We report analyses from a study of gene-environment interaction in adolescent depression. The sample was selected from 1990 adolescents aged 10-20 years: those with depression symptoms in the top or bottom 15% were identified and divided into high or low environmental risk groups. DNA was obtained from 377 adolescents, representing the four quadrants of high or low depression and high or low environmental risk. Markers within, or close to, each of the serotonergic genes 5HTT, HTR2A, HTR2C, MAOA (monoamine oxidase type A) and tryptophan hydroxylase (TPH) were genotyped. Environmental risk group was a nonsignificant predictor and sex was a significant predictor of the depression group. HTR2A and TPH significantly predicted the depression group, independent of the effects of sex, environmental risk group and their interaction. In addition, there was a trend for an effect of 5HTTLPR, which was significant in female subjects. Furthermore, there was a significant genotype-environmental risk interaction for 5HTTLPR in female subjects only, with the effect being in the same direction as another recent study, reaffirming that an important source of genetic heterogeneity is exposure to environmental risk. Molecular Psychiatry (2004) 9, 908-915.

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SummaryBackgroundSleep difficulties might be a contributory causal factor in the occurrence of mental health problems. If this is true, improving sleep should benefit psychological health. We aimed to determine whether treating insomnia leads to a reduction in paranoia and hallucinations.MethodsWe did this single-blind, randomised controlled trial (OASIS) at 26 UK universities. University students with insomnia were randomly assigned (1:1) with simple randomisation to receive digital cognitive behavioural therapy (CBT) for insomnia or usual care, and the research team were masked to the treatment. Online assessments took place at weeks 0, 3, 10 (end of therapy), and 22. The primary outcome measures were for insomnia, paranoia, and hallucinatory experiences. We did intention-to-treat analyses. The trial is registered with the ISRCTN registry, number ISRCTN61272251.FindingsBetween March 5, 2015, and Feb 17, 2016, we randomly assigned 3755 participants to receive digital CBT for insomnia (n=1891) or usual practice (n=1864). Compared with usual practice, the sleep intervention at 10 weeks reduced insomnia (adjusted difference 4·78, 95% CI 4·29 to 5·26, Cohen's d=1·11; p<0·0001), paranoia (−2·22, −2·98 to −1·45, Cohen's d=0·19; p<0·0001), and hallucinations (−1·58, −1·98 to −1·18, Cohen's d=0·24; p<0·0001). Insomnia was a mediator of change in paranoia and hallucinations. No adverse events were reported.InterpretationTo our knowledge, this is the largest randomised controlled trial of a psychological intervention for a mental health problem. It provides strong evidence that insomnia is a causal factor in the occurrence of psychotic experiences and other mental health problems. Whether the results generalise beyond a student population requires testing. The treatment of disrupted sleep might require a higher priority in mental health provision.FundingWellcome Trust.

The objective of this study was to examine the associations between persistent childhood sleep problems and adulthood anxiety and depression. Parents of 943 children (52% male) participating in the Dunedin Multidisciplinary Health and Development Study provided information on their children's sleep and internalizing problems at ages 5, 7, and 9 years. When the participants were 21 and 26 years, adult anxiety and depression were diagnosed using a standardized diagnostic interview. After controlling for childhood internalizing problems, sex, and socioeconomic status, persistent sleep problems in childhood predicted adulthood anxiety disorders (OR (95% CI) = 1.60 (1.05-2.45), p = .030) but not depressive disorders (OR (95% CI) = .99 (.63-1.56), p = .959). Persistent sleep problems in childhood may be an early risk indicator of anxiety in adulthood.

