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PubMedDate not supplied

Oral versus intravenous magnesium supplementation in patients with magnesium deficiency.

The efficacy of oral magnesium supplementation in correcting magnesium deficiency was examined in a group of 40 elderly patients with suspected magnesium deficiency. The patients were randomized in a double-blind, placebo-controlled fashion to oral magnesium-lactate-citrate for 6 weeks. Magnesium status was assessed by an intravenous magnesium-loading test at baseline and after treatment. For comparison, another group of 23 patients received 30 mmol magnesium sulfate intravenously daily for 7 days. A group of 30 patients without known predisposition to magnesium deficiency and a group of 27 young healthy subjects served as controls. The initial magnesium-loading test in the placebo group reduced magnesium retention from a mean 41% (95% confidence intervals 34-49) to 22% (15-29) (p less than 0.01). In the group receiving oral magnesium supplementation for 6 weeks, magnesium retention decreased from 39% (31-47) to 10% (2-18) (p less than 0.01), which was significantly better than with placebo treatment (p less than 0.01). The magnesium retention after oral magnesium supplementation was comparable to that observed after parenteral administration of magnesium for 7 days, 6% (-4 to 16), and to that in the reference groups of patients 4% (-2 to 10) and healthy control subjects 3% (-2 to 8). The study suggests that the bioavailability of orally given magnesium-lactate-citrate is satisfactory, and that oral administration of magnesium for 6 weeks may restore magnesium depots in patients with magnesium deficiency.

Administration, Oral↗
PubMed1993

Magnesium homeostasis and renal magnesium handling.

Magnesium is essentially an intracellular cation, which makes it difficult to evaluate magnesium status. About 1% of total body magnesium is present in serum and interstitial body fluid and only about 1% of the intracellular magnesium is in the free form, Mg2+. Recent studies show that this small fraction of free Mg2+ rapidly changes with the extracellular magnesium. These free Mg2+ levels are carefully controlled within the cell and total cellular magnesium content are maintained at the expense of extracellular fluid and bone magnesium levels. Regulation of magnesium balance is met between intestinal absorption and renal excretion. The excretory side of magnesium balance involves appropriate changes in renal magnesium handling. Present evidence indicates that renal handling of magnesium normally is a filtration-reabsorption process; magnesium is filtered at the glomerulus and reabsorbed along the various segments making up the renal nephron. About 80% of total serum magnesium (0.7-1 mmol/l) is filtered at the glomerular membrane. Of the ultrafilterable magnesium (0.6-0.8 mmol/l) 20-25% is reabsorbed by the proximal tubule, including the convoluted and straight portions. Some 50-60% of the filtered magnesium is reabsorbed in the loop of Henle, specifically by thick ascending limb cells. The terminal nephron segments, including the distal convoluted tubule and collecting ducts, reabsorb only a small portion of the filtered magnesium (about 5-10%). The loop of Henle plays the major role in determining magnesium reabsorption and urinary magnesium excretion. The loop of Henle also is the segment in which the major regulatory factors act to maintain magnesium balance.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1993

Magnesium and ageing. II. Clinical data: aetiological mechanisms and pathophysiological consequences of magnesium deficit in the elderly.

Ageing constitutes a risk factor for magnesium deficit. Primary magnesium deficit originates from two aetiological mechanisms: deficiency and depletion. Primary magnesium deficiency is due to insufficient magnesium intake. Dietary amounts of magnesium are marginal in the whole population whatever the age. Nutritional deficiencies are more pronounced in institutionalized than in free-living ageing groups. Primary magnesium depletion is due to dysregulation of factors controlling magnesium status: intestinal magnesium hypoabsorption, reduced magnesium bone uptake and mobilization, sometimes urinary leakage, hyperadrenoglucocorticism by decreased adaptability to stress, insulin resistance and adrenergic hyporeceptivity. Secondary magnesium deficit in ageing largely results from various pathologies and treatments common to elderly persons, i.e., non-insulin dependent diabetes mellitus and use of hypermagnesuric diuretics. Magnesium deficit may participate in the clinical pattern of ageing, particularly in neuromuscular, cardiovascular and renal symptomatologies. The consequences of hyperadrenoglucocorticism-the simplest marker of which is non-response to the dexamethasone suppression test-may include immunosuppression, muscle atrophy, centralization of fat mass, osteoporosis, hyperglycaemia, hyperlipidaemia, atherosclerosis, and disturbances of mood and mental performance through accelerated hippocampal ageing particularly. It seems very important to point out that magnesium deficit and stress aggravate each other in a true 'pathogenic vicious circle', particularly in the stressful state of ageing. The importance of magnesium deficit in the aetiologies of insulin resistance, and the adrenergic, osseous, oncogenic, immune and oxidant disturbances of ageing is still uncertain. Oral physiological magnesium supplementation (5 mg Mg/kg/d) is the best diagnostic tool for establishing the importance of magnesium deficiency. Too few open and double blind studies on the effects of the treatment of magnesium deficiency and of magnesium depletion in geriatric populations have been done. Further study is necessary to assess the true place of magnesium deficit in the pathophysiology of ageing.

