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G Stendig-Lindberg

Publications and source records attributed to G Stendig-Lindberg.

18 recordsLinked to original sources
PubMed2004

Prolonged magnesium deficiency causes osteoporosis in the rat.

BACKGROUND: Peroral magnesium (Mg) administration, used as the only treatment in postmenopausal osteoporosis, has been shown to cause a significant increase of BD. OBJECTIVES: To gauge the role of magnesium deficiency in the etiology of osteoporosis, we compared rats fed a Mg deficient diet daily with rats fed a Mg adequate diet over a period of one year. METHODS: Sprague-Dawley female rats (mean weight 110, SD 23 g) were divided into two groups of 8 and randomly assigned to an identical semisynthetic diet, containing either 2000 ppm (group A) or 200 ppm Mg (group B). Urine samples were collected every 3 months and blood samples at end of trial. After sacrifice, L3-L5 vertebrae and the femoral regions were examined for bone density (BD) using dual energy X-ray absorptiometry. The femurs were examined for bone fragility, the tibias by histomorphometry and the mineral contents of the bones was estimated. RESULTS: The mean BD of L3-L5 vertebral bone (BDL) was significantly higher in group than in the Mg deficient group B (p = 0.035, 1 tail). The BD of the femoral region (BDF) was also significantly higher in group A (p = 0.045, 1 tail). The stiffness of the femur, as determined by resistance to bending, was slightly greater in group A than in group B, but after correction to diminish the influence of the difference in bone dimensions in the two groups, the stiffness (ie loss of elasticity) in group B became significantly greater than that in group A (p = 0.024). The force needed to break the bone (F-max) was significantly higher in group A, than in group B (p = 0.024) and remained so after correction, although no longer significantly. In Group B, the diminution of the trabecular bone volume, in relation to tissue volume (BV/TV) and the increase in the degree of trabecular interconnection (TBPf) indicated osteoporosis, and focal osteoporosis of the metaphyseal spongy bone was seen on microscopy. CONCLUSION: Experimentally induced prolonged Mg deficiency causes osteoporosis in rats.

Absorptiometry, Photon↗
PubMed1998

How significant is magnesium in thermoregulation?

Nine apparently healthy male subjects, mean age 22.8 yr, SD 4.1, free from disease, medication or addiction who gave informed consent, underwent acclimation process in a heat chamber; exposed during 2 h daily for 10 consecutive days to a temperature of 40 degrees C and 40% relative humidity while walking on a treadmill elevated by 3 degrees at a speed of 5 km/h (VO2 1.2 1.min-1). Serum, mononuclear and erythrocyte magnesium (S-Mg, M-Mg and E-Mg, respectively) were monitored on day 1, 5 and 10 before and after the heat exposure. S-Mg decreased while M-Mg increased after the heat exposures, suggesting a shift of S-Mg to mononuclear cells. The decrease of S-Mg was sustained at the end of the acclimation process. E-Mg increased up to day 5 and decreased gradually approximating the baseline by day 10. Mg appears to play a significant role in heat acclimation.

Adult↗
PubMed1993

Trabecular bone density in a two year controlled trial of peroral magnesium in osteoporosis.

Since magnesium regulates calcium transport, and magnesium replacement in magnesium-deficient postmenopausal patients resulted in unexpected improvement in documented osteoporosis, we investigated the effect of magnesium treatment on trabecular bone density in postmenopausal osteoporosis. Thirty-one postmenopausal patients (mean age +/- SD = 57.6 +/- 10.6 years), consecutively admitted to the Back Rehabilitation Unit with musculoskeletal pain of non-malignant origin and bone density values of < or = 1.19 g/cm3 (measured by Compton Bone Densitometer), received two to six tablets daily of 125 mg each of magnesium hydroxide (Magnesium Magma USP/; 'Mazor', Israel) for 6 months and two tablets for another 18 months in a 2 year, open, controlled therapeutic trial. Twenty-three symptom-free postmenopausal women (mean +/- SD = 61.2 +/- 6.2 years) whose bone density was concurrently assessed at the same laboratory and who were found to have osteoporosis but refused treatment, served as controls. No new fractures occurred. Twenty-two patients (71 per cent) responded by a 1-8 per cent rise of bone density. The mean bone density of all treated patients increased significantly after 1 year (P < 0.02) and remained unchanged after 2 years (P > 0.05). The mean bone density of the responders increased significantly both after one year (P < 0.001) and after 2 years (P < 0.02), while in untreated controls, the mean bone density decreased significantly (P < 0.001). The disparity between the initial mean bone density and bone density after one year in all osteoporotic patients and in the responders differed significantly from that of the controls (both P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Bone Density↗
PubMed1991

Magnesium content of mononuclear cells, erythrocytes and 24-hour urine in carefully screened apparently healthy Israelis.

