Wednesday, March 10, 2010
Don't worry, be happy.
Neuroskeptic has a nice little post about a case study of a man who has a rare genetic condition that severely limits his ability to produce monoamines, most notably the neurotransmitters dopamine and serotonin. Since the deficit of dopamine leads to symptoms very similar to Parkinson's disease, this man was treated, from a very early age, with L-dopa (the precursor to dopamine, and a common treatment for Parkinson's). However, the deficit in serotonin was left unchecked and untreated. The interesting thing about this is that the patient was never diagnosed with depression, which goes against the current idea that depression is all about a lack of serotonin. Since most of the current antidepressants on the market work by preventing the absorption and breakdown of serotonin, the immediate effect is the same as increasing the overall level of serotonin in the synapses. Now, does a single case study of a single individual overturn the successes of drugs like Prozac, Paxil, and Zoloft? No (a much larger sample size would be needed for that to happen). However, when you add this story to what we already know about selective serotonin reuptake inhibitors (SSRIs like Prozac, Paxil, and Zoloft), it lends further credence to the idea that serotonin may be involved in symptoms of depression , but it is certainly not the only, or perhaps not even the primary, factor. As I said, SSRIs have been shown to be effective in relieving symptoms of depression, however, they are not a panacea. Their effects can be best described as modest, and some studies suggest that they only really help in cases of severe depression. Also, we know that it usually takes 2 to 3 weeks for patients to report feeling a benefit from the drugs, despite the fact that they increase serotonin levels almost immediately. So, is serotonin important, or isn't it? Unfortunately, there is no simple answer. It seems that boosting serotonin activity in the brain can lessen symptoms of depression and anxiety, but it may not be the serotonin directly, or serotonin alone. For example, researchers have shown that SSRIs have other effects, like increasing neurogenesis, and that this increased neuronal proliferation may be necessary for the observed therapeutic effects. Ultimately, it seems, depression is a bit more complicated than just a single neurotransmitter, but hopefully, as more information like this case study comes to light, scientists will get a better handle on the underlying physiology, and treatment options will only improve.