Magnesium for Bones & Joints
This guide looks at magnesium’s roles in bone and joint health and why magnesium deficiency can lead to osteoporosis and aching joints.
- Magnesium helps prevent stiff and brittle bones.
- Bone formation and repair requires magnesium.
- Magnesium regulates our bones’ calcium absorption & bone formation.
- Magnesium helps our body absorb calcium from diet.
- Magnesium deficiency can cause brittle bones and calcified joints & organs.
The solutions section then looks at actions we can take to restore and maintain healthy magnesium levels.
1. Magnesium prevents brittle bones...
Calcium is only one of 18 nutrients needed for healthy bones. Our bones need this mix of minerals for sufficient strength and malleability: a physical property opposite of stiffness, which allows bones to absorb mechanical force instead of fully opposing it, thus avoiding breaking.
Considering we need magnesium for more vital bodily processes than any other nutrient, it may come as a surprise to some that magnesium is a metal. Yet metals are known for being malleable, which helps explain why over 60% of our body’s magnesium is found in bone, where it is known to reduce the rate of bone mineral degradation and overall bone loss, and why magnesium-deficient bones are more fragile despite higher levels of other bone minerals.
This also sheds light on why magnesium deficiency and low magnesium intake result in brittle, fragile bones as well as osteoporosis.[7-10]
The relationship between magnesium deficiency and osteoporosis is even more clear when we see how magnesium is ingrained in the very nature of bone metabolism and formation:
Over 60% of our magnesium is in our bones, and it gives them malleability which prevents them from breaking.
Magnesium also reduces bone loss while magnesium deficiency is linked with brittle bones and osteoporosis.
2a. Magnesium forms and repairs bones (video):
Our bone tissue is comprised of two complimentary parts:
- A physical framework or “matrix” called osteoid.
- A mixture of bone minerals stored within this framework.
To see how bone formation requires magnesium, let’s look at the four main cells involved in life’s ongoing cycle of breaking down and rebuilding bone tissue:
- Osteoclasts: break down bone matrix (osteoid) & release the minerals.[12-15]
- Osteoblasts: lay down new bone matrix (build and rebuild our bones).[15-18]
- Osteocytes: which were once osteoblasts,  are embedded in the bone matrix. These cells sense any mechanical stress placed on our bones, and respond by activating functional osteoblasts to build more bone.[20-24]
- Lining cells: dormant osteoblasts on our bones’ outer border.
The video[v1] shows how osteoblasts secrete the collagen-based bone “matrix” onto our bones.[18,25] The matrix solidifies into a physical framework called osteoid, into which a mineral mixture of calcium, phosphate, magnesium and others, is deposited.
Bones are made of a framework called osteoid and a mineral mixture called bone matrix found inside the osteoid.
Osteoclasts are cells that break down bones, and osteoblasts rebuild them.
The video shows how these bone cells are constantly rebuilding our bones.
2b. Bone formation requires magnesium...
Now that we have a grasp on how our osteoblasts build and maintain strong bones, let’s see how this requires magnesium.
Our bones are in a constant dance of being broken down by osteoclasts, and being rebuit or grown by osteoblasts. Thus to prevent osteoporosis and keep healthy bones, we need enough osteoblast activity, so we don’t break down more bone than we make. Our osteoblasts can’t function without magnesium: They depend on it for three main factors:
To make bone matrix, osteoblasts need energy in the form of ATP molecules (adenosine triphosphate)[26-29] which are made from the fat and carbs we eat. Not only is magnesium a physical part of every active ATP molecule[30-34] but the processes of our cells absorbing carbs and fat,[35-42] and then converting them into ATP, both require magnesium.[43-48]
Simply put, without magnesium osteoblasts have no energy. In fact, the calcium:magnesium ratio is so critical to energizing our cells, that if calcium inside our cells rises too high above magnesium, this slows down energy production! In other words, to much calcium in our bone cell prevents proper bone formation!
2. Bone matrix production:
Bone matrix is made of various proteins, over 90% of which are collagen[17,25]. The process of making these proteins is called protein synthesis. It has two phases: copying DNA, and then converting the copy into an actual protein. Both of these phases require magnesium.[50-53] Osteoblasts need magnesium to make bone matrix.
