87%) than Mg2+ (30%) in the cell. The consequences of the double Mg-K depletion are either antagonistic: i.e. versus insulin secretion (increased by K+, decreased by Mg2+) or agonistic i.e. on the membrane: (i.e. Na+K+ATPase), tolerance of glucose oral load, renal disturbances. The real importance of these disorders in the diabetic condition is still poorly understood. Retinopathy and microangiopathy are correlated with the drop of plasma and red blood cell Mg. K deficiency increases the noxious cardiorenal effects of Mg deficiency. The treatment should primarily insure diabetic control.
<>We report 2 cases of true hypocalcemia (not caused by decreased binding protein) associated with metastatic prostate cancer and review previously reported cases. Hypocalcemia is a common but frequently unrecognized complication of prostatic cancer. Estrogen therapy often is associated with the hypocalcemia, which may be asymptomatic. The hypocalcemia is always associated with osteoblastic metastases and usually it is associated with increased serum alkaline phosphatase activity, acid phosphatase activity and serum parathyroid hormone concentration. Serum concentrations of magnesium, phosphorus and vitamin D frequently are decreased. Patients are in a positive calcium balance. The osteoblastic metastases seem to act as a calcium sink, creating a 'hungry tumor phenomenon'. The role of estrogens may be to stop the resorption of normal bone resulting in lower serum calcium concentrations.
<>It is known that the peroxidation of LDL is a trigger for developing arteriosclerosis. The oxidized LDL is produced by either oxidative stress or a few oxidant. Selenium decreased in serum and some organs of stroke-prone spontaneously hypertensive rats (SHRSP), which is a cofactor of glutamine peroxidase. Serum magnesium decreased in patients with diabetes mellitus, with ischemic heart disease, with essential hypertension and with cerebral vascular lesions. Calcium to magnesium ratio was higher in some organs of SHRSP as compared to Wistar Kyoto rats (WKY). These changes accelerated vascular lesions in SHRSP. (21 Refs.)
<>Magnesium ion is of great importance in physiology by its intervention in 300 enzymatic systems, its role in membrane structure and its function in neuromuscular excitability. The skeleton is the first pool of magnesium in the body. Intestinal absorption, renal metabolism, bone accretion and resorption of magnesium are very similar to those of calcium. Magnesium metabolism is accurately controlled, in particular by parathyroid hormone, 25 - dihydroxy vitamin D3, calcitonin, catecholamine and estrogens. The main regulation mechanisms of magnesium metabolism are located in the kidney which is the principal excretory organ.
Osteoporosis International (United Kingdom), 1996, 6/6 (453-461)
<>Osteoporosis and magnesium (Mg) deficiency often occur in malabsorption syndromes such as gluten-sensitive enteropathy (GSE). Mg deficiency is known to impair parathyroid hormone (PTH) secretion and action in humans and will result in osteopenia and increased skeletal fragility in animal models. We hypothesize that Mg depletion may contribute to the osteoporosis associated with malabsorption. It was our objective to determine Mg status and bone mass in GSE patients who were clinically asymptomatic and on a stable gluten-free diet, as well as their response to Mg therapy. Twenty-three patients with biopsy-proven GSE on a gluten-free diet were assessed for Mg deficiency by determination of the serum Mg, red blood cell (RBC) and lymphocyte free Mg2+, and total lymphocyte Mg. Fourteen subjects completed a 3-month treatment period in which they were given 504-576 mg MgCl2 or Mg lactate daily. Serum PTH, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and osteocalcin were measured at baseline and monthly thereafter. Eight patients who had documented Mg depletion (RBC Mg2+ < 150 microM) underwent bone density measurements of the lumbar spine and proximal femur, and 5 of these patients were followed for 2 years on Mg therapy. The mean serum Mg, calcium, phosphorus and alkaline phosphatase concentrations were in the normal range. Most serum calcium values fell below mean normal and the baseline serum PTH was high normal or slightly elevated in 7 of the 14 subjects who completed the 3-month treatment period. No correlation with the serum calcium was noted, however. Mean serum 25-hydroxyvitamin D, 1,25-dihydroxy vitamin D and osteocalcin concentrations were also normal. Despite only 1 patient having hypomagnesemia, the RBC Mg2+ (153 + or - 6.2 microM; mean plus or minus SEM) and lymphocyte Mg2+ (182 plus or minus 5.5 microM) were significantly lower than normal (202 + or - 6.0 microM, P < 0.001, and 198 + or - 6.8 microM, p < 0.05, respectively). Bone densitometry revealed that 4 of 8 patients had osteoporosis of the lumbar spine and 5 of 8 had osteoporosis of the proximal femur (T-scores less than or equal to -2.5). Mg therapy resulted in a significant rise in the mean serum PTH concentration from 44.6 + or - 3.6 pg/ml to 55.9 plus or minus 5.6 pg/ml (p < 0.05). In the 5 patients given Mg supplements for 2 years, a significant increased in bone mineral density was observed in the femoral neck and total proximal femur. This increase in bone mineral density correlated positively with a rise in RBC Mg2+. This study demonstrates that GSE patients have reduction in intracellular free Mg2+, despite being clinically asymptomatic on a gluten-free diet. Bone mass also appears to be reduced. Mg therapy resulted in a rise in PTH, suggesting that the intracellular Mg deficit was impairing PTH secretion in these patients. The increase in bone density in response to Mg therapy suggests that Mg depletion may be one factor contributing to osteoporosis in GSE.
