We need survey data to determine whether comorbidity is increasing or decreasing over time. Third, we need to test existing hypotheses to account for comorbidity via experimental designs, including testing third variables that might account for associations. Replication will be important, as many hypotheses have one or two studies to support them, but no more. Until biological and behavioral mechanisms are elucidated, designing prevention treatment interventions for comorbid smokers will be difficult. Smoking-induced changes in MAO predispose to depression.
Smoking induces tolerance to alcohol, which decreases the aversive effects of alcohol.
Fourth, we need to know whether treatments for psychiatric comorbidity influence smoking. For example, generalizable experimental trials could replicate whether methadone increases smoking, clozapine decreases smoking, and haloperidol increases smoking. Fifth, we need to know whether treatments for smoking influence comorbidity. For example, generalizable experimental trials may show whether cessation increases or decreases drug use or sobriety in abusers of alcohol and other drugs, whether cessation precipitates relapse to depression, and so forth. From Basic Science to Clinical Practice .