Magnesium & Metabolism

This guide looks at how all major phases of metabolism need magnesium, and why prolonged or severe magnesium deficiency can lead to low energy and pre-diabetic symptoms.

  1. Fuel absorption – glucose and fatty acids. (VIDEO)
  2. Fuel preparation – includes converting body fat.
  3. Fuel to energy coversion – includes burning fat.
  4. Protection from metabolic damage and disease.

The solutions section then looks at measures we can take to restore and maintain healthy magnesium levels that support a healthier metabolism.

1. Absorbing fuel requires magnesium:

The cells that make up our body generate energy from the carbs and fats we eat: 

Our intestine breaks down carbs and fats into glucose and fatty acids. These fuel sources then pass into our bloodstream and travel to our cells. Only there can they be converted into energy molecules called ATP: Adenosine Triphosphate[1] What’s critical, is that our cells need magnesium in order to absorb the glucose and fatty acids from our blood stream:

 

Magnesium & insulin: Absorbing glucose

When our pancreas senses that dietary glucose has entered our bloodstream, it releases the hormone insulin into our bloodstream. Insulin interacts with our cells to let them absorb the glucose from our bloodstream.  Magnesium is needed for insulin function in two ways:

1. Insulin production requires magnesium:

Insulin is a protein made in our pancreas’ beta cells[2] via the process of protein synthesis, whose two steps need magnesium: copying the insulin gene, [3-5] and then using the copy to assemble the insulin protein [6,7]. This helps explain why magnesium-chloride supplementation boosts the function of beta cells.[8]

2. Insulin function requires magnesium:

The less magnesium our cells have, the less effective insulin may be [9-11] because magnesium fuels overall cellular function,[12,13] and because it’s critical in the function of the insulin receptor: 

Insulin lets glucose into our cells by binding to their tyrosine kinase receptors.[14] These receptors need magnesium[10,15-17] which explains why magnesium supplements boost insulin function.[18] Once activated, these receptors bring glucose transporters to the cell’s surface, which allow the glucose to enter inside.[19-22] 

Magnesium also supports insulin function by converting cholesterol into the youth hormone DHEA,[23-25] which improves problems of insulin resistance.[26] Simply put, magnesium is critical to energy levels because it helps our cells absorb glucose via its role in insulin production, and insulin receptor function. 

 

Magnesium releases fat for fat-burning

For us to burn body fat, our fat cells must release fat into our blood stream so it can travel to our muscle and organ cells where it is converted to energy. This mobilization of fat requires magnesium:

When we have low blood sugar, our pancreas makes the hormone glucagon which helps our liver release more glucose into our blood, and makes our fat cells release fatty acids into the blood.[27-29] We make glucagon via the magnesium-dependent process of protein synthesis.[3-7]

This release of fat is called lipolysis [30] and human growth hormone is another magnesium-made hormone that triggers it. [31,32] (Fasting and high intensity interval training also stimulate growth hormone production.)

When we look at human energy production, the first step is for our cells to get access to their glucose and fatty acid fuel sources. Magnesium is fundamental to this step because of its role in the critical hormones insulin, glucagon, and human growth hormone.

1. Summary

We have energy only if our cells do.  Magnesium lets our cells absorb fuel sources from carbs and fats because:

1. It creates the hormone insulin which facilitates cellular carb absorption. The cells’ insulin receptors also depend on magnesium.

2. Magnesium creates growth hormone and glucagon which force our fat cells to release stored fat for other cells to use as energy.

2. Preparing fuel requires magnesium:

More ATP means greater health, while low ATP is associated with most major diseases. So we know that our cells convert the fatty acids and glucose we eat into this ATP energy. But where does this happen? Inside our cells’ energy factories , called mitochondria. Mitochondria use the oxygen we breathe to convert glucose and fatty acids into ATP.  However glucose and fatty acids must first be converted into smaller molecules called Acetyl-CoA, in order for our mitochondria to convert them into ATP energy molecules. This preparation of Acetyl Coa requires magnesium:

 

Glucose preparation for mitochondria

Each glucose molecule can be converted into two Acetyl CoA molecules. This ten-step conversion process is called Glycolysis, [33] and it requires magnesium[34]:

No step can occur unless the prior step happens first: In each step, an enzyme slightly changes the glucose molecule until by the last step it has become 2 Acetyl Coa molecules. Seven of the ten enzymes in glycolysis depend on magnesium,[35] making it impossible to prepare glucose for energy production in our mitochondria, without magnesium.