3. Osteoblast production:
Both magnesium and magnesium-dependent ATP are mitogenic to osteoblasts.[28,55,56] This means they help osteoblasts divide and replicate. This can largely be explained by their facilitation of the various enzymes needed for DNA replication before cell division. [57-59] In fact magnesium has been shown to directly raise the number of osteoblasts in bone.
Besides replication, we also get osteoblasts from the process of cell differentiation, when our body’s stem cells transform into osteoblasts, via the magnesium-dependent process of protein synthesis.
When we add the fact that magnesium deficiency is known to increase bone-destroying osteoclasts, it’s no surprise that magnesium increases our overall bone formation:
Simply put, our osteoblasts – the cells responsible for building, repairing and maintain healthy bones – all depend on magnesium for energy, building bone matrix, and replication!
To maintain healthy bones and avoid osteoporosis, our osteoblasts need to make as much or more bone as our osteoclasts break down.
Our bone-building osteoblasts need magnesium for their:
- bone matrix production
- healthy osteoblast population
Magnesium is critical to the function and existence of our bone-building cells.
3. Magnesium for calcium absorption...
Bones need bone matrix to absorb calcium, and magnesium helps make this bone matrix by fueling our osteoblasts. This helps explain why higher dietary and supplemental magnesium intake is linked with higher bone mineral density.[63,64]
Yet magnesium also controls calcium absorption by regulating three important “calciotropic” hormones: calcitonin, parathyroid hormone and calcitriol. These hormones activate our osteoblasts and osteoclasts and thus regulate our calcium absorption/release [66-69]:
This hormone has been studied for over 50 years and still new information is being drawn about its effects on bone metabolism. What we do know is that calcitonin increases osteoblast population and function (and thus bone formation), and it decreases osteoclast function and bone destruction.[70-73] We also know that magnesium increases this hormone.[74-76]
Parathyroid hormone has both opposite effects to calcitonin,[68,77,78] as well as complimentary effects. It stimulates osteoclasts to break down bone matrix and release calcium into our blood stream. However it also exhibits bone-building effects when it is secreted intermittently.[79,80
Magnesium regulates parathyroid hormone production in a way that is favorable to bone formation. While a rise in magnesium can inhibit parathyroid hormone secretion, research also shows that acute drops in magnesium increase parathyroid hormone and acute spikes decreases it.[83,65]
It seems that magnesium’s fluctuational effects on parathyroid fall in line with the hormone’s beneficial effects being tied to its intermittent secretion, especially when we consider magnesium deficiency’s association with osteoporosis.
Magnesium’s intelligent regulation of parathyroid hormone also seems to favor keeping safe levels of calcium in our blood,  which can prevent excess parathyroid production and bone loss. Furthermore, similarly to all other organs, the parathyroid glands still require magnesium to function which is why magnesium deficiency can lead to hypoparathyroidism.
Simply put, magnesium is critical to the function of this complex hormone that regulates bone formation and blood calcium levels.
Calcitriol is the active form of Vitamin D which is in fact a hormone that impacts bone formation and dietary calcium absorption, and which needs magnesium for its activation:
Magnesium allows our bones to absorb calcium by regulating three hormones:
It boosts calcitonin to help our bones absorb calcium.
It prevents parathyroid hormone from stimulating too many osteoclasts and breaking down our bones.
It also has a special role in Vitamin D…
4. Magnesium, vitamin D and calcium absorption...
The vitamin D we get from food or sunlight (whose UVB rays convert our cholesterol into Vitamin D), is in the inactive form [85,86] known as D3 or cholecalciferol.
- Our liver then converts this inactive form into the storage form: calcidiol
- Our kidneys then convert this storage form into the final active form: calcitriol.
We need magnesium for this vitamin D activation, because the enzymes that facilitate the above conversions belong to the cytochrome P450 family of enzymes[88-91] which is magnesium-dependent.
