Family, twin, and adoption studies have been essential in defining the genetic epidemiology of bipolar disorder over the past several decades. Family studies have documented that first-degree relatives of affected individuals have an excess risk of the disorder, while twin studies (and to a lesser extent, adoption studies) suggest that genes are largely responsible for this familial aggregation. We review these studies, including the magnitude of familial risk and heritability estimates, efforts to identify familial subtypes of bipolar disorder, and the implications of family/genetic data for validating nosologic boundaries. Taken together, these studies indicate that bipolar disorder is phenotypically and genetically complex.

A long-standing challenge for scientific and clinical work on suicidal behavior is that people often are motivated to deny or conceal suicidal thoughts. We proposed that people considering suicide would possess an objectively measurable attentional bias toward suicide-related stimuli, and that this bias would predict future suicidal behavior. Participants were 124 adults presenting to a psychiatric emergency department who were administered a modified emotional Stroop task and followed for six months. Suicide attempters showed an attentional bias toward suicide-related words relative to neutral words, and this bias was strongest among those who had made a more recent attempt. Importantly, this suicide-specific attentional bias predicted which people made a suicide attempt over the next six months, above and beyond other clinical predictors. Attentional bias toward more general negatively-valenced words did not predict any suicide-related outcomes, supporting the specificity of the observed effect. These results suggest that suicide-specific attentional bias can serve as a behavioral marker for suicidal risk, and ultimately improve scientific and clinical work on suicide-related outcomes. Keywords suicide; attentional bias; Stroop task; predictionSuicide is a leading cause of death in the United States and worldwide (Nock et al., 2008). Mortality data indicate that one person dies by suicide somewhere around the world every 40 seconds (Krug, Dahlberg, Mercy, Zwi, & Lozano, 2002). The high rate of suicide results in part from the fact that assessment primarily depends on people's explicit self-report, Correspondence to Matthew K. Nock, Ph.D., Department of Psychology, Harvard University, 33 Kirkland Street, 1280, Cambridge, MA 02138, nock@wjh.harvard.edu.. Publisher's Disclaimer: The following manuscript is the final accepted manuscript. It has not been subjected to the final copyediting, fact-checking, and proofreading required for formal publication. It is not the definitive, publisher-authenticated version. The American Psychological Association and its Council of Editors disclaim any responsibility or liabilities for errors or omissions of this manuscript version, any version derived from this manuscript by NIH, or other third parties. The published version is available at www.apa.org/pubs/journals/ABN NIH Public Access which is unreliable because people often are motivated to deny their suicidal thoughts (Busch, Fawcett, & Jacobs, 2003). Developing more objective and scientifically rigorous ways of determining who is at risk for suicidal behavior is essential for both scientific and clinical work addressing this devastating behavior problem.The National Institute of Mental Health (NIMH) Strategic Plan lists as one of its primary objectives the identification of biological and behavioral markers associated with mental disorders and clinical behavior problems (NIMH, 2009). Behavioral markers are objectively observable, behavior-based factors that indicate some underlying disease process and can aid in c...

Suicide is a leading cause of death worldwide, challenging all theories that assume a universal drive for self-preservation. It is difficult to predict and prevent because people who consider killing themselves often are unwilling or incapable of reporting their intention. Advances in the measurement of implicit cognition provide an opportunity to test whether automatic associations of self with death can provide a behavioral marker of suicide risk. We measured implicit associations about death/suicide in 157 people presenting for treatment at a psychiatric emergency department while they awaited medical attention. Results confirmed that suicide attempters hold a significantly stronger implicit association between death/suicide and self than do psychiatrically distressed nonattempters. Moreover, the implicit association of death/suicide with self was associated with an approximately six-fold increase in the odds of making a suicide attempt in the next 6 months, exceeding the predictive validity of known risk factors (e.g., depression or suicide attempt history) and both patients’ and clinicians’ predictions. These results provide the first evidence of a behavioral marker for suicidal behavior and suggest that measures of implicit cognition may be useful for detecting and predicting sensitive clinical behaviors that are unlikely to be reported.

