Magnesium: Energy & Fat Loss (Master Page)

Do you have low energy levels, diabetic symptoms, and trouble maintaining healthy body weight? See why it’s impossible for your body to convert food and body fat into energy without magnesium.

++ Page Overview

This master page looks at how all major phases of metabolism need magnesium, follwed by a solutions section to help you restore and maintain healthy magnesium levels.

  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.

Before the solutions section, we look at how modern farming and stress levels have made it impossible to get enough magnesium from diet alone. 

++ Helpful tip

This page has a lot of powerful info to help you resolve your problems. 

If you’re busy or want to understand things better, please read each section’s quick summary.

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: duplicating the insulin gene, [3-5] and then using the duplicate to assemble the insulin protein [6,7](See our magnesium & protein synthesis video here). 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 is [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] 

Apart from its central role, magnesium also helps with 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 release 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 are good ways to stimulate growth hormone production, and magnesium is needed to produce it.)

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 it’s 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:
Our cells’ energy factories (mitochondria) use the oxygen we breathe to convert glucose and fatty acids into our energy currency: ATP. More ATP means greater health, while low ATP is associated with most major diseases.

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 without the prior step happening 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] Thus it is impossible to prepare glucose for energy production in our mitochondria, without the use of magnesium.

Fat preparation for mitochondria

Fatty acids are converted into Acetyl CoA molecules by a process called Beta-Oxidation.[36] Fatty acids differ in size based on how many carbon atoms are in their tails. For every two carbons in a fatty acid’s tail, the Beta Oxidation process makes one Acetyl CoA molecule. For example, a fatty acid with a 14 carbon tail produces 7 Acetyl CoA molecules.

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 plays a critical role in converting our carbs and fats into the Acetyl CoA molecules that our mitochondria use to make our ATP energy molecules.

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 (energy factories) engage two phases (each with several steps) that convert Acetyl CoA molecules into ATP. The first phase must happen in order for the second phase to start.

The same goes for the steps in each of the two phases; no step can happen without the prior step happening first. The two ATP generation phases 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 a malfunction of mitochondrial function.[42]

Magnesium is also a part of the ATP molecule.

We now know how our body converts food and oxygen into ATP 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 helps 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 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, we can develop almost any major 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 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 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 critical in treating and preventing disease.[98,99]

This becomes even more important as we look at how difficult it has now become to satisfy our body’s daily magnesium requirement from our diet alone:

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.

5. Why Our Magnesium Levels Are Now Dropping:

Figure 1 is a general representation of the trends of the three primary factors that affect the magnesium levels in our body everyday. The fourth line represents our ability to make our own magnesium, which will always stay at zero.

  1. Total environmental stress that drains our magnesium
  2. Magnesium in our soil and healthy foods
  3. Our intestine’s ability to absorb magnesium from food and pills

Our adrenals (stress glands) are magnesium-dependent. Stress depletes magnesium, and inflames our intestine, hindering absorption of dietary magnesium. (Even a healthy gut only absorbs 30-40% of a food’s magnesium.)

This means our metabolism is competing for its magnesium not only with our other vital functions, but also with increasing amounts of environmental stress and poor intestinal Mg absorption.

A magnesium deficiency graph that shows how our magnesium intake has declined since 1950, while our sources of magnesium depletion have increased. The depletion of our soils and the increasing environmental stress show us that we can no longer get enough magnesium without supplementation. This strengthens the importance of magnesium and weight loss.
A magnesium deficiency graph that shows how our magnesium intake has declined since 1950, while our sources of magnesium depletion have increased. The depletion of our soils and the increasing environmental stress show us that we can no longer get enough magnesium without supplementation. This strengthens the importance of magnesium and weight loss.
  1. Total environmental stress that drains our magnesium
  2. Magnesium in our soil and healthy foods
  3. Our intestine’s ability to absorb magnesium from food and pills

Our adrenals (stress glands) are magnesium-dependent. Stress depletes magnesium, and inflames our intestine, hindering absorption of dietary magnesium. (Even a healthy gut only absorbs 30-40% of a food’s magnesium.)

This means our metabolism is competing for its magnesium not only with our other vital functions, but also with increasing amounts of environmental stress and poor intestinal Mg absorption.

Summary & Solutions:

Summary: Magnesium essential to healthy metabolism

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.

Healthy metabolism is simply not possible if we are magnesium deficient. Unresolved deficiency leads to low energy levels, accelerated aging, and metabolic diseases such as diabetes and cancer.