Twenty apparently healthy Israelis aged 16-52, examined for their history of disease and, carefully screened to exclude concurrent infection or medication, abuse of alcohol or drugs, and pathological findings on routine laboratory estimation, were examined to establish the reference range for the magnesium content of mononuclear cells. The magnesium content of mononuclear cells was estimated according to modified method of Elin & Hosseini (Clin. Chem. 31 (1985) 377-380), together with serum magnesium concentration (S-Mg) and erythrocyte magnesium content. In 10 subjects, aged 23-37 years, 24 h urinary magnesium (U-Mg) was also determined. The mean magnesium content of mononuclear cells was 164.8 fg/cell (SD 28.3 fg/cell). The mean erythrocyte magnesium content was 2.02 (SD 0.16) mmol/l. The magnesium content of mononuclear cells was significantly correlated to U-Mg (r = 0.704, p less than 0.01), suggesting that U-Mg may have a potential value as an index of intracellular Mg content.

Adolescent↗
PubMed1991

Long term effects of peak strenuous effort on serum magnesium, lipids, and blood sugar in apparently healthy young men.

Earlier findings showed a sustained lowering of serum magnesium concentration (S-Mg) which indicated the presence of Mg deficit, and a parallel, delayed rise of blood sugar and serum lipids as a sequel to strenuous effort. S-Mg was still significantly decreased 3 months after termination of peak effort. To gain further perspective, we followed the biochemical sequels of exertion over an extended period of observation, while maintaining the same experimental conditions used earlier, which mimicked those employed in the training of military recruits. We examined two groups of military recruits, n = 15 (group 1), n = 16 (group 2), mean age 18.6, SD 1.3 and 18.7, SD 0.6, years respectively, who underwent a graded training programme of 7 months' duration culminating in a 120 km forced march. Blood was sampled for estimation of S-Mg in 20 soldiers on recruitment, 6 and 10 months after the 120 km march in group 1, and 9, 11 and 15 months after the march in group 2. Blood sugar and serum lipids were screened on recruitment and up to 11 months after the 120 km march. A significant lowering of mean S-Mg was found as late as 10 months after completion of the march in group 1, and 11 months in group 2 (P less than 0.01). Mean serum cholesterol and triglycerides showed a delayed rise, especially in group 2 (P less than 0.05 and P less than 0.001, respectively), whereas blood sugar decreased in group 1, but increased in group 2 (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Delayed metabolic changes after strenuous exertion in trained young men.

Twenty apparently healthy, young male volunteers, aged 18-25 (mean 19.3, SD 1.4) years received a 6 months standardized, graded outdoor physical training and were screened for serum magnesium concentration (S-Mg), serum calcium concentration (S-Ca), serum aspartate amino transferase (S-AST), serum alanine amino transferase (S-ALT), serum creatine kinase activity (S-CK), other laboratory variables, weight, and VO2 ml.kg-1.min-1 [corrected] (VO2 max), before a 70 km march, as well as at 1, 24 and 72 h and 18 days after. Maximal aerobic power, body weight, haemoglobin, haematocrit, serum creatinine, total protein and albumin remained unchanged throughout. Immediately after the march, S-Mg did not change, S-AST, S-ALT and S-CK rose, but the rise was not statistically significant, while small but significant rises in S-Ca (P less than 0.05, Student's t-test) and serum cholesterol (P less than 0.01) normalized at 24 h. At 72 h after the march, a significant fall in S-Mg was found (P less than 0.01), together with a second significant rise in S-Ca (P less than 0.05). After 18 days, with no intervening marches or dietary changes, S-Mg remained significantly lowered (P less than 0.05), mean S-ALT and S-CK became significantly raised for the first time (P less than 0.001 and P less than 0.01 respectively), whereas S-Ca normalized. Concomitantly, for the first time there was now a significant rise in blood sugar (P less than 0.001), serum triglycerides (P less than 0.01), and a second rise of serum cholesterol (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Magnesium fluxes in ventricular fibrillation and defibrillation in untreated and dibenzepine HC1 pretreated cats.

