Photo by Adam Nieścioruk on Unsplash
Recently, I read an interesting book, 'We are our brains: from the womb to Alzheimer's' by Dick Swaab. A fascinating book for anyone interested in how our brains work- with facts peppered throughout such as a single brain contains 100 billion neurons (which is fifteen times the number of people on earth!), there are over sixty thousand miles of nerve fibers, and there are 1000 times 1000 billion points that they connect to each other and make us our brains!
Anyway, these 'points of connection' are what makes our brains unique and the central players of these efficient messaging system are the 'neurotransmitters'. These are chemical substances that relay information ('signal') across the neurons, from one part of the brain to another. This 'signaling' is what makes us experience the 'highs' after a run (runners amongst you will know what I am talking about!) and also the 'lows', for example, during depression and anxiety.
Years of neuroscience research have painstakingly teased out the identity of many of these neurotransmitters, how they work and what are their functions. And it was only a matter of time before we learned how to manipulate these functions, ie, block them or make them more active to suit our desired outcome. At the risk of simplifying the tremendous amount of research behind this, simply put, manipulating these pathways are what antidepressants are all about.
One of the most commonly prescribed classes of antidepressant drugs is the 'Selective Serotonin Reuptake Inhibitors or SSRIs for short. You may know them by the brand names - Prozac, Zoloft, Celexa, Lexapro, Paxil, etc. Most SSRIs treat depression by increasing levels of serotonin in the brain. Serotonin is one of the chemical messengers (neurotransmitters) that carry signals between brain nerve cells (neurons). Serotonin, also known as the 'happy chemical' acts as a mood stabilizer, and research suggests that an imbalance in serotonin levels may influence mood in a way that leads to depression.
So how do SSRIs work?
One of the ways in which these neurons send signals to one another is by releasing a little bit of serotonin at a time so that the message can be delivered. They then have to take back the neurotransmitter they released so they can send the next message. This process of replacing the neurotransmitter is called “reuptake.”
SSRIs help make more serotonin available by blocking the reuptake process. This allows serotonin to build up between neurons so messages can be sent correctly as well as have a higher amount of serotonin available in between the neurons. They’re called “selective” serotonin reuptake inhibitors because they specifically target serotonin.
There are many other classes of antidepressants that work differently than SSRIs. However, SSRIs, are interesting to us because they are generally considered safe during pregnancy/breastfeeding and are the most commonly prescribed class of antidepressants during this time. What has been a particularly interesting area of research for Haplomind is exploring why do two pregnant women who take an antidepressant respond very differently to the same antidepressant (in how quickly it makes them feel better or what side effects they experience). Considering how vulnerable this period is, not being able to find out what is the right antidepressant for you from the beginning and having to wait for 8 weeks on average to find out if the current one works (that is how long it takes for an antidepressant to be fully effective), is risky for the woman and her child and is something that we are very interested to work on.
In one of the later posts, I will explore more about why do we not know which antidepressants (SSRIs) are right for someone from the start, especially during pregnancy and what can be done about it.
Comentarios