The cause of mental disorders such as depression remains unknown. However, the idea that neurotransmitter imbalances cause depression is vigorously promoted by pharmaceutical companies and the psychiatric profession at large (emphasis added). We examine media reports referring to this chemical imbalance theory and ask reporters for evidence supporting their claims. We then report and critique the scientific papers and other confirming evidence offered in response to our questions. Responses were received from multiple sources, including practicing psychiatrists, clients, and a major pharmaceutical company. The evidence offered was not compelling, and several of the cited sources flatly stated that the proposed theory of serotonin imbalance was known to be incorrect. The media can play a positive role in mental health reporting by ensuring that the information reported is congruent with the peer-reviewed scientific literature.
It's been known for more than a decade that the 'chemical imbalance/low serotonin' hypothesis was deeply flawed, yet in continues to be promoted not only in the media, but in medical journals by researchers who should know better.
Using the theory as a convenient shorthand explanation might be acceptable, barely, if it wasn't leading people to self-medicating with the potentially dangerous supplements L-Tryptophan and 5-HTP in the mistaken belief that taking these serotonin precursors will achieve the same result as antidepressants without the side effects.
A good starting point to banishing this nonsense might be for medical journals to reject new papers based on it.
The problem here is that, both in the original article and in the later comment posted above, the authors assume that a causative relationship is being presumed between the mental illness - in this case depression - and the neurotransmitter "imbalance".
That simply isn't true, or at least not for the most part and it certainly doesn't need to be true to justify current treatment practices.
As I have stated many times in various contexts, I don't think there is yet any way of determining whether depression (or anxiety, or bipolar disorder, or OCD, or schizophrenia, or any other mental disorder) is caused by an imbalance among the major neurotransmitters, or by too little or too much serotonin, dopamine, norepinephrine, or gaba, or anything else. It is just as possible that the changes we see in neurotransmitters are a result of the mental disorder rather than a cause or precursor.
But we do know several things:
1. Once the mental disorder is established and the individual comes to the attention of mental health practitioners, there are measurable differences in various neurotransmitter levels compared to control subjects without that mental disorder.
2. To some extent, the specific neurotransmitter(s) affected vary across different diagnoses, so there is some (though not complete) specificity.
3. Medications used to treat these disorders do in fact have the effect of changing neurotransmitter levels and these changes are correlated with reduction in symptoms and with recovery from the mental disorder.
4. Recent research has suggested that the observed changes in neurotransmitters may also be associated with the growth of new brain cells and/or neural pathways in the brain. It may be that this new growth is what is critical for recovery but if altering neurotransmitter levels is effective in promoting the new growth the use of current medications to treat these mental disorders is still a primary component of a biologically informed treatment approach to mental illness.
5. Repeatedly, research has demonstrated that the combination of medication plus psychotherapy is the most effective strategy for treating a range of mental disorders, including depression, anxiety disorders, OCD, schizophrenia, and bipolar disorder.
I would agree that the debate about what causes what is relevant, and that it deserves to continue to be the focus of further research, which is what is occurring now.
But, that said, I think it would be absolute folly to ignore the clinical and research evidence for the efficacy of these medications and their role in altering neurotransmitter levels while promoting symptom management and recovery.
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