Serum magnesium concentration (S-Mg) was estimated in 12 anesthetized cats before and after central thoracotomy, during an electrically induced ventricular fibrillation (VF) and after defibrillation (DEF), and again, in the same experimental animals, after the administration of 3 mg/kg of dibenzepine HC1--a tricyclic antidepressant reported to facilitate spontaneous DEF--as well as during a subsequently induced VF and after the spontaneous DEF which followed. In the first part of the experiment, the surgery and the induction of VF caused no significant change of mean serum magnesium concentration (S-Mg) or serum calcium concentration (S-Ca), whereas the DEF was accompanied by Mg efflux (a significant increase of mean S-Mg from 0.824 mmol/l, SD 0.182, n = 12 to 0.991 mmol/l, SD 0.182, n = 12; P less than 0.05). In the second part of the experiment, following the administration of dibenzepine HCl there was Mg influx (a lowering of mean S-Mg to 0.891 mmol/l, SD 0.160, n = 12; P less than 0.05). During VF in the pretreated cats, S-Mg remained unchanged, while S-Ca decreased significantly (P less than 0.05), followed by a rebound Ca++ efflux (a systematic rise of S-Ca) as the animals defibrilated spontaneously. Concomitantly, there was Mg efflux (a systematic rise of S-MG), the mean S-Mg rising from 0.879 mmol/l, SD 0.143, n = 9 to 1.083 mmol/l, SD 0.257, n = 7, ie to virtually the same value as that obtained after electrically induced DEF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Changes in serum magnesium concentration after strenuous exercise.

Serum magnesium concentration (S-Mg) was measured in 20 highly trained young men (mean age 19.5, +/- 0.5, range 18-20.5) before, and at 1 hour, 24 hours, 72 hours, and 3 months after a 120 km hike. As found in previous studies, S-Mg was significantly decreased at the end of the hike (p less than 0.001, [corrected] Student's t-test). In this group S-Mg had risen significantly after 24 hours in relation to the value at 1 hour (but not to starting value); yet, at 72 hours and 3 months later, it was once more significantly lower than the starting value (p less than 0.001 and p less than 0.05, respectively, Student's t-test). A marked elevation in serum creatine kinase activity (CK) suggests that the rise in S-Mg observed at 24 hours is the result of either exertional rhabdomyolysis or loss of membrane integrity, as a result of the strenuous exertion, since the CK had fallen sharply by 72 hours after the hike. The biphasic, statistically significant, lowering of S-Mg which persisted after 3 months suggests that strenuous exertion induces magnesium deficiency.

Adolescent↗
PubMed1984

Comparison of diluents for serum magnesium estimation by atomic absorption spectrophotometry.

In order to determine the optimal diluent for the determination of Mg by atomic absorption spectrophotometry, the following diluents were tested: deionized water, 0.1 mol/l HCl, 2.5 g/l SrCl2, 1.8 g/l LaCl3, 17.7 g/l LaCl3, half-saturated 8-hydroxyquinoline (oxine), 40 g/l trichloroacetic acid (TCA)/17.7 g/l LaCl3, and 100 g/l TCA/0.1 mol/l HCl. The calibration curves, obtained on the same day, were passed through the origin in the form of linear regressions. The variances about the calibration curves did not differ significantly (p greater than 0.05), while the calibration slopes for the diluents differed significantly (p less than 0.001). A standard serum solution was analyzed with the use of the eight diluents and the mean results did not differ significantly (p greater than 0.05). The % coefficient of variation varied from 0.8 to 2.0 and the percent recovery ranged from 95.5 to 102.5. The 99% confidence interval (CI) ranged from 0.02 to 0.09. Since conventional CIs do not take into account the random error of the calibration curve, the inverse CI were also calculated for each diluent. On both the conventional estimates and on the inverse CI, strontium chloride gave the best results, but only marginally in view of the interassay variability of approximately 1%.

Calibration↗
PubMed1980

Stepwise regression analysis of an intensive 1-year study of delirium tremens.

An intensive 1-year study was carried out on 41 male patients, mean age 49, mean hospitalization time 49 days, admitted to a special ward of the Beckomberga Hospital with the diagnosis of delirium tremens and 50 concomitant somatic and psychiatric diagnoses (1--9 per capita), and given a standardized treatment. The mean duration of delirium tremens after admission was 2 days; 76% recovered within 48 h. The duration after admission was positively correlated to age, number of previous delirium tremens, negatively correlated to B-haemoglobin and B-haematocrit for laboratory data obtained within the first 24 h and was positively correlated to blood sugar and S-creatinine on data taken within 40 h (Pearson correlation matrix). Stepwise multiple regression (SWR) based on 46 quantitative and dummy variables (the latter used to represent the presence of various concomitant diseases) was employed to identify the factors predicting the duration of delirium tremens. On final SWR analysis, which limited the number of observations to cases with complete observation vectors, the following regression equation was obtained: Duration after admission = 3.57--0.93 (S-magnesium)--0.29 (B-eosinophils) + 0.62 (liver disease), P greater than 0.05, n = 14. Although the regression coefficients were not statistically significant, S-magnesium, negatively associated with the duration after admission, offered 20% out of the total 38% of explanation given, whereas B-eosinophils, negatively associated, offered 12%, and liver disease, positively associated, 6%. The choice by the SWR program of S-magnesium as the most important factor in predicting the duration of delirium tremens is consistent with clinical evidence that alcohol ingestion causes magnesium diuresis and that magnesium deficiency is present in chronic alcoholism. In view of this knowledge, it is reasonable to assume that the lack of statistical significance is due to the small sample size rather than to the alternative that no explanation is offered by S-magnesium. Furthermore, B-haemoglobin, S-potassium, S-ASAT, and S-ALAT, known to be characteristically altered in delirium tremens, were found on forcing (a variant of SWR) to be of secondary importance to S-magnesium as explaining factors, whereas blood sugar and S-creatinine derived part of their explaining power from S-magnesium. In conclusion, extensive use of SWR analysis based on 46 potential explaining variables points to serum magnesium concentration as the most important factor in predicting the duration of delirium tremens.