 

Fat preparation for mitochondria

Fatty acids are converted into Acetyl CoA molecules by a process called Beta-Oxidation.[36] Beta Oxidation can’t happen without magnesium because the enzyme Acyl Coa-Synthetase which allows fatty acids to enter the Beta Oxidation cycle, requires magnesium to work.[35]

Simply put, magnesium is essential in converting our carbs and fats into the Acetyl CoA molecules that our mitochondria use to make ATP energy.

2. Summary

Once inside our cells, fats and carbs are converted into Acetyl CoA molecules.

Only then can they enter our cells’ energy factories called mitochondria, where they’re turned into usable energy.

Our cells need magnesium to convert fats & carbs into Acetyl CoA molecules.

3. Burning fat & carbs requires magnesium:

Our cells’ mitochondria carry out a sequence of two phases that convert Acetyl CoA molecules into ATP. In each of the two phases; no step can happen without the prior step happening first. The two phases that generate our ATP are:

 

Phase 1: Citric Acid Cycle.[37] Four of the seven steps need magnesium enzymes.[12,35]

Phase 2: Cellular Respiration (oxidative phosphorylation) – 5 steps.[38] The fourth step requires the critical magnesium-dependent enzyme cytochrome C oxidase,[12,35,39,40] and in the fifth step magnesium works with the ATP synthase enzyme.[41]

Have you ever wondered why we eat and breathe? It’s to supply oxygen, glucose, fatty acids and vitamins & minerals to our mitochondria so they can make our ATP energy molecules. Simply put, mitochondrial ATP production keeps every system in our body alive, and magnesium deficiency leads to decreaased mitochondrial function.[42]

 

Magnesium is also a part of each ATP molecule.

We now know how our body converts food and oxygen into ATP energy which keeps us alive. This process occurs non-stop in all the trillions of cells that make up our body. We make many trillions of ATP energy molecules each second we’re alive! Now think about this:

Every single ATP energy molecule we make, must be attached to magnesium in order to be of any use. In fact, the true scientific term for ATP is Mg-ATP. [43] Simply put, magnesium makes, and is a physical component of the ATP molecules that give us energy for life. 

3. Summary

Now inside our mitochondria, Acetyl CoA molecules undergo two consecutive phases to become usable energy:

These two phases are called the Citric Acid Cycle & Cellular Respiration. Neither are possible without magnesium.

Magnesium is also a physical component of each newly made energy molecule, called ATP (adenosine triphosphate).

Magnesium produces, and is a physical part of our body’s energy currency.

4. Magnesium protects mitochondria & prevents disease:

Besides helping our mitochondria make ATP, magnesium also protects them from calcification, inflammation and oxidative stress. Its protective effects on our energy factories help explain why magnesium deficiency is often found in people with chronic fatigue. [44-48]

 

Magnesium prevents calcification

The majority of our calcium should be in bone. While we do also need it for our mitochondria to work[49,50], it’s only in modest amounts.[51] In fact, mitochondrial use of calcium walks such a fine line[52,53], that even a bit too much calcium slows down mitochondrial energy production.[54] Not only do our energy levels drop, but our mitochondria suffer calcification and begin to produce excess harmful molecules called reactive oxygen species.[55,56]

Through various mechanisms such as regulating calcium-controlling hormones[57], magnesium protects our cells and their mitochondria from excess calcium buildup[58] which otherwise lead to dysfunctional mitochondria that produce these reactive oxygen species.[59] These harmful molecules cause cellular and organ inflammation, and if these conditions persist long enough, it can lead to various forms of disease, including metabolic disorders.[60-68]

