Magnesium & Digestion

Do you have low energy, constipation, stomach aches, or heartburn/GERD?

Learn how the digestion of fat, carbohydrate and protein is magnesium-dependent, and how resolving digestive problems also requires magnesium.

This page looks at all of magnesium’s roles in digestion and digestive disorders. This is followed by a solutions section that shows how to restore and maintain healthy magnesium levels for better digestion.

  1. Basics: energy, protection, and physical repair of digestive organs
  2. First phase of digestion: salivary glands
  3. Second phase: stomach & protein digestion
  4. Third phase: pancreatic & intestinal digestion of carbs, fats and proteins
  5. Digestive disorders including SIBO, heart burn, GERD, and cancer?

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

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.

The Three Fundamentals

We can find the following 3 biological roles of magnesium in every tissue of the body, because they are fundamental to life itself: energy production, physical structure, and cellular protection. Let’s take a quick look at how magnesium facilitates these in our digestive organs:

Magnesium & energy

Every digestive organ is made of cells which need energy for the organ to stay alive. Energy is created when cells convert fat molecules (fatty acids) or sugar molecules (glucose) into units of molecular energy called ATP.

Digestive organs don’t work without ATP, and cells can’t convert sugar and fat into energy without magnesium. You can learn more about this on the magnesium & metabolism page.

Magnesium & physical maintenance/repair

Organs are made of functional units called cells. The organ’s structural health is a direct result of it’s cells’ structural health. Cells maintain their structure by assembling our dietary amino acids into the proteins that repair and/or become an actual part of the cells themselves. (The conversion of food into flesh).

This biological process is called protein synthesis, and it requires both magnesium and our DNA, which you can watch a quick video about here.

Magnesium & organ protection

Magnesium protects our digestive organs from their most consistent forms of damage: inflammation, oxidative stress and calcification.

1. Inflammation: Magnesium is naturally antiinflammatory which is linked with its role in producing and positively influencing two of our biggest anti-inflammatory helpers, melatonin and glutathione. This explains why magnesium deficiency leads to inflammation and malfunction of the heart and intestine and why it is found in up to 88% of people suffering from inflammatory bowel disease.

2. Oxidative stress: Magnesium prevents oxidative stress by making ceruloplasmin: the enzyme that keeps iron in our blood instead of building up to toxic levels in our cells. Oxidative stress physically damages organs, and excess iron in the intestine is known to cause inflammation, oxidative stress, and bacterial overgrowth in adults and children.

3. Calcification: Magnesium regulates hormones that encourage bone-calcium absorption and prevent excess calcium build-up in soft tissues and organs, thus helping to prevent a wide variety of cases of damaging calcification in digestive organs. Learn more: magnesium & bones page.

Magnesium & the path of digestion:

Now, as we will follow the path of digestion our food takes until it enters our bloodstream, we will see how magnesium’s role in these fundamental processes helps with each phase of digestion. We also look at how magnesium is involved in other more specific ways for each phase/organ.
Our digestive organs need magnesium to make energy from the food we eat. They also need magnesium to repair themselves daily via protein synthesis.

Magnesium protects our digestive organs from inflammation directly, and by creating glutathione and melatonin.

It also regulates calcium and iron so that neither build up in our organs to cause calcification and rust.
Digestion consists of a mechanical and chemical component. We see magnesium’s involvement in both of these components in the first phase of digestion: in our mouth.

The obvious mechanical component is chewing, which depends on magnesium for nervous and muscular activation of the muscles in our jaw. However the act of chewing plays another critical role:

It activates our vagus nerve, which signals our digestive organs to prepare themselves to handle incoming food by producing digestive enzymes and stomach acid. This increases the importance of magnesium’s central role in chewing.

Magnesium & salivary enzymes – carbohydrates

The chemical component of digestion occurs when a digestive organ produces digestive enzymes: molecules that break down our food into smaller parts.

Our mouth’s digestive organs are the salivary glands. They make saliva which has amylase: the digestive enzyme that breaks down starch into smaller chains of glucose. Salivary glands – like all organs – need magnesium for energy, function and safety. Magnesium’s vitality to salivary function looks even more important when we realize that saliva also plays a role in oral hygiene, wound healing, and enhancing the function and health of other digestive areas.

