Terman et al (SEE ARTICLE) evaluated 2 nonpharmacological treatments for seasonal affective disorder for antidepressant efficacy. Bright diffuse fluorescent light of 10,000 lux was presented daily for 30 minutes in the morning or evening, and negative ions were presented in the morning for 30 minutes at low or high concentration. Morning light produced the highest remission rate, but evening light and high-density ions also were superior to low-density ions, a plausible placebo that was clinically ineffective.
Eastman et al (SEE ARTICLE) showed that a light box produced more remissions in winter depression than a sham negative-ion generator. There were reductions in depression after just 1 week; however, light was not superior to placebo until the third week of treatment.
Lewy et al (SEE ARTICLE) report that morning light is significantly more antidepressant than evening light in winter depression. When bright light exposure occurs in the morning, it corrects an abnormal phase delay in the timing of the circadian rhythms when these patients are depressed in the winter.
Commentaries on light therapy and winter depression by Wirz-Justice (SEE ARTICLE) and Avery (SEE ARTICLE) are included.
A brain thermostat was recently described and reported as dysfunctional in patients with winter depression. Schwartz et al (SEE ARTICLE) found that while both melatonin and serotonin 1A receptors were involved in normal function, neither were involved in the thermostat's observed dysfunction in winter depression. The results suggest several testable hypotheses regarding the role of the thermostat in the development of psychopatholog//ical symptoms.
Pfefferbaum et al (SEE ARTICLE) followed healthy and alcoholic men for 5 years to document brain aging and whether heavy alcohol consumption accelerates and abstinence normalizes age-related brain changes. Healthy men showed cortical, particularly prefrontal, tissue loss and ventricular expansion over 5 years. Alcoholics showed similar changes with particularly marked temporal lobe volume loss; alcoholics who drank more during follow-up lost more cortical tissue, whereas alcoholics who maintained sobriety showed normal ventricular enlargement.
Posttraumatic stress disorder (PTSD) has been linked to substance use disorders. In an epidemiological study of young adults, Chilcoat and Breslau (SEE ARTICLE) found that PTSD increases the risk of abuse or dependence of prescribed drugs 13-fold. The findings support the self-medication hypothesis, and provide little evidence that persons with drug abuse or dependence are at increased risk for traumatic events or PTSD.
Fallon et al (SEE ARTICLE) conducted the first placebo-controlled double-blind study of gradually escalating intravenous clomipramine treatment among patients with obsessive-compulsive disorder who reported an inadequate or no response to oral clomipramine. Intravenous clomipramine treatment was safe and significantly more effective than intravenous placebo.
Women with bulimia nervosa are known to have alterations of brain serotonin activity and mood as well as obsessions with perfectionism. Kaye et al (SEE ARTICLE) found that these alterations and symptoms persisted after recovery from bulimia nervosa, suggesting that they are not merely a consequence of abnormal eating behaviors. While bulimia nervosa is often presumed to be caused by psychosocial factors, these findings suggest that biological risk factors may also contribute to this disorder.
Anxiety is a genetically influenced personality trait, leading to the conclusion that people tend to be more or less anxious owing to inherited differences in genes affecting brain function. Last year, a variant of the serotonin transporter gene promoter was described that showed a relationship to anxiety. With a new genetic study, Mazzanti et al (SEE ARTICLE) support the relationship of the transporter to anxiety.
The relationship between personality disorder traits and the genetic architecture of personality is poorly understood. Livesley et al (SEE ARTICLE) showed that the observed structure of personality disorder is similar across clinical and nonclinical samples, and that this structure closely reflects genetic predisposition. Four broad factors were identified in phenotypic and genetic analyses: emotional dysregulation, dissocial behavior, inhibitedness, and compulsivity. When the effects of these genetic factors were removed from the variability of specific traits, a substantial heritable component remained.
A Commentary by Widiger (SEE ARTICLE) is included.
