Category: Health

Bone health and magnesium

Bone health and magnesium

Magnesium deficiency and vitamin D deficiency Hyperglycemia and kidney disease worsen Bone health and magnesium. In addition to hypomagnesemia, signs magnesiium Bone health and magnesium magnesium deficiency included hypocalcemia, low serum potassium concentrations hypokalemianagnesium of sodiumlow circulating PTH concentrations, neurological and muscular symptoms tremormuscle spasms, tetanyloss of appetite, nausea, vomiting, and personality changes 3. Magnesium is involved in many physiologic pathways, including energy production, nucleic acid and protein synthesision transport, cell signalingand also has structural functions. Vitamin A RE e. Bone health and magnesium

Bone health and magnesium -

Vitamin D is one of the few vitamins that human beings can synthesize themselves. Thus, its name "vitamin" is not fully applicable because it is actually a prohormone. Still the name "vitamin D" was kept due to historical reasons. Vitamin D is activated through sunlight — to be more precise, UV-B radiation — on the skin.

Vitamin D3 is synthesized from dehydrocholesterol. From the blood, it reaches the liver, where it is converted to its storage form. A healthy Central European adult who walks daily for approx.

After about 30 minutes, approx. The body then virtually stops the synthesis to rule out an overdose caused by excessive sunlight. Unneeded vitamin D can be stored in fatty tissue, to be retrieved and activated in the winter months when the sun cannot send us enough UV-B radiation to synthesize new vitamin D.

Therefore, it is important to refuel enough sunshine in the summer so we have a sufficient supply of vitamin D! In order that the body itself can synthesize vitamin D, enough naked skin needs to be exposed to the sun to start synthesizing it. Too many clothes and sunscreen with high sun protection factor can interfere with vitamin D synthesis because they prevent UV-B radiation from reaching the skin.

Then, should we apply less sunscreen? This is a real dilemma in times when there are more justified warnings about the danger of skin cancer. In Central Europe, the angle of incidence of sun rays is too flat, so the needed UV-B radiation cannot even reach us.

North of the 42nd parallel i. the approximate location of Barcelona or Boston , this is the November to February time period; north of the 52nd parallel i. north of Berlin or Edmonton , this is even from October to March. Persons with darker skin have more difficulties to synthesize enough vitamin D 3 than lighter-skinned ones — the darker the skin color, the slower vitamin D synthesis takes place.

To compensate for this, darker skin is better protected from the damaging effects of sunlight, thus allowing sunbathing a little longer without risking sunburn. The solution for this dilemma lies, as always, in the middle: Sun on naked skin is OK — but if you intend to spend several hours outdoors right away, then never forget to apply sunscreen!

Do not expose yourself to the sun too long and only according to your skin type. Luckily, vitamin D 3 can be absorbed from foods — albeit to a limited extent. You may remember the daily spoonful of cod liver oil that to your frustration was given to you as a child in the s.

Vitamin D3 is especially abundant in fatty fish and marine creatures, but is also found in eggs and dairy products. The elderly need more vitamin D due to the higher risk for osteoporosis.

They are often less mobile, something that can shorten outdoor stays. In addition, production in the skin falls considerably with advanced age. Nutritionally speaking, the elderly also have a harder time to satisfy their need for vitamin D or even to compensate for a multiple need.

To counteract vitamin D deficiency, it can be an especially good idea to take vitamin D supplements. Magnesium is known above all for its function in our muscles. All our muscles need magnesium so they can relax again after physical stress.

Therefore, magnesium deficiency quickly manifests itself in nightly calf cramps and arrhythmia — because the heart is as well "only" a muscle. In women's health, it also plays an important role owing to its antispasmodic effect.

Magnesium can be stored in our body; however, not in our fat reservoirs as is the case with vitamin D, but in our bones and teeth. The remaining magnesium is distributed in the muscles and soft tissue, where it is bound, for example, to ATP adenosine triphosphate, the fuel of our cells to perform its tasks.

In the bones the stored magnesium is not passive, but contributes to bone stabilization and to bone growth and mineralization. If there is a lack of it, important functions can no longer be carried out and diseases like osteoporosis can worsen.

Both minerals are therefore important for bone cells. Thus, calcium and magnesium should logically be provided to the body in sufficient quantities both with the daily diet and with beverages like mineral water.