In addition to its influence on the function of our salivary glands, magnesium  itself is also one of the electrolytes found in human saliva – alongside sodium and potassium which are the most critical.  Magnesium’s association with salivary function is also found in human disease:

Magnesium, saliva & diabetes

Chewing and saliva help the entire digestive process. This helps explain why  more  salivary amylase is linked to better blood sugar balance after eating carbs. How well we metabolize carbs is also strongly linked with diabetes. It makes sense then that another link between salivary function, diabetes and magnesium has been found:

Not only do diabetic people have impaired salivary function and make less saliva, but their saliva also has higher concentrations of calcium, and lower concentrations of magnesium than that of healthy people. This brings to mind magnesium’s natural antagonistic relationship with calcium, which shows traces in a health condition specific to our salivary glands:

Magnesium and salivary stones

Like our kidneys, our salivary glands can also develop dense mineral deposits. Salivary gland stones are called sialoliths, and sialolithiasis is a common disorder of the salivary glands.  While not life-threatening, sialoliths can be painful. If untreated they can lead to salivary gland deterioration, and grow to almost an inch in size, requiring surgical removal.

The exact cause of sialolithiasis is not known however symptoms include poor salivary and metabolic function which both require magnesium. Furthermore the stones are primarily composed of calcium, which brings to mind magnesium’s basic role in preventing calcification. This is further highlighted when we look at the environment of the salivary glands and the saliva itself, which show increased levels of calcium, and decreased levels of magnesium.

While magnesium won’t heal sialolithiasis, our goal is to prevent it. Based on magnesium’s role in overall salivary gland function as well as calcium regulation, healthy magnesium levels are essential to preventing salivary stones, and of course to initiating the digestive process, which resumes in our stomach:
Magnesium facilitates chewing which breaks down food, and signals digestive organs to prepare for work.

Magnesium fuels our salivary glands to make saliva that digests carbs. It also regulates calcium to prevent salivary stones (similar to kidney stones).
Our food now passes down our esophagus, into our stomach where protein digestion begins. Just like our salivary glands, our stomach’s cells need magnesium for both the mechanical and chemical componenets of digestion. The mechanical aspect involves the churning of the stomach’s muscles to break down food chunks into smaller pieces. The contraction, relaxation, and activation of these muscles requires magnesium.

The chemical component of the stomach’s protein digestion is also the most critical and energy-demanding: the making of stomach acid by the stomach’s parietal cells, which also requires magnesium:

Magnesium & stomach acid

Stomach acid production is stimulated by hormones & neurotransmitters whose creation (via protein synthesis), and delivery (via nervous and cardiovascular systems) need magnesium. Yet these are only magnesium’s broad roles which highlight its ever-present nature in our body’s systems. We also need magnesium specifically to pump stomach acid to digest protein:

From all the different kinds of cells that make up our stomach, the parietal cells are the ones that pump hydrogen and chloride ions (hydrochloric/stomach acid) into the stomach’s digestive area. This utilizes a special hydrogen/potassium pump called an H+/K+ ATPase pump.

What’s critical here is that this stomach-acid pump is magnesium-dependent. In other words without magnesium, our stomach can’t make the acid that inititates protein digestion. Once the acid is released it performs two critical functions:

First it unfolds (denatures) the proteins we consumed. Second, it converts the digestive enzyme pepsin, into its active form pepsinogen. Pepsinogen is what breaks down our proteins into smaller combinations of amino acids, which can then pass into our small intestine where the final phase of digestion for proteins, carbs and fats takes place:
Our stomach makes acid that begins protein digestion and kills bacteria in our food. The parietal cells of our stomach need magnesium to make this acid, and to activate protein-digesting enzymes.

Magnesium and our pancreas

The fats, amino acid chains and glucose chains now pass from our stomach into our intestine, where more digestive enzymes break them down into fatty acids, single amino acids, and single glucose molecules. Yet while digestion occurs in the intestine, the pancreas is the nearby organ that releases these digestive enzymes into the small intestine. It releases:

  1. Amylase enzymes to break down glucose chains into single glucose units.
  2. Protease enzymes to break down amino acid chains into single amino acids.
  3. Lipase enzymes to break down triglycerides (fats) into fatty acids.