 

Magnesium fights inflammation

Our mitochondria are especially vulnerable to inflammation, and magnesium protects them via its key roles in two of our cells’ most powerful anti-inflammatory molecules: glutathione and melatonin.[69-73] This helps explain why low magnesium intake is linked with inflammation as well as the most common health conditions caused by unhealthy mitochondria and poor metabolism: obesity and diabetes.[74,75]

 

Magnesium prevents cellular RUST

Iron deficiency is rare and often confused with iron misplacement which is very common [76]: Iron is meant to circulate in our blood, not to build up in our cells. Ceruloplasmin is the enzyme that loads iron from cells onto transport molecules in our blood. [77-79] Without enough ceruloplasmin, iron builds up in our cells and causes oxidative stress,[80] which is another way of saying our cells and their mitochondria begin to rust. 

The resulting low iron in our blood (and thus blood tests) misleads many health practitioners who then prescribe iron supplements, making things worse. The key is having enough ceruloplasmin, and magnesium is needed for ceruloplasmin production and recycling.[81] Thus, without enough magnesium our cellular energy factories suffer damage from toxic iron buildup, which is linked to obesity, insulin resistance and diabetes.[82-89] Simply put, magnesium’s role in preventing cellular iron toxicity is critical to maintain healthy energy levels and metabolism.

 

Magnesium deficiency & metabolic disease

As we look at how deeply rooted magnesium is in the function and protection of our carb and fat energy metabolism, it makes sense why low magnesium is associated with metabolic and inflammatory diseases like diabates and fibromyalgia.[74,75,90-93]

And when we realize that healthy energy production is required for every major bodily system, it’s no surprise that magnesium deficiency is associated with most forms of major disease such as heart disease, diabetes, cancer, and neurodegenerative diseases,[94-97] and why magnesium restoration is essential in treating and preventing disease.[98,99]

4. Summary

Magnesium protects our cells and their mitochondrial energy factories from:

Calcification: It regulates “calciotropic” hormones in a way that keeps calcium in bones instead of organ cells.

Inflammation: Magnesium fuels the production of anti-inflammatory helpers like glutathione and melatonin which protect our mitochondria.

RUST: Magnesium keeps iron flowing in our blood instead of building up to toxic levels in our cells, where it can damage and rust our mitochondria.

Magnesium deficiency is linked with obesity, diabetes and all major metabolic diseases.

SUMMARY

All major aspects of human energy production depend on magnesium:

  1. Absorption of glucose and fatty acids into our cells.
  2. Preparation of these building blocks into fuel sources for our mitochondria.
  3. Mitochondrial conversion of fuel sources into cellular energy.
  4. Protection, maintenance and regulation of our mitochondrial energy factories.

A healthy and fast metabolism is simply not possible if the body is deficient in magnesium. Magnesium is essential for burning carbs and fat to make energy. Severe and prolonged magnesium deficiency can lead to low energy levels, accelerated aging, and even metabolic diseases such as diabetes and cancer.

Furthermore, due to lower levels of magnesium in the food supply, and higher levels of environmental stress that depletes the body’s magnesium, scientists now agree that diet alone is not enough to restore and maintain healthy magnesium levels.  A more well-rounded approach is needed.

Solutions to restore magnesium:

While restoring and maintaining healthy magnesium levels may not resolve your metabolic issues on its own, based on magnesium’s essential roles in human metabolism, it is still a major requirement for healthy weight, energy levels and overall metabolism.  A complete magnesium restoration protocol can include:

  • Eating a magnesium-smart dietLearn more
  • 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, consider combining this with an oral magnesium-taurate, magnesium orotate  or magnesium glycinate supplement for added mental, cardiovascular and cellular support. Learn more

