How, you might ask, do antidepressants work?
The easy answer is: We don’t know. This makes drug treatment for depression and anxiety a guessing game where a multitude of drugs are prescribed in a course of trial and error. One person may respond to one drug and not another; it’s difficult to predict individual response. It’s no wonder that people get frustrated and often give up taking meds altogether. Or get kicked off reality TV shows like “Celebrity Rehab”.
Recently scientists discovered a 3D structure of a brain protein receptor, CRF1, a molecule on the outside of cells on the pituitary gland, that releases CRF, hormones involved in regulating our stress response that over time contribute to anxiety and depression.
This is great news, because knowing the structure can help researchers make drugs that mimic CRF1 and block it’s capability of creating the hormone that causing the stress response.
CRF1 is made by the gene CRHR1. I looked up the gene to see if there are any significant known mutations. In mice models, disruption of the gene (knocking it out, or mutating it) reduced anxiety-related behavior under both basal conditions and following alcohol withdrawal. According to the Online Mendelian Inheritance in Man “The results demonstrated a key role of the Crhr1 receptor in mediating the stress response and anxiety-related behavior. CRH had been previously identified as a potent mediator of endocrine, autonomic, behavioral, and immune responses to stress and had been implicated in the stress-like and other adverse consequences of drug abuse, such as withdrawal from alcohol.”
Could this mean the end of television shows like “Celebrity Rehab” and “Intervention”? Probably not. Stress response is a necessary tool for survival, honed over time by evolution. We can’t knock out the gene in people, but drugs may be able to mimic the knockout response.
At this time, a gene test wouldn’t reveal much information, but there could be different forms of the gene that produce more or less amount of the protein.
Link to article on CFR1: