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Vitamin C Deficiency

vitamin c gluten celiac disease symptomWhat Is Vitamin C?

[dropcap]V[/dropcap]itamin C, also called ascorbic acid or ascorbate, is an essential water soluble vitamin.

Fresh supplies of vitamin C are required every day to perform vital roles throughout the body among which are the production of connective tissue such as skin, blood vessels and bone, anti-inflammatory responses and anti-oxidant performance. See below for all roles.

Vitamin C fights for us! It has an anti-cancer effect stemming from its role as a potent anti-oxidant in blood plasma and within cells. It also protects nucleic acids (DNA) from oxidative damage and inhibits the formation of nitrosamines (carcinogenic compounds formed in the digestive tract).

Importantly, vitamin C can regenerate vitamin E from an oxidized state after vitamin E performs its own anti-oxidant role against free radicals and vitamin C works together with other anti-oxidants, such as beta-carotene and glutathione, to increase their overall anti-oxidant effect.

A study investigating the specific anti-inflammatory and anti-oxidant micronutrients that reduce oxidative stress found that in adolescents with metabolic syndrome (MetS) the lower the vitamin C level in blood the worse the MetS status and blood uric acid level.  MetS prevalence was estimated at 7% among boys and 3% among girls.1

Vitamin C reverses osteoporosis by reducing or preventing oxidative stress that destroys living bone tissue. Osteoporosis is a disorder of bone inflammation that results in thin, weak bones that may easily fracture. In normal bone structure, vitamin C is required to form collagen, which is living bone tissue.

In humans, vitamin C reduces the duration of common cold symptoms, even if its effect is not clear.2

Vitamin C must be obtained from food daily because our bodies, unlike monkeys and other animals, cannot produce it.

Urinary excretion of vitamin C 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.3

What Is Vitamin C Deficiency In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. TGBeydoun MA, Canas JA, Beydoun HA, Chen X, Shroff MR, Zonderman AB. Serum antioxidant concentrations and metabolic syndrome are associated among U.S. adolescents in recent national surveys. J Nutr. 2012 Sep;142(9):1693-704. doi: 10.3945/jn.112.160416. [↩]
  2. Shaik-Dasthagirisaheb YB, Varvara G, Murmura G, Saggini A, Caraffa A, Antinolfi P, Tete’ S, Tripodi D, Conti F, Cianchetti E, Toniato E, Rosati M, Speranza L,Pantalone A, Saggini R, Tei M, Speziali A, Conti P, Theoharides TC, Pandolfi F. Role of vitamins D, E and C in immunity and inflammation. J Biol Regul Homeost Agents. 2013 Apr-Jun;27(2):291-5. [↩]
  3. 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. [↩]

Schizophrenia

Collagenous Colitis.
Microscopic Image Showing a Pink Collagen Band in Collagenous Colitis.

What Is Collagenous Colitis?

[dropcap]C ollagenous colitis is a disease of the large intestine (colon) that is characterized by microscopic inflammation of the surface mucosal lining and an abnormally thickened collagen band of tissue that develops wthin the lining of the colon.

The thicker than normal layer of collagen of at least 10 µm (reference value: 2–7 µm) can vary in different locations. Inflammation occurs with increased numbers of lymphocytes (white blood cells) and plasma cells and epithelial (surface cell) damage. These changes can only be seen under microscopic examination of multiple biopsied tissue samples taken during a colonoscopy procedure.

Q: What is collagen?

A: Collagen is a strong, fibrous protein found in connective tissue of the colon and many other tissues such as tendons. The normal basement membrane in the bowel consists mainly of collagen type IV, laminin, and fibronectin. The increased collagen band observed in collagenous colitis consists basically of collagen type I and III, which are the subtypes produced by repair functions, indicating a reactive origin to some irritant or drug.1

The biopsies should preferably be taken from the ascending colon, since the pathological hallmarks may be absent in the descending colon, and in the normally occurring thicker collagen layer in the rectosigmoid region.1 Inflammation of the ileum (last segment of the small intestine next to colon) is common.2

Endoscopy and radiological (x-ray) examinations are usually normal.3

Autoimmune disorders are frequently seen in adult patients with collagenous colitis.4 In the study below by Koskela et al. concomittent autoimmune diseases were present in 53% of patients with collagenous colitis.5

Importantly, the finding of collagenous colitis in patients with autoimmune diseases may reflect the treatment with NSAIDs (non-steroidal anti-inflammatory drugs), such as Ibuprofin and aspirin, PPIs (proton pump inhibitors), and other drugs. However, if secondary forms of collagenous colitis are not taken into consideration, underlying, treatable diseases may be overlooked, while only the gastrointestinal symptoms are treated symptomatically or with budesonide (a steroid).6

Treatment with budesonide steroid is efficacious irrespective of bile acid malabsorption.7

Budesonide at a mean dose of 4.5 mg/day maintained clinical remission for at least 1 year in the majority of patients with collagenous colitis and preserved health-related quality of life without safety concerns. Treatment extension with low-dose budesonide beyond 1 year may be beneficial given the high relapse rate after budesonide discontinuation.8

See below for nutritional deficiency problems caused by steroid usage and steps to be taken for correction.

What Is Collagenous Colitis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Ohlsson B. New insights and challenges in microscopic colitis. Therap Adv Gastroenterol. 2015 Jan;8(1):37-47. doi: 10.1177/1756283X14550134. [↩] [↩]
  2. Bjørnbak C, Engel PJ, Nielsen PL, Munck LK. Microscopic colitis: clinical findings, topography and persistence of histopathological subgroups. Aliment Pharmacol Ther. 2011 Nov;34(10):1225-34. doi: 10.1111/j.1365-2036.2011.04865.x. [↩]
  3. Abdo AA, Urbanski SJ, Beck PL. Lymphotcytic and collagenous colitis: the emerging entity of microscopic colitis. An update on pathophysiology, diagnosis and management. Canadian Journal of Gastroenterology. Jul 2003;17(7):425-32. [↩]
  4. Leung ST, Chandan VS, Murray JA, Wu TT. Collagenous gastritis: histopathologic features and association with other gastrointestinal diseases. Am J Surg Pathol. 2009 May;33(5):788-98. doi: 10.1097/PAS.0b013e318196a67f. [↩]
  5. Koskela RM, Niemela SE, Karttunen TJ, Lehtola JK. Clinical characteristics of collagenous and lymphocytic colitis. Scandanavian Journal of Gastroenterology. Sep 2004;39(9):837-45. [↩]
  6. Ohlsson B. New insights and challenges in microscopic colitis. Therap Adv Gastroenterol. 2015 Jan;8(1):37-47. doi: 10.1177/1756283X14550134. [↩]
  7. Bjørnbak C, Engel PJ, Nielsen PL, Munck LK. Microscopic colitis: clinical findings, topography and persistence of histopathological subgroups. Aliment Pharmacol Ther. 2011 Nov;34(10):1225-34. doi: 10.1111/j.1365-2036.2011.04865.x. [↩]
  8. Münch A, Bohr J, Miehlke S, et al. Low-dose budesonide for maintenance of clinical remission in collagenous colitis: a randomised, placebo-controlled, 12-month trial. Gut. 2014 Nov 25. pii: gutjnl-2014-308363. doi: 10.1136/gutjnl-2014-308363. [↩]