The pancreas’ production of these digestive enzymes requires magnesium, and without them, our intestine is incapable of absorbing most of the nutrients from our food.  In addition to its function, magnesium is also required for our pancreas’ general health:

Not only does magnesium supplementation significantly reduce the severity of pancreatitis (a condition of severe pancreatic inflammation), but magnesium intake also serves as a primary preventative measure against pancreatic cancer.

Magnesium and our intestine’s lifespan

Our small intestine is the gateway for the majority of nutrients to pass into our bloodstream. However it’s also the environment that is most exposed to bacteria and inflammation, which are both extremely damaging to intestinal cells.

This is why intestinal cells (especially the microvilli that absorb nutrients) have some of the shortest lifespans of all cells: between 2-3 days. Every time an intestinal cell dies, an unspecialized stem cell must replicate and transform into a specialized intestinal cell to replace it. Thus we see just how critical magnesium is to our small intestine:

The replication and maturation of the stem cell into an intestinal cell can’t happen without magnesium. This is because the enzymes involved in the process of duplicating the cell’s DNA before it replicates (and the subsequent process of protein synthesis that transforms the newly duplicated cell into an intestinal cell) require magnesium in order to function.

In other words, magnesium is central to the constant renewal of our intestinal cells, and thus the overall health, function and lifespan of our intestine.
As food now enters our intestine, our  pancreas sends enzymes there which digest carbs, proteins, & fats. It needs magnesium to make these enzymes.

Magnesium helps prevent pancreatic inflammation and cancer, and helps our intestine regenerate every few days.
The high amounts of inflammation and bacteria in our small intestine are also two primary contributors to SIBO: Small Intestinal Bacterial Overgrowth which is increasingly common. It’s no coincidence that SIBO numbers are rising as our exposure to stress and synthetic/toxic/iron-enriched foods is also at all-time highs:

Stress and inflammation both physically damage our cells and impair their energy production, especially the cells of our intestine’s immune system. When these damaged, inefficient immune cells are unable to fully control bacteria levels in the gut, we develop bacterial overgrowth.

Magnesium’s central role in fighting inflammation helps explain why correcting magnesium deficiency is a key component of treating SIBO. Furthermore, SIBO, inflammation and magnesium deficiency are also related to digestive disorders of our stomach:
Acid reflux and GERD are the most common digestive disorders in North America. They  include the painful sensation of stomach acid touching our esophagus. Drug companies tell us this is caused by excess stomach acid so they can sell drugs called Proton Pump Inhibitors which  impair stomach acid secretion, and as a side effect cause magnesium deficiency. 

In reality, GERD and acid reflux have nothing to do with excess stomach acid, especially considering these conditions increase with age, yet stomach acid production decreases with age. In fact, over 90% of people over 40 with heartburn have poor stomach acid production, and hydrochloric acid (stomach acid) supplements often resolve the issue! How can excess stomach acid be the root cause if it helps resolve these issues?

The true cause of acid reflux and GERD, is the malfunction of the esophageal sphincter:  the muscular flap at the top of the stomach which prevents stomach acid from entering up into the esophagus above. This esophageal sphincter malfunction is not caused by stomach acid. It’s more likely caused by intra-abdominal pressure.

What leads to this disruptive pressure in our stomach? Research points to the overgrowth of h.pylori bacteria in the stomach and small intestine, which helps explain why antibiotics decrease acid reflux and strengthen the esophageal sphincter.

While anitbiotics help, magnesium has a fundamental role in fighting bacteria, without any side-effects. It fuels immune cells in our intestine and protects them from inflammation. This effect is especially potent via its positive effect on melatonin levels and synthesis, because melatonin is powerfully anti-inflammatory, especially in our intestine, nervous and immune systems, which are all closely connected.

Besides fighting intestinal inflammation, magnesium also helps prevent bacterial overgrowth via its role in stomach acid production because: One of stomach acid’s main roles is to kill bacteria from the food we eat. In other words, stomach acid is the first line of defense against bacterial overgrowth, and we can’t make stomach acid without magnesium!

