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BackgroundDepression rises markedly in adolescence, a time when increased and new genetic influences have been reported.AimsTo examine ‘new’ and ‘stable’ genetic and environmental factors on depressive symptoms in adolescence and young adulthood.MethodA questionnaire survey investigated a sample of twin and sibling pairs at three time points over an approximately 3-year period. Over 1800 twin and sibling pairs reported depressive symptoms at the three time points. Data were analysed using multivariate genetic models.ResultsDepressive symptoms at all time points were moderately heritable with substantial non-shared environmental contributions. Wave I genetic factors accounted for continuity of symptoms at waves 2 and 3. ‘New’ genetic effects at wave 2 also influenced wave 3 symptoms. New non-shared environmental influences emerged at each time point.ConclusionsNew genetic and environmental influences may explain age-related increases in depression across development.

Anxiety and depression share genetic influences, and have been associated with similar cognitive biases. Psychological theories of anxiety and depression highlight threat interpretations of ambiguity. Little is known about whether genes influence cognitive style, or its links to symptoms. We assessed ambiguous word and scenario interpretations, anxiety and depression symptoms in 300 8-year-old twin pairs. There were significant correlations between both negative interpretations of ambiguous words and scenarios and depression symptoms after controlling for anxiety symptoms (r = .13 and .31, respectively), but no significant correlations with anxiety independent of depression. Genetic effects ranged from 16% for depression to 30% for ambiguous word interpretations. Non-shared environmental influences were large (68-70%). Both genetic and environmental influences contributed to the association between depression and ambiguous scenario interpretations. These findings support psychological theories, which emphasise the role of environmental stress both on the development of threat interpretations and on their links with symptoms. The data also support a role for genetic influence on threat interpretations, which may mediate responses to stress.

State and trait anxiety define different aspects of anxiety, and may represent environmentally and genetically mediated components of this phenotype. Furthermore their relationship, where trait anxiety is expressed through levels of state anxiety under threatening circumstances, may represent a process of interplay between a genetic vulnerability factor and an environmental stressor. To test these hypotheses, we explored genetic and environmental influences on measures of state and trait anxiety in a sample of 1058 twins (521 males and 537 females) aged 8-16. The results were consistent with these hypotheses. State anxiety is largely influenced by environmental factors in males and females whereas trait anxiety shows moderate genetic effects and substantial non-shared environment effects. Their association was accounted for by non-shared environmental effects, with modest genetic and shared environmental inputs. The implications of these results for vulnerability mechanisms involving stress reactivity on anxiety are discussed.

The chapter offers some insight into the valuable contribution made by behavioral genetics to the understanding of the family environment. A powerful behavioral genetic tool for examining purely nonshared environmental impact of specific measured aspects of the environment is the MZ differences design. The strength of this design lies in the fact that, like the adoption design, it can give one a clean estimate of one type of effect-nonshared environment. The extent to which MZ twins differ on behavioral and emotional ratings is assumed to be because of nonshared environment only. An adoption research that considered the role of both gene-environment correlation and interaction found that exposure to adversity in the life of the adoptive parents moderated the effects of genetic risk on the child's environment. Information on parental antisocial behavior, child conduct problems, and the degree of father presence in the family home was collated, and used in a regression framework that had traditionally been designed to assess the effects of genetic and shared environmental variance. © 2005 Elsevier Ltd. All rights reserved.

OBJECTIVE: Autism is a diagnostic spectrum of variable severity, with significant comorbidity. No existing standardized interview measures autistic features dimensionally. The authors aimed to develop a parental autism interview that could be administered to unselected clinical and general population samples that measures both symptom intensity and comorbidity across the full range of the autistic spectrum. METHOD: A computerized procedure was devised for administration by trained interviewers that generates symptom and diagnostic profiles for both autism and non-autistic conditions. Test-retest reliability and interrater reliability were assessed in unselected clinical (n = 50) and nonclinical (n = 30) populations. Concurrent validity (n = 120), discriminant validity (n = 120), and criterion validity (n = 29) were evaluated in autistic spectrum and non-autistic patients. RESULTS: Test-retest and interrater reliabilities were excellent (most intraclass correlation coefficients > 0.9). Concurrent validity (agreement with independent clinician formulation) was very good (mean kappa = 0.74). Criterion validity, a comparison with the Autism Diagnostic Interview, was excellent. Discrimination between autistic spectrum versus non-autistic subjects was almost perfect (sensitivity 1.0; specificity > 0.97). CONCLUSIONS: The Developmental, Dimensional and Diagnostic Interview (3di) provides an efficient and accurate means of assessing, in dimensional terms, the presence of autistic symptoms in both clinical and normal populations. It offers novel opportunities for those engaged in research and clinical practice.