BACKGROUND Obesity is one of the leading causes of preventable death worldwide. Circadian rhythms are known to control both sleep timing and energy homeostasis, and disruptions in circadian rhythms have been linked with metabolic dysfunction and obesity-associated disease. In previous research, social jetlag, a measure of chronic circadian disruption caused by the discrepancy between our internal versus social clocks, was associated with elevated self-reported body mass index, possibly indicative of a more generalized association with obesity and metabolic dysfunction. METHODS We studied participants from the population-representative Dunedin Longitudinal Study (N = 1037) to determine whether social jetlag was associated with clinically assessed measurements of metabolic phenotypes and disease indicators for obesity-related disease, specifically, indicators of inflammation and diabetes. RESULTS Our analysis was restricted to N = 815 non-shift workers in our cohort. Among these participants, we found that social jetlag was associated with numerous clinically assessed measures of metabolic dysfunction and obesity. We distinguished between obese individuals who were metabolically healthy versus unhealthy, and found higher social jetlag levels in metabolically unhealthy obese individuals. Among metabolically unhealthy obese individuals, social jetlag was additionally associated with elevated glycated hemoglobin and an indicator of inflammation. CONCLUSIONS The findings are consistent with the possibility that ‘living against our internal clock’ may contribute to metabolic dysfunction and its consequences. Further research aimed at understanding that the physiology and social features of social jetlag may inform obesity prevention and have ramifications for policies and practices that contribute to increased social jetlag, such as work schedules and daylight savings time.

It is anticipated that the novel coronavirus disease 2019 (COVID‐19) pandemic and associated societal response will have wide‐ranging impacts on youth development and mental health. Sleep is crucial for child and adolescent health and well‐being, and the potential for sleep problems to emerge or worsen during and following the pandemic is high. This may be particularly true for children and adolescents who are at heightened risk for the onset of sleep and mental health disturbances and for those whom developmental changes impacting sleep are rapidly occurring. Youth with preexisting psychopathologies (including anxiety and depression) and neurodevelopmental conditions (including attention‐deficit/hyperactivity disorder and autism spectrum disorder) could be especially vulnerable to disturbed sleep during this period of change and uncertainty. It is thus imperative that sleep considerations be part of research and clinical initiatives aimed at understanding and mitigating the impact of the COVID‐19 pandemic in children and adolescents. This article considers ways in which the pandemic may impact sleep, including research and clinical implications.

Context:The close association between generalized anxiety disorder (GAD) and major depressive disorder (MDD) prompts questions about how to characterize this association in future diagnostic systems. Most information about GAD-MDD comorbidity comes from patient samples and retrospective surveys.Objective: To revisit the sequential and cumulative comorbidity between GAD and MDD using data from a prospective longitudinal cohort.Design: Prospective longitudinal cohort study.Setting: New Zealand.Participants: The representative 1972The representative -1973 Dunedin birth cohort of 1037 members was followed up to age 32 years with 96% retention. Main Outcome Measures:Research diagnoses of anxiety and depression were made at ages 11,13,15,18,21,26, and 32 years. Mental health services were reported on a life history calendar.Results: Sequentially, anxiety began before or concurrently in 37% of depression cases, but depression began before or concurrently in 32% of anxiety cases. Cumulatively, 72% of lifetime anxiety cases had a history of depression, but 48% of lifetime depression cases had anxiety. During adulthood, 12% of the cohort had comorbid GADϩ MDD, of whom 66% had recurrent MDD, 47% had recurrent GAD, 64% reported using mental health services, 47% took psychiatric medication, 8% were hospitalized, and 11% attempted suicide. In this comorbid group, depression onset occurred first in one third of the participants, anxiety onset occurred first in one third, and depression and anxiety onset began concurrently in one third. Conclusions:Challenging the prevailing notion that generalized anxiety usually precedes depression and eventually develops into depression, these findings show that the reverse pattern occurs almost as often. The GAD-MDD relation is strong, suggesting that the disorders could be classified in 1 category of distress disorders. Their developmental relation seems more symmetrical than heretofore presumed, suggesting that MDD is not necessarily primary over GAD in diagnostic hierarchy. This prospective study suggests that the lifetime prevalence of GAD and MDD may be underestimated by retrospective surveys and that comorbid GAD ϩ MDD constitutes a greater mental health burden than previously thought. Psychiatry. 2007;64:651-660 T HIS ARTICLE WAS PREPARED in response to a call for research to inform how generalized anxiety disorder (GAD) should be characterized in relation to major depressive disorder (MDD) in forthcoming diagnostic systems. Arch Gen1 Because the 2 disorders are closely related, key nosologic questions concern whether they ought to be classified together and whether GAD ought to be considered a subsyndrome of MDD vs an independent disorder. Substantial literature suggests that GAD ought not be viewed as independent from MDD, pointing to evidence that generalized anxiety generally precedes MDD in sequential order and that most individuals with GAD eventually develop MDD. The present article revisits the sequential and cumulative comorbidity between GAD and MDD using data from a pr...