Adrenocortical Hyperfunction↗
PubMed1990

Serum magnesium concentrations after repetitive magnesium cathartic administration.

Severe hypermagnesemia has been reported by several authors after multiple doses of magnesium-containing cathartic are administered during management of a toxic ingestion. To evaluate the frequency and magnitude of serum magnesium elevations after the use of repetitive magnesium catharsis, we prospectively evaluated 102 patients who received multiple doses of magnesium citrate as a part of treatment of an overdose. Commonly ingested substances for which repetitive cathartic was administered were tricyclic antidepressants in 47%, aspirin in 17%, and phenytoin in 10%. For each case, serial electrolytes, blood urea nitrogen, creatinine, calcium and magnesium were obtained. Mean initial serum magnesium concentration was 1.8 +/- .03 mEq/L. After a mean 960 mL of magnesium citrate (9.22 g magnesium), final mean serum magnesium concentration was 2.5 +/- .05 mEq/L. Forty-seven patients (47%) developed an elevated (greater than 2.4 mEq/L) serum magnesium concentration, with 12 greater than 3.0 mEq/L. No correlation was found between total quantity of magnesium citrate administered and the increment in serum magnesium concentration. Our data indicate that serum magnesium concentrations consistently rise after repetitive magnesium citrate use. However, the magnitude of this rise appears modest. The elevation in serum magnesium concentration does not correlate with the quantity of magnesium administered. We conclude that with close monitoring, repetitive magnesium citrate can be administered without inducing severe hypermagnesemia (serum magnesium concentration greater than 5.0 mEq/L).

Adolescent↗
PubMed2000

Magnesium supplementation in pregnancy.

BACKGROUND: Many women, especially those from disadvantaged backgrounds, have intakes of magnesium below recommended levels. Magnesium supplementation during pregnancy may be able to reduce fetal growth retardation and pre-eclampsia, and increase birthweight. OBJECTIVES: The objective of this review was to assess the effects of magnesium supplementation during pregnancy on maternal, neonatal and paediatric outcomes. SEARCH STRATEGY: We searched the Cochrane Pregnancy and Childbirth Group trials register. SELECTION CRITERIA: Randomised and quasi-randomised trials of dietary magnesium supplementation during pregnancy. DATA COLLECTION AND ANALYSIS: Suitability for inclusion and methodological quality were separately assessed by each reviewer. Data were independently extracted by two reviewers. MAIN RESULTS: Six trials involving 2637 women were included. Only one of these trials was judged to be of high quality. Compared with placebo, oral magnesium treatment from before the 25th week of gestation was associated with a lower incidence of preterm birth (odds ratio 0.71, 95% confidence interval 0.52 to 0.95). There was also less maternal hospitalisation during pregnancy, fewer cases of antepartum haemorrhage, a lower incidence of low birthweight and small for gestational age infants. Poor quality trials are likely to have resulted in a bias favouring magnesium supplementation. REVIEWER'S CONCLUSIONS: There is not enough high quality evidence to show that dietary magnesium supplementation during pregnancy is beneficial.

Dietary Supplements↗
PubMed1997

Effects of magnesium deficiency on magnesium and calcium content in bone and cartilage in developing rats in correlation to chondrotoxicity.

