Do you have social anxiety? Scientists discover that the condition lives in your intestines

Scientists have discovered that social anxiety lives in a person’s gut, which could lead to new treatments affecting 15 million American adults.

Researchers from Ireland’s University College Cork transplanted gut microbes from a human with the condition into mice, which showed social anxiety behavior 10 days after implantation.

The team found that the subjects also had reduced levels of the hormone corticosterone, which is involved in the regulation of energy, immune responses and stress responses.

The findings, according to researchers, have suggested that ‘the microbiota-gut-brain axis is an ideal target for identifying new therapies to improve symptoms’ to reduce social anxiety in humans.

These results add to a growing body of research showing a complex link between the gut and the brain, suggesting that anxiety, depression, autism and other brain disorders can be treated at least in part by addressing problems that start in the gut.

Importantly, immune system markers indicated that the mice had disrupted the immune system after the transplant, suggesting that this so-called ‘gut-brain axis’ involves inflammatory molecules that can travel from the gut to the brain.

This study was an offshoot of an existing research experiment that the scientists did with people.

The gut microbe samples came from people who volunteered for a study on the relationship between gut microbes and social anxiety in humans.

So while they had the samples, they tried something strange.

The scientists behind the study started with twelve microbiome samples – fecal samples – from six people with a formal diagnosis of social anxiety disorder (SAD) and six people without social anxiety.

Before participating in the study, all participants had to confirm that they were not taking any psychiatric medications or nutritional supplements that could affect their microbiome.

Mice were prepared for the study by giving them a mix of four different antibiotics for a week, ‘to deplete the existing microbiota’.

In other words, they got a clean slate.

Then, each participant’s poop donation was split six ways and implanted into six different mice, for a total of 72 mice – 36 received transplants from people with SAD and 36 received transplants from people without.

Scientists implanted the new microbiome into the intestines of each mouse via a feeding tube for three days in a row to ensure that the new microbiome took hold.

Ten days after starting treatment, the mice underwent a series of tests to examine a range of functions, including sociability, general anxiety, gut function, depression and anxiety.

On most tests, the two groups of mice performed similarly.

But there was one test where the transplant group of people with SAD performed significantly worse: a test of social anxiety.

In this experiment, the scientists induced fear in the mice, fear caused by social cues, and then measured how long it took for it to disappear.

Although the SAD group took much longer for their social anxiety to decrease, there was no difference in sociability between the two groups.

So the researchers concluded that what they observed was the mouse version of social anxiety.

Social anxiety can also be present in humans, even if someone has the desire to be social. That is what can make the situation so dire.

Tests of the microbiomes of mice showed that they were significantly different between the two groups, confirming that the two groups of people – those with and without SAD – had significantly different gut microbes.

These mice remained otherwise healthy, but in addition to their new social anxiety, they also showed some unique changes in their brains.

In particular, the brain area called the bed nucleus of the stria terminalis had reduced levels of the so-called ‘love hormone’ oxytocin, which is important for bonding between parent and child and between individuals in both social and romantic settings.

This brain region is important for anxiety and stress responses, and the mice with SAD transplants showed severe changes.

Furthermore, the medial amygdala and prefrontal cortex both had reduced expression of genes linked to oxytocin in the SAD transplant mice. These brain areas are involved in anxiety and personality, respectively.

So it’s clear that the changes in their microbiome had led to some significant behavioral differences.

It’s not entirely clear how one change led to another, but the scientists suspect it has to do with the immune system: markers of inflammation were increased in the SAD transplant mice, and these markers can cross the blood-brain barrier.

The study was published in the magazine Proceedings of the National Academy of Sciences.

Although the study did not identify a treatment, it did open the door for its development in the future.

“This suggests that the microbiota may play a causal role in increased social anxiety responses in the disorder,” the study authors wrote.

‘In the future, the microbiota-gut-brain axis is an ideal target for identifying new therapies to improve symptoms in SAD.’