Magnesium is an essential mineral predominantly found in the body within cells, where it is vital for their functions.
Here is a summary of what magnesium does in our body:
Co-factor for over 300 enzymes involved in the metabolism of food components and synthesis of many compounds.
Required for nerve transmission.
Required for muscle activity (acts to relax muscles in opposition to calcium which acts to contract).
Acts to maintain heart rhythm.
Required for membrane transport and interactions.
Required for glucose metabolism and energy production within cells.
Component of bone mineralization and tooth formation.
Plays a key role in calcium and phosphorus metabolism and management by parathyroid hormone.
Maintains the structural and functional integrity of vital eye tissues such as lens.1
Only 1% of magnesium is found in blood, but the body must keep blood levels of magnesium constant.
What Is Magnesium Deficiency In Celiac Disease and/or Gluten Sensitivity?
Sources:
Agarwal R, Iezhitsa I, Agarwal P, Spasov A. Magnesium deficiency: does it have a role to play in cataractogenesis? Exp Eye Res. 2012 Aug; 101:82-9. doi: 10.1016/j.exer.2012.05.008. [↩]
Chronic constipation is an intestinal motility disorder characterized by abnormal stool formation, consistency, and evacuation.
Motility disorder means the normal rhythmic movement of intestinal muscles, called peristalsis, that moves food matter through the gut is hampered or dysfunctional.
Studies show that methane gas present in the colon induces constipation by delaying transit time, which is the time it takes for stool to pass through the colon.
Researchers investigating the relationship between methane and constipation found that methane positivity was detected in 75% of patients with slow transit, 44% of patients with normal transit and and 28% of the patients who were controls. However, methane positivity was not related with stool consistency.1
Other researchers investigating the total amount of methane produced found that there was significantly more methane production in patients with constipation (21.1 ppm vs. 6.1 ppm, respectively) than in controls without constipation.2
Q. How does methane get into the colon?
A. Methane is produced in the colon by intestinal methanogens (microbes) that metabolize hydrogen, one of the end products of normal anaerobic (meaning without oxygen) bacterial fermentation. Fermentation of the undigested starchy part of carbohydrates produces hydrogen in the intestine which is the substrate (food) for methane production by intestinal methanogens.
Hydrogen and methane are excreted in the flatus and in breath giving the opportunity to indirectly measure their production using breath testing. Methane is detected in 30%-50% of the healthy adult population worldwide.3
Other common causes of constipation include not getting enough exercise, not drinking enough fluids, not eating enough fiber in the diet, not eating foods that supply microbes needed by the colon (probiotics), not eating foods that nourish the good microbe population (prebiotics) and supply minerals needed for healthy movement of stool, and food sensitivities. Too much cows milk is a common cause of stool that forms into balls.
Who is Affected in the General Population? Chronic constipation is a remarkably common and costly condition that can negatively impact the quality of life and result in a major social and economic burden. Based on the definition, either self-reported or using Rome criteria, chronic constipation can affect up to 27% of the population. There is strong evidence that constipation occurs more frequently in women.4
What Is Chronic Constipation In Celiac Disease and/or Gluten Sensitivity?
Sources:
Triantafyllou K, Chang C, Pimentel M. Methanogens, Methane and Gastrointestinal Motility. J Neurogastroenterol Motil. 2014 Jan;20(1):31-40. Epub 2013 Dec 30. [↩]
Triantafyllou K, Chang C, Pimentel M. Methanogens, Methane and Gastrointestinal Motility. J Neurogastroenterol Motil. 2014 Jan;20(1):31-40. Epub 2013 Dec 30. [↩]
Triantafyllou K, Chang C, Pimentel M. Methanogens, Methane and Gastrointestinal Motility. J Neurogastroenterol Motil. 2014 Jan;20(1):31-40. Epub 2013 Dec 30. [↩]
Sanchez MI, Bercik P. Epidemiology and burden of chronic constipation. Can J Gastroenterol. 2011 Oct;25 Suppl B:11B-15B. [↩]
E czema, or atopic dermatitis, is a chronic recurring inflammatory skin disorder characterized by itching, eczematous plaques and a defective epidermal barrier (surface layer of skin cells) that fails to hold moisture, with affected areas becoming dry then inflamed.
Q: Why does eczema develop?
