This well-known theory first gained currency in an article which appeared in The American Journal of Psychiatry in 1965. Was the chemical concerned serotonin? No, it was norepinephrine. The author himself, Joseph Schildkraut, described the theory as ‘at best a reductionist simplification’. He was right, and this is still the case today.
But accepting the theory for argument’s sake, let’s make a comparison. Let us suppose that Madeleine is having trouble with her thyroid gland. She is producing too little thyroxine and so has a chemical imbalance. The extent of the imbalance is measured by blood test and she is prescribed synthetically produced thyroxine to correct it. The amount of thyroxine required is worked out by reference to Madeleine’s test results.
And now a second case. Albert is a worried man. He goes to his doctor and, after a short chat, the doctor concludes that he is suffering from depression. She then prescribes an SSRI (selective serotonin re-uptake inhibitor) which will correct the chemical imbalance in Albert’s brain.
But wait a minute, where is the test in this case? Madeleine was tested, why wasn’t Albert? How can the doctor know there is a chemical imbalance to correct without testing the chemical levels in Albert’s brain?
So, in prescribing an SSRI, the doctor is assuming:
– That the chemical imbalance theory has solid evidence to support it
– That Albert is one of those affected by a chemical imbalance and his ‘depression’ does not have some other cause
– That the SSRI she prescribes, and in the quantity she is prescribing it, will correct this supposed imbalance
When it comes to the prescribing of anti-depressants, bold assumptions like these are now being made on an industrial scale.
[To be fair to the doctor, she errs on the side of caution when it comes to quantity, starting with a small dose of Albert’s SSRI and gradually increasing it: something she would not do with thyroxine, where she would know – as a consequence of testing – how much was required.]