There has been much in the UK news about Prozac and other anti-depressants over the last couple of days. This is because of a recently released study from the University of Hull, which suggests that some of these drugs might not be as effective as we have been previously led to believe. With over 31 million prescriptions being given out for these drugs in England alone, this is a grave statement indeed. In light of this study, this morning I’m bringing you an extract from our book Happiness: The Science Behind Your Smile by Daniel Nettle, which sheds a little light on the history of Prozac and other “happy pills”.
Aldous Huxley’s prophetic novel Brave New World (1931) depicts an England where unhappiness has been eliminated. ‘Everybody’s happy now’ is the mantra repeated to the young 150 times a night for the first twelve years of life. Perfect happiness is ensured by a combination of genetic engineering, artificially controlled growth conditions, and intense mindtraining from an early age. However, for any residual glimmers of dissatisfaction that somehow survive into adulthood, there is soma. Soma is a synthetic drug which the population is encouraged, almost required, to use on a daily basis. It banishes all feelings of discontent; ‘one cubic centimetre cures ten gloomy sentiments’. As well as getting people through their working week, soma can be used for social control. Puffing an aerosol of soma into the air easily disperses a riot that threatens to turn into a revolution.
Though Huxley’s satire is astonishingly perceptive and fresh today, most of the technical aspects of his vision—growing babies in jars, for example—are as farfetched and implausible as they were when he wrote them. What about soma? Could there really be a drug whose specific action would be to produce a state of happiness? This implies that happiness has a specific locus in the brain that it would be possible to manipulate. Is there any evidence of what such a locus might be?
The most obvious equivalents to soma in real life are antidepressants like Prozac. Prozac (the trade name of the compound fluoxetine) was the first of a new generation of antidepressants called the selective serotonin reuptake inhibitors (SSRIs). Before the advent of the SSRIs, antidepressants had been rather effective at dealing with clinical depression, but had produced a wide range of side-effects, often including sedation, weight gain, blurred vision, and a dry mouth. The SSRIs were about equally effective at treating the depression, but with fewer of these side-effects. Indeed, at least a subgroup of patients reported feeling ‘better than well’ with the new drugs. In healthy volunteers with no history at all of depressive illness, taking an SSRI increases measures of extroversion and positive emotion. The effect is not dramatic, but it is detectable. SSRIs proved effective in treating a wide range of conditions, including, for example, social phobia, a disorder of extreme shyness that scarcely existed before the drug was found to cure it.
The reception of the SSRIs has been astonishing. Prozac was launched, in the USA first, in 1988. Over the following ten years, antidepressant use rose by 100–200% in many developed countries, including the UK and USA, and much of this was due to the uptake of the SSRIs. Rates of use continue to grow at 6–10% per year, with over 3% of the population taking SSRIs in the UK and USA at any one time. For sufferers from clinical depression, SSRIs are a lifeline, but there are probably many people out there who seek them simply because they want a chemical shelter from the normal pains of being human. Some evidence for this comes from the fact that rates of use in Germany and France are less than half that in economically comparable Britain.
Prozac is not soma. Its effects in healthy volunteers are subtle, and moreover, it needs a few weeks of taking the drug for the effects to kick in. This is thought to be because the action of the drug on the relevant systems is quite indirect. The SSRI disables a mechanism whose function is to remove the important brain messenger chemical serotonin; levels of serotonin at one end of certain brain cells are augmented; the cells retune and become more active; and this causes an increase in serotonin activity at the other end of the cell. Only then does the antidepressant action follow. Soma, by contrast, produced positive feelings and ended negative thoughts in minutes.