Context Amygdala and ventrolateral prefrontal cortex (vlPFC) dysfunction manifests in adolescents with anxiety disorders when they view negatively valenced stimuli in threatening contexts. Such fear-circuitry dysfunction may also manifest when anticipated social evaluation leads socially anxious adolescents to misperceive peers as threatening. Objective To determine whether photographs of negatively evaluated smiling peers viewed during anticipated social evaluation engage the amygdala and vlPFC differentially in adolescents with and without social anxiety. Design Case-control study. Setting Government clinical research institute. Participants Fourteen adolescents with anxiety disorders associated with marked concerns of social evaluation and 14 adolescents without a psychiatric diagnosis matched on sex, age, intelligence quotient, and socioeconomic status. Main Outcome Measures Blood oxygenation level–dependent signal measured with event-related functional magnetic resonance imaging. Before and during neuroimaging scans, participants anticipating social evaluation completed peer- and self-appraisals. Event-related analyses were tailored to participants' ratings of specific peers. Results Participants classified 40 pictures of same-age peers as ones with whom they did or did not want to engage in a social interaction. Anxious adolescents showed greater amygdala activation than healthy adolescents when anticipating evaluation from peers previously rated as undesired for an interaction. Psychophysiological interaction connectivity analyses also revealed a significant positive association between amygdala and vlPFC activation in anxious vs healthy adolescents in response to these stimuli. Conclusions Anticipating social evaluation from negatively perceived peers modulates amygdala and vlPFC engagement differentially in anxious and healthy adolescents. Amygdala and vlPFC dysfunction manifests in adolescent anxiety disorders in specific contexts of anticipated peer evaluation.

Summary Adolescence is a time of extensive neuroanatomical, functional, and chemical reorganisation of the brain which parallels substantial maturational changes in cognition and affect regulation. This period is characterised by stabilisation of synapses to diminish redundancy and increase efficiency of neural function, fine-tuning of excitatory and inhibitory neurotransmitter systems, beginning of integration between late maturing and early maturing brain structures, and development of effective connections. In effect, these so-called moving parts create a state of dynamic change that might underlie adolescent behaviours. Imbalances or changes in timing of these developmental processes clearly increase the risk for psychiatric disorders. Genetic, environmental, and epigenetic factors that shape brain development and hormonal changes that affect stress reactivity could be reasons why some, but not all, adolescents are at a heightened risk of developing a psychopathological disorder. In this Series paper, we assess the neurobiology of the changing adolescent brain, implications of this knowledge, and future research in major psychiatric disorders, particularly for psychotic disorders.

Worry is a common experience, thought to be maintained by the tendency of interpreting ambiguous information in a consistent (e.g. negative) manner, termed “interpretation bias”. This study explored whether high worriers (Penn State Worry Questionnaire score, PSWQ ≧ 56) and low worriers (PSWQ score ≦ 39) show different interpretation biases, and examined at which stages of information processing these interpretation biases occur. Participants with high and low worry levels completed interpretation assessment tasks yielding behavioural and event-related potential indices. We focused on the N400 component, reflecting whether given interpretations were in line with or violated participants' own interpretations. We found that high worriers lack the benign interpretation bias found in low worriers from the early "online" interpretative stage, reflected by the reaction time in a relatedness judgment task and the N400 in a lexical decision task, to the later "offline" stage at which participants had time for reflection. Our results suggest that a benign interpretation bias may be a protective factor in relation to worry and is likely to remain active across online and offline stages of interpretation processing.