Once hailed as a revolution in treating depression, the benefits of the class of drugs that includes Prozac and Seroxat now look to have been exaggerated. This week’s study showing that selective serotonin reuptake inhibitors (SSRIs) are little better than placebos, at least for mild and moderate depression, is only the latest to challenge their purported effectiveness.

These findings do not necessarily mean, however, that the drugs don’t work. Leaving aside methodological problems raised by some psychiatrists, the evidence could have another explanation. Perhaps they don’t work for everybody.

Some tantalising if preliminary results that could support this hypothesis also emerged this week. A US study found that many patients who do not benefit from one SSRI share a particular genetic variant, which has been linked to their action.

It would be wrong to read too much into this yet, but it suggests poor responses to SSRIs could be attributable to genetic variation. If the drugs help only a subset of people, indiscriminate trials would not show substantial benefits beyond placebos. Participants who are genetically immune to them could easily mask positive effects among others.

This phenomenon has yet to be established for SSRIs, but it certainly applies to other drugs. Herceptin, for example, does not work for every breast cancer patient, but only for the one in five whose tumours have a particular genetic profile.

This bespoke approach to prescribing, known as pharmacogenetics, has great potential for patients, promising medicines that are more likely to work for them. It makes the pharmaceutical industry nervous, however, as it challenges its business model. Its big money-spinners have traditionally been one-size-fits-all drugs, such as SSRIs or statins, which can be sold in vast numbers. Tailor-made medicines for genetic niche groups will have smaller markets.

The fear that this will hit profits is understandable but shortsighted. First, genetic targeting can cut the costs of trials and marketing. If a drug is likely to work only for one patient group, time and money can be saved by using these people for trials. That lowers the risk of conducting expensive research with negative results – the biggest cost of drug development.

Had Herceptin been tested on randomly selected women, it would have been dropped as ineffective. Targeted at a susceptible group, it has become both a life-saver and a profit-maker for its manufacturer, Roche. It has shown, too, how a drug that becomes the best option for a particular genotype can essentially market itself, with obvious relevance for the bottom line.

Pharmacogenetics can also “rescue” drugs that perform poorly at a population level but which work for individuals. Many drugs are abandoned, after heavy spending on development, because they fail trials or cause adverse effects in a minority. If it is possible to identify groups in whom they are safe and effective, some of this investment might still be recouped.

SSRIs could be a case in point. The evidence that they are overprescribed is growing stronger, and the backlash against them is threatening a fertile source of profits. Pharmacogenetics could provide some insurance. If SSRI response does turn out to be linked to DNA – and nothing has been proved yet – the drugs could be remarketed as targeted therapies. They might no longer be blockbusters, but neither would they be lost.

As we understand more about genetic variation, the blockbuster model that fed the SSRI revolution is going to become less sustainable. The pharmacogenetic alternative holds great opportunities not only for patients but also for those drug companies that embrace new ways of doing business.

Mark Henderson is the Science Editor of The Times

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