The association between bullying‐victimisation and sleep disturbances in adolescence: Evidence from a twin study

Bullying‐victimisation has been associated with sleep disturbances. This study investigated the degree to which subtypes of bullying‐victimisation in adolescence are linked with sleep disturbances. Genetic and environmental contributions underlying bullying‐victimisation and sleep disturbances were investigated. Participants (3,242–5,076 pairs) from a longitudinal community twin study reported on their bullying‐victimisation at the age of 14 years, and sleep quality and insomnia symptoms at age 16. Regression analyses were used, accounting for the role of individual and family factors. Structural equation twin model fitting was conducted. Bullying‐victimisation was modestly associated with sleep quality and insomnia symptoms (r = 0.22–0.23) and a similar strength of associations was found across bullying‐victimisation subtypes (r = 0.11–0.22). Bullying‐victimisation, sleep quality and insomnia symptoms were predominantly influenced by genes (25–59%) and non‐shared environments (40–62%). The association between bullying‐victimisation and sleep quality was explained by genetic and non‐shared environmental influences. For insomnia symptoms and sleep quality, the association with bullying‐victimisation was in part explained by a genetic overlap. Associations between bullying‐victimisation and sleep disturbances are not limited to specific aspects of bullying‐victimisation but appear to exist for all subtypes. These findings stimulate research questions regarding the mechanisms underlying these links. For example, could certain heritable traits, such as temperament, increase vulnerability to experiencing sleep disturbances and being bullied? Research on bullying and sleep should aim to take the role of genetic predisposition into account, while also noting that it is not the only causal influence. Understanding more about these pathways could strengthen the development of techniques to prevent these difficulties from occurring

The phenotypic and genetic structure of depression and anxiety disorder symptoms in childhood, adolescence, and young adulthood

Importance: The recently published DSM-5 continues to classify mood and anxiety disorders as separate conditions. However, some studies in adults find a unidimensional internalizing factor that underpins anxiety and depression, while others support a bidimensional model where symptoms segregate into distress (depression and generalized anxiety) and fear factors (phobia subscales). Little is known, however, about the phenotypic and genetic structure of internalizing psychopathology in children and adolescents. Objective: To investigate phenotypic associations between depression and anxiety disorder symptom subscales, and to test genetic structures underlying these symptoms (DSM-5-related, unidimensional and bidimensional), across three developmental stages: childhood, adolescence and early adulthood. Design: Two population-based prospective longitudinal twin/sibling studies. Setting: United Kingdom Participants: Child sample: 578 twins, mean ages approximately 8 and 10 years at waves 1 and 2 respectively. Adolescent and early adulthood sample at 3 waves: 2619 twins, mean ages 15, 17 and 20 years at each wave respectively. Main Outcome Measures: Self-report symptoms of depression and anxiety disorders. Results: Phenotypically, when controlling for other anxiety subscales, depression symptoms were only associated with generalized anxiety disorder symptoms in childhood; this association broadened to panic and social phobia symptoms in adolescence; and all anxiety subscales in young adulthood. The genetic associations were in line with phenotypic results. In childhood, anxiety subscales were influenced by a single genetic factor that did not contribute to genetic variance in depression symptoms, suggesting largely independent genetic influences on anxiety and depression. In adolescence, genetic influences were significantly shared between depression and all anxiety subscales, in agreement with DSM-5 conceptualization. In young adulthood, a genetic internalizing factor influencing depression and all anxiety subscales emerged, alongside a small significant genetic fear factor. Conclusions and Relevance: These results provide preliminary evidence for different phenotypic and genetic structures of internalizing disorder symptoms in childhood, adolescence and young adulthood, with depression and anxiety becoming more associated from adolescence. The results inform molecular genetics research and transdiagnostic treatment approaches. Findings affirm the need to continue examining the classification of mood and anxiety disorders in diagnostic systems

Sub-types of insomnia in adolescents: insights from a quantitative/ molecular twin study

