Your Gut Microbiome Might be Giving You Social Anxiety
Recent scientific research has shown that bacteria in the gut microbiome is related to having Social Anxiety Disorder. The research is anticipated to revolutionize future treatment.
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As you talk to your classmate, your body begins to feel weird. Suddenly, your palms feel sweaty, your knees feel weak, and your arms feel heavy. Chances are, you’re experiencing social anxiety. Social anxiety is characterized by the intense fear of judgment and scrutiny from others, which can interfere with the ability to make new friends, maintain relationships, and get through everyday social interactions.
The 2001 to 2004 National Comorbidity Survey-Adolescent Supplement Report states that a third of teenagers 13 to 18 years old in the U.S. have been diagnosed with Social Anxiety Disorder (SAD), and it remains one of the most common anxiety disorders among teenagers today. Both genetic and environmental factors contribute to the development of the disorder. Environmental factors such as traumatic past experiences like bullying, abuse, family conflict, or growing up around an overbearing parent correlate with the development of SAD in early childhood or adolescence. This is because a lack of socialization early on deprives you of the chance to develop your social skills, and becoming excessively reliant on a hovering parent prevents you from learning how to regulate your emotions. Scientists know that genetics also play a role; someone who has an immediate family member with SAD is about five times more likely to develop the condition than someone with no family history of SAD, but the gene that causes this has yet to be identified as the culprit.
Those with SAD feel irrational fear when undergoing social interactions. This fear response starts in the amygdala, a part of the brain that assesses the “vibe” of our surroundings and lets us read body language and facial expressions. When we’re faced with a threat, the amygdala sends signals to the hypothalamus, a different part of the brain that tells the body to release hormones. The hypothalamus then activates the sympathetic nervous system, which in turn makes us physically alert by signaling to glands in our kidneys to release adrenaline and noradrenaline—hormones that increase our heart rates. The hypothalamus also activates the pituitary gland, which communicates to the same glands in our kidneys to release about 30 other types of stress hormones, including cortisol. Using new neuroimaging technology, scientists have observed increased blood flow to the amygdala in the brains of people with SAD, which can help explain why the fear response is so extreme—an over-activated amygdala would naturally escalate the body’s physical responses to fear.
Currently, SAD is treated with selective serotonin reuptake inhibitors (SSRIs), designed to help the brain better retain the neurotransmitter serotonin. Serotonin is responsible for helping neurons communicate and also plays a large role in mood regulation. A study done by researchers from the Institute of Human Genetics at the University of Bonn has identified a serotonin transporter gene that amplifies the severity of SAD, offering insight into the role serotonin plays in the disorder and how SSRIs manage to help. The transporter gene codes for transporter proteins, which control how much serotonin a transmitter cell located in the brain absorbs when serotonin carries neural signals. Transmitter cells are responsible for scooping up excess serotonin as it jumps between neurons, and SSRIs stop transmitter cells from doing so; this increases the amount of serotonin available and makes neuron signaling more efficient.
Another common medication is serotonin and norepinephrine reuptake inhibitors (SNRIs), which act similarly to SSRIs by targeting the transmitter cells of serotonin and norepinephrine (a neurotransmitter that keeps you alert). SNRIs increase and maintain the amounts of serotonin and norepinephrine in the brain. Increased serotonin levels have been found to improve cognitive function and increased norepinephrine levels have been found to provide greater clarity of mind.
Another resource for patients is cognitive behavioral therapy, where patients speak to a professional about underlying issues that may have triggered the development of SAD. While these mainstream methods are the most effective treatments up to date, the majority of patients suffer from SAD for a lifetime. Most medications come with a multitude of inconvenient side effects that are especially prominent in the beginning of treatment: SSRIs and SNRIs can induce indigestion, dizziness, sleep trouble (insomnia or fatigue), or low libido. People also respond differently to these drugs, meaning there isn’t a “one-size-fits-all” solution. The search to make current treatment options as effective as possible while developing new methods is still ongoing. Recently, research has directed scientists toward the gut microbiome as a potential way to enhance modern care.
The gut microbiome is the collection of all the microorganisms (bacteria, viruses, and fungi) that live in your intestines. These microorganisms serve a wide range of functions — some of them are pathogens that cause sickness, and others facilitate bodily functions like processing fiber from food and helping the immune system combat diseases. Gut microbes do this by releasing bacteriocin, which are proteins that target harmful bacteria in the digestive tract by directly competing with these pathogens for nutrients. Gut microbes also signal to immune cells whether or not to release inflammatory agents in response to foreign matter, which can prevent under or over immune responses. The gut microbiome also plays an important role in mental health, as some of the important neurotransmitters that exist in the brain, including serotonin, are primarily produced by gut bacteria.
A recent report on the effects of the gut microbiome on sociability in mice by Professor John Cryan and fellow researchers explains what has led scientists to believe that mental health is connected to the gut microbiome. In Cryan’s experiment, scientists used the antibiotics ampicillin, vancomycin, and imipenem to neutralize the natural gut microbiomes of mice and split them into two groups. One group received the microbiomes of people with SAD, while the other group was given the microbiomes of healthy people. Both groups were then electrically shocked when they approached new social stimuli, or new mice, for two days. Once the shocks were no longer being administered, their social interactions were observed. Researchers observed that the mice who received SAD microbiomes continued to struggle to engage with others, while those that received healthy microbiomes were gradually able to continue approaching new mice. Scientists also observed that mice with the SAD microbiomes experienced reduced levels of oxytocin (the “love hormone”), lower concentrations of the Bacteroides nordii and Bacteroides cellulosiyticus, and increased levels of Phocaeicola massiliensi in their feces. This observation was interpreted to be evidence of a difference in the microbiomes of healthy people and those suffering from SAD.
While the relation between gut microbiome to social anxiety is relatively unexplored, current research is promising. Studies have singled out two bacteria from the gut in recent years: those with SAD have abnormally high levels of Anaeromassilibacillus An250 and abnormally low levels of Parasutterella excrementihominis.
By isolating a biological factor behind social anxiety, scientists are able to engineer more effective treatments. A recent study published in Translational Psychiatry speculates that D-cycloserine has benefited patients going through exposure therapy for SAD. D-cycloserine is an antibiotic that inhibits the enzyme kynurenine aminotransferase from turning the compound kynurenine into kynurenic acid (KYNA). This is an important step in the tryptophan-kynurenine pathway, where the amino acid tryptophan (supplied by the gut microbiome) is broken down. Scientists have observed a correlation between elevated levels of KYNA in the brain and the development of SAD and other psychological disorders. This correlation remains unexplained but poses the reduction of KYNA as a potential way to alleviate the symptoms of SAD. Some psychologists are also exploring the intake of gut-friendly foods as an option for preventing those who are genetically predisposed to SAD from developing the condition.
Despite being one of the most common mental health issues in this day and age, social anxiety is rarely thought of in physiological terms. While it’s true that personal circumstances and experiences affect the way patients develop SAD, the biological processes are just as important in finding a solution. The ongoing research on gut microbes and the role they play in relevant neurological pathways gives scientists and patients hope for future SAD treatment.