Coid et al Article confirm the belief of most clinicians of a strong relationship between delusions and violence in a UK first-episode psychosis sample. Few direct associations were found but a subset of highly prevalent delusional beliefs (persecution, being spied on, and conspiracy) were associated with serious violence. However, the association was mediated by anger due to the delusions.
Using a combination of neuroimaging approaches in a carefully matched sample, followed by confirmation in a larger population-based sample, Voineskos et al Article show that patients with the schizophrenia deficit subtype show alterations in neural circuitry important for emotion recognition, emotion expression, and socioemotional function compared with patients with nondeficit schizophrenia and healthy controls.
In a multisite, randomized, placebo-controlled clinical trial, Roffman et al Article found that 16 weeks of folate and B12 supplementation improved negative symptoms of schizophrenia, but only when accounting for the effects of genetic variants in the folate metabolic pathway. A common variant in FOLH1, which mediates folate absorption through the intestinal lumen, influenced both blood folate levels and treatment response.
Wisner et al Article screened 10 000 women for depression at 4 to 6 weeks post partum and evaluated those with positive screen findings for timing of episode onset, self-harm ideation, and primary and secondary DSM-IV disorders. A positive screen finding was an Edinburgh Postnatal Depression Scale score of 10 or more, which was found in 14.0%. More episodes began post partum (40.1%), followed by during pregnancy (33.4%), and before pregnancy (26.5%). In this population, 19.3% had self-harm ideation. About sixty-eight percent had unipolar depressive disorders, two-thirds had comorbid anxiety disorders, and 22.6% had bipolar disorders.
Pechtel and Pizzagalli Article report that, relative to women with a history of depression alone, women with past depression and childhood sexual abuse were characterized by behavioral and neural deficits in using positive reinforcements to optimize decision making. Disrupted reward-based decision making predicted more frequent engagement in self-harm and suicidal behaviors. No differences emerged for learning from punishments, providing evidence for reward-specific deficits following childhood sexual abuse, irrespective of past depression.
Roberts et al Article report an association between mother's childhood experience of physical, emotional, and sexual abuse and a greater risk of autism in her children. The study examined 9 potential perinatal mediators of this association, including smoking, gestational diabetes, toxemia, birth weight, gestation length, selective serotonin reuptake inhibitor use, alcohol use, prior abortion, and intimate partner violence victimization. These factors explained only a small part of increased risk of autism in children of women who experienced abuse.
Frans et al Article report that paternal age not only has an impact on autism risk in offspring but also affects subsequent generations. This study used population-based Swedish longitudinal registers to identify individuals with and without childhood autism and link them to their parents and grandparents. The analyses show that individuals with autism have older grandfathers than healthy controls.
In this randomized clinical trial of 294 community volunteers, Cinciripini et al Article demonstrate that both varenicline tartrate and bupropion hydrochloride sustained release increase abstinence rates from smoking at the end of treatment and at the 3-month postquit follow-up visit but by 6 months only the varenicline vs placebo comparison remained significant. Importantly, however, they also found that relative to placebo varenicline has a favorable (suppressive) effect on symptoms of depression and other affective measures, with no clear adverse neuropsychiatric events in this community sample.
Belsky et al Article studied genetic influences on the development of smoking behavior using a multilocus genetic risk score. Follow-up of a 1037-member birth cohort through age 38 years revealed that genetic risk was not associated with smoking initiation but did predispose to rapid progression from initiation toward a pathological pattern of use, including persistent heavy smoking, nicotine dependence, and cessation failure. Interventions that target the onset of smoking behavior in adolescence may mitigate genetic risks.