Anti-depressants and the placebo effect
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By M Parrott
Article ID: 1319
It’s a growing trend to believe that a pill can cure anything. Any aches, any pains, any sores. It’s a big reason why people are still looking for a pill to make you thin. While I think we have become far too reliant on pills, I’m not saying to scrap all drugs. They save lives, they save the economy money and they stop your pain. However, there is a specific type of drug that I have a problem with – the anti-psychotic. Or, to be even more specific, the anti-depressant. There are at least seventy-three anti-depressants on the market. For something that is supposed to “cure” depression, that’s a lot of drugs.
Let me explain where this idea comes from, that a drug will cure a psychological disorder. It relies upon a theory called the “monoamine hypothesis“. This theory suggests that depression is caused by low levels of three neuro-chemicals from a group called monoamine neurotransmitters in the central nervous system. In bi-polar patients, the subject’s levels of monoamine neuro-chemicals will fluctuate depending on whether they are in a depressed or manic state (low levels for depression, high for mania). What evidence do we have for this effect? Urine. No, honestly, urine. When studying the urine of people with depression we find they have low levels of by-products of dopamine, noradrenaline and serotonin. Autopsies show that those who commit suicide have these same low levels. It therefore seems plausible that depression is caused by low levels of the three neuro-transmitters.
However, correlation does not equal causation: there are no ill effects when artificially inducing low-levels of these three neuro-chemicals. The participants do not become depressed. This suggests that low-levels of serotonin, noradrenalin and dopamine do not cause depression. If this is the case, then the whole idea of anti-depressant drugs is a fallacy.

What about the drugs themselves? Proponents of the monoamine hypothesis argue that anti-depressants work, therefore proving that the theory is correct. However, this justification by circular reasoning doesn’t fly. More on that later. Let me first outline what anti-depressants are. There are four main types; SSRIs (selective serotonin reuptake inhibitors or serotonin-specific reuptake inhibitors), MAOIs (monoamine oxidase inhibitors), SNRIs (serotonin-norepinephrine reuptake inhibitors) and TCAs (tricyclic antidepressants). Medical doctor Arif Khan (1979-1999) tested the effectiveness of three substances; Sertraline hydrochloride (an SSRI), St John’s Wort (a plant from which most anti-depressants are made) and sugar pills (a placebo). The effectiveness test came back with a surprising result: sertraline hydrochloride was effective 25% of the time, St John’s Wort was at 24% and sugar pills were at 35%. Actual anti-depressant drugs were less effective than a placebo.
That’s depressing.
More research supporting these results is by Professor Irving Kirsch et al. (1998, 2002 and 2008), who showed that anti-depressants do not have enough statistical significance in comparison to placebos. Another point is that TCAs are also used to treat ADHD. You should treat ADHD with depressants, and yet TCAs – anti-depressants – are used to treat depression. I question any group of drugs used as depressants and anti-depressants at the same time.
After studying these drugs and the monoamine hypothesis, it appears that the lack of serotonin, noradrenalin and dopamine is a psychological disorder manifesting itself in a physiological symptom. For example, we don’t say that Tourette syndrome is caused by sudden inappropriate language, but that Tourette syndrome causes the inappropriate statements. Some argue that if anti-depressant drugs are placebos, at least they seem to do something. This is not a good plan. We should instead pursue other treatments for depression, rather than assuming one little tablet can cure such a complex thing as a psychological disorder.
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