The idea of prescribing drugs according to patients' genetic profiles is considered to be one of the next frontiers for medicine. It is an approach already used in cancer treatment, where several drugs have been developed that work only when tumours carry particular mutations.

Herceptin, for example, can prolong the survival of breast-cancer patients when their tumours have mutations in a gene called Her-2, and Glivec is given to people with chronic myeloid leukaemia (CML) who have a particular chromosomal defect.

DNA tests can also detect rare disorders caused by faulty genes, such as familial hypercholesterolaemia, which increases greatly the risk of early-onset heart disease. Carriers of the mutation can then be given preventive treatment.

What has been missing from healthcare so far has been an ability to use genetics to break down common chronic diseases into narrower categories and to predict how individuals will respond to particular drugs. Much as it is now understood that cancer is not one illness but hundreds, conditions such as type 2 diabetes and heart disease are also thought to be broad diagnostic labels that encompass many distinct sub-groups of disease.

While symptoms are similar, these often have different genetic roots and may benefit from different treatment strategies. Individuals' genes can also affect the way they metabolise drugs, such as statins for heart disease or metformin for type 2 diabetes, which can influence effectiveness or side-effects.

Pharmacogenetics aims to refine diagnosis and prescription according to these genetic factors. It will replace a one-size-fits-all model of medicine with a more nuanced, personalised version that is more likely to work.

The Mody gene test is the most successful application yet beyond cancer and very rare conditions. It is also one of the first that can switch patients to a cheap, generic drug, saving the NHS money: drugs such as Herceptin, designed with particular genetic profiles in mind, are extremely expensive.

But it is one of the low-hanging fruit: only a single gene is involved, so it is comparatively simple to test for and then change people's treatment. Most diseases, including most forms of type 2 diabetes, do not work like that. They are influenced by dozens of common genetic variants, each of which does not cause disease directly but contributes slightly to risk. Identifying what these combinations mean for therapy remains a considerable challenge.

Another potential barrier to pharmacogenetics is the attitude of drug companies. At present, their business model is based primarily on searching for blockbusters that can be sold in their millions, such as statins and the SSRI group of antidepressants. The whole point of pharmacogenetics, however, is to do the reverse - to provide drugs to niche groups of patients for whom they are most effective.

This makes the industry nervous: its financial interests are not well served by research that could reduce the potential market for a product. This fear is understandable but may be short-sighted as pharmacogenetics can actually reduce the costs of drug development. Genetic targeting can make clinical trials cheaper to run, and can “rescue” drugs that have serious side-effects for a minority.

Another likely saving is on marketing. A drug such as Glivec is known to be so effective for patients with a particular type of CML that it is almost always chosen as the frontline treatment. There is no need to spend vast sums on promotion because the product promotes itself.

It is interesting to note that many scientists working for the leading pharmaceutical companies are excited about pharmacogenetics and recognise these potential savings. It is often the marketing men who are most sceptical.

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