In This Issue

A treatment study by Fenton and Chavez (p. 1697 ) discusses the care of patients who develop the metabolic syndrome while taking second-generation antipsychotic drugs. Obesity, hypertension, and abnormal lipid, triglyceride, and glucose levels can be managed through both lifestyle and medication. The psychiatrist’s role thus expands to include monitoring of weight and pertinent laboratory test results. The physiology behind the metabolic effects of second-generation antipsychotics is not clear, and risk varies among drugs. Olfson et al. (p. 1821 ) found that hyperlipidemia among California Medicaid recipients was most strongly associated with clozapine, followed by risperidone, quetiapine, olanzapine, ziprasidone, and first-generation antipsychotics. Aripiprazole did not increase risk.

Recognition that attention deficit hyperactivity disorder (ADHD) occurs in adults is helping refine illness characteristics. Faraone et al. (p. 1720 ) provide evidence that the diagnostic requirement of onset by age 7 could be modified to include late-onset cases. Adults with late-onset ADHD were similar to those with the full diagnosis in terms of co-occurring psychiatric disorders, familial transmission, and functional impairment. Biederman et al. (p. 1730 ) found that problems in executive functioning—how well the frontal cortex executes mental activities—were more common in adults with ADHD (31%) than in healthy subjects (16%). These deficits were associated with academic, work, and social dysfunction, conferring even greater disability than ADHD alone. In an editorial, Drs. James McGough and James McCracken (p. 1673 ) relate these findings to issues in diagnosis of ADHD.

An experimental study by H�d et al. (p. 1739 ) suggests that patient attributes may help explain why different types of psychotherapy often produce seemingly equivalent outcomes. Patients received 1 year of dynamic psychotherapy with or without interpretations of “transference,” the interaction between the patient and psychotherapist. The two forms of psychotherapy produced similar improvements overall. However, there was a difference for a subgroup of patients, those with poor interpersonal relationships, who unexpectedly benefited more from the therapy including transference interpretations. Dr. Glen Gabbard discusses this study in an editorial on p. 1667 .

Injury severity may be an important indicator of risk for posttraumatic stress disorder (PTSD), report Grieger et al. (p. 1777 ). Among 243 U.S. soldiers seriously injured in Iraq or Afghanistan, PTSD symptoms and physical symptoms at 1 month were associated with both PTSD and depression at 7 months. However, 79% of the soldiers with PTSD or depression at 7 months had not had either condition at 1 month.

Three articles present genetic evidence for molecular mechanisms underlying specific clinical phenomena: cognitive dysfunction in schizophrenia, responsiveness to antipsychotic drugs, and mania as the presenting feature of bipolar disorder. Hirvonen et al. (p. 1747 ) demonstrated a genetic influence on dopamine transmission in the prefrontal cortex, which is related to cognitive deficits in schizophrenia. The unaffected monozygotic twins in pairs discordant for schizophrenia had higher densities of dopamine D ₁ receptors in the medial prefrontal cortex than healthy comparison subjects. This twin strategy allowed researchers to assess a genetic abnormality in dopamine receptors, free of the confounding effects of antipsychotic medication. Among patients receiving antipsychotic drugs, Reynolds et al. (p. 1826 ) found that one of three possible genotypes for a variable region of the serotonin 5-HT _1A receptor gene was associated with greater improvement in negative and depressive symptoms than were the other two genotypes. Kassem et al. (p. 1754 ) report that manic onset of bipolar disorder is linked to chromosome 16p and that the polarity of the first episode (manic or depressive) is transmitted in families. A postmortem study by Paz et al. (p. 1829 ) presents evidence for cerebellar hyperactivity based on mRNA levels of three activity-dependent genes. As Kendler and Greenspan (p. 1683 ) describe, the genetic underpinnings of psychiatric illness have several commonalities with the genetics of behavior in “simpler” organisms, such as fruit flies and rodents. The editorial by Drs. David Lewis and Ahmad Hariri (p. 1676 ) provides further perspective on the field of psychiatric genetics.