[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?
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. [↩]
[dropcap]N[/dropcap]iacin is an essential water-soluble B vitamin that is required by all cells of the body.
During digestion of food containing it, niacin (the form in food) is changed in the small intestines to the active form niacinamide (niacin plus an amide group), which is then absorbed into the bloodstream.
Niacinamide is converted by the body into co-enzymes which are present in all cells. These are niacinimide adenine dinucleotide (NAD) and NADP. NADP is formed when the body adds a phosphate to NAD.
Q: How do these enzymes work?
A: These enzymes function in oxidation-reduction reactions essential for release of energy from carbohydrates, fats, and proteins and are needed as components for more than 200 enzymes involved in metabolism.
In addition to producing energy, niacinamide is essential for healthy skin and the mucosal lining of the digestive tract, normal functioning of the brain and nervous system, and production of steroid hormones in adrenal glands and hormones in sex glands. Functions are more fully described below.
Urinary excretion of niacin cannot be detected when vitamin intake is below the required levels. On the other hand, when intake exceeds saturation in the body, the vitamin and/or its metabolites are actively excreted into urine to prevent excessive toxicity of the vitamins.1
What Is Niacin Deficiency In Celiac Disease and/or Gluten Sensitivity?
Sources:
Shibata K, Hirose J, Fukuwatari T. Relationship Between Urinary Concentrations of Nine Water-soluble Vitamins and their Vitamin Intakes in Japanese Adult Males. Nutr Metab Insights. 2014 Aug 5;7:61-75. doi: 10.4137/NMI.S17245. eCollection 2014. [↩]
Testing the Eye for Tear Production (L) and Damage to Conjunctiva from Dryness (R).
What Is Sjögren’s Syndrome?
[dropcap]S jögren’s syndrome is a systemic inflammatory autoimmune disease with a chronic, progressive course that primarily attacks the lacrimal glands of the eye and the salivary glands of the mouth, which are exocrine glands. Exocrine glands secrete the substances they produce through a duct.
Sjögren’s syndrome is ordinarily characterized by dysfunction of the lacrimal glands to produce tears causing dry eye and the salivary glands to produce saliva causing dry mouth, but is not limited by or to these features.
Besides involvement of these exocrine glands, there may be involvement of other parts of the body, termed extraglandular, which may be more severe than eye or mouth features.
There is not yet agreement on classifying Sjögren’s syndrome. Primary and secondary are the two forms generally accepted.1 Both forms can cause mild to severe disease, called the spectrum:
Primary Sjögren syndrome. Disease occurs without involvement of other linked autoimmune disorders. In addition to the eyes and mouth, the nose, throat and skin may also be affected and joints, lungs, kidneys, blood vessels, digestive organs and nerves as well.2 Systemic manifestations (other than eyes and mouth) concern a third of patients, including lymphoma in 5% of the patients.3
Secondary Sjögren’s syndrome. Disease complicates other autoimmune disease such as systemic lupus erythematosus, rheumatoid arthritis, primary biliary cirrhosis, and celiac disease.
Diagnosis of Sjögren’s syndrome is made by most doctors based on Schimer’s test for tears and unstimulated whole salivary flow to assess objective eye and oral involvement, since these are the tests most physicians use in clinical practice.4 Specific antibody tests would be positive for anti-Ro (SSA)/anti-La (SSB) autoantibodies. Sjögren’s syndrome should also be considered when extraglandular manifestations such as vasculitis, polyneuropathy or arthritis occur, even when the patients do not complain of dry eyes and mouth.5
There is no cure for Sjögren’s syndrome. Treatment is aimed to diminish symptoms. For example, steroids and Ibupropen are used to decrease inflammation and pain in joints. Artificial tears and ointments are used for dry eye.
Most people who develop Sjogren’s syndrome are older than 40 years. Nine of ten people with Sjögren’s syndrome are women.2
What Is Sjögren’s Syndrome In Celiac Disease and/or Gluten Sensitivity?
Sources:
Huang YF, Cheng Q, Jiang CM, An S, Xiao L, Gou YC, Yu WJ, Lei L, Chen QM, Wang Y, Wang J. The immune factors involved in the pathogenesis, diagnosis, and treatment of Sjogren’s syndrome. Clin Dev Immunol. 2013;2013:160491. doi: 10.1155/2013/160491. Epub 2013 Jul 9. [↩]
Fazaa A, Bourcier T, Chatelus E, Sordet C, Theulin A, Sibilia J, Gottenberg JE. Classification criteria and treatment modalities in primary Sjögren’s syndrome. Expert Rev Clin Immunol. 2014 Apr;10(4):543-51. doi: 10.1586/1744666X.2014.897230. [↩]
Cornec D, Saraux A, Cochener B, Pers JO, Jousse-Joulin S, Renaudineau Y, Marhadour T, Devauchelle-Pensec V. Level of agreement between 2002 American-European Consensus Group and 2012 American College of Rheumatology classification criteria for Sjogren’s syndrome and reasons for discrepancies. Arthritis Res Ther. 2014 Mar 19;16(2):R74. [↩]
Witte T. Pathogenesis and diagnosis of Sjögren’s syndrome. Z Rheumatol. 2010 Feb;69(1):50-6. doi: 10.1007/s00393-009-0519-2. [↩]
What Is Carbohydrate Malabsorption? [dropcap]C[/dropcap]arbohydrate malabsorption is a digestive disorder characterized by the inability to properly digest and absorb carbohydrates within the small intestine to supply needed energy to the body. Q: What carbohydrates should be normally…
Intestinal Edema of Duodenum in an 11 Month Old Baby. Courtesy: Nature.com
What Is Small Intestinal Edema?
[dropcap]S[/dropcap]mall intestinal edema is characterized by fluid accumulation within the intestinal mucosa so that the intestinal wall appears thick and swollen.
Intestinal edema hampers peristalsis that can result in pain and gas build-up. Peristalsis is the normal rhythmic muscular wave-like action that moves residue along the gastrointestinal tract.
Q: What part of the small intestinal lining is swollen?
A: Any part of the small intestine may be affected. Some causes of edema include allergic reactions, enteropathies such as celiac disease, cow milk enteropthy, yeast infection, parasite infection, inflammatory bowel disease such as Crohn’s disease, and certain medications.
For example, the anti-hypertensive drugs known as Angiotension Converting Enzyme (ACE) inhibitors can cause intestinal angioedema and therefore the patient may present with gastrointestinal complaints.1
What Is Small Intestinal Edema In Celiac Disease and/or Gluten Sensitivity?
Sources:
LoCascio E J, Mahler S A, and Arnold TC. Intestinal Angioedema Misdiagnosed as Recurrent Episodes of Gastroenteritis. West J Emerg Med. Sep 2010; 11(4): 391–394. [↩]
Small Bowel Volvulus Caused the Enlarged Dark Loops. Courtesy African Journal of Pediatric Surgery.
What Is Volvulus?
[dropcap]V[/dropcap]olvulus is twisting of a loop(s) of bowel onto itself which effectively closes it thus preventing digested matter from passing and causing engorgement of the closed loop with gas and fluid.
Q: How does the bowel get untwisted?
A: This condition usually necessitates surgical correction although some do return to their proper position.
The danger is that there may develop necrosis of the twisted loop(s) in which case, if left untreated,death will ensue.
What Is Volvulus In Celiac Disease and/or Gluten Sensitivity?
Fluid accumulation within small intestinal mucosa resulting from inflammation that may cause abdominal pain and distention because of hampering peristalsis. Click Small Intestinal Edema for full description.
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What Are Essential Amino Acids?