If a deficiency has already been detected; it should be treated with suitable medications. Last but not least, magnesium also plays an important role in vitamin D activation. Vitamin D — or to be more precise — calcitriol in turn regulates calcium and magnesium resorption in the small intestine.

Because of that, both biofactors directly and crucially influence their absorption from foods. Since there is relatively little magnesium in the average Western European diet, a slight magnesium deficiency is quite common. Many other factors of our everyday life make us use up more magnesium or excrete it more than usual.

When exercising, for example, increased muscle function consumes magnesium, which is also excreted with the sweat. Persons with chronic diseases such as diabetes also excrete more magnesium. Depending on age and gender, healthy individuals should take between mg and mg of magnesium, as recommended by the German Nutrition Society.

Those who belong to a risk group or have a higher need owing to medications should consult with their physician before taking more magnesium to prevent a deficiency. Magnesium sources include grains, nuts and sprouts. Examples are the South American crops quinoa and amaranth, as well as pumpkin and sunflower seeds, sesame and almonds.

Seaweed and naturally some mineral waters contain magnesium. Thus, when buying mineral water, in addition to the calcium content, pay attention to the magnesium content per liter so you can easily satisfy your magnesium needs.

Good news for chocoholics: g of cocoa powder contains mg of magnesium. Therefore, eat a little dark chocolate frequently for the benefit of your bones, as bittersweet chocolate still contains about mg of magnesium, depending on cocoa content.

Vegetarians are better off than meat eaters — at least if they like to eat tofu. Soy products have a magnesium content of approx. When thinking about the subject of osteoporosis, don't just think of your bones and the necessary calcium — the complex processes in our body need more than that for functioning well.

Trends for a positive Mg effect were evident in the pre- and early puberty and in mid-late puberty. Lumbar spinal BMC accrual was slightly but not significantly greater in the Mg-treated group. Serum mineral levels, calciotropic hormones, and bone markers were similar between groups.

Conclusions: Oral Mg oxide capsules are safe and well tolerated. A positive effect of Mg supplementation on integrated hip BMC was evident in this small cohort.

DIETARY INTAKE, PHYSICAL activity, and genetic factors have been described as potential determinants of osteoporosis in later life 1 — 6. The dependence of bone mass throughout adulthood upon the attainment of bone mass in late adolescence is not well studied.

Nevertheless, the establishment of optimal nutrition during growing years is a targeted strategy for decreasing the incidence of osteoporosis in future decades.

Whereas several studies have concentrated on the importance of calcium nutrition on the skeleton in children 7 — 11 , only limited investigations of magnesium Mg nutrition have been undertaken in this regard. Mg is an important component of the mineral phase of bone 12 — Approximately one half of total body Mg is in bone, adsorbed to the hydroxyapatite surface 15 , Mg plays a central role in mineral homeostasis, regulating PTH secretion and action 17 , 18 and vitamin D activation Mg interacts with the extracellular calcium-sensing receptor on parathyroid and renal tubular cells, providing one direct mechanism by which Mg affects organs essential to mineral homeostasis Nutritional monitoring programs have consistently demonstrated inadequate dietary Mg intake in young American women.

Limited human intervention studies indicate decreased bone turnover 23 , and improved bone mass with Mg supplementation in targeted groups of adults 24 , Furthermore, Mg deprivation in rats during rapid bone growth directly contributes to an osteoporotic phenotype Impaired bone growth with decreased osteoblasts, increased osteoclasts, and loss of trabecular bone occurs in Mg-deprived mice We therefore hypothesized that Mg undernutrition may contribute to suboptimal attainment of bone mass during adolescence, and we designed a pilot study to address this issue.

Our Mg supplementation regimen was well tolerated with optimal compliance, and resulted in a favorable incremental gain of bone mineral content BMC at the hip in premenarchal girls. We designed this study to determine whether oral Mg supplementation was safe and acceptable to adolescents.

Identification of effect size and determination of compliance with Mg supplements were primary objectives.

We directed the study toward 8- to yr-old girls because of the coincident rapid bone accretion and relative Mg undernutrition. Subjects were recruited from local pediatricians. Parents were informed of the purpose of the study and dietary Mg status after screening. The study was a randomized, placebo-controlled, double-blind, year-long interventional trial of magnesium oxide compared with placebo.