A: Patients with atopic dermatitis have genetically determined risk factors that affect the barrier function of the skin and immune responses that interact with environmental factors.1
Atopic eczema is associated both with an abnormal skin matrix and impaired systemic immune response. Therefore, isolated topical treatment may have suboptimal effect.2
Atopic eczema is a common presentation of immune response towards food proteins in infancy.3
Global evidences reflect a marked increase in prevalence, which has tripled since 1960. In the United States, the current prevalence rates range from 10% to 20% in children and 1 to 3% in adults.4
What Is Eczema In Celiac Disease and/or Gluten Sensitivity?
Sources:
Mesquita Kde C, Igreja AC, Costa IM. Atopic dermatitis and vitamin D: facts and controversies. An Bras Dermatol. 2013 Nov-Dec;88(6):945-53. doi: 10.1590/abd1806-4841.20132660. [↩]
Caffarelli C, Santamaria F, Vottero A, Bernasconi S. Progress in Pediatrics in 2012: choices in allergy, endocrinology, gastroenterology, hematology, infectious diseases, neurology, nutrition and respiratory tract illnesses. Ital J Pediatr. 2013 May 8;39(1):26. [↩]
Ho MH, Wong WH, Chang C. Clinical Spectrum of Food Allergies: a Comprehensive Review. Clin Rev Allergy Immunol. 2012 Nov 16. [↩]
Mesquita Kde C, Igreja AC, Costa IM. Atopic dermatitis and vitamin D: facts and controversies. An Bras Dermatol. 2013 Nov-Dec;88(6):945-53. doi: 10.1590/abd1806-4841.20132660. [↩]
A cquired ichthyosis is an uncommon, nonhereditary cutaneous disorder characterized by dry, rough skin with prominent symmetrical scaling that involves significant portions of the body.
Most microscopic studies of acquired ichthyosis exhibit hyperkeratosis (thickened skin) with a reduced or absent granular layer.1
Q: What is the granular layer of skin?
A: The granular layer is the third cell layer(of five) composing the epidermis, or outer surface of skin.
Acquired icthyosis has been associated with internal disease including malignancies, autoimmune/inflammatory, metabolic, endocrine, and infectious diseases, and medication use.
What Is Acquired Ichthyosis In Celiac Disease and/or Gluten Sensitivity?
Sources:
Patel N, Spencer LA, English JC 3rd, Zirwas MJ. Acquired ichthyosis. J Am Acad Dermatol. 2006 Oct;55(4):647-56. [↩]
Close-up shows inflammation and infected patches on roof and back of the mouth caused by candidiasis. Uvula is swollen, hanging near the tongue. Courtesy: Wikimedia.
What Is Candida Albicans Infection?
Candida albicans infection, called candidosis or candidiasis, is an opportunistic invasion of mucous membrane or skin by candida albicans, an endogenous yeast found in 40 to 80% of normal human beings. A former name for this small, budding fungus is monilia albicans.
Opportunistic means that yeast living on mucosal and skin surfaces does not invade (infect) unless these tissues become unhealthy and therefore cannot protect themselves.
Q: How does candida albicans cause infection?
A: Candida albicans lives on the mucosal surfaces and skin in most people without causing infection (colonizes) because of our normal defenses against invasion. In fact, candida albicans is a very effective colonizer of humans. For example, Russell and Lay found that 47% of 1-month-old infants were orally colonized with candida albicans, and 49% were colonized with other fungi.
During growth within the intestinal tract, the organism senses pH (acidity), oxygen, carbon sources, and the presence of surfaces allowing it to optimize gene expression for a particular environment. With these mechanisms for sensing, candida albicans is able to efficiently colonize humans in infancy.1
Candida Infection Of The Esophagus (White Area) On X-ray. Courtesy Radiology Assistant.nl
Lowered host defenses allow yeast already present on mucosal and skin surfaces to take advantage and can grow rapidly, becoming pathogenic (disease producing) so that infection results.
Infection is characterized by superficial, irregular white patches on mucosal surfaces and possible invasion of the bloodstream by a filamentous form (thread-like structures) that can rapidly develop.
Candida albicans is unique among oral pathogens in its ability to invade cornified layers of stratified squamous epithelium of the tongue, mouth surfaces, hard and soft palate, esophagus, and gut. Stratified squamous epithelium is the tough surface cells that ordinarily protect underlying tissues from damage or invasion by microbes.