Because bacteria in our intestine feed on carbohydrates, stomach acid also prevents bacterial overgrowth another way: It signals our pancreas to release digestive enzymes into our intestine which break carbs down into glucose. In fact not only does stomach acid prevent bacterial overgrowth, but on the other hand, h.pylori bacteria also inhibits stomach acid secretion. This means if we don’t make enough stomach acid, the resulting bacterial overgrowth can further reduce stomach acid production, starting a dangerous cycle. Let’s sum up the entire issue:

  • GERD and acid reflux are caused by a malfunctioning esophageal sphincter, which allows stomach acid to enter where it should never be found: the esophagus.
  • This sphincter’s malfunction is caused by intra-abdominal pressure.
  • This intra-abdominal pressure is caused by bacterial overgrowth.
  • This bacterial overgrowth is caused by low stomach acid.
  • Stomach acid production requires magnesium.

Once stomach acid is impaired (either by insufficient nutrients or PPI drugs) and bacterial overgrowth has begun, the condition becomes a self-perpetuating cycle. For those taking antacid drugs, the pain of acid in the esophagus subsides because they lose the ability to make acid. However they don’t solve the problem, thus the bacterial overgrowth (caused by low stomach acid in the first place) continues to progress, and the malfunctioning esophageal sphincter never improves. What’s worse is that continued bacterial overgowth can lead to worse conditions including stomach ulcers and IBS – irritable bowel sundrome. These are more serious conditions than GERD and heartburn.

Digestive health needs magnesium

Is it a coincidence that as these digestive disorders are at all-time highs, so is magnesium deficiency? While deficiency isn’t the only cause of digestive disorders, and it may not resolve the entire issue on its own, the fact is that healthy magnesium levels are a necessity for optimal digestive health. Magnesium is simply far too ingrained in the function and health of our digestive organs, for such issues to be resolved while in a magnesium-deficient state.

This only further increases the importance of why and how difficult it has now become to satisfy our daily magnesium needs from diet alone:

6. 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 the human body’s ability to make its 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 digestive system is competing for its much needed magnesium with our other vital functions AND with increasing amounts of environmental stress and poor intestinal Mg absorption.

  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 digestive system is competing for its much needed magnesium with our other vital functions AND with increasing amounts of environmental stress and poor intestinal Mg absorption.

Summary & Solutions:

Summary: Magnesium ingrained in digestion

Magnesium is not just a natural digestive aid. Rather, it is the mineral ingrained in the nature and function of our digestive system. Without magnesium, we simply cannot:

  1. Fuel, repair, and protect our digestive organs.
  2. Perform the mechanical aspects of digestion.
  3. Make hydrochloric acid (stomach acid).
  4. Make any digesting enzymes for carbs, proteins and fats.
  5. Prevent disease in our salivary glands, intestines, pancreas, esophagus, and stomach.

With a magnesium-depleted food supply, and experts stressing the importance of magnesium supplementation, a well-rounded approach is optimal to restore magnesium levels for a healthy digestive tract:

Solutions: Safe & smart magnesium restoration

To restore and maintian healthy magnesium, several measures may be taken, including using a quality magnesium-chloride supplement which contains two key components for the stomach’s hydrochloric acid (stomach acid). Other beneficial measures include:

  • Eat less refined carbohydrates to prevent excess fuel for intestinal bacteria.
  • Consume ginger tea made form raw organic ginger.
  • Eat a magnesium-smart diet and avoid the tricky magnesium-rich foods.
  • Do your best to reduce the environmental, psychological and physical factors that cause stress and thus deplete magnesium.

Click here to learn more about the different types of magnesium supplements including magnesium chloride.