Adult↗
PubMed1977

Hypomagnesaemia and muscle electrolytes and metabolites.

Ten patients, aged 39-61 years, with hypomagnesaemia due to chronic alcoholism (7 cases) or malabsorption (3 cases), have been investigated by assessing the maximum isometric voluntary contraction force (MVC) of the quadriceps femoris muscle (7 cases), laboratory screening (9 cases) and estimating the electrolyte and metabolite content of biopsy specimens from the quadriceps femoris muscle. The MVC ranged from 0.5 to 34 kp and was significantly lower than in 12 apparently healthy normomagnesaemic controls (p is less than 0.001). The results of the laboratory screening, apart from a significant lowering of the serum magnesium concentration (p is less than 0.01), were mainly within the range of normal values, apart from signs of liver damage, such as an elevated activity of S-OCT (3 cases), alkaline phosphatease(3 cases), S-ALAT (1 case) and an elevation of bilirubin and blood ammonia (2 cases). Low serum iron-binding capacity occurred in 4 cases, a finding reported in protein-calorie malnutrition. Muscle magnesium content was significantly lower than in healthy controls (p is less than 0.001). Muslce sodium and chloride contents were significantly increased (p is less than 0.05). Total H2O content and the extracellular H2O content were both significantly increased (p is less than 0.05). Pyruvate and lactate values were within the normal range. The apparent equilibrium constant for creatine kinase differed significantly ( is less than 0.01). ATP values were within the normal range, but there were slight decreases for ADP (p is less than 0.05) and creatine phosphate ( is less than 0.01), whcih is of interest in view of the lowering of the MVC and the diminished capacity for sustained muscular effort in hypomagnesaemic patients reported earlier.

Adenosine Diphosphate↗
PubMedDate not supplied

Is physical working capacity determined by optimal magnesium concentration?

Two lines of research originated in the mid-seventies; one attempted to gauge the effect of strenuous effort on serum magnesium concentration (S-Mg) and the second, the effect of S-Mg on the indices of physical working capacity. In apparently healthy trained young Israeli men, long-term studies of the effect of strenuous effort on S-Mg showed that after a moderately strenuous effort (70 km forced march), there was a decrease of S-Mg which became statistically significant after 72 h, whereas after a severely strenuous effort (120 km forced march), the decrease was biphasic, being significant after 1 h, with a second fall after 72 h. In repeated experiments, the decrease of S-Mg was found to persist over time parallel 1. Since chronic lowering of S-Mg signifies a concomitant lowering of intracellular Mg content, these findings showed that Mg deficiency was a sequel to strenuous effort. Studies of the effect of S-Mg on the indices of physical working capacity showed that: (1) S-Mg determines the maximal voluntary muscle contraction force (MVC); (2) S-Mg affects, among other things, the maximal aerobic capacity (VO2max). The estimated daily Mg intake in the Israeli population is inadequate and a widely prevalent marginal to overt Mg deficiency is found in apparently healthy Israelis. It is proposed that an optimal physical working capacity in the Israeli population will be achieved only under conditions of Mg saturation of metabolism. Studies to validate this hypothesis are under progress.

Adolescent↗
PubMedDate not supplied

Sudden death of athletes: is it due to long-term changes in serum magnesium, lipids and blood sugar?

In young, apparently healthy, trained Israeli men, strenuous effort was reported to give rise to persistent magnesium (Mg) deficiency and a parallel long-term increase of cholesterol, triglycerides and blood sugar parallel 1-3. The relationship of Mg deficiency to the pathogenesis of cardiovascular disease has been increasingly documented during the last decade. Several authors have highlighted the phenomenon of sudden deaths in sport and have suggested that it is associated with cardiovascular disease. The association is discussed between Mg deficiency and increase of blood lipids and sugar, found as a sequel to strenuous effort, and cardiovascular morbidity and mortality risk reported in athletes. It is postulated that sudden death of athletes and other intensely training individuals during exertion, is mediated by the deleterious cardiovascular effects of persistent magnesium deficiency and the resultant hyperlipaemia and hyperglycaemia, which, as we have documented, follows strenuous effort.

Adolescent↗