Is Stomach Bacteria Causing Depression and Anxiety?
People who struggle with depression are often told “it’s all in your head” by people who don’t understand mental illness and underestimate the severe reality of depression. But, while depression isn’t all in your head, a new study suggests a significant factor in depression and anxiety may be in your stomach.
Researchers from the Farncombe Family Digestive Health Research Institute at McMaster University say they have discovered intestinal bacteria play an important role in inducing anxiety and depression. Additionally, manipulating this bacteria could potentially help treat these conditions, according to study published in Nature Communications.
The researchers say this is the first study to explore the role of intestinal microbiota in the altered behavior that results from early life stress.
“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.”
Past research has drawn strong associations between intestinal bacteria and behavior, but that past research used healthy mice. This study used techniques to subject the mice to early life stress using maternal separation. From day three to day 21, newborn mice were separated from their mothers for three hours a day, then returned.
From there, the team of researchers confirmed that conventional mice with complex microbiota, which had been maternally separated, showed anxiety and depression-like behaviors as well as abnormal corticosterone levels. Corticosterone is a stress hormone. The researchers also saw the mice showed gut dysfunction based on the release of the neurotransmitter acetylcholine.
The team then repeated the experiment in germ-free conditions. They noticed the mice without complex microbiota still showed gut dysfunction and abnormal stress hormone levels, but they did not show signs of depression or anxiety.
From there, the researchers found that when the maternally separated germ-free mice are colonized with bacteria from control mice, the bacterial composition and metabolic activity changed. Within weeks, the mice began to show signs of 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.
He said that with this new research, “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.”
For Bercik, the next step is to find whether these findings translate to humans.
“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.