References
  1. PubChem: Adenosine Triphosphate  https://pubchem.ncbi.nlm.nih.gov/compound/Adenosine_triphosphate
  2. The islet beta-cell. http://www.ncbi.nlm.nih.gov/pubmed/14687913
  3. The linkage between magnesium binding and RNA folding.  http://www.ncbi.nlm.nih.gov/pubmed/11955006
  4. Bidentate RNA-magnesium clamps: on the origin of the special role of magnesium in RNA folding.  http://www.ncbi.nlm.nih.gov/pubmed/21173199
  5. A thermodynamic framework for the magnesium-dependent folding of RNA.  http://www.ncbi.nlm.nih.gov/pubmed/12717727
  6. RNA-magnesium-protein interactions in large ribosomal subunit.  http://www.ncbi.nlm.nih.gov/pubmed/22712611 
  7. A recurrent magnesium-binding motif provides a framework for the ribosomal peptidyl transferase center.  http://www.ncbi.nlm.nih.gov/pubmed/19279186
  8. 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
  9. Intracellular magnesium and insulin resistance. http://www.ncbi.nlm.nih.gov/pubmed/15319146
  10. Magnesium in Human Health and Disease. 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
  11. Magnesium responsiveness to insulin and insulin-like growth factor I in erythrocytes from normotensive and hypertensive subjects. https://www.ncbi.nlm.nih.gov/pubmed/9851785?dopt=Abstract
  12. Biochemistry of magnesium http://www.uwm.edu.pl/jold/poj1532010/jurnal-16.pdf
  13. Magnesium basics. http://ckj.oxfordjournals.org/content/5/Suppl_1/i3.full
  14. The insulin receptor: structure, function, and signaling. http://www.cogsci.ucsd.edu/~mboyle/COGS163/pdf-files/W2-AR-The%20insulin%20receptor%20structure,%20function%20and%20signaling.pdf
  15. Magnesium metabolism in type 2 diabetes mellitus, metabolic syndrome and insulin resistance. http://www.ncbi.nlm.nih.gov/pubmed/16808892
  16. Separate effects of Mg2+, MgATP, and ATP4- on the kinetic mechanism for insulin receptor tyrosine kinase. http://www.ncbi.nlm.nih.gov/pubmed/2157363
  17. Role of divalent metals in the activation and regulation of insulin receptor tyrosine kinase. http://www.ncbi.nlm.nih.gov/pubmed/2847822
  18. 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
  19. Insulin Signaling and the Regulation of Glucose Transport. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1431367/
  20. Regulation of GLUT4 and Insulin-Dependent Glucose Flux. http://www.hindawi.com/journals/isrn/2012/856987/
  21. Molecular Basis of Insulin-stimulated GLUT4 Vesicle Trafficking. http://www.jbc.org/content/274/5/2593.full
  22. Sustained activation of insulin receptors internalized in GLUT4 vesicles of insulin-stimulated skeletal muscle. http://www.ncbi.nlm.nih.gov/pubmed/11078443
  23. Biochemistry. 5th edition. Section 26.4Important Derivatives of Cholesterol Include Bile Salts and Steroid Hormones.http://www.ncbi.nlm.nih.gov/books/NBK22339/
  24. Hormonal regulation of cytochrome P450 enzymes, cholesterol side-chain cleavage and 17 alpha-hydroxylase/C17-20 lyase in Leydig cells.  http://www.ncbi.nlm.nih.gov/pubmed/2160293
  25. Consider Magnesium Homeostasis: III: Cytochrome P450 Enzymes and Drug Toxicity.  http://online.liebertpub.com/doi/abs/10.1089/pai.1994.8.7
  26. Dehydroepiandrosterone (DHEA) replacement decreases insulin resistance and lowers inflammatory cytokines in aging humans. https://www.ncbi.nlm.nih.gov/pubmed/21566261
  27. Glucagon and Adipose Tissue Lipolysis. http://link.springer.com/chapter/10.1007%2F978-3-642-68866-9_19
  28. Physiological effect of glucagon in human isolated adipocytes. https://www.ncbi.nlm.nih.gov/pubmed/7590626/
  29. Effects of Glucagon on Lipolysis and Ketogenesis in Normal and Diabetic Men. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC301453/
  30. Regulation of Lipolysis in Adipocytes. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2885771/
  31. Effects of cortisol and growth hormone on lipolysis in human adipose tissue. https://www.ncbi.nlm.nih.gov/pubmed/10690893
  32. Role of Growth Hormone in Regulating Lipolysis, Proteolysis, and Hepatic Glucose Production during Fasting. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2453052/
  33. Carb burning: 10 Steps of glycolysis  http://biology.about.com/od/cellularprocesses/a/aa082704a.htm
  34. Magnesium regulation of the glycolytic pathway and the enzymes involved.  http://www.ncbi.nlm.nih.gov/pubmed/2931560