Quinolone-induced arthropathy has been described in juvenile rats between 3 and 6 weeks of age, but not in adult rats. The mechanism of this chondrotoxic effect is probably related to the Mg2+-chelating properties of the drugs, since identical cartilage lesions were observed in magnesium-deficient juvenile rats without quinolone treatment. However, the reasons for the phase-specificity of the effect are unknown. In the present study, we fed a magnesium-deficient diet to Wistar rats at different postnatal developmental stages. Cartilage lesions were only observed in magnesium-deficient rats between 3 and 5 weeks of age, but not in rats receiving the magnesium-deficient diet during weeks 5 to 8, weeks 8 to 11, or months 15 to 16. The formation of cartilage lesions was not related to the magnesium concentration in plasma, since magnesium concentrations in plasma were similarly reduced in rats with and without cartilage lesions. However, chondrotoxicity correlated with magnesium content in articular cartilage. In articular cartilage (articular and epiphyseal cartilage in immature rats) and bone, magnesium content was more reduced in rats receiving the magnesium-deficient diet between 3 and 5 weeks of age as compared with rats receiving the magnesium-deficient diet during weeks 8 to 11 postnatally. It was not possible to reduce the magnesium content in bone tissue of 15-month-old Wistar rats, which suggests a lower magnesium turnover in aged rats. Magnesium content in epiphyseal cartilage of 2-week-old rats (total femoral head) was 41.9 +/- 16.9 mmol/kg dry weight. The magnesium content in joint hyaline cartilage was significantly lower in 4-week-old rats (19.5 +/- 3.6 mmol/kg dry weight) and increased subsequently again to 48.5 +/- 9.2 mmol/kg dry weight (mean +/- SD; n = 8 to 16). Increase of the magnesium content in femoral bone between weeks 4 and 6 postnatally was less pronounced (139 +/- 10 and 175 +/- 15 mmol/kg dry weight, respectively). Taken together, these data show that in 4-week-old rats, magnesium concentration in joint hyaline cartilage is significantly lower than at other times during postnatal development. Only at this developmental stage can cartilage lesions be induced by feeding rats a magnesium-deficient diet. This period correlates well with the sensitive phase of immature rats toward the chondrotoxic action of quinolones.

Aging↗
PubMed1996

Brain ionized magnesium and calcium levels during magnesium supplementation and deficiency in female Long-Evans rats.

OBJECTIVE: To examine the effect of changes in the state of magnesium balance on ionized magnesium and ionized calcium in serum and brain tissue of female rats. METHODS: Forty-two mature rats were used in the study. To induce hypermagnesemia, 12 rats received 270 mg/kg of magnesium sulfate intraperitoneally, followed every 20 minutes for 2 hours with 27 mg/kg magnesium sulfate. Ten control rats received an equal volume of saline. To induce hypomagnesemia, ten rats were placed on a magnesium-deficient diet for 4 (n = 5) or 8 (n = 5) days. Ten control rats were placed on basal diets of equal duration. Following treatment, rats were euthanized and serum and brain tissue were analyzed for ionized magnesium and calcium content. RESULTS: Hypermagnesemia produced a significant increase in serum ionized magnesium (P < .05) and calcium (P < .05). In addition, brain levels of ionized magnesium were significantly increased (P < .05), whereas calcium levels significantly decreased (P < .05) particularly in the hippocampus, parietal cortex, and cerebellum. Hypomagnesemia induced by 4 days on a magnesium-deficient diet led to decreased serum ionized magnesium (P < .01) and total magnesium (P < .05) but did not affect brain magnesium levels. Brain levels remained unaltered even after 8 days of hypomagnesemia. Serum and brain ionized calcium were not affected during peripheral magnesium deficiency. CONCLUSION: During peripheral magnesium deficiency, brain levels of ionized magnesium and ionized calcium are tightly regulated and appear unaffected. However, central levels of these electrolytes are altered under hypermagnesemic conditions. Thus, magnesium administration may change biologically active portions of magnesium and calcium in the brain.

Animals↗
PubMedDate not supplied

Some magnesium status indicators and oxidative metabolism responses to low-dietary magnesium are affected by dietary copper in postmenopausal women.