<>Background: Nutritional assessment and management remain important issues in the treatment of CF patients despite newer developments as lung transplantation, inhalation with DNase and gene therapy. Methods: The nutritional status of 26 patients (mean age 15,8 years; 16 male; 46% homozygous, 38% heterozygous for DeltaF 508, remaining unknown; 3 pancreas sufficient, Shwachman score intermediate to excellent) of our CF clinic was analyzed using a three days protocol, the precise weighing method and comparison of data with the official dietary recommendations. Results: The average energy intake was below the 130% officially recommended and the fat intake was below the aimed 40% of total energy intake. The regression analysis revealed positive correlations between energy intake and SDS(Height) and Shwachman score and SDS(Weight) respectively. Food contained an insufficient amount of unsaturated fatty acids. Water soluble vitamins were supplemented adequately besides folic acid, but intake of fat soluble vitamins E and A often was insufficient despite extra vitamin capsules. Every second patient did not take enough minerals as calcium, magnesium or iron. Conclusions: This analysis underlines how important the regular assessment of the nutritional status can be for the individual nutritional management of CF patients even if clinical symptoms of deficiencies could not be detected. An increase of fat intake as a main source of energy, essential fatty acids and fat soluble vitamins has to be encouraged as well as the increased use of milk and milk products for the prevention of osteoporosis. Iron and folic acid are further critical nutrients.
Netherlands Tijschrift voor de Klinische Chemie (Netherlands), 1996, 21/1 (8-10)
<>Experiences are described at a kidney stone clinic which was established as part of the Department of Clinical Biochemistry ten years ago. During this period, the investigational protocol has changed from an in-patient to an out-patient scheme. The most important metabolic abnormalities among calcium oxalate kidney stone formers were hypercalciuria, hypernatriuria, hyperuricosuria, increased blood urate, decreased blood phosphate and hyperphosphaturia with decreased renal phosphate threshold. These abnormalities were found in the majority of patients. Oxalate output was, however, increased in less than 50 percent of the patients. The effectivity of thiazides, allopurinol, magnesium and phosphate supplementation was tested, and it was concluded that (a) the effect of thiazides was significant, but calciuria normalized only in a few cases, (b) the withdrawal of allopurinol led to a significant increase of urate parameters only in patients without a low-purine diet, (c) a sufficient dose of magnesium and phosphate is necessary to achieve a therapeutie effect. Preliminary data indicate that some patients with hypercalciuria and kidney stones are at risk of decreased bone mass, and the role of bone markers monitoring is mentioned.
<>We measured plasma Cu, Zn and Mg levels in 40 women suffering from premenstrual tension syndrome (PMTS) and in 20 control subjects by atomic absorption spectrophotometer. Mean plasma Cu, Zn and Mg levels, the Zn/Cu ratio were 80.2 plus or minus 6.00 microg/dl, 112.6 plus or minus 8.35 microg/dl, 0.70 plus or minus 0.18 mmol/l, and 1.40 plus or minus 0.10 in the PMTS group; and 77.0 plus or minus 4.50 microg/dl, 117.4 plus or minus 9.50 microg/dl, 0.87 plus or minus 0.10 mmol/l, and 1.51 plus or minus 0.05 in the control group respectively. The mean Mg level and the Zn/Cu ratio were significantly lower in PMTS patients than in the control group. Plasma Mg and Zn levels were diminished significantly during the luteal phase compared to the follicular phase in PMTS group. Mg deficiency may play a role in the etiology of PMTS.