Remember: when we have low calcium in our blood, parathyroid hormone takes calcium from our bones to replenish our blood. Calcitriol helps prevent this by increasing our gut’s dietary calcium absorption[93-95] while decreasing our kidneys’ excretion of calcium. This maintenance of blood calcium prevents high levels of parathyroid hormone which otherwise cause bone loss. Thus magnesium’s activation of vitamin D can help prevent excess bone loss.
However this brings up an important issue: it may not be ideal to supplement with vitamin D when we are severely deficient in magnesium, because supplemenets have non-active vitamin D, whose conversion into the active form depletes our body’s magnesium further. In fact, a low vitamin D level may indicate magnesium deficiency.[97-99]
This is why experts say 3 different tests should be done for vitamin D status, to show how much active and inactive vitamin D we have, and if we have healthy levels of magnesium for the conversion. The tests are:
- Calcidiol (storage vitamin D) also called 25(OH)D or 25 hydroxyvitamin D
- Calcitriol (active vitamin D) also called 1,25(OH)2 D3 or 1,25 hydroxyvitamin D
- Magnesium red blood cell test
Now, because magnesium is needed for vitamin D activation and most people are magnesium-deficient to some degree, this helps explain why taking vitamin D supplements without magnesium supplementation to prevent and treat bone diseases is not recommended.[100,101]
Magnesium’s role in calcium regulation also explains why calcium supplementation while severely magnesium-deficient, may actually increase the onset of various health conditions:
Vitamin D helps our body absorb dietary calcium. Our body makes Vitamin D from cholesterol.
It needs magnesium for this conversion.
Vitamin D has two forms: active and non-active. When testing Vitamin D, it’s important to test both, because excess vitamin D supplementation can deplete our magnesium and cause calcification.
5. Magnesium, osteoporosis, & organ calcification...
We now know that magnesium is vital to the three main factors of bone health:
- It provides malleability and prevents brittle bones.
- It allows our osteoblasts to form bone.
- It regulates our hormones in favor our bones’ calcium absorption & formation.
This explains why magnesium deficiency causes dysregulated and misplaced calcium, leading to eventual problems such as osteoporosis. But weak bones aren’t the only result. Calcification and damage of tissues like our heart, arteries, kidneys and brain are also consequences of calcium misplacement caused by magnesium deficiency.
As we look at magnesium’s natural ability to keep excess caclium out of the cells of our soft organs, tissues and joints, it explains why some experts say that calcium supplements on their own are actually not that effective in treating and preventing osteoporosis,[100,104] and why taking them is at times linked to increased risk of heart disease. [105-107]
Magnesium’s central role in calcium regulation means that its deficiency reaches beyond our bones, with negative effects being found in other major organs. This sheds light on why scientists are now finding links between osteoporosis and heart disease. [108-110]
Rather than these specific diseases occurring mostly due to genetic mutations, perhaps the human body is simply experiencing the consequences of calcium being taken out of its rightful place (bones) and being put in vulnerable places it doesn’t belong: soft tissues.
Magnesium is our body’s natural calcium regulator:
It keeps calcium in our bones, and out of our soft tissues like our heart, brain and liver, where it can otherwise cause damage and serious diseases.
Calcium supplementation is linked with increased risk of heart disease! It is critical to supplement with magnesium before taking calcium or vitamin D.
Without magnesium, calcium absorption and bone formation in our body both suffer. We need magnesium to keep calcium in our bones, and out of our soft organs and tissues, where it can cause calcification, inflammation and damae..
Unfortunately, scientists agree that due to modern agriculture and environmental stress levels, it is now very difficult to get enough magnesium without supplementation, which helps explain why over 50 million people in the U.S. alone have osteoporosis, with many more at risk. Magnesium supplementation can be a major aid in supporting strong healthy bones:
Solutions to restore magnesium:
While restoring and maintaining healthy magnesium levels may not resolve all bone and joint issues on its own, based on magnesium’s essential roles in skeletal health, it is still a major requirement. A complete magnesium restoration protocol can include:
- Eating a magnesium-smart diet. Learn more.
- Engaging in regular light exercise (30 minutes daily) with a wide variety of ranges of motion to maintain functionality and stimulus in your nerves, bones and joints.
