Low Magnesium Diet Research Articles

Effects of low dietary magnesium intake on development of hypertension in stroke-prone spontaneously hypertensive rats: role of reactive oxygen species.

To investigate whether low dietary Mg2+ intake influences the development of hypertension in stroke-prone spontaneously hypertensive rats (spSHRs) and whether these effects are associated with vascular functional and structural changes, and to assess the role of reactive oxygen species and the activation of vascular mitogen-activated protein (MAP) kinases in these processes. Six-week-old male spSHRs (n = 18) were divided into three groups: control (normal chow, 0.21% Mg2+ ), low Mg2+ group (Mg2+ -free diet), and high Mg2+ group (Mg2+ -rich diet, 0.75%). Systolic blood pressure (SBP) was assessed weekly for 16 weeks. In a second series of experiments, 6-week-old spSHRs (n = 18) were divided into three groups and studied weekly for 7 weeks: control group, low Mg2+ group, and low Mg2+ group receiving the superoxide dismutase mimetic, tempol (1 mmol/l). The low Mg2+ diet caused an initial decrease in SBP followed, 5 weeks later, by an exacerbated development of hypertension. This was associated with a transient reduction in the plasma concentrations of substances associated with the thiobarbituric acid reaction (markers of oxidative stress), which increased rapidly 2 weeks later. In the low Mg2+ group, acetylcholine-induced vasodilatation was decreased compared with that in controls ( P<0.05). The media : lumen ratio was greater in rats receiving a low Mg2+ diet than in those fed a high Mg2+ diet ( P<0.05). Mg2+ depletion was associated with increased vascular superoxide anion compared with that in Mg2+ -supplemented rats (1.2 0.24 compared with 0.65 0.1 nmol/min per mg). Phosphorylation of MAP kinases was increased two- to threefold in Mg2+ -deficient rats. Tempol prevented the progression of hypertension and normalized the vascular changes in rats fed a low Mg2+ diet. Chronic Mg2+ deficiency leads to development of severe hypertension, endothelial dysfunction and vascular remodelling. These processes are associated with oxidative stress and upregulation of redox-dependent MAP kinases. Tempol normalized vascular changes and attenuated the development of hypertension. Our findings suggest that reactive oxygen species play an important part in vascular processes that are associated with progression of hypertension in Mg2+ -deficient spSHRs.

Medication and Dietary Practices of Independent Living Healthy African-American Older Persons

The main objective of this study was to determine the dietary and medication practices of independent-living African-Americans aged 55 years and older. Forty-one women and 19 men completed a detailed in-home drug survey. A questionnaire was used to gather demographic information and a 3-day dietary record. Results indicate that on a daily basis 17% of the respondents were taking four prescribed medications and 7% were taking four over-the-counter medications. In addition, on a daily basis 7% of the respondents were taking five prescribed medications and 14% were taking five over-the-counter medications. Respondents with less than a high school education reported the total percentage of calories ingested from fat was 36%, at the p < 0.01 level, while respondents with a high school education or greater reported a 30% indigestion. The results also indicate a low caloric intake and a low dietary calcium, magnesium, zinc, and copper intake. Research indicates drugs often deplete these minerals.

Risk Factors for Kidney Stones in Older Women in the Southern United States

The occurrence of kidney stones is disproportionate in the southern region of the United States. Risk factors for the occurrence of kidney stones in this geographic area have not been reported previously. The Women's Health Initiative (WHI) is an ongoing multicenter clinical investigation of strategies for the prevention of common causes of morbidity and mortality among postmenopausal women. A case-control ancillary study was conducted on 27,410 (white or black) women enrolled in the 9 southern WHI clinical centers. There were 1,179 cases (4.3%) of kidney stones at the baseline evaluation. Risk factors for stone formation were assessed in cases versus age- and race-matched control subjects. Risk factors (univariate) included low dietary potassium (2,404 versus 2,500 mg/day, P = 0.006), magnesium (243 versus 253 mg/day, P = 0.003) and oxalate (330 versus 345 mg/day, P = 0.02) intake, as well as increased body mass index (28.5 versus 27.7 kg/m2, P = 0.001) and a history of hypertension (42% versus 34%, P = 0.001). A slightly lower dietary calcium intake (683 versus 711 mg/day, P = 0.04) was noted in case subjects versus control subjects, but interpretation was confounded by the study of prevalent rather than incident cases. Supplemental calcium intake >500 mg/day was inversely associated with stone occurrence. Multivariate risk factors for the occurrence of kidney stones in postmenopausal women include a history of hypertension, a low dietary intake of magnesium, and low use of calcium supplements.

