Mental illness is the 21st century’s leading cause of disability, affecting an estimated billion people across the world. Depression is the number one contributor: more than 250 million people have this condition globally. The number of people prescribed antidepressant medications, the first-line treatment for depression, increases each year, and the market for them is valued at approximately $15bn (£11bn). Yet depression prevalence rates have not decreased since accurate record-keeping began. One reason for this paradox is the failure of science to adequately explain how and why depression occurs.
Psychiatry has long sought and failed to find a compelling biomedical explanation for depression. One popular idea, the “serotonin hypothesis”, was inspired by the observation that drugs that increase the activity of this naturally occurring brain chemical have antidepressant effects. First produced in the mid-1980s, Prozac (chemical name fluoxetine) is the most famous selective serotonin reuptake inhibitor (SSRI) antidepressant. Of these, Cipralex (escitalopram) is one of the newest and best performing.
While the serotonin hypothesis has some scientific foundation, it has been massively oversold by the pharmaceutical industry. This has stoked scepticism about one-sided, neurochemical explanations for depression, which suggest, for instance, that people are depressed because their serotonin levels are too low. The latest evidence indicates that SSRIs such as escitalopram are only marginally more effective at treating depression than a placebo, with response rates tending to average around 50-60%. Other limitations of SSRIs include poor compliance, symptoms when people stop taking them, unpleasant side-effects and a sluggish onset of antidepressant effects.
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