Tests were performed in the Clinical Research Centers at Yale University School of Medicine. The study protocol was approved by the Yale Human Investigation Committee. After baseline evaluation, subjects were evaluated at 1, 6, and 12 months after initiating supplementation.

Subjects were contacted at 1- to 2-month intervals to assess safety and compliance. If any untoward events occurred during the study, subjects were instructed to contact the study coordinator. After initial contact of eligible subjects by pediatricians via office posting or letter, we explained the project in detail by telephone.

The eligible study population consisted of premenarchal healthy Caucasian adolescent females, aged 8—14 yr. A registered dietitian interviewed the parent and child to obtain dietary details.

Those participating underwent physical examination by a research nurse trained in pediatric endocrinology. Tanner stage of breast development was recorded. Inclusion criteria were as follows: Caucasian ethnicity, a ratio of weight-to-height between the third and 97th centiles, and the absence of bone disease.

Exclusion criteria were as follows: scoliosis, onset of menses, use of chronic medications retinoids, thyroid hormone, GH, glucocorticoids, oral contraceptives, anticonvulsants, diuretics, or supplements providing pharmacological dosages of vitamins A or D. Subjects were randomized in blocks of four to receive either Mg oxide or placebo ratio , using a random number table.

Study personnel and subjects were blinded to treatment. Mg was supplemented twice daily in a capsule containing powdered magnesium oxide mg of elemental Mg per day. Identically appearing encapsulated methylcellulose powder served as placebo. Capsules were provided in calendar-coded cards with two capsules in each sealed blister.

One- to 3-month supplies were distributed throughout the study. Monthly telephone contact by the study coordinator assessed safety and encouraged compliance. At entry and after 6 and 12 months of supplementation, densitometric measures of the lumbar spine and hip were performed.

BMC was chosen as the primary skeletal outcome variable because it is a direct measure and is not confounded by changes in bone area that occur during growth. Height and weight were recorded, and a complete biochemical profile was obtained at these times and additionally after 1 month of supplementation, as shown in Tables 1 and 5.

Follow-up visits and blood sampling generally occurred in the mid-afternoon as to not interrupt school schedules. To convert to SI units, multiply calcium value by 0. BUN, Blood urea nitrogen.

Biochemistry values through the course of Mg supplementation mean ± sd. Anterio-posterior scans of the lumbar spine were obtained and were analyzed using pediatric software Legacy Low Density Spine-revision C; Hologic.

All scans were performed by one of two technicians with experience in performing bone densitometry in children. All scans were reviewed to ensure comparable definition of regions of the hip for serial scans within the same subject.

A questionnaire on general food preferences was used to estimate daily Mg intake. Instructions for completing the food record were provided in a face-to-face meeting using food models, and printed descriptions of portion sizes.

Subjects were asked to record brand names of consumed foods, estimate portion sizes using household measurements, and describe food preparation. Subjects were asked to record their intake over two weekdays and one weekend day.

The completed record was reviewed by the registered dietitian, and any incomplete information was clarified by telephone contact. A second 3-d food record was completed by participants midway through the study to assess consistency of intake.

Nutrient analysis was performed by a registered research dietitian using the Food Processor Program ESHA Research, Inc. Statistical analyses for BMC and bone mineral density BMD were performed in SAS version 8.

A P value of 0. The primary objective of the analysis was to evaluate the magnitude and variability of the incremental BMC changes in the treatment group compared with the placebo group after 12 months of treatment. The secondary objectives were to assess trends in BMC and BMD as related to treatment for each maturity group and for each skeletal site examined.

Maturity groups consisted of a prepubertal-early pubertal group Tanner stage 1 or 2 at enrollment and a mid-late pubertal group Tanner stage 3 or 4 at enrollment. In the model, the incremental BMC change from baseline to 12 months was the outcome variable.

The treatment which has two levels and maturity group which has two levels served as fixed effects, and baseline BMC served as a covariate to adjust the baseline effect. Within-subject covariance was adjusted by an unstructured variance-covariance pattern matrix. In addition to the factors and covariates described above, we also tested the following interactions: treatment by maturity group, treatment by location, and treatment by baseline BMC or BMD.