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

  1. PubChem: Adenosine Triphosphate.   https://pubchem.ncbi.nlm.nih.gov/compound/Adenosine_triphosphate
  2. Biochemistry of magnesium.   http://www.uwm.edu.pl/jold/poj1532010/jurnal-16.pdf
  3. Magnesium regulation of the glycolytic pathway and the enzymes involved.  http://www.ncbi.nlm.nih.gov/pubmed/2931560
  4. THE EFFECT OF MAGNESIUM DEFICIENCY ON OXIDATIVE PHOSPHORYLATION  http://www.jbc.org/content/228/2/573.full.pdf
  5. Section: “ELEMENTS OF MAGNESIUM BIOLOGY” Subsection: 1.13 Synthesis and activity of enzymes. http://www.mgwater.com/durex01.shtml
  6. Role of magnesium in genomic stability.  http://www.ncbi.nlm.nih.gov/pubmed/11295157
  7. Magnesium basics. http://ckj.oxfordjournals.org/content/5/Suppl_1/i3.full
  8. Magnesium Decreases Inflammatory Cytokine Production: A Novel Innate Immunomodulatory Mechanism. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3884513/
  9. Magnesium sulfate increases intracellular magnesium reducing inflammatory cytokine release in neonates. https://www.ncbi.nlm.nih.gov/pubmed/23590581
  10. Magnesium Intake in Relation to Systemic Inflammation, Insulin Resistance, and the Incidence of Diabetes. http://care.diabetesjournals.org/content/33/12/2604.abstractijkey=f923c1120dc6636d93fa39d29c797bee45949288&keytype2=tf_ipsecsha
  11. 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
  12. Effects of oral magnesium supplementation on inflammatory markers in middle-aged overweight women. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3685774/
  13. 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
  14. Dietary factors and fluctuating levels of melatonin. http://www.foodandnutritionresearch.net/index.php/fnr/article/view/17252/23292
  15. Dietary magnesium deficiency decreases plasma melatonin in rats. http://www.ncbi.nlm.nih.gov/pubmed/17172005
  16. Glutathione Biosynthesis. https://en.wikipedia.org/wiki/Glutathione
  17. Glutathione Synthesis in Human Erythrocytes. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC442063/
  18. Effects of Glutathione on Red Blood Cell Intracellular Magnesium. http://hyper.ahajournals.org/content/34/1/76.full
  19. Intestinal inflammation caused by magnesium deficiency alters basal and oxidative stress-induced intestinal function.  https://www.ncbi.nlm.nih.gov/pubmed/17657590
  20. The role of magnesium deficiency in cardiovascular and intestinal inflammation.  https://www.ncbi.nlm.nih.gov/pubmed/20971697
  21. Magnesium and inflammatory bowel disease.  https://www.ncbi.nlm.nih.gov/pubmed/3294519
  22. The Role of Ceruloplasmin in Iron Metabolism. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC322742/pdf/jcinvest00228-0276.pdf
  23. Multi-Copper Oxidases and Human Iron Metabolism. http://www.mdpi.com/2072-6643/5/7/2289/htm
  24. Biological effects of mutant ceruloplasmin on hepcidin-mediated internalization of ferroportin. http://www.sciencedirect.com/science/article/pii/S0925443910001481
  25. 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
  26. Nutritional iron turned inside out: intestinal stress from a gut microbial perspective. http://femsre.oxfordjournals.org/content/38/6/1202
  27. Iron fortification adversely affects the gut microbiome, increases pathogen abundance and induces intestinal inflammation in Kenyan infants.  http://gut.bmj.com/content/early/2014/08/20/gutjnl-2014-307720.short
  28. The effects of iron fortification on the gut microbiota in African children: a randomized controlled trial in Côte d’Ivoire.  http://ajcn.nutrition.org/content/92/6/1406.short
  29. The relationship between magnesium and calciotropic hormones. http://www.ncbi.nlm.nih.gov/pubmed/7669510
  30. Calcium regulation. http://www.ncbi.nlm.nih.gov/pubmed/7037224
  31. Metastatic Calcification of Multiple Visceral Organs in Non-Hodgkin’s Lymphoma. http://jnm.snmjournals.org/content/36/5/820.full.pdf
  32. Organ calcification in renal hyperparathyroidism. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1296968/
