[dropcap]A[/dropcap]mino acids are small molecules, or subunits, that link together in various combinations to make up big, complicated proteins. As such, amino acids are commonly referred to as “the building blocks” of proteins.
Q: How many amino acids are used in our body?
A: There are 20 amino acids that are used within our body to synthesize or produce our unique human proteins. Of these amino acids, 9 are termed essential, meaning our bodies require them to live but cannot make them. Therefore, the essential amino acids must come from the food we eat, whether from plant or animal sources.
The essential amino acids include histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine.
What Is Deficiency Of Essential Amino Acids In Celiac Disease and/or Gluten Sensitivity?
This photo taken during laparoscopy shows the gall bladder (small white organ in middle) surrounded by yellow fat. Liver (dark red organ) is overlying.
What Is Impaired Gall Bladder Motility?
[dropcap]I[/dropcap]mpaired gall bladder motility means the gall bladder is slow to empty or is dysfunctional.
The functional disorder of the gallbladder is caused initially either by metabolic abnormalities or by an alteration in its muscular ability to contract (motility dysfunction).
The diagnostic criteria based on symptoms of motility dysfunction of the gallbladder are episodes of moderate to severe steady pain located in the epigastrium and right upper abdominal quadrant that last at least 30 minutes.
Gallbladder motility disorder is suspected after gallstones and other structural abnormalities have been excluded.1
Q: What does the gallbladder do?
A: The gallbladder is a small pouch-like organ about the size of a pear that receives bile produced by the liver and stores it until needed during digestion. It lies just under the liver.
Bile is a complex fluid containing water, electrolytes and many organic molecules including bile acids, cholesterol, phospholipids and bilirubin. Bile acids are critical for digestion and absorption of fats and fat-soluble vitamins in the small intestine. Many waste products, including bilirubin, are eliminated from the body by secretion into bile and elimination in feces.2
Before a meal, the gallbladder is usually full of bile. In response to fat in the diet, the gallbladder squeezes stored bile into the small intestine through a series of ducts. When emptied after meals, the gallbladder is flat.
What Is Impaired Gall Bladder Motility In Celiac Disease and/or Gluten Sensitivity?
Sources:
Behar J, Corazziari E, Guelrud M, Hogan W, Sherman S, Toouli J. Functional gallbladder and sphincter of oddi disorders. Gastroenterology. 2006 Apr;130(5):1498-509. [↩]
[dropcap]A nti-endomysium antibodies (EmA) are connective tissue autoantibodies produced in persons who have inherited the genes for celiac disease, an autoimmune disease, and are reacting to gluten in their diet.
Autoantibodies are abnormal in that they attack the body’s own tissue.
Q: What is endomysium?
A: Endomysium is the delicate connective tissue that surrounds individual muscle fibers. The autoantigen, or target, that stimulates the autoimmune response is the naturally occuring enzyme in endomysium called tissue transglutaminase (tTG), or more specifically tranglutaminase-2 (TG2). Anti-tissue transglutaminase antibodies recognize the same antigen as EmA, from which they differ in terms of detection method.
Anti-endomysium antibodies (EmA) are tested by the indirect immunofluorescence method and directed against “reticulin-like” fibres in connective tissue around smooth muscle fibres in the esophagus, liver, stomach, and bladder of monkeys, in the sections of the jejunum and kidneys of rats and in sections of the human umbilical cord. In comparison, for the determination of anti-tissue transglutaminase IgA and IgG antibodies, ELISA with human extractive or recombinant transglutaminase is recommended.1
EmA‐binding patterns in serum samples from patients with celiac disease have proved to be exclusively TG2‐targeted and the correlation between EmA and TG2 antibodies is therefore good. Evidence shows that celiac autoantibodies are produced in the small‐bowel mucosa.2
What Are Anti-Endomysium Antibodies In Celiac Disease and/or Gluten Sensitivity?
Sources:
Trigoni E, Tsirogianni A, Pipi E, Mantzaris G, Papasteriades C. Celiac disease in adult patients: specific autoantibodies in the diagnosis, monitoring, and screening. Autoimmune Dis. 2014;2014:623514. doi: 10.1155/2014/623514. [↩]
Salmi TT, Collin P, Korponay-Szabó IR, Laurila K, Partanen J, Huhtala H, Király R, Lorand L, Reunala T, Mäki M, Kaukinen K. Endomysial antibody‐negative coeliac disease: clinical characteristics and intestinal autoantibody deposits.Gut. 2006 Dec;55(12):1746-53. [↩]
What Is Irritable Bowel Syndrome? [dropcap]I[/dropcap]rritable bowel syndrome (IBS) is a motility disorder without anatomic cause involving the entire gastrointestinal tract that is characterized by these four features: 1) Abdominal pain usually relieved by defecation…
[dropcap]H[/dropcap]ypomagnesemia means the level of magnesium in the bloodstream is too low to meet metabolic needs of the body for this mineral.