Due to the depletion of magnesium in our agricultural soil and thus food, scientists now agree it is near impossible to get enough magnesium without supplementation:

Solutions: Safe and smart magnesium restoration

To restore our magnesium and keep it at the levels needed for healthy metabolism, several measures should be taken:

  1. Take a natural, quality magnesium-chloride supplement to boost insulin function, energy production, and whole-body magnesium levels. This is the basis of any magnesium restoration protocol.
  2. Take a secondary magnesium supplement for added mental and cardiovascular support, such as magnesium-orotate, taurate, or glycinate.
  3. Eat a magnesium-smart diet and avoid the tricky magnesium-rich foods.
  4. Do your best to reduce the environmental, psychological and physical factors that cause stress and thus deplete magnesium.

Click here to see the magnesium-chloride supplement we trust and recommend.

Click here to learn more about the other types of secondary supplements, including magnesium orotate, glycinate and taurate.

Click here to learn more about magnesium deficiency and the rest of your body parts.

++ References
  1. PubChem: Adenosine Triphosphate
  2. The islet beta-cell.
  3. The linkage between magnesium binding and RNA folding.
  4. Bidentate RNA-magnesium clamps: on the origin of the special role of magnesium in RNA folding.
  5. A thermodynamic framework for the magnesium-dependent folding of RNA.
  6. RNA-magnesium-protein interactions in large ribosomal subunit. 
  7. A recurrent magnesium-binding motif provides a framework for the ribosomal peptidyl transferase center.
  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).
  9. Intracellular magnesium and insulin resistance.
  10. Magnesium in Human Health and Disease.  or  see this excerpt:
  11. Magnesium responsiveness to insulin and insulin-like growth factor I in erythrocytes from normotensive and hypertensive subjects.
  12. Biochemistry of magnesium
  13. Magnesium basics.
  14. The insulin receptor: structure, function, and signaling.,%20function%20and%20signaling.pdf
  15. Magnesium metabolism in type 2 diabetes mellitus, metabolic syndrome and insulin resistance.
  16. Separate effects of Mg2+, MgATP, and ATP4- on the kinetic mechanism for insulin receptor tyrosine kinase.
  17. Role of divalent metals in the activation and regulation of insulin receptor tyrosine kinase.
  18. Oral magnesium supplementation improves insulin sensitivity in non-diabetic subjects with insulin resistance. A double-blind placebo-controlled randomized trial.
  19. Insulin Signaling and the Regulation of Glucose Transport.
  20. Regulation of GLUT4 and Insulin-Dependent Glucose Flux.
  21. Molecular Basis of Insulin-stimulated GLUT4 Vesicle Trafficking.
  22. Sustained activation of insulin receptors internalized in GLUT4 vesicles of insulin-stimulated skeletal muscle.
  23. Biochemistry. 5th edition. Section 26.4Important Derivatives of Cholesterol Include Bile Salts and Steroid Hormones.
  24. Hormonal regulation of cytochrome P450 enzymes, cholesterol side-chain cleavage and 17 alpha-hydroxylase/C17-20 lyase in Leydig cells.
  25. Consider Magnesium Homeostasis: III: Cytochrome P450 Enzymes and Drug Toxicity.
  26. Dehydroepiandrosterone (DHEA) replacement decreases insulin resistance and lowers inflammatory cytokines in aging humans.
  27. Glucagon and Adipose Tissue Lipolysis.
  28. Physiological effect of glucagon in human isolated adipocytes.
  29. Effects of Glucagon on Lipolysis and Ketogenesis in Normal and Diabetic Men.
  30. Regulation of Lipolysis in Adipocytes.
  31. Effects of cortisol and growth hormone on lipolysis in human adipose tissue.
  32. Role of Growth Hormone in Regulating Lipolysis, Proteolysis, and Hepatic Glucose Production during Fasting.
  33. Carb burning: 10 Steps of glycolysis
  34. Magnesium regulation of the glycolytic pathway and the enzymes involved.
  35. Section: “ELEMENTS OF MAGNESIUM BIOLOGY” Subsection: 1.13 Synthesis and activity of enzymes
  36. Fat burning: Beta Oxidation
  37. Citric acid cycle
  38. The Mechanism of Oxidative Phosphorylation.
  39. The subunit location of magnesium in cytochrome c oxidase.
  40. The Role of Magnesium and Its Associated Water Channel in Activity and Regulation of Cytochrome cOxidase.
