My other blog includes occasional posts about telepathy because the hero of my other novel, x0, is a budding telepath. Last night I made an attempt to understand how telepathy might be possible without requiring magic that defies the laws of the known universe. (Please understand that I have no objection to law-defying magic.) I realized that much of my arguement came from my research for y1 into the workings of the human brain. Zane, the hero of y1, is a student of neuroscience because he desperately wants to understand how he can alter his appearance. Once he begins working for a pharmaceutical company dedicated to mental health issues, however, other aspects of the brain begin to intrigue him. Like, what happens in your brain when you are happy?
A brain works by chemistry and by electrical impulse, and it directs hundreds of chemical substances called neurotransmitters that travel in-between the brain’s cells, delivering messages about thoughts and feelings. I share Zane’s amazement that such a system even works, much less with the precision that it does.
We do know that different substances deliver certain kinds of messages, like a FedEx that only does books or a UPS that exclusively delivers clothing. One of these messengers, serotonin, generally likes to blab to the nearest neuron about anxiety, mood, sexuality, and appetite. Another, norepinephrine, appears to focus on delivering messages about fatigue, alertness, and stress. Dopamine likes to communicate about motivation and reward. The theory behind antidepressants is that the neurotransmitters that like to communicate about feelings should be linked to a person’s happiness. So when people are depressed perhaps it is because they do not have enough of these particular messengers running around to spread the joy.
The very first antidepressants created in the ‘50s tried to raise the brain’s levels of serotonin and norepinephrine, to play with this mental message system. A second class of anti-depressants was based on inhibiting the enzyme that breaks down these guys in order to leave more of the good stuff in the brain. Basically the same idea. Next came the less side-effect-plagued successor, known as selective serotonin re-uptake inhibitors (SSRI), the most frequently prescribed antidepressants today. First developed in the ‘70s, and continuously improved upon by different pharmaceutical companies, SSRI’s work by stopping the process of reuptake, a fancy name for when a responsible neuron absorbs the neurotransmitter it has sent out, to take the messenger back off the streets once the message has been sent. The theory here is that by keeping the sending neuron from doing its re-absorbing, more of this “happy” chemical stays running around the brain. Again, the same idea.
While it sounds great to say that taking this medication is “fixing chemical imbalances in the brain,” the problem is that no one gets to do experiments on a live human brain. Thankfully. And dead human brains don’t send chemical messages and can’t be depressed. Neither really can animals, at least those generally accepted for grisly lab experiments. So no one actually knows whether depressed people have less serotonin in their brains. Or whether they reabsorb it too fast without medication. In fact, no one knows how much serotonin a generally joyful person has. Can one really have too little? Or too much? Because a few antidepressants lower serotonin levels, and they appear to work too.
Trying to figure out what makes for a happy brain is complicated even more because there is no way to tell how much these medications change a person’s serotonin levels, because there is no way to measure those levels in a live human. Which means that, in the end, the only evidence we have that serotonin levels might be related to human depression at all is that in more cases than not, the medication works.
Is it working because it is based on an accurate analysis of how chemicasl in our brains keep us happy? Or not? That will be subject of another post.