Postmortem biochemical markers of experimentally induced hypomagnesaemic tetany in cattle

Severe hypomagnesaemia and tetany were induced in 10 lactating cows by feeding them semi-synthetic low magnesium diets and the animals were used to study the stability of postmortem markers of...

Postmortem biochemical markers of experimentally induced hypomagnesaemic tetany in sheep

Hypomagnesaemic tetany was induced in non-lactating and lactating ewes by feeding them semi-synthetic low magnesium diets containing additional potassium chloride and citric acid. Aqueous and vitreous humour were sampled from...

The impact of diets with different magnesium contents on magnesium and calcium in serum and tissues of the rat

The impact of three different magnesium diets (70, 1000 and 9000 ppm) on total, ionized and bound magnesium as well as ionized calcium in serum and total calcium and magnesium in femoral bone, skeletal muscle, heart and liver of male Sprague-Dawley rats was investigated. The percentage of ionized serum magnesium was unproportionally high in rats fed a low magnesium (70 ppm) diet. Femoral magnesium was correlated with ionized and total serum magnesium. In contrast, there was generally no correlation between total serum magnesium and the magnesium fractions in skeletal muscle, heart and liver. In rats fed the magnesium deficient diet, total cardiac concentration of magnesium was even significantly increased along with total calcium content, while there were no effects on total muscle and liver magnesium. Within the single groups, ionized serum calcium was never proportional to dietary magnesium, but in all three magnesium diet groups together, it was inversely correlated with dietary magnesium. Moreover, ionized serum calcium was inversely correlated with both ionized and total serum magnesium. In all 3 groups together, the concentrations of total calcium and magnesium in heart and skeletal muscle were correlated, within the single groups correlation existed only in the 1000 ppm group. Magnesium influx via calcium channels during low magnesium intake has been seen in non cardiac tissues [35,36], but nothing similar is known about non selective channels for divalent cations in the heart [33]. Thus, magnesium uptake by cardiac cells along with calcium seems to be possible, especially at low intracellular magnesium concentrations, but is still poorly investigated. We suggest that the calcium-antagonistic effect of magnesium is related to the turnover rate of magnesium rather than to its tissue concentrations.

The Interaction Between Dietary Fructose and Magnesium Adversely Affects Macromineral Homeostasis in Men

Objective: Studies with rats have found that an interaction between fructose and magnesium affects macromineral metabolism; high dietary fructose significantly increased kidney calcification in both male and female rats, particularly when dietary magnesium was low. This study tests the hypothesis that an interaction between dietary fructose and magnesium adversely affects macromineral homeostasis in men.Methods: Eleven men aged 22 to 40 years were fed a mixed, Western diet for four 42-day dietary periods in which dietary magnesium was either approximately 170 or 370 mg/day and dietary fructose was either 4% or 20% of energy. A decaffeinated beverage containing high fructose corn syrup replaced cornstarch, bread and rice in the low fructose diet to give the high fructose diet.Results: High dietary fructose significantly (p<0.01) increased magnesium balance during both low and high dietary magnesium intakes. Ultrafilterable and ionized serum magnesium also apparently were related to magnesium and fructose intakes; they were higher when fructose was fed and when Mg intakes were high. High fructose depressed calcium balance: the effect tended to be more marked when dietary Mg was low. High dietary fructose also significantly (p<0.005) decreased phosphorous balance. Urinary phosphorous losses were significantly (p<0.001) higher when high dietary fructose was fed. High dietary fructose also increased the concentration of serum alkaline phosphatase (p<0.005).Conclusion: These findings indicate that dietary fructose adversely affects macromineral homeostasis in humans and suggest further studies to see if a high fructose diet coupled with low dietary magnesium and marginal calcium leads to bone loss.

Serum and dietary magnesium and the risk for type 2 diabetes mellitus: the Atherosclerosis Risk in Communities Study.