  35. Section: “ELEMENTS OF MAGNESIUM BIOLOGY” Subsection: 1.13 Synthesis and activity of enzymes http://www.mgwater.com/durex01.shtml
  36. Fat burning: Beta Oxidation  https://en.wikipedia.org/wiki/Beta_oxidation
  37. Citric acid cycle https://en.wikipedia.org/wiki/Citric_acid_cycle
  38. The Mechanism of Oxidative Phosphorylation. http://www.ncbi.nlm.nih.gov/books/NBK9885/
  39. The subunit location of magnesium in cytochrome c oxidase. http://www.ncbi.nlm.nih.gov/pubmed/8408083
  40. The Role of Magnesium and Its Associated Water Channel in Activity and Regulation of Cytochrome cOxidase. http://link.springer.com/chapter/10.1007/978-1-4615-4827-0_38
  41. 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
  42. THE EFFECT OF MAGNESIUM DEFICIENCY ON OXIDATIVE PHOSPHORYLATION  http://www.jbc.org/content/228/2/573.full.pdf
  43. Thiamine and magnesium deficiencies: keys to disease.  http://www.ncbi.nlm.nih.gov/pubmed/25542071
  44. Seelig M. Presentation to the 37th Annual Meeting, American College of Nutrition, October 13, 1996./li>
  45. Red blood cell magnesium and chronic fatigue syndrome. https://www.ncbi.nlm.nih.gov/pubmed/1672392
  46. Magnesium and chronic fatigue. https://www.ncbi.nlm.nih.gov/pubmed/1676129
  47. Magnesium and chronic fatigue syndrome. https://www.ncbi.nlm.nih.gov/pubmed/1715504
  48. Nutritional strategies for treating chronic fatigue syndrome. https://www.ncbi.nlm.nih.gov/pubmed/10767667
  49. Mitochondria and calcium: from cell signalling to cell death. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2270168/
  50. Mitochondria: The calcium connection. http://www.sciencedirect.com/science/article/pii/S0005272810005797
  51. Mitochondrial calcium uptake. http://www.pnas.org/content/110/26/10479
  52. Mitochondria as all-round players of the calcium game. https://www.ncbi.nlm.nih.gov/pubmed/11080249
  53. Mitochondrial calcium signalling: message of life and death. https://www.ncbi.nlm.nih.gov/pubmed/19192620
  54. 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
  55. Inflammation, CRP, calcium overload and a high calcium–phosphate product: a ‘liaison dangereuse’. http://ndt.oxfordjournals.org/content/17/2/201.full
  56. Calcium, ATP, and ROS: a mitochondrial love-hate triangle. https://www.ncbi.nlm.nih.gov/pubmed/15355853
  57. The relationship between magnesium and calciotropic hormones. http://www.ncbi.nlm.nih.gov/pubmed/7669510
  58. Magnesium: Nature’s physiologic calcium blocker. http://www.ahjonline.com/article/0002-8703(84)90572-6/references
  59. THE CALCIUM CONTROVERSY.  http://www.mgwater.com/gacontro.shtml
  60. Recent Advances in Obesity-Induced Inflammation and Insulin Resistance. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3737462/
  61. “Introductory remarks,” in Oxidative Stress. https://books.google.ca/books?hl=en&lr=&id=BEoXBQAAQBAJ&oi=fnd&pg=PA1&ots=hj_a7MjyYC&sig=duAUcqYnGLuUML9q1SVRPPlZ0z4&redir_esc=y#v=onepage&q&f=false
  62. Free Radicals in Biology and Medicine. https://www.amazon.ca/Radicals-Biology-Medicine-Barry-Halliwell/dp/019856869X
  63. Which comes first: Renal inflammation or oxidative stress in spontaneously hypertensive rats? http://www.tandfonline.com/doi/full/10.1080/10715760601059672
  64. Hypertension Induces Oxidative Stress but Not Macrophage Infiltration in the Kidney in the Early Stage of Experimental Diabetes Mellitus. http://www.karger.com/Article/Abstract/95707
  65. Hypertension Increases Pro-Oxidant Generation and Decreases Antioxidant Defense in the Kidney in Early Diabetes. http://www.karger.com/Article/Abstract/109993
  66. Oxidative Stress and Inflammation: Essential Partners in Alcoholic Liver Disease. https://www.hindawi.com/journals/ijh/2012/853175/
  67. Oxidative stress and inflammation, a link between chronic kidney disease and cardiovascular disease. https://www.scopus.com/record/display.uri?eid=2-s2.0-57049146797&origin=inward&txGid=4410BBAF77E42B5CB05A79C7C19BF999.wsnAw8kcdt7IPYLO0V48gA%3a2
  68. Chronic Kidney Disease Influences Multiple Systems: Describing the Relationship between Oxidative Stress, Inflammation, Kidney Damage, and Concomitant Disease. https://www.hindawi.com/journals/omcl/2015/806358/
  69. Glutathione Synthesis in Human Erythrocytes. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC442063/
  70. Effects of Glutathione on Red Blood Cell Intracellular Magnesium. http://hyper.ahajournals.org/content/34/1/76.full