Candida albicans is also capable of invading the lungs and causing pneumonia and septicemia, which is the spread of infection into the bloodstream.
Here is a time honored simple do-it-youself test for infection of the mouth or throat: First thing in the morning before brushing your teeth or eating, fill a small see through glass with water then gently spit onto the surface. If after an hour the spit remains on the water surface, it is unlikely you have candida in the mouth. If it grows legs downward, it indicates that yeast is growing. If the spit sinks to the bottom, you have this problem. Yeast in the mouth can quickly travel down the esophagus and into the gut.
Medical diagnosis. Difinitive diagnosis for the oral cavity is made by your clinician by swabbing the areas of your mouth and/or throat and viewing under a microscope for evidence of candida.
Infections of the esophagus and gut require inspection by gastroscopy or endoscopy procedure and the taking of samples to be examined under microscope. This examination also give the opportunity to rule out other problems. Barium swallow can show the extent of infection and any disfiguration of the esophagus that results.
What Is Candida Albicans Infection In Celiac Disease and/or Gluten Sensitivity?
Sources:
Rosenbach A, Dignard D, Pierce JV, Whiteway M, Kumamoto CA. Adaptations of Candida albicans for growth in the mammalian intestinal tract. Eukaryot Cell. 2010 Jul;9(7):1075-86. doi: 10.1128/EC.00034-10. Epub 2010 Apr 30. [↩]
Dementia is the term used to describe a group of symptoms that show significant deterioration of an individual’s intellectual and social abilities.
The deterioration in intellectual function is progressive and is characterized by memory and cognitive impairment involving deficits in reasoning, judgment, abstract thought, comprehension, learning, use of language, and task execution.
Some types of dementia can be reversed, while most types of dementia are degenerative or nonreversible.
Q: What causes dementia?
A: There are many differing causes of dementia. Here are some causes according to nonreversible and reversible:
Nonreversible dementia may not be turned back due to these conditions:
Alzheimer’s disease is the most common type of degenerative dementia caused by abnormal protein structures in certain areas of the brain.
Lewy body disease is a leading cause of dementia in elderly adults.
Vascular dementia due to many small strokes.
Medical conditions: Huntington’s disease, multiple sclerosis, infections that can affect the brain, such as HIV/AIDS and Lyme disease, Parkinson’s disease, Pick’s disease, and progressive supranuclear palsy.
Reversible dementia may be stopped or reversed if these conditions are found soon enough:
Brain injury.
Brain tumors.
Chronic alcohol abuse.
Changes in blood sugar, sodium, and calcium levels.
Changes that can occur with celiac disease, diabetes, thyroid disease, and other metabolic disorders.
Nutritional deficiencies.
Use of certain medications, including cimetadine and some cholesterol-lowering medications.1
What Is Dementia In Celiac Disease and/or Gluten Sensitivity?
Photo by gastroscopy showing ulcer in the antrum area of the stomach (lower area).
What Is A Gastric Ulcer?
G astric ulcer is a painful stomach disorder characterized by an open sore involving the mucosa lining and deeper muscle layer of the stomach.
Gastric ulcer is associated with lymphocytic gastritis which is inflammation of the mucosal lining of the stomach. The thick mucosal lining normally protects the stomach from the erosive action of stomach acid.
Q: How do ulcers develop?
A: Ulcers develop if hydrochloric acid secreted by the gastric glands of the stomach for the purpose of digesting food damages the normally resistant mucosal walls of the stomach. In the reverse, ulcers may be accompanied by achlorhydria (insufficient acid production).
Damage occurs when there is a predisposing factor that alters the health of the mucosal lining. The most common cause is infection with a bacteria called h. pylori bacter, stress and chronic use of the pain relievers aspirin and non-steroidal drugs like ibuprofen.
Smoking tocacco and consuming alcohol aggravate an ulcer but do not cause it to develop.
The most common location for ulcer formation is along the stomach antrum which is the area of the stomach before the pylorus, the lower region that empties liquid stomach contents into the small intestine.
What Is A Gastric Ulcer In Celiac Disease and/or Gluten Sensitivity?
Malnourished Infant With Acute Diarrhea and Swollen Belly.
What Is Acute Diarrhea?
A cute diarrhea is a small intestinal motility disorder characterized by excessively rapid movement of intestinal contents through the small intestine with excessive loss of fluid and electrolytes that leads rapidly to a life threatening hypokalemia (low potassium blood level) and acidosis.