Experimental studies in animals and cross-sectional studies in humans have suggested that low serum magnesium levels might lead to type 2 diabetes; however, this association has not been examined prospectively. We assessed the risk for type 2 diabetes associated with low serum magnesium level and low dietary magnesium intake in a cohort of nondiabetic middle-aged adults (N = 12,128) from the Atherosclerosis Risk in Communities Study during 6 years of follow-up. Fasting serum magnesium level, categorized into 6 levels, and dietary magnesium intake, categorized into quartiles, were measured at the baseline examination. Incident type 2 diabetes was defined by self-report of physician diagnosis, use of diabetic medication, fasting glucose level of at least 7.0 mmol/L (126 mg/dL), or nonfasting glucose level of at least 11.1 mmol/L (200 mg/dL). Among white participants, a graded inverse relationship between serum magnesium levels and incident type 2 diabetes was observed. From the highest to the lowest serum magnesium levels, there was an approximate 2-fold increase in incidence rate (11.1, 12.2, 13.6, 12.8, 15.8, and 22.8 per 1000 person-years; P = .001). This graded association remained significant after simultaneous adjustment for potential confounders, including diuretic use. Compared with individuals with serum magnesium levels of 0.95 mmol/L (1.90 mEq/L) or greater, the adjusted relative odds of incident type 2 diabetes rose progressively across the following lower magnesium categories: 1.13 (95% CI, 0.79-1.61), 1.20 (95% CI, 0.86-1.68), 1.11 (95% CI, 0.80-1.56), 1.24 (95% CI, 0.86-1.78), and 1.76 (95% CI, 1.18-2.61) (for trend, P = .01). In contrast, little or no association was observed in black participants. No association was detected between dietary magnesium intake and the risk for incident type 2 diabetes in black or white participants. Among white participants, low serum magnesium level is a strong, independent predictor of incident type 2 diabetes. That low dietary magnesium intake does not confer risk for type 2 diabetes implies that compartmentalization and renal handling of magnesium may be important in the relationship between low serum magnesium levels and the risk for type 2 diabetes.

Low dietary magnesium is associated with insulin resistance in a sample of young, nondiabetic black Americans

In both humans and experimental animals, dietary induced magnesium deficiency is correlated with insulin resistance. The purpose of this study was to determine whether dietary magnesium intake is associated with insulin sensitivity or blood pressure in a sample of nondiabetic, young adult black Americans. We also examined dietary calcium, potassium, and sodium intake. The study was conducted on a sample (n = 179) of young adults aged 30 ± 3.4 years who had been followed longitudinally. Nutrient intake was assessed by obtaining a 24-h recall interview of dietary intake. Intake data were entered in a nutrient analysis program (Nutritionist III), which quantitated micronutrients, macronutrients, and minerals. We classified the sample into insulin-sensitive (IS) and insulin-resistant (IR) groups, according to insulin-stimulated glucose use (M) measured during insulin clamp. M correlated positively with magnesium intake in mg/kg of fat-free mass (r = 0.15, P < .05 overall; in men, r = 0.25, P < .02). There was a significant negative correlation of total dietary magnesium intake with the sum of insulin levels measured during an oral glucose tolerance test (OGTT) (r = −0.13, P < .05). When corrected for body fat, in men there was also a significant correlation of dietary magnesium intake, measured in mg/kg of fat-free mass, with the sum of insulin concentrations on the OGTT (r = −0.22, P < .05). When cases were categorically classified as IS versus IR, magnesium intake in mg/kg of fat-free mass was lower in IR (2.97 ± 1.4) than in IS (3.68 ± 2.2; P = .022). These results suggest a possible role for dietary magnesium in insulin resistance.

The bioavailability of magnesium from Wakame (Undaria pinnatifida) and Hijiki (Hijikia fusiforme) and the effect of alginic acid on magnesium utilization of rats.