  71. Melatonin Metabolism in the Central Nervous System. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3001211/
  72. Melatonin and its relation to the immune system and inflammation. http://www.ncbi.nlm.nih.gov/pubmed/11268363
  73. The Magnesium Factor – melatonin biosynthesis – oxidative stress, pg 172. https://books.google.ca/books?id=BuW6xwqlQfkC&pg=PA172&lpg=PA172&dq=melatonin+biosynthesis+magnesium&source=bl&ots=vaxoOEyveq&sig=hwjGTCJch53S_NIo6Te8zvJHRww&hl=en&sa=X&ved=0ahUKEwiXwJGExKvOAhVE9x4KHToeAe0Q6AEIQjAF#v=onepage&q=melatonin%20biosynthesis%20magnesium&f=false
  74. Magnesium Intake in Relation to Systemic Inflammation, Insulin Resistance, and the Incidence of Diabetes  http://care.diabetesjournals.org/content/33/12/2604.abstract?ijkey=f923c1120dc6636d93fa39d29c797bee45949288&keytype2=tf_ipsecsha
  75. Dietary magnesium intake is inversely associated with serum C-reactive protein levels: meta-analysis and systematic review:   http://www.ncbi.nlm.nih.gov/pubmed/24518747
  76. Ferrotoxic Disease: The Next Great Public Health Challenge. http://clinchem.aaccjnls.org/content/clinchem/60/11/1362.full.pdf
  77. The Role of Ceruloplasmin in Iron Metabolism. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC322742/pdf/jcinvest00228-0276.pdf
  78. Multi-Copper Oxidases and Human Iron Metabolism. http://www.mdpi.com/2072-6643/5/7/2289/htm
  79. Biological effects of mutant ceruloplasmin on hepcidin-mediated internalization of ferroportin. http://www.sciencedirect.com/science/article/pii/S0925443910001481
  80. Iron, Free Radicals, and Oxidative Injury. http://jn.nutrition.org/content/134/11/3171S.full.pdf+html
  81. Reconstitution of ceruloplasmin by the Cu(I)-glutathione complex. Evidence for a role of Mg2+ and ATP. https://www.ncbi.nlm.nih.gov/pubmed/8567646
  82. The role of iron in type 2 diabetes in humans. https://www.ncbi.nlm.nih.gov/pubmed/18501198
  83. Back to past leeches: repeated phlebotomies and cardiovascular risk. link.springer.com/article/10.1186/1741-7015-10-53
  84. Dietary iron overload induces visceral adipose tissue insulin resistance. https://www.ncbi.nlm.nih.gov/pubmed/23578384
  85. Iron, Human Growth, and the Global Epidemic of Obesity. www.mdpi.com/2072-6643/5/10/4231/htm
  86. Mutual interaction between iron homeostasis and obesity pathogenesis. www.sciencedirect.com/science/article/pii/S0946672X14000716
  87. Iron metabolism in obesity: How interaction between homoeostatic mechanisms can interfere with their original purpose. Part I: Underlying homoeostatic mechanisms of energy storage and iron metabolisms and their interaction. www.sciencedirect.com/science/article/pii/S0946672X14001916
  88. Iron status in obesity: An independent association with metabolic parameters and effect of weight loss. www.sciencedirect.com/science/article/pii/S0939475315000551
  89. Iron Chelation Prevents Obesity by Increasing Hypothalamic Hypoxia-Inducible Factor-1α, Metabolic Rate and Adipose Tissue Browning. esa-srb-2012.m.asnevents.com.au/schedule/session/114/abstract/753
  90. Magnesium Intake and Risk of Type 2 Diabetes in Men and Women. http://care.diabetesjournals.org/content/27/1/134.abstract
  91. Management of Fibromyalgia: Rationale for the Use of Magnesium and Malic Acid. www.tandfonline.com/doi/abs/10.3109/13590849208997961
  92. Glycolysis abnormalities in fibromyalgia. www.tandfonline.com/doi/abs/10.1080/07315724.1994.10718387
  93. Magnesium Deficiency in Fibromyalgia Syndrome. www.tandfonline.com/doi/abs/10.3109/13590849409034552
  94. Magnesium in Man: Implication for Health and Disease http://physrev.physiology.org/content/95/1/1.full
  95. Magnesium in Health and Disease: http://link.springer.com/chapter/10.1007%2F978-94-007-7500-8_3
  96. Hypomagnesemia is Associated with Increased Mortality among Peritoneal Dialysis Patients.  http://www.ncbi.nlm.nih.gov/pubmed/27023783
  97. Magnesium Deficiency: A Cause of Heterogenous Disease in Humans: http://www.magtabsr.com/content/dr-resources-pdfs/Magnesium-Deficiency-A-Cause-of-Heterogenous-Disease-in-Humans.pdf
  98. Magnesium in Prevention and Therapy  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4586582/#B5-nutrients-07-05388
  99. Magnesium: physiology and pharmacology http://bja.oxfordjournals.org/content/83/2/302.full.pdf