- Reducing the environmental, psychological and physical stressors that deplete magnesium from your body. Learn more
- Using a quality trans-dermal magnesium supplement to restore whole-body magnesium levels. Also, because skeletal and heart conditions occurr frequently together, consider combining this with an oral magnesium-taurate or magnesium orotate supplement which are both beneficial to heart health. Learn more.
v1: Audio done by imagnesium.com. All visuals/digital animation/footage have been taken from Amgen Science. We thank them for their phenomenal work! You can visit their website at https://www.amgenscience.com/.
- Determinants of Bone Health. http://www.ncbi.nlm.nih.gov/books/NBK45503/
- The human “magnesome”: detecting magnesium binding sites on human proteins. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3439678/
- Magnesium Supplementation and Bone Turnover. http://www.ncbi.nlm.nih.gov/pubmed/10453178
- Influence of magnesium substitution on a collagen-apatite biomaterial on the production of a calcifying matrix by human osteoblasts. http://www.ncbi.nlm.nih.gov/pubmed/9827688
- Daily oral magnesium supplementation suppresses bone turnover in young adult males. http://www.ncbi.nlm.nih.gov/pubmed/9709941
- [The interplay of magnesium and vitamin K2 on bone mineralization]. http://www.ncbi.nlm.nih.gov/pubmed/15995297
- Magnesium and Osteoporosis: Current State of Knowledge and Future Research Directions. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3775240/
- Skeletal and hormonal effects of magnesium deficiency. http://www.ncbi.nlm.nih.gov/pubmed/19828898
- Effect of short-term hypomagnesemia on the chemical and mechanical properties of rat bone. http://www.ncbi.nlm.nih.gov/pubmed/1403290
- The effect of moderately and severely restricted dietary magnesium intakes on bone composition and bone metabolism in the rat. http://www.ncbi.nlm.nih.gov/pubmed/10655958
- The role of magnesium in osteoporosis and idiopathic hypercalcaemia. https://www.cabdirect.org/cabdirect/abstract/19611400775
- The cell biology of osteoclast function. http://www.ncbi.nlm.nih.gov/pubmed/10639325
- Major progress in understanding osteoclast function. http://www.mayoclinic.org/medical-professionals/clinical-updates/endocrinology/research-explores-mechanisms-regulate-bone-resorption-formation
- Osteoclast Migration, Differentiation and Function. http://www.medscape.com/viewarticle/781508_4
- Perspectives on Osteoblast and Osteoclast Function. http://ps.oxfordjournals.org/content/79/7/1005.full.pdf
- Osteoblasts and bone formation. http://www.ncbi.nlm.nih.gov/pubmed/17572649
- Control of osteoblast function and regulation of bone mass. http://www.ncbi.nlm.nih.gov/pubmed/12748654
- Osteoblast Differentiation and Mineralization. http://www.promocell.com/fileadmin/knowledgebase/pdf-xls/Osteoblast_Differentiation_and_Mineralization.pdf
- Buried alive: how osteoblasts become osteocytes. http://www.ncbi.nlm.nih.gov/pubmed/16258960
- Function of osteocytes in bone. http://www.ncbi.nlm.nih.gov/pubmed/7962159
- [Recent progress in studies on osteocytes–osteocytes and mechanical stress]. http://www.ncbi.nlm.nih.gov/pubmed/11155692
- Osteocyte and bone structure. http://www.ncbi.nlm.nih.gov/pubmed/16036059
- Osteocytes, Mechanosensing and Wnt Signaling. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2349095/
- Osteocyte signaling in bone. http://www.ncbi.nlm.nih.gov/pubmed/22552701
- The bone microenvironment in metastasis; what is special about bone? http://www.ncbi.nlm.nih.gov/pubmed/18071636/
- Adenosine triphosphate. https://en.wikipedia.org/wiki/Adenosine_triphosphate
- Adenosine and Bone Metabolism. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3669669/
