It is often assumed, and sometimes defended fanatically by certain
“groups”, that humans cannot digest gluten, and therefore no single human (with
or without CD) should be eating gluten-containing foods, such as wheat. For them
the story ends here. But there is a lot more to it.
Abstract
There is a large variety of bacteria capable of digesting gluten with
gluten-degrading proteases naturally present in the upper human
gastro-intestinal tract. The oral cavity is colonised with microorganisms that
produce proteases capable of hydrolysing peptides rich in proline and glutamine
residues. Intestinal dysbiosis is
present in celiac disease patients, characterized by increased
Gram-negative bacteria, other potentially pro-inflammatory bacteria and reduced
bifidobacteria.
Small-intestinal bacterial overgrowth (SIBO) and infections have been suggested to contribute to CD
pathogenesis with persistence of
gastrointestinal symptoms after gluten withdrawal. Pathogenic
enterobacteria could play a role in
the switch from tolerance to an inflammatory immune response to gluten, by
altering the permeability of the intestinal mucosa.
A lack of maturation of the gut microbiota is observed within the first 2 years of life in
infants at risk of CD. The early introduction of gluten and the lack of
maturity in the GI microbiota could trigger or accelerate the development of
autoimmunity. Bacterial groups related to gluten metabolism are altered in
patients with CD.
Either Bifidobacterium could protect against CD, or inherent features of the
CD intestine influence Bifidobacterium colonization. Reduced IgA-coated
bacteria is associated with intestinal
dysbiosis suggesting the
existence of a barrier defect, which fails to stabilize the gut microbiota
and prevent the host from the invasion of harmful antigens and pathogens.
The induction of gliadin proteolysis in the
human gut might not be the solution but the origin of CD, since gliadinases
are CD specific. Gliadinases might
have a bacterial origin within the duodenum of patients with CD. Gliadin-metabolising bacteria could be absent, or
present to a much lower degree, in the duodenum of all non-predisposed
individuals.
In CD the mucosal tolerance to
the gut microbiota is deregulated. Reductions in beneficial Gram-positive
bacteria could favor the residence and interactions of harmful Gram-negative
bacteria within the mucosal surface thereby contributing to loss of gluten tolerance.
Either a
particular glycosylation pattern in predisposed individuals favors harmful
bacterial adhesion, which contributes to CD pathogenesis or modifications in
the composition of the intestinal microbiota lead to alterations in the
glycosylation pattern and its defensive role of the mucus layer against
infections and CD.
Read the Free Full Article @ http://sciencedrivennutrition.com/gluten-manisfesto/ and learn a ton about gluten with myself and Brad Dieter, PhD
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Summary of 34 articles with
36.528 words and 1121 references on
Exercise and nutrition
