Gut microbiota as a risk factor for psychiatric disorders - Annissa DeSilva



This week, the papers focused on the relationship between the gut microbiome and the brain, known as the gut-brain axis as potential risk factors for stress related psychological disorders and neurodevelopmental disorders. Buffington et al found that offspring of mice who were fed high fat diets during pregnancy (MHFD) had social behavior deficits, repetitive behaviors and anxiety which are all ASD associated behaviors. The deficits in social behavior were directly related to dysbiosis of the MHFD gut, specifically the absence of lactobacillus reuteri (L.reuteri) accounted for this phenotype. What I found to be the most interesting result was that when L.reuteri was given through drinking water the MHFD social deficits were restored however their anxious and repetitive behavior were not remedied. This made me think about the MHFD model and its potential relation to the Reber et al paper. Could the microbiome dysregulation and more specifically the lack of L.reuteri have effects in the realm of the old friend’s hypothesis tested in the Reber et al paper? ( i.e. is reduction of L.reuteri considered a considerable lack of exposure to immunoregulatory microorganisms). The idea that lack of a microbiota disrupts social behavior and could lead to inflammation which is a major risk factor for affective disorders in combination with maternal high fat diet may compound to produce severe dysbiosis of the gut related to both ASD and other symptoms of psychological disorder. Youth with ASD have a much higher prevalence rates of anxiety and ASD has a high comorbidity with depression. To test this, you could combine the 2 paradigms together, give an MHFD rat the M.Vaccae immunization to see if it produces an anxiolytic effect. Interestingly the Reber paper references lactobacillus reuteri probiotics, stating that its mechanism to increase testosterone and its metabolite 17β-estradiol produces an anxiolytic effect through increases in neuronal firing rates in the dorsal raphe, Reber suggesting that this anti-anxiety producing mechanism of L.reuteri may be similar the M.Vaccae immunization mechanism of action for ani-anxiety effects. The authors also mention that L.reuteri has been noted to reduce intestinal inflammation, thus it’s not unreasonable to hypothesize that this lack of bacterium could be responsible for not only the social symptoms of ASD but also may be an additional risk factor (lack of L.reuteri causes increased inflammation) to stress related psychological disorders that have high comorbidity with ASD. Although Buffington et al found no reduction in anxiety with L.reuteri treatment perhaps the difference lies in the age of the mice tested and the relative amount of sex hormones circulating, it would be interesting as a follow up to see if treatment with L.reuteri in the MHFD adult rats produces anxiolytic effects similar to the studies cited by Reber et al.

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