- Adenosine Triphosphate stimulates differentiation and mineralization in human osteoblast-like Saos-2 cells. http://onlinelibrary.wiley.com/doi/10.1111/dgd.12288/abstract
- ATP and UTP at low concentrations strongly inhibit bone formation by osteoblasts: a novel role for the P2Y2 receptor in bone remodeling. http://www.ncbi.nlm.nih.gov/pubmed/12210747
- Pubchem: MgATP https://pubchem.ncbi.nlm.nih.gov/compound/15126#section=Top
- Biochemistry of magnesium http://www.uwm.edu.pl/jold/poj1532010/jurnal-16.pdf
- Magnesium in biology (Mg-ATP) https://en.wikipedia.org/wiki/Magnesium_in_biology
- Magnesium basics. http://ckj.oxfordjournals.org/content/5/Suppl_1/i3.full
- MAGNESIUM IN MAN: IMPLICATIONS FOR HEALTH AND DISEASE pg 2 paragraph 2. http://www.physiomics.eu/media/181616/de_baaij_magnesium_in_man.full.pdf
- Magnesium improves the beta-cell function to compensate variation of insulin sensitivity: double-blind, randomized clinical trial.(While magnesium’s role in the beta cell’s actual release of insulin is less established than its role in the beta cells creating insulin, this study makes ground on the overall impact of magnesium on beta cells). http://www.ncbi.nlm.nih.gov/pubmed/21241290
- Separate effects of Mg2+, MgATP, and ATP4- on the kinetic mechanism for insulin receptor tyrosine kinase. http://www.ncbi.nlm.nih.gov/pubmed/2157363
- Role of divalent metals in the activation and regulation of insulin receptor tyrosine kinase. http://www.ncbi.nlm.nih.gov/pubmed/2847822
- Substitution Studies of the Second Divalent Metal Cation Requirement of Protein Tyrosine Kinase CSK. http://pubs.acs.org/doi/abs/10.1021/bi982793w
- Intracellular magnesium and insulin resistance. (Insulin’s function is magnesium dependent): http://www.ncbi.nlm.nih.gov/pubmed/15319146
- Magnesium in Human Health and Disease. (Insulin’s function is magnesium dependent): http://www.springer.com/gp/book/9781627030434 or see this excerpt: https://books.google.ca/books?id=iUCx1dwWr7kC&pg=PA132&lpg=PA132&dq=tyrosine+kinase+Mg&source=bl&ots=y2ITN0DdKo&sig=d9F3WRCchZ2_2wQhvW9fe2faqtk&hl=en&sa=X&ved=0ahUKEwj7jJ3fxdTMAhVM1oMKHQDFAKkQ6AEIYzAJ#v=onepage&q=tyrosine%20kinase%20Mg&f=false
- Oral magnesium supplementation improves insulin sensitivity in non-diabetic subjects with insulin resistance. A double-blind placebo-controlled randomized trial. http://www.ncbi.nlm.nih.gov/pubmed/15223977
- Fatty acid transport across the cell membrane: regulation by fatty acid transporters. http://www.ncbi.nlm.nih.gov/pubmed/20206486
- Magnesium regulation of the glycolytic pathway and the enzymes involved. http://www.ncbi.nlm.nih.gov/pubmed/2931560
- Fat burning: Beta Oxidation https://en.wikipedia.org/wiki/Beta_oxidation
- Section: “ELEMENTS OF MAGNESIUM BIOLOGY” Subsection: 1.13 Synthesis and activity of enzymes http://www.mgwater.com/durex01.shtml
- ATP production: Oxidative phosphorylation. https://en.wikipedia.org/wiki/Oxidative_phosphorylation
- THE EFFECT OF MAGNESIUM DEFICIENCY ON OXIDATIVE PHOSPHORYLATION. http://www.jbc.org/content/228/2/573.full.pdf
- Chemical mechanism of ATP synthase. Magnesium plays a pivotal role in formation of the transition state where ATP is synthesized from ADP and inorganic phosphate. http://www.ncbi.nlm.nih.gov/pubmed/10506126
- Calcium inhibition of the ATP in equilibrium with [32P]Pi exchange and of net ATP synthesis catalyzed by bovine submitochondrial particles. https://www.ncbi.nlm.nih.gov/pubmed/2145974
- The linkage between magnesium binding and RNA folding. http://www.ncbi.nlm.nih.gov/pubmed/11955006
- Bidentate RNA-magnesium clamps: on the origin of the special role of magnesium in RNA folding. http://www.ncbi.nlm.nih.gov/pubmed/21173199
