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Don't be misled: "The total area of the human adult gut mucosa is not in the order of tennis lawn, rather is that of half a badminton court."
(Reason for sharing: total mucosal surface of the GI tract ā¼32 m2, of which only 2 m2 is the large intestine.) https://www.tandfonline.com/doi/full/10.3109/00365521.2014.898326
(Reason for sharing: total mucosal surface of the GI tract ā¼32 m2, of which only 2 m2 is the large intestine.) https://www.tandfonline.com/doi/full/10.3109/00365521.2014.898326
In line with area size and physiological differences, the small intestinal microbiota is distinct from that of the colon, not to mention fecal. Whatās even more different is its reaction to dietary changes. https://www.nature.com/articles/s41598-019-44994-7
One of the many great references with a very telling title:
The human small intestinal microbiota is driven by rapid uptake and conversion of simple carbohydrates https://www.nature.com/articles/ismej2011212
The human small intestinal microbiota is driven by rapid uptake and conversion of simple carbohydrates https://www.nature.com/articles/ismej2011212
āa low fiber, high simple sugar diet triggered FGID-related symptoms and decreased small intestinal microbial diversity while increasing small intestinal permeability.ā
SIBO is just a special case of dysbiosis, therefore lack of it means almost nothing. https://www.nature.com/articles/s41467-019-09964-7
SIBO is just a special case of dysbiosis, therefore lack of it means almost nothing. https://www.nature.com/articles/s41467-019-09964-7
Increased permeability means increasing small intestinal inflammation. Look at the correlations between the most effective T2D remitting bariatric surgery procedures and changes in inflammatory markers & insulinemia. https://twitter.com/gerdosi/status/1158658068567220224?s=21
This study measured intestinal NLRP6 activation before and after RYGB in rats. It was lower before and increased after, together with taurine. Iām wondering whether it has a connection to IL-23 and IL-17 (as seen above). https://link.springer.com/article/10.1007/s11695-019-04152-4
Differences in type of small intestinal dysbiosis might explain (some of) the variations seen in metabolic disease outcomes. SIBO is just a narrow subtype of dysbiosis. https://www.sciencedirect.com/science/article/abs/pii/S0306987719307418
A pair of recent studies strengthen the importance of identifying and quantifying mucosa-associated bacteria instead of luminal or, even less relevant, fecal. Most important interactions happen at mucosal surfaces.
https://onlinelibrary.wiley.com/doi/full/10.1111/jgh.14910
https://link.springer.com/article/10.1186/s12866-019-1617-1
https://onlinelibrary.wiley.com/doi/full/10.1111/jgh.14910
https://link.springer.com/article/10.1186/s12866-019-1617-1
So excess protein putrefies in the colon. Whatās more, if itās milk protein it causes inflammation. No and nope. Look what happens in the small intestines! What a difference it makes when important parameters are measured in the right place. https://www.sciencedirect.com/science/article/abs/pii/S0955286314002058
Uh-oh. Looks like these rats are severely starved of fiber. @KetoCarnivore Link in the above post.
Chronic alcohol intake causes small intestinal dysbiosis with high LPS producers, increased serum LPS and subsequent immune activation. Thereās little difference between alcoholic and non-alcoholic liver disease. Lactobacillus granule fixes the problem.
https://www.liebertpub.com/doi/abs/10.1089/jmf.2018.4357
https://www.liebertpub.com/doi/abs/10.1089/jmf.2018.4357
Targeting Gram-negative bacteria with specific antibiotics "modulated the gut microbiota, and reduced serum LPS and triglycerides, which prevented the progression of IR and inflammation"
https://pubs.rsc.org/en/content/articlelanding/2018/RA/C8RA03774D#!divAbstract
https://pubs.rsc.org/en/content/articlelanding/2018/RA/C8RA03774D#!divAbstract
āsmall and large intestine display close microbiota composition early in life but distinct mucosal phenotype and follow very different postānatal development.ā https://onlinelibrary.wiley.com/doi/full/10.1096/fj.201902514R
"Qualitative and quantitative differences between the corresponding jejunal and fecal samples indicate the inability of fecal samples to represent the microbiotas present in the upper gut." https://aem.asm.org/content/71/8/4169.full
āThe small bowel microbiome is markedly different from that in stool and also varies between segments. These findings may be important in determining how compositional changes in small intestinal microbiota contribute to human disease states.ā https://link.springer.com/article/10.1007/s10620-020-06173-x
āresearchers have discovered that a certain species of bacteria behaves differently depending on where in the gut it takes up residence.ā
I think that ALL strains behave differently at mucosal surfaces then in the lumen. 90 % of this surface is in the SIā¦
https://twitter.com/caltech/status/1237500207581073410?s=21 https://twitter.com/Caltech/status/1237500207581073410
I think that ALL strains behave differently at mucosal surfaces then in the lumen. 90 % of this surface is in the SIā¦
https://twitter.com/caltech/status/1237500207581073410?s=21 https://twitter.com/Caltech/status/1237500207581073410