OBJECTIVE: A study with human volunteers was conducted to ascertain whether a low intake of copper (Cu) would exacerbate the response to a deficient intake of magnesium (Mg). METHODS: Nineteen postmenopausal women, age 47 to 78 y, completed a metabolic unit study as designed. For 162 d, nine women were fed a diet containing 1.0 mg of Cu/2000 kcal and 10 women were fed 3.0 mg of Cu/2000 kcal. Diets contained 99 or 399 mg of Mg/2000 kcal for 81 d in a randomized, double-blind, crossover design. Differences were considered significant when statistical analysis yielded P </= 0.05. RESULTS: Magnesium balance was highly positive when the dietary magnesium was high but non-positive when dietary magnesium was low. Copper balance was more positive when dietary copper was high than when it was low. Plasma ionized magnesium was decreased by magnesium deprivation. Several variables measured indicated that low dietary copper affected the response to magnesium deprivation or vice-versa. Red blood cell magnesium was lower when dietary copper was low than when it was high. When dietary magnesium was low, serum copper was lower in the women fed marginal copper than in those fed luxuriant copper. When dietary magnesium was high, low dietary copper did not affect serum copper. Magnesium deprivation decreased red blood cell superoxide dismutase when dietary copper was luxuriant; when dietary copper was low, magnesium deprivation did not have much of an effect. Apolipoprotein A1 was lowest when dietary magnesium and copper were low. The order in which the magnesium restriction occurred affected the response of a number of variables to this treatment including concentrations of serum magnesium and total and low-density lipoprotein cholesterol. CONCLUSIONS: The findings indicated that, in short-term magnesium depletion experiments, the response to depletion can be influenced by other dietary factors including copper intake and a high magnesium intake before depletion, and that 100 mg of Mg/d is inadequate for postmenopausal women.

Aged↗
PubMed1980

Effect of magnesium deficiency on renal magnesium and calcium transport in the rat.

Recollection of micropuncture experiments were performed on acutely thyroparathyroidectomized rats rendered magnesium deficient by dietary deprivation. Urinary magnesium excretion fell from a control of 15 to 3% of the filtered load after magnesium restriction. The loop of Henle, presumably the thick ascending limb, was the major modulator for renal magnesium homeostasis. The transport capacity for magnesium, however, was less in deficient rats than control animals. Absolute magnesium reabsorption increased with acute infusions of magnesium chloride but was always less in magnesium-deficient rats than control rats for any given filtered load, which suggests either a defect of a resetting of the reabsorption mechanism. Recollection micropuncture demonstrated that this was a characteristic of the loop of Henle. Proximal magnesium reabsorption remained unchanged at 15% of the filtered load and was unaffected by magnesium deficiency or acute magnesium repletion. Distal tubular magnesium reabsorption was limited during depletion and increased to a similar extent in control and deficient rats with enhanced magnesium delivery. Calcium reabsorption was not altered in magnesium deficiency; however, elevations of extracellular magnesium resulted in a specific inhibition of calcium reabsorption within the loop of Henle. These data suggest that overall control of renal magnesium reabsorption occurs within the loop of Henle and that the proximal tubule reabsorbs a constant fraction of the filtered load despite variations in body magnesium status.

Animals↗
PubMed2004

The alteration of magnesium, calcium and phosphorus metabolism by dietary magnesium deprivation in postmenopausal women is not affected by dietary boron deprivation.