Q: What are the metabolic needs of the body for magnesium?
A: The metabolic needs of the body for magnesium are numerous which gives rise to very many distressing symptoms when this mineral is deficient.
A major function of magnesium is to stabilize the structure of an enzyme called adenosine triphosphate (ATP) within cells for the production of energy. In the brain, magnesium plays important roles in all the major metabolisms such as oxidation-reduction and regulation of ions (charged minerals).1
What Is Hypomagnesemia In Celiac Disease and/or Gluten Sensitivity?
Sources:
Bourre JM. Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients. J Nutr Health Aging. 2006 Sep-Oct;10(5):377-85. [↩]
[dropcap]Z[/dropcap]incemia means the zinc level in blood plasma is too low to meet metabolic needs of the body for this mineral.
Q: How important is a normal blood level of zinc?
A: A low blood level of zinc is characterized by widespread alterations in energy metabolism, growth, hemoglobin, carbon dioxide transport, hormone activity, insulin storage, many enzyme activities, prostaglandin function, collagen production, male fertility, protein synthesis, and vitamin A metabolism.
What Is Zincemia In Celiac Disease and/or Gluten Sensitivity?
[dropcap]U rticaria is an immune based skin disorder characterized by multiple eruptions of well-demarcated edematous, intensely pruritic (itchy) plaques that may be small or reach the diameter of many centimeters with surrounding erythema (redness) each lasting less than 24 hours.1
Q: What is the immune reaction in hives?
A: Hives form when, in response to histamine, blood plasma leaks out of small blood vessels in the skin. Histamine is a chemical released from specialized cells along the skin’s blood vessels. Allergic reactions, chemicals in certain foods, insect stings, sunlight exposure, or medications can all cause histamine release.2
In many patients, in spite of extensive investigations, the cause remains elusive. The term idiopathic is often used to denote this category. Now it is known that autoimmunity is the cause of chronic urticaria in 50% of cases.
Treatment is generally started with nonsedating antihistamine in the daytime and sedating antihistamine in the night.3
What Is Chronic Urti caria In Celiac Disease and/or Gluten Sensitivity?
Sources:
Scala E, Giani M, Pirrotta L, Guerra EC, DePita O, Puddu P. Urticaria and adult celiac disease. Allergy. 1999;54:1008-9. [↩]
Gluten sensitive enteropathy is active celiac disease characterized by inflammation of the small intestinal mucosa that results from an inherited immunologic intolerance to ingested gluten.
Q: What does the inflammation do to the mucosa in the small intestine?
A: Inflammation is a cell level immune response to gluten that has these effects on the mucosa:
Damages the barely visible villi (multitudinous finger-like structures) by causing atrophy or loss.
Likely affects the structural support and microcirculation of the villus, leading to collapse of the villus.
Elongates the crypts between villi. The thickening of the crypt is not so much a response to loss of surface enterocytes but represents inflammation of the mucosa.1
Increases round cells in the lamina propria and surface epithelial cells leaving few, irregular microvilli (brush border) on the surface of villi.
Damage is most intense in the duodenum and decreases toward the large intestine.
The extent of the damage to the intestine determines the malabsorptive consequences of the disease. Both gastric and small intestinal permeability are disrupted in patients with celiac disease.2
Relationship between active celiac disease and intestinal permeability: There is a clear association between degree of mucosal damage and the intestinal-permeability ratio, and a normal ratio generally implies near-normal small intestinal structure. A raised intestinal permeability of the mucosal lining (leaky gut) could predispose to a high absorption of gluten and exacerbate an existing lesion and hence convert a latent to an overt enteropathy.3
Relationship between active celiac disease and tight junction proteins: A study of intestinal permeability showed that the expression of all junction proteins of the small intestinal lining (occludin, claudin 3, zonula occludens 1, and E-cadherin) was already decreased in early stage celiac disease when compared with non-celiac controls, showing leaky gut and confirming the above earlier study by Johnston et al. Junction protein expression correlated positively with mucosal villus structure and negatively with the number of intraepithelial lymphocytes (IELs), the intensity of small-intestinal autoantibody deposits, and serum autoantibodies. The expression of claudin 3 showed a negative correlation with diarrheal score.4
Relationship between active celiac disease and inflammation. In celiac disease there is an over production of inflammatory interleukin-15 (IL-15) which inhibits the correct removal of damaged intraepithelial lymphocytes caused by the reaction to gluten. Serum levels of IL-15 are directly correlated with the seriousness of tissue damage.5
Relationship between active celiac disease and gut microbiota. Results of a study investigating intestinal microbiota (normal bacterial residents) in patients with celiac disease suggest that with lower levels of the genus bifidobacteria, celiac patients have an imbalance in the intestinal microbiota even while on a gluten-free diet. This fact could favor the pathological process of the disorder. The concentration of bifidobacteria per gram of feces was significantly higher in healthy subjects (2.5 ± 1.5 x107 CFU/g) when compared to celiac patients (1.5 ± 0.63 x108 CFU/g).6
Relationship between active celiac disease and endoscopy technique. The most severe degree of villous atrophy was detected when distal duodenal biopsy specimens were taken in addition to a duodenal bulb biopsy specimen from either the 9- or 12-o’clock position (96.4% sensitivity; 95% CI, 79.7%-100%). The difference between the 12-o’clock position biopsy and the 3-o’clock position biopsy in detecting the most severe villous atrophy was 92% (24/26 patients) versus 65% (17/26 patients).7
Relationship between active celiac disease and diet adherence. Patients with consistent gluten free diet adherence experience symptomatic responses to dietary gluten (SRDG) faster and more severe in comparison to their prior gluten exposure possibly demonstrating an adept immunological response. Anxiety and depression also enhance the speed of symptom onset and co-existing visceral hypersensitivity is a risk factor for severe reactions to dietary gluten.8
Relationship between active celiac disease and atrial fibrillation: Patients with celiac disease, verified by intestinal biopsy, are at increased risk of atrial fibrillation. This observation is consistent with previous findings that elevation of inflammatory markers predicts atrial fibrillation.9
How Prevalent Is Gluten Sensitive Enteropathy?