All interactions were tested at the 0. If none of the interactions was significant, the absolute difference of increase between baseline and the month parameters for treatment and placebo groups was tested by the above-described ANCOVA model in an overall analysis.

Least squares means and se values of BMC and BMD increases were calculated in the model and were plotted for each treatment group as a whole as well as for each Tanner group.

If a significant treatment and maturity group interaction was found, we applied the same model for each maturity group to assess the treatment effect. Lumbar spine changes were of a markedly different magnitude and were therefore analyzed separately, using similar methodology.

Biochemical data were analyzed using analysis of covariance, employing SAS. Treatment comparisons of these parameters over the time frame of the study were made using a model that accounts for dependence of observations obtained from the same patient by modeling the correlation structure.

Treatment, time, the interaction between treatment and time, and baseline levels of the outcome were included in the model as fixed effects. A secondary subgroup analysis was performed examining the effects of treatment and time of therapy with pubertal staging.

Where appropriate, result of biochemical data are expressed as least squares means. A one-sided significance level of 0.

placebo groups, unless otherwise stated. A total of subjects were screened, 50 subjects enrolled, and 44 completed the study. Reasons given for withdrawal included moving away, excessive time commitment, and difficulty with compliance with treatment.

Anthropomorphic measures, average dietary intake, biochemical variables Table 1 , and bone mass measures were not different between treatment groups at enrollment Table 2. Measures of bone mass were comparable at baseline between the placebo and Mg-treated groups.

placebo-treated girls, respectively; Fig. The least square means calculated for both the less mature Tanner 1 and 2 group 0. BMC at each location showed the same treatment trend favoring Mg supplementation as found with the overall combined hip data, although no individual site reached the 0.

Although the Mg-supplemented group had a slightly greater mean incremental gain in spinal BMC, these differences were not statistically significant data not shown.

A, Net change in BMC during the year of the study, over all hip locations measured, expressed in grams. The least square mean of the change in BMC is represented for subjects receiving Mg by the hatched bars , and for subjects receiving placebo by the solid gray bars.

Data for the entire cohort is shown in the pair of bars on the right , and by Tanner grouping in the first and second pairs. Subgroup analysis by maturity rating confirmed that the direction of the effect on BMC with Mg treatment was evident in both less and more mature girls. B, Net change in BMC during the year of the study by specific anatomical sites.

As described above, data are presented as least square means, and subjects receiving Mg are represented by the hatched bars , and subjects receiving placebo by the dark gray bars.

The difference in incremental gain in BMC at each site favored the Mg-supplemented group, although a statistically significant difference could not be shown when each site was analyzed separately. BMD was examined using the same methods as performed for BMC.

Similar results were seen when analyzing BMD corrected for height and BMD corrected for BMI data not shown. The incremental gain in spinal BMD, as with BMC, was also slightly, but not significantly, greater in the Mg-supplemented group compared with the placebo group.

Biochemical parameters at 1, 6, and 12 months of therapy are listed in Table 5. No significant effects of Mg supplementation on any of these parameters were evident, except FEMg see Safety and compliance , which was consistently greater during Mg supplementation. A trend toward a greater decrement in urinary excretion of N-telopeptide of type 1 collagen was present at 1 month, suggesting an acute effect of Mg on decreasing bone resorption; however, the absolute excretion of this marker was not different at this or other time points.

Only two subjects reported side effects; both developed loose bowel movements upon starting supplementation. This resolved upon halving the treatment dose with resumption of full dose after 7 d. In three subjects after 6 months of supplementation, we examined intracellular free Mg content of the gastrocnemius muscle, as determined by 31 P-nuclear magnetic resonance spectroscopy, adapting the methods of Ryschon et al.

This methodology uses the chemical shift of ATP peaks in the setting of variable concentrations of intracellular Mg. No differences were evident between Mg-treated or placebo treated subjects data not shown. This study provides data supporting the hypothesis that Mg supplementation has positive effects on accrual of bone mass in adolescents with suboptimal Mg intake.

The incremental gain in overall hip BMC in subjects receiving Mg was significantly greater than in placebo-supplemented subjects. Subgroup analysis of these effects as stratified by maturity Tanner pubertal stage 1 and 2 girls as a contrast to Tanner stage 3 and 4 girls was performed, demonstrating that changes favoring Mg supplementation held for each maturity group although the effects in either group alone did not reach statistical significance.

