The Anxiety and Depression Association of America claims anxiety disorders are the most common mental illness in the United States, affecting over 18% of the population. That’s a staggering 40 million adults in the nation and an estimated 264 million that are six times more likely to be hospitalized for psychiatric disorders than those who don’t suffer from such disorders, and yet under 37% of those people receive treatment for what are considered highly treatable illnesses.
When we feel stressed, our nervous system starts to gear up, preparing itself for potential danger and preparing the body to take action. The parasympathetic nervous system, one of three divisions of the autonomic nervous system, steps in at this moment to stabilize all those hormones and calm you down. But when the parasympathetic nervous system isn’t able to do this, a person only continues to rev up with more energy and hormones in preparation of danger. Adrenaline, for example, is the very hormone produced to prepare your muscles for a fight or for running. What’s happening during an anxiety attack is an overwhelming rush of hormones being sent or restricted through different parts of the body to fight off whatever threat may be around. The anxiety becomes unmanageable and turns into a full-fledged attack when all those signals aren’t controlled by the brain properly, sending you down that rabbit hole of anxiety.
Recently, scientists at the Max Planck Institute for Experimental Medicine in Göttingen identified a synaptic protein which, when inactivated, has an anxiolytic effect in mice. Translation: these researchers have found a brain protein that can be targeted more directly for treating patients with anxiety disorders.
Now, if you’re a little thrown off by the language, an anxiolytic is a medication or other intervention that inhibits anxiety. This effect is in contrast to anxiogenic agents, which increase anxiety. Typically, anxiolytic medications like Benzodiazepines strengthen the function of inhibitory synapses in the amygdala, a brain region that influences how we process emotions like anxiety and fear. Overactivation of the amygdala is known to result in severe anxiety and panic attacks. And these Benzodiazepines are very common in modern society for treating people with anxiety. Xanax, Ativan, Valium, and Klonopin among others are used widely and effectively, to the point that the National Institute on Drug Abuse says 13.5 million people filled a prescription for one of the medications in 2013. And that number grew drastically from 8.1 million in 1996.
Stephen Taylor, chief medical officer at Pathway Healthcare in Birmingham, Alabama and the medical director of the Player Assistance/Anti-Drug Program of the National Basketball Association compares the use of benzodiazepines to drinking, offering a quick but temporary relief of anxiety. They create a calming effect when they affect the brain’s GABA receptor, a neurotransmitter that works to suppress nerve activity.
“These medications have limited duration of effect and people often feel even more anxious after the medication wears off,” says David Hu, the medical director at Behavioral Health of the Palm Beaches in Florida. “This can lead to people taking the medication continuously to avoid feeling anxious.”
This new study, however, could aid in developing medications that are A) targeted on more specific areas of the brain that influence anxiety and B) can potentially avoid some of the negative side effects found with the use of benzos, for example, impacting parts of the brain that are not targeted for anxiety treatment, sometimes resulting in pronounced sedation and impaired concentration.
“Our research shows that protein structures at inhibitory synapses in the centromedial amygdala, and particularly the protein IgSF9b, constitute promising new targets for potential treatments,” said ilja Krueger-Burg, who led a study. “It thus provides an important contribution toward understanding the biological causes of anxiety disorders and for the development of new anxiolytic medications.”
While benzos are a highly effective short-term resolution for anxiety, their also potentially dangerous to longterm health, with up to 44 percent of benzo users developing a dependency on them. Knowing this, it’s also important to understand how these drugs affect your brain and how and why the use of them sometimes goes wrong. This can lead patients to lower the threshold for which they decide to take anxiety medications over time. “While a patient may have taken the pill initially to prevent panic symptoms, now they’re taking it for even the mildest symptoms,” says Neeraj Gandotra, chief medical officer at Delphi Behavioral Health Group in Florida. “They start taking it prophylactically — when they wake up, before a meeting, when they go to the grocery store.”
Olga Babaev from the Max Planck Institute for Experimental Medicine, said of the new developments, “Blocking IgSF9b in pathologically anxious mice has an anxiolytic effect and normalizes anxiety behavior in these animals. This protein could, therefore, be a target for pharmacological approaches to treating anxiety disorders.”
The researchers at the Max Planck Institute for Experimental Medicine in Göttingen accomplished this by studying the behavior of mice that were placed into an empty test chamber. Healthy mice were found to investigate the test chamber, actively moving about as if curious about their surroundings. The rodents with a pathological anxiety phenotype, however, split into a corner because they were afraid, and when the scientists inhibited the production of the IgSF9b protein, these same mice were found to start wandering around the chamber again, seemingly less afraid and less anxious.
This new research, while useful, seems to be opening doors to new forms of treatment in the future. With more and more people choosing to avoid prescribed medications like Xanax, Ativan, Valium, and Klonopin, and opt instead for more natural remedies like CBD or even “anxiety hacks,” the need and desire for new treatments are apparent. It’s still just as important for individuals to recognize and be informed of their own individual anxiety triggers like specific foods, social triggers, and even sleep deprivation, for example, in which a person gradually loses sleep over time and brain activity brain activity mirrors brain activity indicative of anxiety disorders.