Actually it might. A recent study on mice found that gut bacteria are important for their social behaviour. The study discovered that mice without a gut microbiome (the germ-free mice) showed significant antisocial behavior, such as avoiding a stranger mouse rather than interacting with it.
The researchers established a complex gut microbiome – hormones – neurons – social behaviour connection through the HPA (hypothalamus–pituitary–adrenal) axis. They found that lack of gut microbiome in mice has led the adrenal gland to produce more corticosterone (the analog of our ‘stress hormone’ cortisol), which then influenced specific neurons in the brain (glucocorticoid receptor-positive neurons). These neurons control social behavior in the brain and make the mice perform antisocial behavior.
The good news is that when the same ‘antisocial’ mice received fecal transplants from mice with healthy gut microbiome, their social behaviour improved as the result of more gut microbiome, less stress hormone (corticosterone) and activity changes of the glucocorticoid receptor-positive neurons. The researchers highlighted the role of the neurons in this complex connection. They showed that even with lacking gut microbiome, mice demonstrated more normal social behavior when their neurons were not able to respond to the stress hormone.
The researchers were also able to identify a specific bacterial species that are responsible for sociability. These turned to be the gut bacteria Enterococcus faecalis that play a mediator role between social behavior and corticosterone levels. Germ-free mice that received E. faecalis showed improved social behavior and lowered corticosterone levels. How exactly E. faecalis is able to mediate this improvement will be further investigated.
These are exciting findings, aren’t they? Of course, they are needed to be confirmed on people but they give a hope that our social behaviour and social deficits might be corrected by treating our gut, which is much easier to influence compared to our brain.
Curious? HERE is the source