<>Reduced magnesium (Mg) levels have been reported in women affected by premenstrual syndrome (PMS). To evaluate the effects of an oral Mg preparation on premenstrual symptoms, we studied, by a double-blind, randomized design, 32 women (24-39 years old) with PMS confirmed by the Moos Menstrual Distress Questionnaire. After 2 months of baseline recording, the subjects were randomly assigned to placebo or Mg for two cycles. In the next two cycles, both groups received Mg. Magnesium pyrrolidone carboxylic acid (360 mg Mg) or placebo was administered three times a day, from the 15th day of the menstrual cycle to the onset of menstrual flow. Blood samples for Mg measurement were drawn premenstrually, during the baseline period, andin the second and fourth months of treatment. The Menstrual Distress Questionnaire score of the cluster 'pain' was significantly reduced during the second month in both groups, whereas Mg treatment significantly affected both the total Menstrual Distress Questionnaire score and the cluster 'negative affect'. In the second month, the women assigned to treatment showed a significant increase in Mg in lymphocytes and polymorphonuclear cells, whereas no changes were observed in plasma and erythrocytes. These data indicate that Mg supplementation could represent an effective treatment of premenstrual symptoms related to mood changes.
<>Plasma and erythrocyte magnesium were measured in 105 patients with premenstrual syndrome (PMS) using a simple atomic absorption spectroscopy method. The erythrocyte magnesium concentration for the patients with PMS was significantly lower than that of a normal population. The plasma magnesium did not show this difference. The significant of this apparent cellular deficiency of magnesium is discussed.
<>Magnesium (Mg) concentrations were studied in the brains of 4 patients with definite multiple sclerosis (MS) and 5 controls. The magnesium contents were determined by inductively coupled plasma emission spectrometry in autopsy samples taken from 26 sites of central nervous system tissues, and visceral organs such as liver, spleen, kidney, heart and lung. The average Mg content in the CNS tissues, as well as visceral organs except for spleen, of MS patients showed a significantly lower value than that seen in control cases. The most marked reduction of Mg content was observed in CNS white matter including demyelinated plaques of MS samples. Whether or not these significantly lower Mg contents found in CNS and visceral organs of MS patients may play an essential role in the demyelinating process remain unclear, requiring further studies on MS pathogenesis from the point of metal metabolism.
<>Zinc (Zn), copper (Cu) and magnesium (Mg) concentrations in cerebrospinal fluid (CSF) and serum were determined with atomic absorption spectrophotometry in 74 patients suffering from various neurological diseases, and in 28 healthy controls. Increased CSF zinc levels were found in the group of peripheral nervous system diseases (P < 0.01) and in the cases of different neurological syndromes with increased CSF protein concentration (P < 0.001). Increased CSF and serum copper levels were found in the cases with increased CSF protein levels (P < 0.05). It is probable that damaged blood-brain-barrier (BBB) permits the passage of the trace elements Zn, Cu and of Mg into the subarachnoid space. Decreased serum Cu levels (P < 0.01) were found in the group of multiple sclerosis (MS). The findings are correlated to those of previous communications.
<>A study of the action of magnesium on the centrocecal scotoma in multiple sclerosis revealed that the scotomas were transiently reduced by magnesium infusions or that calcium ionization was modified by alkalinization or Na EDTA.
<>The proposed aetiologies of multiple sclerosis (MS) have included immunological mechanisms, genetic factors, virus infection and direct or indirect action of minerals and/or metals. The processes of these aetiologies have implicated magnesium. Magnesium and zinc have been shown to be decreased in central nervous system (CNS) tissues of MS patients, especially tissues such as white matter where pathological changes have been observed. The calcium content of white matter has also been found to be decreased in MS patients. The interactions of minerals and/or metals such as calcium, magnesium, aluminium and zinc have also been evaluated in CNS tissues of experimental animal models. These data suggest that these elements are regulated by pooling of minerals and/or metals in bones. Biological actions of magnesium may affect the maintenance and function of nerve cells as well as the proliferation and synthesis of lymphocytes. A magnesium deficit may induce dysfunction of nerve cells or lymphocytes directly and/or indirectly, and thus magnesium depletion may be implicated in the aetiology of MS. The action of zinc helps to prevent virus infection, and zinc deficiency in CNS tissues of MS patients may also be relevant to its aetiology. Magnesium interacts with other minerals and/or metals such as calcium, zinc and aluminium in biological systems, affecting the immune system and influencing the content of these elements in CNS tissues. Because of these interactions, a magnesium deficit could also be a risk factor in the aetiology of MS. (51 Refs.)
