Celiac disease

People with celiac disease react to gluten, which is found in wheat, rye, spelt and barley. Villus atrophy in the small intestine is one of the most significant findings in celiac disease, rendering the patient with a poor absorptive capacity. The vast majority of celiac patients produce antibodies to tissue transglutaminase and have either the gene variant HLA-DQ-2 or HLA-DQ-8. However, these gene variants are much more common than the occurence of celiac disease. Thus, there must be additional factors that can explain why celiac disease develops. ¹⁾

After birth, an infant's environment shifts from a sterile space to one colonized by bacteria. Almost immediately, microbial products and live bacteria can be seen, but only in a part of the baby's intestine. The arrival of solid food several months later establishes a complex bacterial flora throughout the entire bowel. The composition of the flora has been shown to vary significantly depending on whether the birth was vaginal or cesarean.

“Differences in the microbial flora and impaired priming of the enteric epithelial surface in individuals who are born by cesarean delivery might therefore contribute to inflammatory conditions of the intestinal mucosa later in life,” write lead author Evalotte Decker, from the Department of Pediatrics, Institute for Medical Microbiology and Hospital Epidemiology, Hannover Medical School, Germany, and colleagues. “Indeed, the rate of cesarean delivery as well as the incidence of [inflammatory bowel disease] and celiac disease have increased in recent decades.”

Cesarean delivery is associated with celiac disease but not inflammatory bowel disease in children.

Abstract OBJECTIVES: The aim of this study was to analyze a possible association between cesarean delivery and enteric inflammatory diseases in children.

METHODS: A retrospective, multicenter, case-control study that included 1950 children was performed in cooperation with 26 university and 16 nonacademic children's hospitals. Information on intestinal disease manifestation, together with mode of delivery and gestational age at birth, postnatal complications, and breastfeeding, was collected by the attending physician from children and their parents who were visiting a gastrointestinal outpatient clinic for Crohn disease (CD; 516 cases), ulcerative colitis (250 cases), celiac disease (157 cases), and other gastrointestinal diseases (165 cases) and control subjects who were visiting ophthalmologic, orthodontic, and dental outpatient clinics (862 cases).

RESULTS: Whereas the rate of cesarean delivery of children with Crohn disease or ulcerative colitis was similar to that of control subjects, a significantly enhanced likelihood of being born by cesarean delivery was found in children with celiac disease compared with control subjects (odds ratio: 1.8 [95% confidence interval: 1.13-2.88]; P = .014).

CONCLUSIONS: The mode of delivery and associated alterations in the development of the enteric homeostasis during the neonatal period might influence the incidence of celiac disease. ²⁾

The emerging data on viral and bacterial microbe-host interactions and their alterations in celiac disease provides a plausible mechanism linking environmental risk and disease development. ³⁾

Some patients with celiac disease have low/normal 25D but elevated 1,25D apparently related to celiac. ⁴⁾

Our patient had hypocalcemia caused by celiac disease and values for serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol. that were normal and elevated, respectively. Correction was demonstrated after dietary gluten withdrawal. ⁵⁾

Calcium and vitamin D supplement intake may increase arterial stiffness in systemic lupus erythematosus patients. ⁶⁾

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“The finding of rod-shaped bacteria attached to the small intestinal epithelium of some untreated and treated celiac-disease patients, but not to the epithelium of healthy controls, ignites the notion that bacteria may be involved in the pathogenesis of celiac disease.” Am J Gastroenterol. 2004 May;99(5):905-6. A role for bacteria in celiac disease? Sollid LM, Gray GM ⁸⁾

“As presence of Campylobacter jejuni in other diseases with antigangliosides antibody formation has been established, we propose the possible role of Campylobacter jejuni in development of CD in association with other genetic and environmental factors by the mechanism that molecular mimicry of gangliosides-like epitopes common to both lipo-polysacharide coats of certain strains of Campylobacter jejuni and gangliosides in cell structure of gastrointestinal mucosa may cause an autoimmuneA condition or disease thought to arise from an overactive immune response of the body against substances and tissues normally present in the body response and consequently lead to atrophy and degeneration of mucosa possibly by apoptosis.” World J Gastroenterol. 2007 Sep 21;13(35):4784-5. Can Campylobacter jejuni play a role in development of celiac disease? Sabayan B, Foroughinia F, Imanieh MH ⁹⁾

Specific duodenal and faecal bacterial groups are associated with paediatric celiac disease.¹⁰⁾

Lymphocytic gastritis and celiac disease in indian children: evidence of a positive relation.¹¹⁾

Autoantibodies involved in celiac disease are not specific, as infection may increase levels of anti-transglutaminase antibodies. These antibodies are not detectable once the infection is gone.¹²⁾

Could a common virus trigger coeliac disease in some children? Tye-Din JA et al, Norway February 2019

study in humans supports a role for infection with reovirus, a seemingly innocuous virus, in triggering the development of CeD ^{13) 14)}

Findings suggest that neither olmesartanMedication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. Also known by the trade name Benicar. nor other ARBs were associated with diarrhea among patients undergoing endoscopy. The spruelike enteropathy recently associated with olmesartan is likely a rare adverse effect and milder presentations are unlikely. ¹⁵⁾

In 2015 I saw that 6 individuals in the USA were suing maker of Benicar. (presumably for bowel immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed. caused by cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system.). Somewhere else I found that 1.9 million individuals are currently taking Olmesartan Medoxomil. 6 in 1.9 million ? Seems pretty rare to me. (Editor)

Gluten in “gluten-free” manufactured foods in Australia: a cross-sectional study. ¹⁶⁾ PMID 30404591

2018 data show that OLM is an Nrf2 activator, NFkB inhibitor and apoptosis inhibitor in an experimental model of ulcerative colitis. Overall, the study indicates that OLM shows promise as a potential therapy for the treatment of human inflammatory bowel diseases. ¹⁷⁾

Research associated with J Tye-Din ¹⁸⁾ , ¹⁹⁾ , ²⁰⁾ , ²¹⁾ , ²²⁾ , ²³⁾ , ²⁴⁾

  Romain Bouziat1,2,*, Reinhard Hinterleitner1,2,*, Judy J. Brown3,4,*, Jennifer E. Stencel-Baerenwald3,4, Mine Ikizler4,5,