Identification With All Humanity (IWAH) relates to higher levels of concern and supportive behavior toward the disadvantaged, stronger endorsement of human rights, and stronger responses in favor of global harmony. So far, IWAH has been conceptualized as a one‐dimensional construct describing the degree with which one identifies with all humans as a superordinate ingroup. However, recent group identification models suggest a multi‐dimensional model to provide a more differentiated approach toward the understanding of the highest level of social identification. Using principal axis (Study 1) and confirmatory (Study 2) factor analyses, we suggest that IWAH sub‐divides into two dimensions—global self‐definition and global self‐investment. Study 2 revealed that global self‐investment was a stronger predictor for both convergent measures (e.g., social dominance orientation and authoritarianism) and behavioral intentions than global self‐definition. Finally, in Study 3, we manipulated IWAH to test its causal effect on donation behavior. Participants in the experimental condition, compared with the control condition, showed higher global self‐investment, which in turn predicted greater giving to global charity. These findings suggest that two dimensions with different behavioral outcomes underlie IWAH.

Human intelligence is a trait that is known to be significantly influenced by genetic factors, and recent linkage data provide positional evidence to suggest that a region on chromosome 6p, previously associated with schizophrenia, may be linked to variation in intelligence. The gene for dysbindin-1 (DTNBP1) is located at 6p and has also been implicated in schizophrenia, a neuropsychiatric disorder characterized by cognitive dysfunction. We report an association between DTNBP1 genotype and general cognitive ability (g) in two independent cohorts, including 213 patients with schizophrenia or schizo-affective disorder and 126 healthy volunteers. These data suggest that DTNBP1 genetic variation influences human intelligence.

Linkage and association studies have recently implicated dystrobrevin-binding protein 1 (DTNBP1) in the etiology of schizophrenia. We analyzed seven previously tested DTNBP1 single-nucleotide polymorphisms (SNPs) in a cohort of 524 individuals with schizophrenia or schizoaffective disorder and 573 control subjects. The minor alleles of three SNPs (P1578, P1763, and P1765) were positively associated with the diagnosis of schizophrenia or schizoaffective disorder in the white subset of the study cohort (258 cases, 467 controls), with P1578 showing the most significant association (odds ratio 1.76, P =.0026). The same three SNPs were also associated in a smaller Hispanic subset (51 cases, 32 controls). No association was observed in the African American subset (215 cases, 74 controls). A stratified analysis of the white and Hispanic subsets showed association with the minor alleles of four SNPs (P1578, P1763, P1320, and P1765). Again, the most significant association was observed for P1578 (P =.0006). Haplotype analysis supported these findings, with a single risk haplotype significantly overrepresented in the white sample (P =.005). Our study provides further evidence for a role of the DTNBP1 gene in the genetic etiology of schizophrenia.

No abstract

substantial body of evidence over the past several decades has established that many psychiatric dis-Objective: Knowledge about the genetic basis of psychiatric illness is growing rapidly, and psychiatrists may be called upon to incorporate this information into clinical practice. The goal of this study was to assess psychiatrists' familiarity with and attitudes toward genetic information.Method: We surveyed 844 participants, the majority of whom were psychiatrists, attending a continuing medical education course in the fall of 2002 and measured knowledge, opinions, and current practice patterns in regard to psychiatric genetics.Results: Responses were received from 352 psychiatrists (54% of those surveyed). Most psychiatrists correctly answered fewer than half of survey items assessing general and psychiatric genetic knowledge. While 83% considered it their role to discuss genetic information with patients and families, fewer than 25% felt prepared or competent to do so. In response to hypothetical questions regarding genetic testing, a substantial proportion of psychiatrists indicated willingness to use such tests for diagnostic clarification, as well as presymptomatic and even prenatal risk prediction. The majority of respondents expressed interest in further genetics education.Conclusions: Our results suggest that psychiatrists view genetic information as clinically relevant, but have limitations in knowledge that may impact the incorporation of psychiatric genetics into clinical practice. (J Clin Psychiatry 2005;66:821-830) for their helpful feedback in the development of the survey. We also thank Mason Freeman, M.D., William Crowley, M.D., and Virginia Hughes, M.S., for their collaboration. Corresponding author and reprints: Christine T.