Krystal et al (SEE ARTICLE) review evidence that ethanol effects on 
-aminobutyric acid (GABA) systems associated with social drinking may arise from actions at an extrasynaptic subpopulation of GABA type A (GABAA) receptors with a distinctive subunit composition. Preclinical and new neuroimaging data suggest that ethanol tolerance and dependence are associated with shifts in GABAA receptor subunit composition that affect the function of these receptors and that the adaptations in GABA systems associated with ethanol dependence appear to be attenuated by smoking. Genetic variation in GABAA receptor subunits contributes to the risk for alcoholism.
Wood et al (SEE ARTICLE) used magnetic resonance spectroscopy to predict functional outcome 18 months after entry to an early psychosis clinic. Better outcomes across a range of measures were associated with higher levels of N-acetylaspartate, a putative neuronal marker, in the prefrontal cortex at intake. This study suggests that prefrontal neuronal integrity is an important component of outcome from a first psychotic episode and may allow tailoring of treatment regimens to improve recovery.
Using positron emission tomography and measures of depression, Neumeister et al (SEE ARTICLE) studied the relative contribution of a functional-length triallelic polymorphism in the promoter of the serotonin transporter, designated 5-HTTLPR, to the behavioral neural responses to tryptophan depletion in individuals with major depressive disorder. They found that genetic variants of the 5-HTTLPR differentiate between patients and controls and show that the 5-HTTLPR polymorphism has a direct effect on the regulation of glucose metabolism in a corticolimbic circuit that has been implicated in major depressive disorder.
Some people have a bias toward negative emotionality but never develop depression; others do. In a female cohort study, Jacobs et al (SEE ARTICLE) examined if a functional polymorphism of the serotonin transporter gene (5-HTTLPR) moderated the tendency of negative affectivity in daily life to contribute to the onset of symptoms of depression. Their findings shed new light on previous reports suggesting a moderating effect of the 5-HTTLPR genotype on the depressogenic effect of stressful life events.
Volkow et al (SEE ARTICLE) tested the hypothesis that high levels of D2 receptors may be protective against alcoholism and showed that subjects who, despite a dense family history for alcoholism, were not alcoholics had significantly higher D2 receptor levels in the striatum than subjects without family histories. D2 receptor level increases were associated with metabolism in frontal regions involved in emotional regulation, inhibitory control, and positive emotionality. Thus, D2 receptors may protect against alcoholism by modulating circuits involved in emotional responses.
In a large population-based birth cohort study of mothers and children followed up into adulthood, Alati et al (SEE ARTICLE) found that exposure of the fetus to 3 or more glasses of alcohol was associated with both early- and late-onset alcohol disorders in young adults. Their findings suggest that the association is not explained solely by maternal drinking or smoking during the childhood and adolescence of the subjects at risk.
In a large population-based study of 9- to 16-year-old youth from the southeastern United States, Foley et al (SEE ARTICLE) found that the severity of symptom-related impairment, and, in some cases, total symptom load, explained risk for suicidality associated with all current psychiatric profiles except depression comorbid with generalized anxiety disorder. Severity of impairment and poverty defined by federal guidelines for families were both independent risk factors irrespective of psychiatric profile.
In a population-based cohort study of individuals born in Israel, Reichenberg et al (SEE ARTICLE) report that advancing paternal age, but not maternal age, was associated with increased risk for autism. Advancing paternal age was also associated with the male-female sex ratio in autism. The sex ratio in the offspring with autism of fathers younger than 40 years was noticeably higher than the sex ratio of the offspring with autism of fathers older than 40 years. Possible biological mechanisms might include de novo mutations or alterations in genetic imprinting.
In a large Korean student sample, Kim et al (SEE ARTICLE) demonstrate that psychopathologic behavior is a consequence, rather than a cause, of bullying. This causal relation was supported by strength and specificity of associations with bullying and findings that bullying preceded the appearance of psychopathologic behavior. These findings have implications for understanding the role of environment in the genesis of psychopathologic behavior as well as for identification of and intervention for school bullying.
Pickett-Schenk et al (SEE ARTICLE) examined the efficacy of an 8-week, family-led education intervention for family members of adults with mental illness. In a randomized controlled trial, compared with wait-list controls, intervention participants reported fewer depressive symptoms, greater emotional role functioning, and fewer negative views of their relationships with their ill relatives. These improved outcomes were maintained over time.