The skeletal effects occurred with no major changes in mineral levels or markers of bone turnover. Finally, the Mg-supplemented group had slightly higher but not statistically significant incremental gain in spinal BMC and BMD than the placebo group.

Daily supplementation of mg of Mg given as two divided doses of encapsulated Mg oxide was safe and well tolerated and met with reasonable compliance. There was no significant difference in weight gain between placebo and Mg-supplemented groups.

Previously correlations of dietary Mg intake with BMD have been demonstrated 31 — Spinal BMD varied with quartile of Mg intake in premenopausal Scottish women 34 ; Mg intake in early adolescence correlates with calcaneal bone mass in young adulthood 35 , suggesting a role for Mg in bone mineral accretion in early adolescence.

Our examination of NHANES data demonstrated an association of dietary Mg and hip BMD in selected groups e. younger non-Hispanic white men Interventional studies examining Mg effects on bone are limited.

A placebo-controlled study of patients with gluten-sensitive enteropathy demonstrated increased BMD after 6 months of Mg supplementation, compared with placebo-supplemented subjects Thus, Mg intervention studies to date have demonstrated positive effects on bone mass, although they have been performed in older populations with underlying illness and not in a healthy young population.

Thus, Mg supplementation may be an important consideration in the periadolescent group, given the suboptimal dietary Mg intake documented in U. food surveys 21 , 22 , We reasoned that early adolescence is an important time to affect Mg intake and therefore designed a pilot study to determine the effects of Mg supplementation in this group.

We included only Caucasian females as to limit variance in bone mass explained by gender and race. We enrolled subjects with Mg intake in the lower half of the screened subjects to select for those most likely to respond to the intervention.

A primary limitation to this study is its small size. We did not have sufficient preliminary data to predict true sample size requirements and did not have sufficient statistical power to detect changes in solitary anatomical sites.

The data should not be overinterpreted given the marginal significance of the differences. However, we suggest that more robust findings would have been possible with a larger study, because the trends favoring Mg supplementation are consistent across all pubertal groups and all anatomical sites studied.

In summary, we have successfully carried out a pilot study demonstrating a positive effect of Mg supplementation for 12 months on accrual of bone mass in peripubertal Caucasian girls selected for suboptimal daily Mg intake.

The supplement was well tolerated and safe. This study will serve as a model for designing future studies on skeletal effects of Mg in children.

We thank Dr. Cynthia Brandt for her assistance with data management and are grateful for the assistance in recruitment provided by the following pediatricians in the New Haven area: Drs.

Jonathan Harwin, Alan Meyers, Dawn Torres, Linda Waldman, Richard Whelan, Joseph Avni-Singer, Deborah Ferholt, Craig Summers, Craig Keanna, Doug McGregor, Laurie Glassman, Kirstin Baker, Mary Porter, Fred Anderson, Anne Hoefer, Robert Nolfo, Nancy Czarkowski, Christopher Canny, Richard Halperin, Lucille Semeraro, Kathleen Fearn, Margaret Dilloway, Dennis Durante, Frank Gruskay, Jeffrey Gruskay, Harry Kipperman, Roberta Lockhart, Howard Sadinsky, Michael Barron, Margaret Ikeda, Robert Dorr, Raymond Seligson, Luis Alonso, Joseph Zelson, James Morgan, Marie Robert, Elizabeth Weisner, Ron Angoff, Nancy Brown, Carol Dorfman, Greg Germain, Elsa Stone, Sidney Spiesel, Christine Butler, Cynthia Mann, Robert Anderson, Liesel Gould, Kenneth Burke, Christopher Goff, Nicholas Condulis, and Michelle DiLorenzo.

from the Patrick and Catherine Weldon Donaghue Medical Research Foundation, NIH Award KHD to T. Wasnich RD Epidemiology of osteoporosis.

In: Favus MJ , ed. Primer on the metabolic bone diseases and disorders of mineral metabolism. Philadelphia-New York : Lippincott-Raven Publishers ; Melton III LJ Epidemiology of vertebral fractures in women. Am J Epidemiol : — Google Scholar.

