as someone who has suffered from depression in the past, I can relate to much of what is being discussed here. Furthermore, I have both an academic background in psychology relating to drugs and behaviour, providing me with experience in pharmacokinetics as well as a political science background which has left me with an infinite desire to question power.
Strangely, despite intensive research on depression (not to mention other psychological disorders), not much is known about the nature of the human brain, or the causes of our emotions. Importantly, much in psychology is correlation, not causation. While studies have linked depression to abnormal levels of monoamine neurotransmitters like serotonin and norepinephrine, the exact science behind it is not clear. It is also not just a simple explanation of low levels. For years drug companies have sold low levels of monoamines as a simple explanation for a complex problem; it’s easy to understand: you do not have a serious problem, your serotonin levels are low is all…we’ll just boost them back up and things will be ok…this is a theory, that although inherently wrong, seems to make sense.
Funnily enough, manipulating the re-uptake of other monamine neurotransmitters seem to have similar effects. For example, one of the first antidepressants, iprozinaid, a MAOI, (MonoAmineOxidaze Inihibtor), affected all of the major monoamines, dopamine, serotonin and norepinephrine (as did all the MAOIs). Interestingly, iproniazid, was originally designed as a drug for TB, but it was noticed that it made patients surprisingly happy. Now, while SSRIs (Selective Serotonin Reuptake Inihbitors) like paxil, prozac, wellbutrin etc, now the most commonly used antidepressants, were supposed to be “cleaner” than the MAOIs, being “selective”, and they did seem to be effective, nobody was quite sure why. Yes, serotonin levels seemed low in depression, and raising them seemed to correlate with feelings of happiness…but is/was it causation? Oddly enough, now increasingly popular are SNRIs (Serotonin-Norephinephrine Reuptake Inihibtors), a combination seemingly “dirtier” than the SSRIs in that two monoamine neurotransmitters are affected…a seeming step backward to a more MAOI like drug but, surprisingly perhaps more effective
On a more personal note, I have long in the past had experiences using an SSRI, paxil. Initially I felt paxil produced a significant improvement in my world outlook. However, as I continued treatment over the span of a month, I began to feel agitated constantly; I had this sense of nervous energy that I could not expend. I have since discovered in trials paxil, and other SSRIs have been attributed to a feeling of “activation;” a sensation that many patients found disturbing. Indeed, many SSRIs have actually been linked to a higher levels of aggression and violence against oneself and others.
If anyone wants further information an excellent book is Let them Eat Prozac by David Healy, a professor at the U of T…Healy was infamously fired by the U of T when he first spoke out against prozac, Eli Lilly being a major sponsor of research at the UofT. Healy was later re-hired after outspoken criticism of the university’s actions was voiced by the Canadian Association of University Teachers.