  33. Multiple organ failure associated with extensive metastatic calcification in a patient with an intermediate state of human T lymphotropic virus type I (HTLV-I) infection: report of an autopsy case.  https://www.ncbi.nlm.nih.gov/pubmed/9648162
  34. CT of Schistosomal Calcification of the Intestine. http://www.ajronline.org/doi/pdf/10.2214/ajr.144.1.75
  35. Calcifying Bowel Inflammation: A Case Report. https://www.hindawi.com/journals/grp/2010/526486/
  36. Extensive peritoneal calcification and small intestinal perforation in a peritoneal dialysis patient: A case report.  http://www.sciencedirect.com/science/article/pii/S1607551X11000210
  37. Idiopathic colonic calcification: a case report. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3687241/
  38. A Case of Isolated Small Intestinal Wall Calcification on Patient with Continuous Ambulatory Peritoneal Dialysis. http://synapse.koreamed.org/DOIx.php?id=10.4166/kjg.2013.62.1.55&vmode=PUBREADER
  39. An unusual cause of intra-abdominal calcification: A lithopedion. http://www.sciencedirect.com/science/article/pii/S2352047714000082
  40. Cephalic reflexes: their role in digestion and possible roles in absorption and metabolism. https://www.ncbi.nlm.nih.gov/pubmed/3302135
  41. Studies on the role of cephalic-vagal stimulation in the acid secretory response to eating in normal human subjects. https://www.ncbi.nlm.nih.gov/pubmed/874101
  42. Saliva Composition and Functions: A Comprehensive Review. https://www.unc.edu/courses/2008ss2/obio/720/001/2008_Readings/070308_saliva_review.pdf
  43. Saliva: its role in health and disease. https://www.ncbi.nlm.nih.gov/pubmed/3053879/
  44. INFLUENCE OF MAGNESIUM ON SALIVARY GLAND SECRETION: PHYSIOLOGICAL AND PATHOPHYSIOLOGICAL STUDIES. https://core.ac.uk/download/pdf/18581530.pdf
  45. .  https://www.ncbi.nlm.nih.gov/pubmed/5227000
  46. High Endogenous Salivary Amylase Activity Is Associated with Improved Glycemic Homeostasis following Starch Ingestion in Adults. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3327743/
  47. Effects of diabetes mellitus on salivary secretion and its composition in the human. http://link.springer.com/article/10.1023/B:MCBI.0000028748.40917.6f
  48. Magnesium: Nature’s physiologic calcium blocker. http://www.ahjonline.com/article/0002-8703(84)90572-6/references
  49. Sialolithiasis. https://www.ncbi.nlm.nih.gov/pubmed/3318353
  50. Sialolithiasis: mechanism of calculi formation and etiologic factors. https://www.ncbi.nlm.nih.gov/pubmed/12867283
  51. Salivary gland diseases: infections, sialolithiasis and mucoceles. https://www.ncbi.nlm.nih.gov/pubmed/24862601
  52. Diagnosis and treatment of sialolithiasis. https://www.ncbi.nlm.nih.gov/pubmed/15696881
  53. Current opinions in sialolithiasis diagnosis and treatment. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2639864/
  54. Increased calcium and decreased magnesium and citrate concentrations of submandibular/sublingual saliva in sialolithiasis. https://www.ncbi.nlm.nih.gov/pubmed/19962126
  55. Micromorphology of sialoliths in submandibular salivary gland: a scanning electron microscope and X-ray diffraction analysis.  https://www.ncbi.nlm.nih.gov/pubmed/15452813
  56. Physiology and pharmacology of the parietal cell. https://www.ncbi.nlm.nih.gov/pubmed/3048449
  57. Cell biology of acid secretion by the parietal cell. https://www.ncbi.nlm.nih.gov/pubmed/12500969
  58. The gastric HK-ATPase: structure, function, and inhibition. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079481/
  59. Acid secretion and the H,K ATPase of stomach. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2589780/
  60. Magnesium and the pancreas. http://ajcn.nutrition.org/content/26/3/362.abstract
  61. Effect of magnesium supplementation and depletion on the onset and course of acute experimental pancreatitis. http://gut.bmj.com/content/early/2013/11/25/gutjnl-2012-304274.abstract
  62. Magnesium intake and incidence of pancreatic cancer: the VITamins and Lifestyle study.  https://www.ncbi.nlm.nih.gov/pubmed/26554653
  63. Innate immunity in the small intestine.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3502877/