<>There are few reports of Mg in MS and none dealing with Mg content in erythrocytes. Mg concentration was determined in serum and in erythrocytes with the help of a BIOTROL Magnesium Calmagite colorimetric method (average sensitivity: 0.194 A per mmol/I) and a Hitachi autoanalyzer in 24 MS patients (7 men and 17 women, age 29-60; 37 years on average with the duration of the disease: 3-19; 11 years on average, at clinical disability stages according to the Kurtzke scale: 1-7; 3.2 on average, in remission stage. A statistically significant decrease (p < 0.001) of Mg concentration in erythrocytes and no changes in plasma of MS patients were found. The results obtained suggest the presence of changes in membrane of erythrocytes which could be connected with their shorter life and with affection of their function.
SCAND. J. CLIN. LAB. INVEST. SUPPL. (United Kingdom), 1994, 54/217
<>It is clear now that although different ionophores for ionized Mg (Img2+) have been designed by several groups, each of these has a distinctly different K(MgCa). In view of this, it is important to determine whether each of these ion selective electrodes (ISE's) yield identical results for IMg2+ in sera from healthy and diseased humans. Using such an approach, we determined, in a blinded-and random manner, IMg2+ with both the NOVA and KONE ISE's for IMg2+ in two independent laboratories. No significant differences were found either for sera from healthy human volunteers or diseased patients. We did, however, note several interesting findings: 1. randomly, selected hospitalized patients exhibit a much higher incidence of abnormalities for IMg2+ (57-71%) than that noted previously for total Mg (TMg) measurements; and 2. coronary heart disease, rectal cancer and multiple sclerosis patients exhibit extracellular deficits in ionized free Mg.
<>Migraine is caused by intermittent brain dysfunction. Attacks result in severe unilateral headache with nausea, vomiting, photophobia, phonophobia and general weakness. The prevalence of migraine is 12 to 20% in women and 8 to 12% in man. Treatment of an acute attack is done by antiemetics in combination with analgesics. Severe migraine attacks are treated with ergotamine or sumatriptan. Parenteral treatment is performed most efficiently and safely with i.v. ASA. Frequent and severe attacks require prophylaxis. Drugs of first choice are metoprolol, propranolol, flunarizine and cyclandelate. Substances of second choice are valproic acid, DHE, pizotifen, methysergide and magnesium. Homeopathic remedies are not superior to placebo. Nonpharmacological treatment consists of sport therapy and muscle relaxation techniques.
<>In order to evaluate the prophylactic effect of oral magnesium, 81 patients aged 18-65 years with migraine according to the International Headache Society (IHS) criteria (mean attack frequency 3.6 per month) were examined. After a prospective baseline period of 4 weeks they received oral 600 mg (24 mmol) magnesium (trimagnesium dicitrate) daily for 12 weeks or placebo. In weeks 9-12 the attack frequency was reduced by 41.6% in the magnesium group and by 15.8% in the placebo group compared to the baseline (p < 0.05). The number of days with migraine and the drug consumption for symptomatic treatment per patient also decreased significantly in the magnesium group. Duration and intensity of the attacks and the drug consumption per attack also tended to decrease compared to placebo but failed to be significant. Adverse events were diarrhea (18.6%) and gastric irritation (4.7%). High-dose oral magnesium appears to be effective in migraine prophylaxis.
<>Headache has often been described in the hyperexcitability syndrome which recognizes an alteration of calcium and magnesium status in its etiopathogenesis. Moreover, in migraine patients magnesium has been shown to play an important role as a regulator of neuronal excitability and, therefore hypothetically, of headache. The present research involves a neurophysiological evaluation and magnesium status assessment of a group of headache patients. Nineteen patients (15 women and 4 men) with episodic tension-type headache and 30 patients (27 women and 3 men) with migraine without aura were examined. An ischemic test was carried out on the right arm with electromyographic (EMG) recording of motor unit potential activity during the interictal period. The determination of extracellular (serum and saliva) and intracellular (red and mononuclear blood cells) magnesium was also performed. The EMG test was positive in 25 of 30 migraine patients and in 2 of 19 tension-type headache patients. Between the two patient groups, there were no significant variations in the concentration of extracellular and white blood cell magnesium, while the red blood cell concentration of this mineral in the group with migraines experienced significantly reduced levels with respect to that in the group of tension-type headache patients (P < 0.05). The positive EMG test was significantly associated with a low concentration of red blood cell magnesium (P < 0.0001). These results confirm previous findings by demonstrating different etiopathogenic mechanisms as the basis of migraine and tension-type headache. Migraine seems to be related to an altered magnesium status, which manifests itself by a neuromuscular hyperexcitability and a reduced concentration in red blood cells.
<>Among other things, magnesium regulates active calcium transport. As a result, there has been a growing interest in the role of magnesium (Mg) in bone metabolism. A group of menopausal women were given magnesium hydroxide to assess the effects of magnesium on bone density. At the end of the 2-year study, magnesium therapy appears to have prevented fractures and resulted in a significant increase in bone density.
