The lining of the GI tract is the body’s largest barrier to the outside environment.
As the first line of defense against the potentially harmful substances present in the foods we ingest, it provides a permeable barrier that limits what substances can cross into the body while allowing nutrients to be absorbed.
The spaces between epithelial cells along the intestinal boundary are called tight junctions, and they play a key role in regulating gut permeability.
It has been suggested that a breach to these junctions allows substances that wouldn’t otherwise enter the bloodstream to permeate the wall of the GI tract, triggering an inflammatory response both in the gut and throughout the body.
This is sometimes referred to as intestinal permeability, or “leaky gut.”
Rather than being a condition in of itself, leaky gut may be more symptomatic of a larger issue at hand. Specifically, there is some evidence to suggest that when individuals suffer from conditions related to systemic inflammation, they are more likely to experience “tight junction dysfunction”.
As a central part of the inflammatory response, mucosal barriers become more permeable to allow the passage of immune cells, but this consequently permits access of other molecules as well.
For instance, people diagnosed with digestive disease such as Inflammatory Bowel Disease (IBS) face a heightened threat to intestinal permeability and related inflammation.
However, it is unclear if this circumstance also occurs in people with GI symptoms who do not have a diagnosable disease [1,2].
Determining the progression of common symptoms may help to answer this.
For example, while gut permeability and subsequent inflammation have been linked to dysbiosis, it has yet to be determined if the inflammation causes the dysbiosis or vice versa [3].
Once weight loss is achieved, markers of intestinal permeability have been shown to decrease in extremely obese subjects with a BMI greater than 44 [4], suggesting that either the obesity or the diet related to the obesity may have caused the permeability.
It does appear that leaky gut is not just associated with a disease state. Evidence suggests that diet may also trigger intestinal permeability.
Specifically, a high-fat, high-sugar “Western Diet” has been shown to promote
the development of a pro-inflammatory gut microbiota, and consequently increase intestinal permeability [6]. However the specific relationship between the two is unclear [5].
Ongoing studies will help to clarify the connections between diet, obesity, dysbiosis and leaky gut.
In the meantime, it is one more reason to eat a healthy plant-based diet to support a healthy gut, and therefore a healthy body.
References:
1. Ahmad R, Sorrell MF, Batra SK, Dhawan P, Singh AB.Gut permeability and mucosal inflammation: bad, good or context dependent. Mucosal Immunol. 2017 Jan 25. doi: 10.1038/mi.2016.128. [Epub ahead of print]
2. Michielan A, D’Incà R. Intestinal Permeability in Inflammatory Bowel Disease: Pathogenesis, Clinical Evaluation, and Therapy of Leaky Gut. Mediators of Inflammation. 2015;2015:628157. doi:10.1155/2015/628157.
3. Stecher B. The Roles of Inflammation, Nutrient Availability and the Commensal Microbiota in Enteric Pathogen Infection. Microbiol Spectrum.2015; 3(3):MBP-0008-2014. doi:10.1128/microbiolspec.MBP-0008-2014.
4. Damms-Machado A1, Louis S1, Schnitzer A1, Volynets V1, Rings A1, Basrai M1, Bischoff SC2. Gut permeability is related to body weight, fatty liver disease, and insulin resistance in obese individuals undergoing weight reduction. Am J Clin Nutr. 2017 Jan;105(1):127-135. doi: 10.3945/ajcn.116.131110. Epub 2016 Nov 9.
5. Gil-Cardoso, K., Ginés, I., Pinent, M., Ardévol, A., Terra, X. and Blay, M. ‘A cafeteria diet triggers intestinal inflammation and oxidative stress in obese rats’. British Journal of Nutrition. 2017; 1–12. doi: 10.1017/S0007114516004608.
6. Pendyala S, Walker JM, Holt PR. A high-fat diet is associated with endotoxemia that originates from the gut. Gastroenterology 2012;142: 1100–1. e2.
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