The bioavailability of magnesium from Wakame and Hijiki, and the effects of alginic acid on absorption of dietary magnesium were examined in five groups of rats fed either control, Wakame, Hijiki, AW (containing the same amount of alginate as in the Wakame) and AH (containing the same amount of alginate as in the Hijiki) diets, and animals fed a low magnesium diet (LMg) (twentieth amount of magnesium in the original mineral mixtures as the control). Food intake and body weight gain were decreased by adding sodium alginate to the diets. A large amount of calcium accumulated only in the kidneys of the rats fed the LMg diet. Serum magnesium concentration decreased only in the LMg group. The magnesium content in the defatted left femurs did not differ between the control and Wakame fed animals and also among the animals eating Wakame, Hijiki and AW diets. The breaking force of the right femurs did not differ among all the groups except the LMg group. The ratio of apparent magnesium absorption (%) of the control, LMg, Wakame, Hijiki, AW and AH groups was 82.2, 72.7, 66.9, 50.8, 69.3 and 54.2 in the first experimental period, and was 75.3, 52.1, 57.7, 46.9, 62.6 and 60.5 in the second experimental period, respectively. It was clear that the bioavailability of magnesium in the Wakame fed rats was higher than in those eating the Hijiki. Large amounts of sodium alginate lowered magnesium absorption from the diet.

The influence of dietary phosphorus and magnesium concentrations on the calcium content of heart and kidneys of DBA/2 and NMRI mice.

Dystrophic cardiac calcification (DCC) is often found in DBA/2 mice, reportedly in association with low plasma magnesium levels in this mouse strain. It was hypothesized that high-phosphorus diets and low-magnesium diets that are known to lower plasma magnesium concentrations would promote the development of DCC. DBA/2 mice were fed diets with either low-magnesium (0.02%, w/w) or high-phosphorus (0.8%) concentrations or a combination of the two variables. NMRI mice were given either a low- (0.2%) or high- (0.6%) phosphorus diet. Female, but not male, NMRI mice accumulated calcium in the heart when fed the high-phosphorus diet; neither gender developed kidney calcification. DBA/2 mice with either a low-magnesium or a high-phosphorus intake developed marked cardiac calcifications. The combination of low-magnesium and high-phosphorus intake caused severe calcification of the heart, kidney and tongue. Increasing the dietary magnesium content (0.08%) and reducing phosphorus (0.2%) did not fully prevent cardiac calcification, but reduced heart calcium concentrations in male DBA/2 mice. It is concluded that diets for DCC-susceptible mice should contain adequate amounts of magnesium and low, but sufficient amounts of phosphorus in order not to additionally stimulate cardiac calcification.

Dietary magnesium improves endothelial dependent relaxation of balloon injured arteries in rats

The purpose of the present study was to examine the importance of magnesium in endothelial function after arterial balloon injury. Male Wistar rats were fed normal, high or low concentrations of magnesium. Three weeks later the animals underwent endothelial injury of the thoracic aorta by a balloon catheter or a sham operation. Biochemical, histological and endothelial function analysis were performed 15 days after the surgical treatment. The animals fed a low magnesium diet presented the lowest level of serum magnesium and the highest ionized blood calcium levels. Histomorphometric analysis revealed no differences among groups neither regarding the magnitude of intimal thickening nor the recovery of endothelial coverage. However, when vasoreactivity responses were compared in the balloon-injured group, those animals fed a high magnesium diet had the better endothelium-dependent vascular relaxation. In conclusion, a higher magnesium level in the diet was beneficial to vessels that underwent endothelial injury by balloon catheter.

Magnesium transport in freshwater teleosts

The magnesium handling of freshwater teleost fish is discussed, with an emphasis on the role of branchial, intestinal and renal transport. In response to the eminent threat of constant diffusive losses of minerals such as magnesium, freshwater fish have developed efficient mechanisms for magnesium homeostasis. Magnesium losses are overcome by the uptake of magnesium from the food, making the intestine an important route for magnesium uptake. Some evidence suggests that intestinal magnesium uptake in fish is a regulated, cellular process. The ambient water is an additional magnesium source for fish, implicating the gills as a secondary route for magnesium uptake. Certainly, in some species, direct uptake from the water, probably via branchial routes, ameliorates the effects of a low-magnesium diet. The hard tissues, representing over 50 % of the total body magnesium pool, form a reservoir from which magnesium can be recruited to perform its functions in the cellular metabolism of soft tissues such as muscle. In fish, as in terrestrial vertebrates, the balance of a variety of elements becomes disturbed when the magnesium homeostasis of the soft tissues is disrupted. However, fish appear to be less sensitive than terrestrial vertebrates to these perturbations. Magnesium is reabsorbed in the kidneys to minimise losses. For renal cells, part of a cellular pathway has been elucidated that would allow absorptive magnesium transport (a magnesium conductive pathway in renal brush-border membranes). In some euryhaline teleosts, the kidneys appear to switch instantaneously to rapid magnesium secretion upon magnesium loading, a response common to marine fish that are threatened by diffusive magnesium entry. This enigmatic mechanism underlies the capacity of some euryhaline species to acclimate rapidly to sea water. Despite the progress made over the last decade, much of the cellular and molecular basis of magnesium transport in the gills, intestine and kidneys remains obscure. The application of fluorescent, radioactive and molecular probes, some of which have only recently become available, may yield rapid progress in the field of magnesium research.