A study with human volunteers was conducted to test the hypothesis that naturally occurring inadequate intakes of magnesium induce negative magnesium balance and undesirable changes in calcium metabolism variables, and that these changes are influenced by dietary boron. Diets composed of ordinary Western foods providing approximately 118 and 318 mg Mg/d and approximately 0.25 and 3.25 mg B/d were fed in a double-blind Latin square design to 13 healthy, post menopausal Caucasian women (aged 50-78 years) living in a metabolic unit. Magnesium balance, which was positive when dietary magnesium was 318 mg/d, became negative when dietary magnesium was 118 mg/d. Magnesium deprivation decreased urinary calcium excretion, and significantly increased calcium balance when balance data analyzed came from all collections during the 42-day periods. Urinary phosphorus excretion was increased, but fecal phosphorus excretion was decreased, thus phosphorus balance was not significantly affected by magnesium deprivation. Magnesium deprivation did not affect manganese or zinc balance. The balance data indicated that 700 mg of calcium, 1.0 mg of manganese, and 10 mg of zinc were adequate for post menopausal women. Magnesium deprivation increased serum 25-hydroxycholecalciferol and decreased serum total cholesterol concentrations. Boron deprivation increased but magnesium deprivation decreased urinary potassium excretion. Boron supplementation decreased serum 17beta-estradiol and progesterone when dietary magnesium was low. The dietary treatments did not affect serum calcitonin, parathyroid hormone, osteocalcin or alkaline phosphatase concentrations. One woman placed on consecutive magnesium-low dietary periods exhibited heart ventricular ectopy after consuming the magnesium-low diet for 72 days; the ectopy disappeared upon consuming the magnesium-adequate diet. The findings indicated that consuming an ordinary diet deficient in magnesium, resulting in negative magnesium balance, can affect calcium, potassium, and cholesterol metabolism. Dietary boron did not have an obvious effect on the response to magnesium deprivation.

Aged↗
PubMed2000

Ionized magnesium supplementation in critically ill patients: comparing ionized and total magnesium.

PURPOSE: The purpose of this study was to assess the effect of magnesium supplementation on total magnesium, ionized magnesium, ionized calcium, potassium, and pH in critically ill cancer patients and to compare the validity of the measurements. MATERIALS AND METHODS: Thirty-three consecutive critically ill patients receiving magnesium supplementation were placed in this prospective observational study at the Comprehensive Cancer Center, University Hospital. One gram (4.1 mmol) magnesium in 50 mL D5W was administered to critically ill patients, and the following were measured: total magnesium, ionized magnesium, ionized calcium, potassium, albumin, pH, BUN, creatinine, creatinine. RESULTS: Total magnesium and ionized magnesium increased by a mean of .11 +/- .02 and .05 +/- .01 mmol/L, respectively, after supplementation with 4.1 mmol of magnesium sulfate (P = .0001). Total magnesium, ionized magnesium, albumin, ionized calcium, potassium, and pH did not change significantly by the administration of 1 g of magnesium sulfate. CONCLUSION: The mean ionized magnesium (IMg+2) relationship to total magnesium (TMg) cannot be predicted before the supplementation with the available technology. After supplementation of 4.1 mmol/L the ionized magnesium level increased by .05 +/- .01 mmol/L. Magnesium supplementation had no significant effect on ionized calcium, potassium, and pH. TMg and IMg+2 should be followed independently.

Adult↗
PubMed1980

Maximum safe dietary magnesium and effects of high dietary magnesium on zinc metabolism in Holstein calves.

Fifteen male Holstein calves were fed diets containing .25 (control), .7, or 1.15% magnesium (from supplemental magnesium oxide) for 28 days. Feed consumption and growth rate were not affected adversely by .7% magnesium but were depressed with 1.15% magnesium. Fecal dry matter percentage was reduced slightly with .7% magnesium and substantially decreased with 1.15% magnesium. However, feces from calves fed .7% magnesium were more fluid in consistency. Urinary and fecal magnesium content increased in calves fed .7 and 1.15% magnesium, with changes closely related to dietary magnesium. Magnesium in plasma increased slightly with .7% magnesium and materially with 1.15%. Magnesium in liver, kidney, and heart was not affected by diets. Apparently calves can tolerate safely .7% magnesium, but 1.15% is detrimental. On day 21 of treatment, all calves received zinc-65 orally and were killed 7 days later. Calves fed .7 and 1.15% magnesium excreted less zinc-65 and retained more, especially in liver and large intestine. Liver and kidney of calves receiving higher percents magnesium had elevated stable zinc. Calcium and copper in tissue were not elevated. The effect of high dietary magnesium on zinc metabolism appears to be systemic in tissues.

Animal Feed↗
PubMed1982

Effects of magnesium infusions on magnesium and nitrogen balance during parenteral nutrition.

