[dropcap]F[/dropcap]olate, also called folic acid or vitamin B9, is a family group of essential water-soluble B vitamins needed to produce healthy blood cells and other tissue cells.
Folate is required for healthy blood cells, the metabolism of at least 5 amino acids, the production of DNA, RNA and tRNA (genetic material), the normal development of a baby in the womb, male and female fertility, and regulation of homocysteine (amino acid) by reduction of harmful blood levels in conjunction with vitamin B6 and vitamin B12.
Urinary excretion of folate cannot be detected when vitamin intake is below the required levels. On the other hand, when intake exceeds saturation in the body, the vitamins and/or their metabolites are actively excreted into urine to prevent excessive toxicity of the vitamins.1
What Is Folate 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. [↩]
[dropcap]V[/dropcap]itamin B12, also called cobalamin, is a highly complex vitamin that functions in two coenzyme forms: adenosylcobalamin and methylcobalamin.
These forms of the vitamin play important roles in the physical and chemical processes by which amino acids become proprionate, proprionate that becomes acetate, and single carbons.
Q: Why are these steps important?
A: These steps are essential for normal function in the workings of all cells, especially for those of the digestive tract, bone marrow and nervous tissue.
Vitamin B12 is mainly excreted through bile into the duodenum (first part of the small intestine) for excretion in stool.1 However, if vitamin B12 is needed, it is reabsorbed in the ileum (end of the small intestine) while excess is excreted in stool and very little in urine.2
The blood level of vitamin B12 in healthy people ranges between 140 and 750 pg/ml.
What Is Vitamin B12 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. [↩]
Shinton N K. Vitamin B 12 and folate metabolism. Br Med J. Feb 26, 1972; 1(5799): 556–559. [↩]
What Is Milk Intolerance (Bovine Beta Casein Enteropathy)?
[dropcap]B ovine beta casein enteropathy is characterized by raised serum IgA antibodies to bovine beta casein found by blood testing and damage to mucosa of the jejunum found by biopsy.
The jejunum is the second section of the small intestine, between the duodenum and the ileum.
Mucosa damage is similar to damage caused by gluten.
Q: What is bovine beta casein?
A: Bovine beta casein is a protein found in cow’s milk.
An immune reaction to protein in milk is totally different from lactose intolerance. Lactose intolerance develops from deficiency of an intestinal enzyme called lactase which is required to digest lactose, the sugar in milk.
What Is Milk Intolerance In Celiac Disease and/or Gluten Sensitivity?
Hypoglycemia means the level of glucose within cells is too low to meet metabolic needs of the body for this essential sugar.
Q: What are the metabolic needs for glucose?
A: Glucose is the most important simple sugar in human metabolism mainly because it is the primary source of energy for most cells of the body.
Energy contained in the glucose molecule is obtained by the body from its reaction with oxygen (oxidation). This oxidation reaction occurs in power producing mitochondria structures that are located within cells.1
Hypoglycemia is characterized by alterations in neurologic, metabolic and muscular functions:
Neurologic function because brain tissue is particularly dependent on glucose for energy,
Metabolic function of glucose-dependent tissues which include red blood cells, white blood cells, bone marrow, eye, inner heart of the kidney, and peripheral nerves because these tissues cannot metabolize fatty acids as an alternate source of energy, and
Muscle function because muscle cells continually require glucose for energy production.
Glucose is made available to cells through the regulating action of insulin, a hormone produced by specialized cells located on the surface of the pancreas.
What Is Hypoglycemia In Celiac Disease and/or Gluten Sensitivity?
[dropcap]U[/dropcap]nexpected weight loss is unintentional loss of body mass composition or inability to gain weight marked by decreased serum proteins and increased stool fat.1
What Is Unexpected Weight Loss In Celiac Disease and/or Gluten Sensitivity?
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:
Ohlsson B. New insights and challenges in microscopic colitis. Therap Adv Gastroenterol. 2015 Jan;8(1):37-47. doi: 10.1177/1756283X14550134. [↩] [↩]
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. [↩]
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. [↩]
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. [↩]
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. [↩]
Ohlsson B. New insights and challenges in microscopic colitis. Therap Adv Gastroenterol. 2015 Jan;8(1):37-47. doi: 10.1177/1756283X14550134. [↩]
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. [↩]
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. [↩]
Paleness and Tendon Problem: Symptoms of Hypocupremia.
What Is Hypocupremia?
[dropcap]H[/dropcap]ypocupremia, or low plasma copper, means the level of copper is too low to meet metabolic needs of the body for copper and is characterized by these many features:
Impaired energy production causing weakness.
Impaired ability as part of an enzyme to oxidize vitamin C which is required to breakdown histamine.
Faulty blood cell formation and instability of blood cell membranes causing anemia, shortened life span of neutrophils causing susceptibility to infection, faulty platelet formation causing impaired blood clotting.
[dropcap]C[/dropcap]achexia is a state of ill health involving deteriorating body composition that is characterized by general malnutrition and loss of lean tissue such as muscle.
Q: What are typical findings in cachexia?
A: Arm muscle triceps (the muscles at the back of the upper arm), skin folds, subscapular skin folds, fat area index, and bone mineral content are significantly lower than normal.
Cachexia may develop in protein-losing enteropathy such as celiac disease, chronic or severe infection such as pneumonia, tuberculosis, malaria, or many chronic diseases such as heart failure and cancer.
Cachexia can develop in persons of any age.
What Is Cachexia In Celiac Disease and/or Gluten Sensitivity?