Q: What is hypokalemia?
A: Hypokalemia is characterized by dehydration that may result in vascular collapse, muscular malfunction that may result in paralytic ileus (bowels do not move), paralysis (cannot stand), and respiratory hypoventilation (shallow breathing) or failure, metabolic acidosis resulting from diarrhea, and impaired nerve conduction.1
While diarrhea may be a common symptom of small bowel mucosal disease, the consequent malabsorption can lead to substantial malnutrition and nutrient deficiencies. The small intestine, unlike the colon, has been relatively inaccessible, and systematic evaluation is often necessary to identify and treat small intestinal mucosal diseases that lead to diarrhea. All patients with severe diarrhea or diarrhea associated with features suggestive of malabsorption may have a disease of the small intestinal mucosa that requires careful evaluation and targeted management.2
What Is Acute Diarrhea In Celiac Disease and/or Gluten Sensitivity?
Murray JA1, Rubio-Tapia A. Diarrhoea due to small bowel diseases. Best Pract Res Clin Gastroenterol. 2012 Oct;26(5):581-600. doi: 10.1016/j.bpg.2012.11.013. [↩]
What Are Erosions In The Second Part Of The Duodenum?
E rosions in the second part of the duodenum typically are superficial excoriations (sores) in the mucosal lining that do not penetrate into the muscle layer as does an ulcer.
Of note, most erosions develop in the first part of the duodenum rather than the second part.
Q: Are duodenal erosions serious?
A: Yes duodenal erosions are serious and can be life-threatening for the following reasons:
Duodenal erosions may occur together with gastric erosions, therefore they can jointly induce massive bleeding.
Duodenal erosions may be associated with duodenal ulcer but hemorrhage originates from the erosion and the ulcer itself does not bleed.
Duodenal erosion in itself might induce bleeding. The intensity of bleeding, if there is no hemorrhage from other places, is not so severe, as the one originating from gastric erosions.1
What Are Erosions In The Second Part Of The Duodenum In Celiac Disease and/or Gluten Sensitivity?
Sources:
Preisich P, Farkas I, Konyár EJ. The role of duodenal erosions in the occurrence of upper gastrointestinal haemorrhage. Scand J Gastroenterol Suppl. 1989;167:36-8. [↩]
Endoscopic Image of Crohn’s Disease Showing Deep Ulceration in the Sigmoid Colon.
What Is Crohn’s Disease?
Crohn’s disease is an inflammatory bowel disease characterized by patchy inflamed areas involving the full thickness of the intestinal wall that can occur anywhere in the intestinal tract, in addition to, mucosal disease.
In Crohn’s disease there is ongoing immune activation which produces inflammation and ulceration but the cause is not known and the severity varies among patients. At diagnosis of Crohn’s disease, factors predictive of subsequent 5-year aggressive disease are an age below 40 years, the presence of perianal disease, and the initial requirement for steroids.1
Dysbiosis is a factor that develops in and worsens Crohn’s disease and stress is a factor in both of these conditions. Psychological stress activates multiple physiological processes aimed at maintaining balance within the body. These physiological processes also have the capacity to influence the composition of microbial communities in the digestive tract, and research now indicates that exposure to stressful stimuli leads to gut microbiota dysbiosis.2
While the relative abundance of many different bacterial types can be altered during stressor exposure, findings in nonhuman primates and laboratory rodents, as well as humans, indicate that bacteria in the genus Lactobacillus are consistently reduced in the gut during stress.2
Q: Is there a cure for Crohn’s disease?
A: Presently, Crohn’s disease cannot be cured. This condition has a course of remissions, when symptoms subside, and flares, when symtpoms get worse. Treatment is aimed to reduce flares and promote remission.
What Is Crohn’s Disease In Celiac Disease and/or Gluten Sensitivity?
Sources:
Beaugerie L, Seksik P, Nion-Larmurier I, Gendre JP, Cosnes J. Predictors of Crohn’s disease. Gastroenterology. 2006;130:650–656. [↩]
Galley JD, Bailey MT. Impact of stressor exposure on the interplay between commensal microbiota and host inflammation. Gut Microbes. 2014 May 1;5(3):390-396. Epub 2014 Apr 1. [↩] [↩]
