Gut bacteria might play a role in inducing anxiety and depression, according to a new study carried out by researchers from the Farncombe Family Digestive Health Research Institute at McMaster University. The findings have been published in the journal Nature Communications.
The new research marks the first time the role of intestinal bacteria bas been analysed in stimulating abnormal behaviour pertaining to anxiety and depression.
“We have shown for the first time in an established mouse model of anxiety and depression that bacteria play a crucial role in inducing this abnormal behaviour,” said Premysl Bercik, senior author of the paper and an associate professor of medicine with McMaster’s Michael G. DeGroote School of Medicine.
“But it’s not only bacteria, it’s the altered bi-directional communication between the stressed host — mice subjected to early life stress — and its microbiota, that leads to anxiety and depression.”
According to Bercik, mostly only healthy and normal mice were used in previous researches showing that intestinal bacteria have an impact on behaviour. Therefore, his team did the opposite: they subjected mice to maternal separation categorised as early life stress. Newborn mice were separated from their mothers for three hours everyday from day 3 to day 21. After the period of 3 hours were over, they were put back with their mothers.
It was then found that those mice which had been maternally separated displayed anxiety and depression-like behaviour. The levels of the stress hormone corticosterone were also found to be abnormal. Furthermore, these mice which had complex microbiota demonstrated gut dysfunction on account of the release of an important neurotransmitter acetylcholine.
The same experiment was then repeated in germ-free conditions. Without the bacteria, the mice which were maternally separated did show modified stress hormone concentrations and gut dysfunction but they showed no sign of anxiety or depression.
Another step in the experiment entailed colonising the maternally separated germ-free mice. This changed the bacterial composition and metabolic activity of the mice in a matter of weeks. The mice thereafter displayed anxiety and depression.
“However, if we transfer the bacteria from stressed mice into non stressed germ-free mice, no abnormalities are observed. This suggests that in this model, both host and microbial factors are required for the development of anxiety and depression-like behavior. Neonatal stress leads to increased stress reactivity and gut dysfunction that changes the gut microbiota which, in turn, alters brain function,” said Bercik.
Bercik believes their study helps to understand the impact of microbiota on host behaviour.
“We are starting to explain the complex mechanisms of interaction and dynamics between the gut microbiota and its host. Our data show that relatively minor changes in microbiota profiles or its metabolic activity induced by neonatal stress can have profound effects on host behaviour in adulthood,” he added.
He also thinks that the observations might be extended to the field of psychiatry.
“It would be important to determine whether this also applies to humans. For instance, whether we can detect abnormal microbiota profiles or different microbial metabolic activity in patients with primary psychiatric disorders, like anxiety and depression,” said Bercik.