Zanchetta JR , Plotkin H , Filgueira MLA Bone mass in children: normative values for the 2—year-old population. Bone 16 : S — S. Matkovic V , Jelic T , Wardlaw GM , Ilich JZ , Goel PK , Wright JK , Andon MB , Smith KT , Heaney RP Timing of peak bone mass in Caucasian females and its implication for the prevention of osteoporosis.

J Clin Invest 93 : — Ettinger B , Sidney S , Cummings SR , Libanati C , Bikle DD , Tekawa IS , Tolan K , Steiger P Racial differences in bone density between young adult black and white subjects persist after adjustment for anthropometric, lifestyle, and biochemical differences.

J Clin Endocrinol Metab 82 : — Marcus R Physical activity and regulation of bone mass. Bonjour J-P , Carrie A-L , Ferrari S , Clavien H , Stosman D , Theintz G , Rizzoli R Calcium-enriched foods and bone mass growth in prepubertal girls: a randomized, double-blind, placebo-controlled trial.

J Clin Invest 99 : — Johnston CC , Miller JZ , Slemenda CW , Reister TK , Hui S , Christian JC , Peacock M Calcium supplementation and increase in bone mineral density in children. Lloyd T , Andon MB , Rollings N , Martel JK , Landis JR , Demers LM , Eggli DF , Kieselhorst K , Kulin HE Calcium supplementation and bone mineral density in adolescent girls.

JAMA : — Lee WTK , Leung SSF , Wang SH , Xu YC , Zeng WP , Lau J , Oppenheimer SJ , Cheng JC Double-blind, controlled calcium supplementation and bone mineral accretion in children accustomed to a low-calcium diet.

Am J Clin Nutr 60 : — Lee WTK , Leung SSF , Leung DMY , Tsang HSY , Lau J , Cheng JCY A randomized double-blind controlled calcium supplementation trial, and bone and height acquisition in children.

Br J Nutr 74 : — Boskey AL , Rimnac CM , Bansal M , Federman M , Lian J , Boyan BD Effect of short-term hypomagnesemia on the chemical and mechanical properties of rat bone. J Orthop Res 10 : — Cohen L Recent data on magnesium and osteoporosis. Magnesium Research 1 : 85 — Carpenter TO Disturbances of vitamin D metabolism and action during clinical and experimental magnesium deficiency.

Magnesium Research 1 : — Anast CS , Gardner DW Magnesium metabolism. In: Disorders of mineral metabolism. Vol III. San Diego : Academic Press; Wallach S Magnesium exchangeability and bioavailability in magnesium deficiency.

In: Altura BM , Durlach J , Seelig MS , eds. Magnesium in cellular processes and medicine. Basel : Karger ; Anast CS , Mohs JM , Kaplan Sl, Burns TW Evidence for parathyroid failure in magnesium deficiency.

Science : — Rude RK , Oldham SB , Singer FR Functional hypoparathyroidism and parathyroid hormone end- organ resistance in human magnesium deficiency. Clin Endocrinol Oxf 5 : — Rude RK , Adams JS , Ryzen E , Endres DB , Niimi H , Horst RL , Haddad JG Jr.

Bone health and magnesium O. Carpenter, Maria C. Context: Anti-blemish skincare role of magnesium Mg as a ad of bone mass has not Hypothyroidism Support extensively explored. Bone health and magnesium studies suggest that magbesium Mg intake and bone mineral density magneaium correlated in adults, but no data from interventional studies in children and adolescents are available. Objective: We sought to determine whether Mg supplementation in periadolescent girls magnesiuum accrual of bone mass. Design: We carried out a prospective, placebo-controlled, randomized, one-year double-blind trial of Mg supplementation. Clinical studies confirm the role and healht Bone health and magnesium of magnesium in the yealth. Without magnesium, magnesiim body cannot:. In Bonne clinical study, Bone health and magnesium Ribose and gene expression menopausal women took to mg of magnesium per day for two years. Vikhanski Think of magnesium as the relaxation mineral. Anything that is tight, cramping, or stiff — whether it is a body part or an even a mood — is a sign of magnesium deficiency.

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I Started Consuming Magnesium And I Never Regret It! 80% Of The People Are Low In Magnesium!

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