Weekly series! As per previous discussion, I will be publishing a big information blog on each Friday. Unfortunately, it’s midterms for me, which means a shorter post for you. Blame the paper(s) and exams and readings and stuff. I promise to be back on schedule next week. Also, I’ve commissioned a post on bulimia from Tetyana, who runs the spectacular Science of Eating Disorders blog, a skeptical look at research on ED’s.
Anyways, today we look at the types of antidepressants.
Selective Serotonin Reuptake Inhibitors (SSRI’s)
[Note to neurobiologists: I am simplifying massively here. I know that.]
These are the most popular medications for depression, and include a bunch of names you probably recognize: Zoloft, Prozac, Paxil, Celexa, Lexapro.
How do they work?
Neurons don’t connect directly to each other–they have a very tiny space (the synaptic cleft) between each end of one and beginning of the next. Neurotransmitters (like serotonin, dopamine, GABA, etc) are released from the presynaptic neuron, and partially absorbed by the postsynaptic neuron. The neurotransmitter that isn’t absorbed is mainly taken back by the presynaptic neuron. SSRI’s work by blocking the reuptake mechanism for serotonin, leaving more available serotonin in the brain, which seems to relieve depression in some people.
But, this is grossly oversimplified, and depression is not as basic as not having enough serotonin. In the words of Ozy, brain chemicals are not fucking magic.
Side effects of SSRI’s can include lack of sex drive, hyperactivity or lowered energy, etc. In some, these are so life-disrupting that other medications are preferred.
Serotonin-Norepinephrine Reuptake Inhibitors (SNRI’s)
SNRI’s include Cymbalta, Effexor, and Pristiq. They work very much like SSRI’s, except they inhibit both the reuptake mechanism for norepinephrine and serotonin.
The effectiveness of SSRI’s lends support to the Monoamine Hypothesis–an incomplete explanation for depression, suggesting that several neurotransmitter systems (including serotonergic) are responsible. The hypothesis does hold up to scrutiny, but doesn’t explain why many antidepressants also help with anxiety and obsessive-type disorders.
Color me happy to have done my research before publishing–turns out I didn’t have all of my facts straight. Tricyclics are antidepressants that operate somewhat like SSRI’s by inhibiting the reuptake of serotonin–but they also have a laundry list of possible side effects, and, like MAOI’s, are used more and more rarely.
Monoamine Oxidase Inhibitors (MAOI’s)
MAOI’s can be super effective! However, they come with hefty diet restrictions, and resultingly, are used rarely–mostly as a last resort.
People taking MAOI’s need to avoid all sorts of things, like pickled foods, most cheeses, wine, decongestants, and SSRI’s. Failure to do so can cause a stroke–the result of buildup of tyramine in the brain. Since other antidepressants are available, MAOI’s have fallen out of favor.
Norepinephrine and dopamine reuptake inhibitors (NDRIs)
Wellbutrin! NDRI’s are good because they usually don’t have the sexual side effects. They too, lend support to the Monoamine Hypothesis, by altering the dopaminergic and norandronergic pathways.
St. Johns Wort
Okay. This is alt-med, but it’s been gaining mainstream popularity. It’s one of those that might work on mild to moderate depression. And if taken without doctor supervision and with other medications it can cause you all sorts of problems. In combination with SNRI’s, it can cause Serotonin Syndrome–an excess of the neurotransmitter which overloads the central nervous system. It also appears to decrease the effectiveness of oral contraceptives, might cause problems if you’re breast-feeding, and oh, right, as an herbal supplement, isn’t all that regulated. What I’m saying is, self-prescribing this stuff is not a great idea, and right now, there’s not evidence that it works for major depression. But some people do use it, so I’ll include it.