  64. The intestinal stem cell. http://genesdev.cshlp.org/content/22/14/1856
  65. Renewal of cell populations. https://www.ncbi.nlm.nih.gov/pubmed/13322651?dopt=Abstract&holding=npg
  66. Adult intestinal stem cells: critical drivers of epithelial homeostasis and regeneration.  http://www.nature.com/nrm/journal/v15/n1/full/nrm3721.html
  67. Small Intestinal Bacterial Overgrowth.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099351/
  68. Epidemiology of gastro-oesophageal reflux disease: a systematic review.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1774487/?tool=pubmed
  69. Severe hypomagnesemia in long-term users of proton-pump inhibitors. https://www.ncbi.nlm.nih.gov/pubmed/18221401
  70. Hypomagnesemia due to use of proton-pump inhibitors–a review.  https://www.ncbi.nlm.nih.gov/pubmed/19581665
  71. .  https://www.ncbi.nlm.nih.gov/pubmed/19930736
  72. Fundic atrophic gastritis in an elderly population. Effect on hemoglobin and several nutritional indicators.  https://www.ncbi.nlm.nih.gov/pubmed/3771980
  73. Aging, the gastrointestinal tract, and risk of acid-related disease. https://www.ncbi.nlm.nih.gov/pubmed/15478847
  74. Why stomach acid is good for you: Natural relief from heartburn, indigestion, reflux and GERD.  https://www.amazon.com/Why-Stomach-Acid-Good-You/dp/0871319314/ref=sr_1_1?ie=UTF8&s=books&qid=1269752363&sr=8-1
  75. Pathophysiology of gastroesophageal reflux disease. http://www.nature.com/gimo/contents/pt1/full/gimo21.html
  76. Increased Intra-abdominal Pressure and GERD/Barett’s Esophagus. http://www.gastrojournal.org/article/s0016-5085(07)01843-4/abstract
  77. Effect of erythromycin on postprandial gastroesophageal reflux in reflux esophagitis. https://www.ncbi.nlm.nih.gov/pubmed/9079271
  78. Erythromycin strengthens the defective lower esophageal sphincter in patients with gastroesophageal reflux disease. https://www.ncbi.nlm.nih.gov/pubmed/8311129
  79. Oxidative damage in the central nervous system: protection by melatonin. http://www.sciencedirect.com/science/article/pii/S0301008298000525
  80. Antiinflammatory Activity of Melatonin in Central Nervous System http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3001216/
  81. Anti-inflammatory actions of melatonin and its metabolites, N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) and N1-acetyl-5-methoxykynuramine (AMK), in macrophages. http://www.ncbi.nlm.nih.gov/pubmed/15975667
  82. Melatonin and its relation to the immune system and inflammation. http://www.ncbi.nlm.nih.gov/pubmed/11268363
  83. The Therapeutic Potential of Melatonin: A review of the science. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1395802/
  84. The role of gastric acid in preventing foodborne disease and how bacteria overcome acid conditions.  https://www.ncbi.nlm.nih.gov/pubmed/12870767
  85. Heartburn Cured: The Low Carb Miracle. https://www.amazon.com/Heartburn-Cured-The-Carb-Miracle/dp/0976642506/ref=sr_1_1?ie=UTF8&qid=1352653327&sr=8-1&keywords=heartburn+cured
  86. Helicobacter pylori infection and chronic gastric acid hyposecretion. https://www.ncbi.nlm.nih.gov/pubmed/9207257
  87. Peptic Ulcers; U.S. Department of Health and Human Services. https://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/peptic-ulcer/Pages/overview.aspx
  88. Peptic Ulcer Disease and H. pylori. http://www.ibdclinic.ca/media/uploads/h_pylori_and_peptic_ulcers.pdf
  89. Abdominal pain: Helicobacter Pylori and Gastritis. http://www.starpoli.com/helio
  90. H. pylori infection and visceral hypersensitivity in patients with irritable bowel syndrome.  https://www.ncbi.nlm.nih.gov/pubmed/11549828

Symptoms of magnesium deficiency can affect any body part. See if you have any of them.

Magnesium BEGINNER’S GUIDE: The 4 magnesium facts you need to know.

COMMON HEALTH CONCERNS:

  1. Depression and mental function
  2. Heart disease
  3. Muscular performance
  4. Weight loss & energy
  5. Sleep
  6. Digestion
  7. Skin 

 

FREQUENT QUESTIONS:

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