- A thermodynamic framework for the magnesium-dependent folding of RNA. http://www.ncbi.nlm.nih.gov/pubmed/12717727
- RNA-magnesium-protein interactions in large ribosomal subunit. http://www.ncbi.nlm.nih.gov/pubmed/22712611
- A recurrent magnesium-binding motif provides a framework for the ribosomal peptidyl transferase center. http://www.ncbi.nlm.nih.gov/pubmed/19279186
- ATP and adenosine act as a mitogen for osteoblast-like cells (MC3T3-E1). http://www.ncbi.nlm.nih.gov/pubmed/8998680/
- Nitric oxide mediates low magnesium inhibition of osteoblast-like cell proliferation. http://www.ncbi.nlm.nih.gov/pubmed/22209000
- Critical role of magnesium ions in DNA polymerase beta’s closing and active site assembly. http://www.ncbi.nlm.nih.gov/pubmed/15238001
- Structural and catalytic chemistry of magnesium-dependent enzymes. http://www.ncbi.nlm.nih.gov/pubmed/12206389
- ATP activates DNA synthesis by acting on P2X receptors in human osteoblast-like MG-63 cells. http://www.ncbi.nlm.nih.gov/pubmed/10913018
- Magnesium directly stimulates osteoblast proliferation. https://www.scienceopen.com/document?10&vid=bd91dfa3-092b-44f9-a6cd-980c5db2f795
- Immunolocalization of RANKL is Increased and OPG Decreased During Dietary Magnesium Deficiency in the Rat. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1266035/
- Effect of magnesium ion on human osteoblast activity. http://www.ncbi.nlm.nih.gov/pubmed/27383121
- Magnesium Intake from Food and Supplements Is Associated with Bone Mineral Density in Healthy Older White Subjects. http://www.mgwater.com/Ryder.pdf
- Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women. http://ajcn.nutrition.org/content/69/4/727.full.pdf
- The relationship between magnesium and calciotropic hormones. http://www.ncbi.nlm.nih.gov/pubmed/7669510
- Calcium regulation. http://www.ncbi.nlm.nih.gov/pubmed/7037224
- [Hormones in bone metabolism. I. Calcitropic hormones]. http://www.ncbi.nlm.nih.gov/pubmed/2272073
- [Parathyroid hormone and calcitonin]. http://www.ncbi.nlm.nih.gov/pubmed/1337117
- [Hormonal regulation of bone metabolism]. http://www.ncbi.nlm.nih.gov/pubmed/8243730
- Effect of calcitonin on bone cell ultrastructure. http://www.sciencedirect.com/science/article/pii/016960099290896L
- Effects of calcitonin on bone quality and osteoblastic function. http://link.springer.com/article/10.1007/BF00310194
- Calcitonin, the forgotten hormone: does it deserve to be forgotten? http://ckj.oxfordjournals.org/content/8/2/180.full
- [Effects of calcitonin on osteoblast cell proliferation and OPG/RANKL expression: experiment with mouse osteoblasts]. http://www.ncbi.nlm.nih.gov/pubmed/17785093
- Magnesium Deficiency in the Pathogenesis of Disease. Early Roots of Cardiovascular, Skeletal, and Renal Abnormalities. http://annals.org/article.aspx?articleid=694784
- THE CALCIUM CONTROVERSY. http://www.mgwater.com/gacontro.shtml
- Magnesium: A Key to Calcium Absorption. http://www.mgwater.com/calmagab.shtml
- Induction of osteoclast formation by parathyroid hormone depends on an action on stromal cells. http://joe.endocrinology-journals.org/content/158/3/341.full.pdf
- Effects of parathyroid hormone on osteoclasts in vivo. http://link.springer.com/article/10.1007/BF00307123
- Parathyroid hormone temporal effects on bone formation and resorption. http://www.ncbi.nlm.nih.gov/pubmed/10824426
- The roles of parathyroid hormone in bone remodeling: prospects for novel therapeutics. http://www.ncbi.nlm.nih.gov/pubmed/21985975
- Magnesium and the parathyroid. http://www.ncbi.nlm.nih.gov/pubmed/12105390
- Parathyroid hormone secretion in magnesium deficiency. http://www.ncbi.nlm.nih.gov/pubmed/263326
- Effect of magnesium on phosphorus and calcium metabolism. http://www.ncbi.nlm.nih.gov/pubmed/1331782