The effects of magnesium infusions on urinary and fecal magnesium excretion, serum magnesium and nitrogen balance were examined in seven well-nourished and three nutritionally depleted adult surgical patients receiving total parenteral nutrition. They were maintained on constant nitrogen and caloric intake for 14 +/- 2 days. Magnesium doses ranged from 0 to 664 mg/d and were given in varying crossover patterns. In both groups, urinary magnesium excretion increased as the amount of magnesium infused increased but, at comparable magnesium infusions, depleted patients excreted significantly less magnesium. Renal conservation was most pronounced in well-nourished patients on magnesium-free intake and in depleted patients given 70 mg magnesium daily. Urinary magnesium losses were 40 +/- 5 mg/d and 33 +/- 8 mg/d, respectively, in these two groups. Endogenous fecal magnesium excretion was minimal and ranged from 2 to 38 mg/d. At each level of magnesium intake, serum levels of well-nourished patients were normal. With infusions of less than 200 mg/d, serum magnesium concentrations in depleted subjects averaged 1.6 mg/dl. Reduced urinary magnesium excretion as well as borderline serum levels measured in depleted adults suggest that the magnesium dosage should be higher than that usually recommended during total parenteral nutrition. In both groups a positive correlation between magnesium and nitrogen balance was noted.

Humans↗
PubMed1998

Intracellular and extracellular blood magnesium fractions in hemodialysis patients; is the ionized fraction a measure of magnesium excess?

To establish the best measure for determining magnesium overload, we measured ionized and total magnesium in serum and mononuclear blood cells and total magnesium in erythrocytes in blood of 23 hemodialysis patients, known for their disturbed magnesium homeostasis. When comparing the mean magnesium values obtained in the patient population with those of a control population, all of these magnesium markers, including the biologically active fractions, were significantly (P < 0.05) increased. Because serum total magnesium was not increased in all dialysis patients studied, the population was divided into two groups, according to total serum magnesium > 1.0 mmol/L or less than that. Results in these two populations showed that ionized serum magnesium and ionized magnesium in mononuclear blood cells might give a better indication about the magnesium status of the tested patients than the currently used total serum magnesium data. However, neither of the two markers, especially ionized serum magnesium, was able to discriminate fully between normal magnesium homeostasis and magnesium excess. We therefore conclude that the two ionized magnesium markers offer minimal advantage for this discrimination, and that the total magnesium concentration in serum remains the measurement of choice.

Adult↗
PubMed2000

Free and total magnesium in lymphocytes of migraine patients - effect of magnesium-rich mineral water intake.

Dietary surveys performed in Western countries show magnesium intakes lower than the recommended dietary allowances, suggesting a large prevalence of magnesium deficiency. Low brain magnesium as well as impaired magnesium metabolism have also been reported in various diseases such as migraine. To detect these deficiencies, a non-invasive and sensitive test assessing magnesium status is needed. Because magnesium is an intracellular cation, either total or ionized magnesium (Mg(2+)) of blood cells were suggested as the most adequate tests. Total magnesium levels in plasma, erythrocytes and lymphocytes and Mg(2+) in lymphocytes were analyzed in a group of 29 migraine patients and 18 control subjects. Results show significantly lower concentrations of total magnesium in erythrocytes (50.7+/-4.7 vs. 53.5+/-2.9 mg/l; P<0.01) and of Mg(2+) in lymphocytes (12.0+/-3.5 vs. 14.2+/-3.8 mg/l; P<0.05) in migraine patients as compared to controls. While a significant difference of mean values was noted between migraine patients and controls, an overlap of individual values was observed. These analyses were repeated on migraine patients before and after a 2-week intake of a mineral water containing 110 mg/l magnesium, and a significant increase in all intracellular magnesium concentrations with no effect on plasma magnesium was observed. These increased intracellular magnesium concentrations demonstrate the bioavailability of magnesium from this mineral water. Among the analyzed parameters, Mg(2+) in lymphocytes appears to be the most sensitive index of magnesium deficiency with a 15% decrease in migraine patients when compared to controls and a 16% increase after 2 weeks of a magnesium-rich mineral water intake.

Adult↗
PubMed1991

Bioavailability of potassium and magnesium, and citraturic response from potassium-magnesium citrate.