  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.
  43. Thiamine and magnesium deficiencies: keys to disease.
  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.
  46. Magnesium and chronic fatigue.
  47. Magnesium and chronic fatigue syndrome.
  48. Nutritional strategies for treating chronic fatigue syndrome.
  49. Mitochondria and calcium: from cell signalling to cell death.
  50. Mitochondria: The calcium connection.
  51. Mitochondrial calcium uptake.
  52. Mitochondria as all-round players of the calcium game.
  53. Mitochondrial calcium signalling: message of life and death.
  54. Calcium inhibition of the ATP in equilibrium with [32P]Pi exchange and of net ATP synthesis catalyzed by bovine submitochondrial particles.
  55. Inflammation, CRP, calcium overload and a high calcium–phosphate product: a ‘liaison dangereuse’.
  56. Calcium, ATP, and ROS: a mitochondrial love-hate triangle.
  57. The relationship between magnesium and calciotropic hormones.
  58. Magnesium: Nature’s physiologic calcium blocker.
  60. Recent Advances in Obesity-Induced Inflammation and Insulin Resistance.
  61. “Introductory remarks,” in Oxidative Stress.
  62. Free Radicals in Biology and Medicine.
  63. Which comes first: Renal inflammation or oxidative stress in spontaneously hypertensive rats?
  64. Hypertension Induces Oxidative Stress but Not Macrophage Infiltration in the Kidney in the Early Stage of Experimental Diabetes Mellitus.
  65. Hypertension Increases Pro-Oxidant Generation and Decreases Antioxidant Defense in the Kidney in Early Diabetes.
  66. Oxidative Stress and Inflammation: Essential Partners in Alcoholic Liver Disease.
  67. Oxidative stress and inflammation, a link between chronic kidney disease and cardiovascular disease.
  68. Chronic Kidney Disease Influences Multiple Systems: Describing the Relationship between Oxidative Stress, Inflammation, Kidney Damage, and Concomitant Disease.
  69. Glutathione Synthesis in Human Erythrocytes.
  70. Effects of Glutathione on Red Blood Cell Intracellular Magnesium.
  71. Melatonin Metabolism in the Central Nervous System.
  72. Melatonin and its relation to the immune system and inflammation.
  73. The Magnesium Factor – melatonin biosynthesis – oxidative stress, pg 172.
  74. Magnesium Intake in Relation to Systemic Inflammation, Insulin Resistance, and the Incidence of Diabetes
  75. Dietary magnesium intake is inversely associated with serum C-reactive protein levels: meta-analysis and systematic review:
  76. Ferrotoxic Disease: The Next Great Public Health Challenge.
  77. The Role of Ceruloplasmin in Iron Metabolism.
  78. Multi-Copper Oxidases and Human Iron Metabolism.
  79. Biological effects of mutant ceruloplasmin on hepcidin-mediated internalization of ferroportin.
  80. Iron, Free Radicals, and Oxidative Injury.
  81. Reconstitution of ceruloplasmin by the Cu(I)-glutathione complex. Evidence for a role of Mg2+ and ATP.
  82. The role of iron in type 2 diabetes in humans.
  83. Back to past leeches: repeated phlebotomies and cardiovascular risk.
  84. Dietary iron overload induces visceral adipose tissue insulin resistance.
  85. Iron, Human Growth, and the Global Epidemic of Obesity.
  86. Mutual interaction between iron homeostasis and obesity pathogenesis.
  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.
  88. Iron status in obesity: An independent association with metabolic parameters and effect of weight loss.
  89. Iron Chelation Prevents Obesity by Increasing Hypothalamic Hypoxia-Inducible Factor-1α, Metabolic Rate and Adipose Tissue Browning.
  90. Magnesium Intake and Risk of Type 2 Diabetes in Men and Women.
  91. Management of Fibromyalgia: Rationale for the Use of Magnesium and Malic Acid.
  92. Glycolysis abnormalities in fibromyalgia.
  93. Magnesium Deficiency in Fibromyalgia Syndrome.
  94. Magnesium in Man: Implication for Health and Disease
  95. Magnesium in Health and Disease:
  96. Hypomagnesemia is Associated with Increased Mortality among Peritoneal Dialysis Patients.
  97. Magnesium Deficiency: A Cause of Heterogenous Disease in Humans:
  98. Magnesium in Prevention and Therapy
  99. Magnesium: physiology and pharmacology

Video References:

v1. Digital animation for insulin video created by the great team at Sanofi. 2017 Ι This website is designed by the artists at  Ι Contact us at