- Magnesium modulates parathyroid hormone secretion and upregulates parathyroid receptor expression at moderately low calcium concentration. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3910342/
- The Relationship between Ultraviolet Radiation Exposure and Vitamin D Status. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257661/
- Vitamin D: The “sunshine” vitamin. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3356951/
- Vitamin D Metabolism, Mechanism of Action, and Clinical Applications. http://www.sciencedirect.com/science/article/pii/S1074552114000246
- Cytochrome P450 enzymes in the bioactivation of vitamin D to its hormonal form (review). http://www.ncbi.nlm.nih.gov/pubmed/11172626
- Overview of regulatory cytochrome P450 enzymes of the vitamin D pathway. http://www.ncbi.nlm.nih.gov/pubmed/11179747
- Cytochromes P450 are essential players in the vitamin D signaling system. http://www.ncbi.nlm.nih.gov/pubmed/20619365
- Cytochrome P450-mediated metabolism of vitamin D. http://www.ncbi.nlm.nih.gov/pubmed/23564710
- Consider Magnesium Homeostasis: III: Cytochrome P450 Enzymes and Drug Toxicity. http://online.liebertpub.com/doi/abs/10.1089/pai.1994.8.7
- Effect of 1,25-dihydroxyvitamin D3 on calcium and magnesium absorption in the healthy human jejunum and ileum. http://www.ncbi.nlm.nih.gov/pubmed/6689108
- Molecular mechanisms for regulation of intestinal calcium absorption by vitamin D and other factors. http://www.ncbi.nlm.nih.gov/pubmed/21182397
- Molecular aspects of intestinal calcium absorption. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4476875/
- [Calciotropic actions of parathyroid hormone and vitamin D-endocrine system]. http://www.ncbi.nlm.nih.gov/pubmed/18019603
- Low serum concentrations of 1,25-dihydroxyvitamin D in human magnesium deficiency. https://www.ncbi.nlm.nih.gov/pubmed/3840173
- Magnesium, vitamin D status and mortality: results from US National Health and Nutrition Examination Survey (NHANES) 2001 to 2006 and NHANES III. bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-11-187
- Magnesium deficit – overlooked cause of low vitamin D status? bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-11-229
- Calcium supplements with or without vitamin D and risk of cardiovascular events: reanalysis of the Women’s Health Initiative limited access dataset and meta-analysis. https://www.ncbi.nlm.nih.gov/pubmed/21505219
- Should we prescribe calcium or vitamin D supplements to treat or prevent osteoporosis? https://www.ncbi.nlm.nih.gov/pubmed/26473773
- Elevated brain lesion volumes in older adults who use calcium supplements: a cross-sectional clinical observational study. https://www.ncbi.nlm.nih.gov/pubmed/24787048
- Magnesium: Nature’s physiologic calcium blocker. http://www.ahjonline.com/article/0002-8703(84)90572-6/references
- Prevention of osteoporosis: the calcium controversy. https://www.ncbi.nlm.nih.gov/pubmed/2631941
- Cardiovascular effects of calcium supplementation. https://www.ncbi.nlm.nih.gov/pubmed/21409434
- Calcium supplements and cardiovascular risk: 5 years on. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4125316/
- Cardiovascular Effects of Calcium Supplements. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3738985/
- Cardiovascular disease and osteoporosis: Balancing risk management. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2291312/
- The link between osteoporosis and cardiovascular disease. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781192/
- Ischemic heart disease is associated with lower cortical volumetric bone mineral density of distal radius. link.springer.com/article/10.1007/s00198-015-3132-z
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