Dietary Magnesium Supplementation Ameliorates Anemia in a Mouse Model of β-Thalassemia

AbstractTo ascertain the quantitative effect on the disease β-thalassemia of a low-magnesium (Mg) diet compared with a high-Mg diet and a standard-Mg diet, we studied the effect these diets had over a 4-week period on β-thalassemic (β thal) mice compared with normal C57BL/6 mice used as controls. The low-Mg diet consisted of 6 ± 2 mg Mg/kg body weight/d, the high-Mg diet 1,000 ± 20 mg Mg/kg body weight/d, and the standard-Mg diet 400 ± 20 mg Mg/kg body weight/d. β thal mice that were fed the low-Mg diet became more anemic, had reduced serum and erythrocyte Mg, and had decreased erythrocyte K. Their K-Cl cotransport increased, followed by commensurate cell dehydration. The high-Mg group showed a significant improvement of the anemia, increased serum and erythrocyte Mg, increased erythrocyte Mg, increased erythrocyte K, reduced K-Cl cotransport, and diminished cell dehydration. C57BL/6 control mice that received the low-Mg diet experienced anemia with erythrocyte dehydration, whereas the high-Mg diet had little effect on the hematologic parameters. β thal and C57BL/6 control mice that were fed a standard diet showed no changes. These results indicate that dietary Mg supplementation corrects hypomagnesemia and improves anemia in murine β thal and should be assessed in human β-thalassemia.

Dietary Magnesium Supplementation Ameliorates Anemia in a Mouse Model of β-Thalassemia

To ascertain the quantitative effect on the disease β-thalassemia of a low-magnesium (Mg) diet compared with a high-Mg diet and a standard-Mg diet, we studied the effect these diets had over a 4-week period on β-thalassemic (β thal) mice compared with normal C57BL/6 mice used as controls. The low-Mg diet consisted of 6 ± 2 mg Mg/kg body weight/d, the high-Mg diet 1,000 ± 20 mg Mg/kg body weight/d, and the standard-Mg diet 400 ± 20 mg Mg/kg body weight/d. β thal mice that were fed the low-Mg diet became more anemic, had reduced serum and erythrocyte Mg, and had decreased erythrocyte K. Their K-Cl cotransport increased, followed by commensurate cell dehydration. The high-Mg group showed a significant improvement of the anemia, increased serum and erythrocyte Mg, increased erythrocyte Mg, increased erythrocyte K, reduced K-Cl cotransport, and diminished cell dehydration. C57BL/6 control mice that received the low-Mg diet experienced anemia with erythrocyte dehydration, whereas the high-Mg diet had little effect on the hematologic parameters. β thal and C57BL/6 control mice that were fed a standard diet showed no changes. These results indicate that dietary Mg supplementation corrects hypomagnesemia and improves anemia in murine β thal and should be assessed in human β-thalassemia.

Toxic and essential metal interactions.

Cadmium, lead, mercury, and aluminum are toxic metals that may interact metabolically with nutritionally essential metals. Iron deficiency increases absorption of cadmium, lead, and aluminum. Lead interacts with calcium in the nervous system to impair cognitive development. Cadmium and aluminum interact with calcium in the skeletal system to produce osteodystrophies. Lead replaces zinc on heme enzymes and cadmium replaces zinc on metallothionein. Selenium protects from mercury and methylmercury toxicity. Aluminum interacts with calcium in bone and kidneys, resulting in aluminum osteodystrophy. Calcium deficiency along with low dietary magnesium may contribute to aluminum-induced degenerative nervous disease.