<>Qualitative and quantitative differences in the dietary habits of postmenopausal women were studied to assess their influence on bone health and osteoporosis. A total of 194 postmenopausal women were studied with forearm DEXA densitometry. 70 were osteoporotic and 124 served as controls. Women had been menopausal for 5-7 years and had never been treated with hormone replacement or drug therapy. A 3-day dietary recall was completed on Sunday, Monday and Tuesday after the examination: the results were processed by computer and daily calcium, phosphorus and magnesium intakes were related to bone mineral content (BMC). Data were compared with Student's t-test and significance was assessed at p < 0.05. Regression analysis was performed to correlate BMC and intake levels. The dietary intake of calcium phosphorus and magnesium was significantly reduced in osteoporotic women and correlated with BMC. Calcium and magnesium intakes were lower than the recommended daily allowance even in normal women. The results suggest that nutritional factors are relevant to bone health in postmenopausal women, and dietary supplementation may be indicated for the prophylaxis of osteoporosis. Adequate nutritional recommendations and supplements should be given before the menopause, and dietary evaluation should be mandatory in treating postmenopausal osteoporosis.
<>The inhibitory effect of magnesium on the first stages of renal calcium stone formation is modest in vitro and more pronounced in experimental in vivo studies. Magnesium deficiency has not yet been convincingly demonstrated in man. However, urinary magnesium concentrations are abnormally low in relation to urinary calcium concentrations in more than 25% of patients with kidney stones. A supplementary magnesium intake corrects this abnormality and prevents the recurrence of stones. Magnesium seems to be as effective against stone formation as diuretics. The modalities of magnesium therapy still have to be determined and its results confirmed. Magnesium, possibly added to drinking water, may well play a role in the primary prevention of renal calcium stones.
KLIN. WOCHENSCHR. (Germany, Federal Republic of), 1988, 66/3 (87-91)
An increased frequency of kidney stone formation is reported in patients with imflammatory bowel disease. In order to investigate its pathogenesis, the concentrations of factors known to enhance calcium oxalate stone formation (oxalate, calcium, uric acid) as well as of inhibitory factors for nephrolithiasis (magnesium, citrate) were determined in the urine of 86 patients with Crohn's disease and compared with those of 53 metabolically healthy controls. Six patients with Crohn's disease already had experienced calcium oxalate nephrolithiasis. Patients with Crohn's disease had significantly higher urinary oxalate and lower magnesium and citrate concentrations. Among all patients magnesium and citrate were significantly lower in those with a positive history of kidney stones. Our results demonstrate that the increased propensity for renal stone formation in patients with Crohn's disease is a result not only of increased urinary oxalate, but also of decreased urinary magnesium and citrate concentrations.
Kidney stones are more common in patients with inflammatory bowel disease (IBD) than in the general population. The main lithogenetic risk factors were evaluated in patients affected by Crohn's disease and ulcerative colitis. Our results show the presence of several factors, besides hyperoxaluria, in patients with IBD although their behaviour appears different in Crohn's disease and ulcerative colitis at pre- and post-operative stages. Before surgery in patients with Crohn's disease we found a decreased citrate (p < 0.001) and magnesium (p < 0.005) excretion together with a low urinary volume (p < 0.001) and pH (p < 0.005). After surgery patients with Crohn's disease showed a further reduction of magnesium and citrate. Patients with ulcerative colitis before surgery showed a reduced citrate excretion (p < 0.05) and a more acidic pH (p < 0.05) than healthy subjects. Surgical treatment of proctocolectomy with ileal pouch-anal anastomosis seems to increase the risk of stone formation; in fact, after surgery we observed a relevant decrease of urinary volume (p < 0.001), pH (p < 0.0001) and urinary excretion of citrate (p < 0.0001) as well as magnesium (p < 0.005). Patients with IBD seem to be at greater risk of stone formation than patients with idiopathic calcium lithiasis; in fact, they show a lower excretion of citrate (p < 0.001) and magnesium (p < 0.001) together with a low urinary pH (p < 0.001) and volume (p < 0.001). Urinary volume reduction is probably one of the major risk factors together with the decrease of small molecular weight inhibitors that is a constant finding in all patients with IBD.
The studies above collectively present the great importance in a person having a sufficient Magnesium intake. Magnesium is a necessary mineral to process calcium, in physical and mental process, in 300 enzymatic systems, in membrane structure and in the neuromuscular system and in proper kidney functions. They clearly establish that Magnesium is a cornerstone mineral in virually every human body function.Some of the studies additionally point to key minerals of magnesium, zinc, potassium, calcium and the importance of trace minerals.
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