Gutierrez, Graciela. “Microbial Based Treatment Reverses ASD's Social Deficits: Mouse Study.” Neuroscience News, Neuroscience News, Baylor College of Medicine, National Institutes of Health, Sammons Enterprise , 4 Dec. 2018, neurosciencenews.com/asd-microbial-treatment-120204/.

Recent experiments performed by researchers at Baylor College of Medicine give support to an unconventional idea that could finally allow for the treatment of the core symptoms of Autism Spectrum Disorder. The researchers found in 2016 that mice offspring of mothers fed high-fat diets had social deficits and changes in their gut microbiome characterized by reduction of the gut bacterium L. reuteri. The important revelation of this finding was that the researchers could reverse the social deficits caused by autism by restoring this bacteria. Additionally, since the tested model was only for one of the many underlying mechanisms of autism, the researchers investigated whether this finding applied to other mechanisms of autism with different causes (idiopathic- or spontaneous/unknown occurrence of disorder or condition- genetic, and environmental models), and adding L. reuteri worked in all tested models of the condition. Afterwards the researchers explored the mechanisms that mediate the rescue of social behavior in mice models of ASD with L. reuteri, and they discovered that the bacteria works in vagus nerve, which bidirectionally (in both directions) connects the gut microbiome to the brain. This is interesting because the supplication of a gut bacteria that was deficient would be expected to restore the composition of the gut microbiome, but rather this bacteria is actually restoring proper functionality to a pathway of a specific connection to the brain, which in turn promotes social interaction. Furthermore, when vagus nerve is active, oxytocin- a social interaction promoting hormone that activates “social reward” when it binds to neuron receptors- is released, so researchers tested whether genetically engineering mice without the oxytocin receptors on their reward neurons, blocking those receptors with certain drugs, cutting the connection between the gut and the brain, or interfering with oxytocin’s binding to the receptors would affect the bacteria’s ability to restore proper social behavior in the mice models of autism: in all cases, the bacteria could not restore social behavior in mice. This corroborates the finding that it is the oxytocin released by the vagus nerve that restores social behavior in mice models, not just the presence of this bacteria. These findings are important because not only does it change the way that neuroscientists and psychiatrists think about the treatment of autism and related disorders, but it gives support to the relatively new idea that it may be possible to control or alter specific behaviors through the gut microbiome by selecting specific strains of bacteria.

This final idea is hugely important because the ability to manipulate people’s gut microbiomes is turning out to have a wide variety of implications. The gut microbiome, which consists of trillions of types of bacteria, not only function in the brain, but they digest food, process nutrients, make vitamins B and K (I know personally that vitamin B makes all of the difference in emotional wellbeing), and produce immune system substances to fight inflammation and heal wounds. In addition to all of these functions, the microbiome is in constant, direct contact with the brain through immune and nerve cell pathways collectively known as the gut-brain axis. One of the neuroactive compounds made in the microbiome and sent to the brain is 90% of the brain’s serotonin, which helps stabilize emotions and prevent depression. In addition to autism, shifts in the composition of the gut microbiome through certain bacterias outcompeting other, necessary ones have been linked to inflammatory bowel disease, blood cancers, and dementia-causing conditions. With such a diverse functionality, the ability to alter specific behaviors through a more advanced understanding of the types of bacteria may fix a wide range of health related problems before the ethical and practical concerns of genetic engineering ever have to be considered. In the foreseeable future, the race to discover and study all of the various bacteria in the microbiome could be the modern day version of the race to sequence the human genome, both in the sense that it will be a literal race and that there may be a gold mine of information in accomplishing such a task that could drastically improve the conditions of many people (the citation for the microbiome information is in the footnote).

In conclusion, this article was well-written in the sense that it highlighted the important points, especially in the beginning to grab attention, and synthesized important quotes from the experts in the topic for the analytical side of the research. This use placement of expert quotes gives credibility to the article. However, one weakness of the article is that it somewhat places a positive spin on the research, using only the most optimistic facts about the research to make the reader think that the experimental results were more full proof than they actually were (ie “Surprisingly, they discovered that, indeed, L. reuteri can trigger the recovery of social behaviors in all the models they tested, suggesting that this microbial-based approach could improve social behavior in a wider subset of ASD.”) Indeed, the abstract of the actual paper paints a more realistic view of the findings by stating that, “However, whether the effect of L. reuteri on social behavior is generalizable to other ASD models and its mechanism(s) of action remains unknown. Here, we found that treatment with L. reuteri selectively rescues social deficits in genetic, environmental, and idiopathic ASD models.” Note that unlike the article, the abstract concedes that the tests were limited with respect to the models it used versus all of the possible ASD models that exist, that the way the L. reuteri work in the vagus nerve is still unknown, and that the bacterial treatment only selectively rescued social deficits in the tested models. When writing to a scientifically curious audience, it is important that an article paints a realistic picture of the research so that the average reader won’t just think that one finding can do something as grand as automatically cure an important ASD symptom. The lesson that research is a long, cumulative process is important for any budding scientist to learn.