Intended for healthcare professionals

Editorials

Serotonin and depression

BMJ 2015; 350 doi: https://doi.org/10.1136/bmj.h1771 (Published 21 April 2015) Cite this as: BMJ 2015;350:h1771

Healy does a disservice to psychiatrists

David Healy does a great disservice to jobbing psychiatrists with this editorial. By portraying them as 'co-opted into a myth' about low levels of serotonin being the sole cause of depression he paints them as gullible, and by stating that the same theory is 'an easy shorthand for communication with patients' he paints us as lazy and reductionist in our appraisal of the complex and diverse causes of depression.

In reality, good psychiatrists are and always have been only too ready to admit that they are unsure how antidepressants work. Serotonin does play an important role - likely via factors like neurogenesis and gene expression downstream from synapses - but modern psychiatry is way ahead of where Healy seems to think it is. The picture is far more complex. The fact that ketamine has been shown to be useful in depression does not 'cast doubt on the link between serotonin and depression', it rather confirms that the neurobiological underpinnings are as multifaceted as we think.

In any case, whatever their mode of action, SSRIs do work. Even the most stringent of analyses (i.e. Kirsch) support this. There is no good evidence that SSRIs work any less well than TCAs for depression , and the SSRIs have not become so commonplace in clinical practice due to some form of pharma-doctor conspiracy, as Healy would suggest, but because the older TCAs have a far less admirable side-effect profile and were also lethal in overdose. The safety of our patients should always come first, and they are far less safe without treatment for their depression.

Competing interests: No competing interests

25 April 2015
Alexander E Langford
Core Trainee in Psychiatry
South London and the Maudsley NHS Foundation Trust