Sources:
Murray JA, the widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999; 69(3):354-365. [↩]
Murray JA, the widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999; 69(3):354-365. [↩]
Johnston SD, Smye M, Watson RGP. Intestinal permeability and morphometric recovery in coeliac disease. Lancet. Jul 28, 2001;358(9278):259, 2p. [↩]
Rauhavirta T, Lindfors K, Koskinen O, Laurila K, Kurppa K, Saavalainen P, Mäki M, Collin P, Kaukinen K. Impaired epithelial integrity in the duodenal mucosa in early stages of celiac disease. Transl Res. 2014 Sep;164(3):223-31. doi: 10.1016/j.trsl.2014.02.006 [↩]
Stazi AV, Trinti B. Selenium status and over-expression of interleukin-15 in celiac disease and autoimmune thyroid diseases. Ann Ist Super Sanita. 2010;46(4):389-99.DOI: 10.4415/ANN_10_04_06. [↩]
Golfetto L, de Senna FD, Hermes J, Beserra BT, França Fda S, Martinello F. Lower bifidobacteria counts in adult patients with celiac disease on a gluten-free diet. Arq Gastroenterol. 2014 Apr-Jun;51(2):139-43. [↩]
Kurien M, Evans KE, Hopper AD, Hale MF, Cross SS, Sanders DS. Duodenal bulb biopsies for diagnosing adult celiac disease: is there an optimal biopsy site? Gastrointest Endosc. 2012 Jun;75(6):1190-6. doi: 10.1016/j.gie.2012.02.025. [↩]
Barratt SM, Leeds JS, Sanders DS. Factors influencing the type, timing and severity of symptomatic responses to dietary gluten in patients with biopsy-proven coeliac disease. J Gastrointestin Liver Dis. 2013 Dec;22(4):391-6. [↩]
Emilsson L, Smith JG, West J, Melander O, Ludvigsson JF. Increased risk of atrial fibrillation in patients with coeliac disease: a nationwide cohort study. Eur Heart J. 2011 Oct;32(19):2430-7. doi: 10.1093/eurheartj/ehr167. [↩]
[dropcap]O[/dropcap]bnoxious gas, or flatus, is gas that is not only offensive when passed but also lingers in the air longer than ordinary gas does.
Gas is a natural digestive product within the colon that is composed mainly of hydrogen and carbon dioxide gases. These gases are given off in the necessary bacterial breakdown of undigested fermentable food entering the colon from the small intestine.
Q: What makes gas obnoxious?
A: The production of obnoxious gas depends on the type and quantity of undigested food residue that is passed into the colon from the small intestine, dysfunctional motility instead of normal peristalsis, and dysbiosis. Dysbiosis is the condition of having unhealthy or insufficient populations of microbes responsible for digesting (fermenting) foodstuffs in the lower gut or colon.
Gases produced by intestinal microbes may modulate intestinal motor function (muscle movement) in individuals with functional bowel disease. Methane, produced by enteric bacteria in the human gut, is associated with slowed intestinal transit and constipation.1
What Is Obnoxious Gas In Celiac Disease and/or Gluten Sensitivity?
Sources:
Jahng J, Jung IS, Choi EJ, Conklin JL, Park H. The effects of methane and hydrogen gases produced by enteric bacteria on ileal motility and colonic transit time. Neurogastroenterol Motil. 2012 Feb;24(2):185-90, e92. doi: 10.1111/j.1365-2982.2011.01819.x. Epub 2011 Nov 20.
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 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. ((Triantafyllou K, Chang C, Pimentel M. Methanogens, Methane and Gastrointestinal Motility. J Neurogastroenterol Motil. 2014 Jan;20(1):31-40. Epub 2013 Dec 30. [↩]
What Are Essential Amino Acids?
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