Mg 2+ modulates membrane lipids in vascular smooth muscle: a link to atherogenesis

Epidemiological studies associate low dietary magnesium intake with an increased incidence of ischemic heart disease and sudden cardiac death. We have used proton-magnetic resonance ( 1H-NMR) techniques and Mg 2+-selective electrodes to monitor changes in lipid extracts of aortic and cerebrovascular smooth muscle as extracellular ionized magnesium ion concentration ([Mg 2+] o) is lowered. We have found that, within the pathophysiological range of Mg 2+ concentrations, fatty acid chain length and double bond content are progressively reduced as [Mg 2+] o is lowered. In contrast, the plasmalogen content is progressively increased. A concomitant decrease in fatty acid chain length and double bonds indicates oxidation of double bonds resulting in truncation of the fatty acids. A decrease in lipid oxidation in the presence of elevated Mg 2+ could contribute to the apparent protective role of increased Mg 2+ intake on vascular function in humans.

L33 Low dietary magnesium is associated with insulin resistance in a sample of young, non-diabetic, African Americans

L33 Low dietary magnesium is associated with insulin resistance in a sample of young, non-diabetic, African Americans

Effect of Low Dietary Magnesium on Immune Response and Osmoregulation of Atlantic Salmon

Abstract The influences of dietary magnesium on immune response and on osmoregulation in parr of Atlantic salmon Salmo salar were determined. Groups of fish were fed a casein–gelatin diet unsupplemented (containing about 200 mg Mg/kg) or supplemented with either 300 or 500 mg Mg/kg dry diet (as MgSO4) for 12 weeks before vaccination to produce fish with different Mg levels, and the feeding regime was continued throughout the study. No differences were observed between the treatment groups in serum-specific antibody levels every second week for 8 weeks after vaccination against Vibrio anguillarum serotypes O1 and O2. Both lysozyme levels and spontaneous hemolytic activities in serum were elevated in vaccinated fish compared with unvaccinated fish. Neither lysozyme activity, complement hemolytic activity, total protein in serum nor blood hemoglobin were affected by dietary Mg. The spontaneous hemolytic activity in serum was lower in fish fed the unsupplemented diet and highest in fish fed the diet supplemen...

Effects of dietary fluoride and magnesium supplements on cyclic adenosine monophosphate (cAMP), calcium and magnesium levels in aorta of genetically hypercholesterolaemic RICO rats

Previous observations have suggested that low intakes of fluoride prevent pathological calcifications of internal organs, including the aortic wall, in experimental animals, fed a basically low magnesium diet. Our group found recently that fluoride has some potentially preventive effect against atherosclerotic serum lipid profiles in genetically hypercholesterolaemic rats. To study whether the apparently positive potential of fluoride against atherosclerosis is also reflected in aortic tissue, through its well known activation of adenylate cyclase, the aortic cAMP content of the rats used in our recent study was determined. Out of a total of 56 male RICO rats, mean weight 160 g, the control group C was fed an adequate diet, with 44% sucrose, a magnesium content of 883 p.p.m. and with 0.5% cholesterol. Group D had the same diet as group C except that the magnesium content was reduced to 200 p.p.m. Group E had the same diet as group D but with the fluoride content elevated from 1.9 to 12 p.p.m. Group G had the same diet as group E but with the magnesium content elevated from 200 to 300 p.p.m. After a feeding period of 6 weeks, the aortas of the animals were removed, cleaned and kept at -70°C until analysed. The mean cAMP content of the aortas, measured by radioimmunoassay, in groups C, D, E and G was 439, 546, 681, and 1394 μmol mg-1 protein, respectively. In group G only, the cAMP content was significantly higher than that of the other groups (p<0.001). The mean calcium and magnesium contents of the aortas of different groups did not significantly differ from each other. Thus in RICO rats, fed a high-sugar low-magnesium diet with cholesterol, supplementation of the diet with a small amount of fluoride elevates the cAMP content of the aorta, provided that the intake of Mg is not very low.