To the Editor: Patients with chronic schizophrenia smoke at substantially higher prevalence rates (70%–80%) than the general population (25%–30%) R1567BCFBHFGG, R1567BCFDDFDI. Reasons suggested to explain this include the following: 1) smoking lowers antipsychotic blood levels (and extrapyramidal side effects R1567BCFDDFDI) by stimulating hepatic microsomal enzymes R1567BCFEADFF, and 2) nicotine reverses antipsychotic-induced cognitive slowing R1567BCFBDBDJ. However, there is also evidence that smoking produces direct "therapeutic" effects (i.e., independent of its interactions with antipsychotics) for patients with schizophrenia. For example, nicotine corrects abnormalities in sensory gating seen in many patients with schizophrenia and in 50% of their first-degree relatives R1567BCFECBCH.

If patients with schizophrenia smoke primarily to reverse the effects of antipsychotic drugs, those with chronic schizophrenia should smoke at substantially higher prevalence rates than first-episode patients.

We interviewed and observed 22 consecutively admitted, first-episode patients with schizophrenia or schizophreniform disorder; all patients gave written informed consent after the procedures were explained to them. The patients had less than 30 days’ previous lifetime exposure to antipsychotics; 17 (77%) smoked. Twelve of these 22 patients had no previous exposure to antipsychotics; 11 of these 12 (92%) smoked.

The fact that first-episode patients smoke at the same prevalence rate as chronic patients suggests that it is schizophrenia, not its treatment with antipsychotic drugs, that determines this prevalence. Pharmacologic agents with therapeutic effects on nicotine-sensitive pathophysiologic mechanisms in schizophrenia may decrease a patient’s drive to smoke and reduce the associated health risks.