Video References:

v1. Digital animation for insulin video created by the great team at Sanofi. http://en.sanofi.com/company/company.aspx

Terms of Use

Our aim is to empower people with information and natural health solutions. The information and products provided by this website and company are not intended to diagnose, treat, cure, or prevent any disease, and are not a substitute for a face-to-face consultation with your physician, and should not be construed as individual medical advice. The statements on this website have not been evaluated by the Food and Drug Administration. We do not make any representations or warranties in regard to any information offered or provided on or through this website, be it regarding treatment, action, or application of any natural treatments. Nothing said on this site is intended to encourage or promote the discontinuation of any medical treatment or prescribed medication. Any changes in your medication should only be considered under the supervision and consultation of your doctor or health care provider. Abrupt discontinuance of some medications can cause serious health complications. We take no credit for the footage and music used in the videos and graphics of this website. All credit goes to its respective media owners. Reliance on any information provided by mgpedia.org, our affiliates, or others referenced or linked to on this Site, is solely at your own risk.

This disclaimer governs your use of this website. By using the mgpedia.org website, you accept this disclaimer in full. If you disagree with any part of this disclaimer, do not use or read this website. If you do use or read this website, you are stating that you agree with this disclaimer.

MgPedia.org 2019   Ι   This website is designed and powered by empaths.io