The bioavailability of potassium and magnesium, and the citraturic response were determined for the new compound, potassium-magnesium citrate, in 14 normal volunteers. Results were compared to those of potassium citrate and magnesium citrate. Each subject participated in 4 phases of study: potassium-magnesium citrate, potassium citrate, magnesium citrate and potassium chloride. After stabilization on a metabolic diet, each subject ingested a single load of a test medication followed by timed urine collections for the next 24 hours. Test loads included potassium-magnesium citrate (49 mEq. potassium, 24.5 mEq. magnesium and 73.5 mEq. citrate), potassium citrate (50 mEq.), potassium chloride (50 mEq.) and magnesium citrate (25 mEq.) Urinary potassium, magnesium and citrate were measured for each collection period. Potassium-magnesium citrate provided an equivalent potassium bioavailability as potassium citrate and potassium chloride, and a comparable magnesium bioavailability as magnesium citrate. However, it gave the highest citraturic response, since the cumulative increment in urinary citrate post-load was 129 mg. daily for potassium-magnesium citrate, 105 mg. daily for potassium citrate and 35 mg. daily for magnesium citrate. Thus, potassium-magnesium citrate gave an optimum citraturic response in addition to providing absorbable potassium and magnesium.

Adult↗
PubMed2006

Magnesium requirements: new estimations for men and women by cross-sectional statistical analyses of metabolic magnesium balance data.

BACKGROUND: Current recommendations for magnesium requirements are based on sparse balance data. OBJECTIVE: To provide new estimates of the average magnesium requirement for men and women, we pooled magnesium data from 27 different tightly controlled balance studies conducted at the US Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center, Grand Forks, ND. DESIGN: Magnesium balance data (magnesium intake - [fecal magnesium + urinary magnesium]) (664 data points) were collected from 243 subjects (women: n = 150; weight: 71.6 +/- 16.5 kg; age: 51.3 +/- 17.4 y; men: n = 93, weight: 76.3 +/- 12.5 kg; age: 28.1 +/- 8.1 y). Data from the last 6-14 d of each dietary period (> or =28 d) of each study were analyzed and were excluded if individual intakes of calcium, copper, iron, phosphorus, or zinc fell below respective estimated average requirements (EARs) or exceeded 99th percentiles of usual intakes of those elements (iron: above the upper limit) from the 1994 Continuing Survey of Food Intakes by Individuals. Daily intakes of magnesium ranged between 84 and 598 mg. The relation between magnesium intake and magnesium output was investigated by fitting random coefficient models. RESULTS: The models predicted neutral magnesium balance [defined as magnesium output (Y) equal to magnesium intake (M)] at magnesium intakes of 165 mg/d [95% prediction interval (PI): 113, 237 mg/d; Y = 19.8 + 0.880 M], 2.36 mg . kg(-1) . d(-1) (95% PI: 1.58, 3.38 mg . kg(-1) . d(-1); Y = 0.306 + 0.870 M), or 0.075 mg . kcal(-1) . d(-1) (95% PI: 0.05, 0.11 mg . kcal(-1) . d(-1); Y = 0.011 + 0.857 M). Neither age nor sex affected the relation between magnesium intake and output. CONCLUSION: The findings suggest a lower magnesium requirement for healthy men and women than estimated previously.

Adult↗
PubMed1989

Early adaptation of renal magnesium reabsorption in response to magnesium restriction.

Dietary magnesium restriction with hypomagnesia is normally associated with diminished urinary magnesium excretion. Young rats were pair fed control magnesium diets (0.05% MgSO4) and magnesium-restricted diets (less than 0.01% Mg), and tubular magnesium reabsorption was assessed to determine the importance of filtered load (plasma magnesium) and to establish the presence of cellular adaptation of magnesium transport. Urinary magnesium excretion decreased from 17.2 +/- 2.7 to 5.9 +/- 1.2% over 20 h on low-magnesium diets without a change in plasma concentration (0.61 +/- 0.02 mM). This cellular adaptation was rapid (within 5 h), specific (without effect on sodium and calcium), and sensitive (without change in plasma concentration). Micropuncture studies demonstrated that cellular adaptation occurred within the loop of Henle. After 20 h, plasma magnesium fell with an associated further decrease in fractional magnesium excretion. Accordingly, cellular adaptation of magnesium transport occurs with magnesium-deficient diets, and alterations in filtered magnesium and plasma magnesium concentration are not necessary for magnesium conservation.

Acclimatization↗