Leaky Gut & Gluten Belly: Bacterial Firebugs Translocate from Your Gut to Your Ever-Growing Visceral Fat Depots

Image 1: Gluttony or a victim of bacterial translocation from an unrecognized gluten-sensitive leaky gut (img from COPD Lighthouse)

"Leaky gut", for decades one of those concepts, the belief in which divided self-proclaimed "real scientists" from their "hippie" counterparts, has eventually found its way to mainstream science. What began with a few tentative studies into the role of a pathologically increased gut permeability in Crohn's disease and co., is about to become a recognized research area with about 150 related publications within the first 9 month of 2011, alone. Out of these 150 publications, a study by Professor Pierre Desreumaux, and his colleagues from the Universitè Lille Nord de France (Desreumaux. 2011) is unquestionably among those, which could have a major impact on the established image of the gut and its biota as an isolated system that sustains the rest of the body with nutrients and has - due to the insulating epithelial layer - little or no direct impact on all the ailments and illnesses by which the Western civilization has been befallen in the course of its quest for highly palatable, optically pleasant, economic and convenient (franken-)food.

The study comprised 22 patients with Chron's disease, 17 patients with ulcerative colitis and 21 controls, who were normal weight, had no history of diabetes mellitus and were not being treated with speci fic medications known to modulate visceral fat. All patients had been scheduled for operations, during which - with their consent - the required subcutaneous/mesenteric fat specimens were taken and the ileal and colonic transparietal biopsies were performed.

Figure 1: CRP mRNA expression [arbitrary units] in mesenteric and subcutaneous fat pads of control, Crohn's disease (CD), and ulcerative colitis (UC) patients (data adapted from Desreumaux. 2011)

While the result that the mRNA expression of c-reactive protein (CRP) in the Crohn's disease group was 83x higher than in the patients with ulcerative colitis (UC) and 3000x higher than in the control group, alone would probably have been worth the whole procedure, a way more interesting result is that the 83x increase over the UC group is fat-depot specific. This means, only the mesenteric fat that is situated right next to the organs of the intestinal tract produces this 83x exaggerated amount of the acute phase protein CRP that is released in response to acute profound inflammation and has been implicated as a marker for peripheral vascular disease (Abdellaui. 2007), liver inflammation (Rodrigez-Leal. 2006), and other unwanted metabolic consequences of the rampant obesity-pandemic (Oda. 2008). This novel observation led the scientists to believe that CRP expression may be enhanced by inflammatory and bacterial stimuli related / subsequent to the pathologically increased gut permeability in Chron's patients.

Image 6: Could Glutamine be
the cheap colostrum?

Can you take measures to decrease your gut permeability and spare your visceral fat e.coli and other bacterial infections? Yes you can! And if you are a diligent student of the SuppVersity, who does not miss a single "course" (i.e. blogpost), you already know that

• glutamine (e.g. dos Santos. 2010), and
• colostrum (Marchbank. 2011)

have been shown to increase gut integrity and to reverse the negative effects of strenuous exercise (such as heavy weight lifting and marathon running ;-) on intestinal permeability.

And in fact, Desreumaux et al. were able to show that in Crohn's disease patients, bacterial translocation, which is usually defined as the migration of bacteria from the gastrointestinal tract to mesenteric lymph nodes and then to peripheral organs such as the liver and spleen, can also affect the mesentric fat pads and increases during experimental ileitis (i.e. inflammation of the ilium, of which a permanently increased mucosal permeability is a characteristic feature; Kroesen. 2008):

Bacterial translocation to mesenteric adipose tissue occurred in 80% of indomethacin-treated rats [model for inflammatory bowel diseases] compared with 11% of control rats. Higher rates of bacterial translocation to mesenteric lymph nodes were also noted in rats following intraperitoneal administration of indomethacin when compared to control animals (67% vs 22%, p < 0.089). The rates of bacterial trans-location were broadly similar in mesenteric adipose tissue and mesenteric lymph nodes (80% vs 67%) in indomethacin-treated rats, as well as in control animals (11% vs 22%).

With 27% the rate in the Crohn's patients was lower, yet still more than two 2x higher than in the "healthy" controls (13%). Basically, this means that a healthy gut keeps >87% of the bacteria from wreaking havoc on your visceral fat depots (and other organs) a "leaky" one, on the other hand, may allow up to 80% of these tiny firebugs to make themselves at home in the fat tissue next to your digestive organs. Now, that would not be a problem, if the local "fire" your new subtenant are sparking within those fat pads would not results in chronic and systemic inflammation (the scientists were able to show a linear relation between visceral CRP and systemic CRP levels) and thus predispose you to obesity, diabetes, heart disease, Alzheimer's, cancer and all the other plagues of the 21st century.