nd to Prozac with decreased anxiety. The clear implication is that people with this variant will not be able to respond to any SSRI, which requires normal neurotrophic-factor function to work.

A psychiatrist could identify this genetic variant and then steer his patient to a different class of antidepressants. Furthermore, other genes may play a role in the adverse effects of antidepressants that have made recent headlines: suicidal behavior. Recent evidence shows that a small number of depressed adolescents and young adults experience an increase in suicidal feelings and thoughts when they are treated with SSRIs, compared with a placebo.

It is entirely possible that a genetic variation in one or more genes that regulate serotonin function makes these people feel briefly more suicidal, rather than less, when exposed to the drugs. This new field of pharmacogenomics will also enable psychiatrists to predict which drugs might produce toxic side effects for certain patients. Nearly all drugs are metabolized by a group of enzymes that vary greatly in activity from person to person.

If patients have a genetic mutation that results in either deficient enzyme activity or none, they would be likely to have serious side effects if exposed to the drug that is metabolized by the enzyme. Within a few years, patients could be routinely screened for these genetic variations, which will tell a doctor which drugs to avoid. This could potentially prevent unnecessary drug toxicity, a major cause of illness and death.

Aside from the potential to transform clinical psychiatric practice, these new developments will surely change the relationship between doctors and the drug industry and between the industry and the public. Direct-to-consumer advertising will become nearly irrelevant because the drugs will no longer be interchangeable, but will be prescribed based on an individuals biological profile.

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