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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