Background: Insomnia with short sleep duration has been postulated as more severe than that accompanied by normal/long sleep length. While the short duration subtype is considered to have greater genetic influence than the other subtype, no studies have addressed this question. This study aimed to compare these subtypes in terms of: 1) the heritability of insomnia symptoms; 2) polygenic scores (PGS) for insomnia symptoms and sleep duration; 3) the associations between insomnia symptoms and a wide variety of traits/disorders. Methods: The sample comprised 4,000 pairs of twins aged 16 from the Twins Early Development Study. Twin models were fitted to estimate the heritability of insomnia in both groups. PGS were calculated for self-reported insomnia and sleep duration and compared among participants with short and normal/long sleep duration. Results: Heritability was not significantly different in the short sleep duration group (A=0.13 [95%CI=0.01, 0.32]) and the normal/long sleep duration group (A=0.35 [95%CI=0.29, 0.40]). Shared environmental factors accounted for a substantial proportion of the variance in the short sleep duration group (C=0.19 [95%CI= 0.05, 0.32]) but not in the normal/long sleep duration group (C=0.00 [95%CI=0.00, 0.04]). PGS did not differ significantly between groups although results were in the direction expected by the theory. Our results also showed that insomnia with short (as compared to normal/long) sleep duration had a stronger association with anxiety and depression (p<.05) - although not once adjusting for multiple testing. Conclusions: We found mixed results in relation to the expected differences between the insomnia subtypes in adolescents. Future research needs to further establish cut-offs for ‘short’ sleep at different developmental stages and employ objective measures of sleep

Association between stressful life events and psychotic experiences in adolescence: evidence for gene-environment correlations

- Background: Stressful life events (SLEs) are associated with psychotic experiences (PEs). SLEs might act as an environmental risk factor, but may also share a genetic propensity with PEs. - Aims: Estimate the extent to which genetic and environmental factors influence the relationship between SLEs and PEs. - Method: Self and parent-reports from a community-based twin sample (4,830 16-year-old pairs) were analysed using structural equation model-fitting. - Results: SLEs correlated with positive PEs (r = .12-.14, all p<. 001). Modest heritability was shown for PEs (25-57%) and dependent SLEs (32%). Genetic influences explained the majority of the modest covariation between dependent SLEs and paranoia and cognitive disorganisation (bivariate heritabilities = 74-86%). The relationship between SLEs and hallucinations and grandiosity was explained by both genetic and common environmental effects. - Conclusion: Further to dependent SLEs being an environmental risk factor, individuals may have an underlying genetic propensity increasing their risk of dependent SLEs and positive PEs

The Genesis 12–19 (G1219) Study: A Twin and Sibling Study of Gene–Environment Interplay and Adolescent Development in the UK

The Genesis 12–19 (G1219) Study is an ongoing longitudinal study of a sample of UK twin pairs, non-twin sibling pairs, and their parents. G1219 was initially designed to examine the role of gene–environment interplay in adolescent depression. However, since then data have continued to be collected from both parents and their offspring into young adulthood. This has allowed for longitudinal analyses of depression and has enabled researchers to investigate multiple phenotypes and to ask questions about intermediate mechanisms. The study has primarily focused on emotional development, particularly depression and anxiety, which have been assessed at multiple levels of analysis (symptoms, cognitions, and relevant environmental experiences). G1219 has also included assessment of a broader range of psychological phenotypes ranging from antisocial behaviors and substance use to sleep difficulties, in addition to multiple aspects of the environment. DNA has also been collected. The first wave of data collection began in the year 1999 and the fifth wave of data collection will be complete before the end of 2012. In this article, we describe the sample, data collection, and measures used. We also summarize some of the key findings to date

Shared etiology of psychotic experiences and depressive symptoms in adolescence: a longitudinal twin study

Psychotic disorders and major depression, both typically adult-onset conditions, often co-occur. At younger ages psychotic experiences and depressive symptoms are often reported in the community. We used a genetically sensitive longitudinal design to investigate the relationship between psychotic experiences and depressive symptoms in adolescence. A representative community sample of twins from England and Wales was employed. Self-rated depressive symptoms, paranoia, hallucinations, cognitive disorganization, grandiosity, anhedonia, and parent-rated negative symptoms were collected when the twins were age 16 (N = 9618) and again on a representative subsample 9 months later (N = 2873). Direction and aetiology of associations were assessed using genetically informative cross-lagged models. Depressive symptoms were moderately correlated with paranoia, hallucinations, and cognitive disorganization. Lower correlations were observed between depression and anhedonia, and depression and parent-rated negative symptoms. Nonsignificant correlations were observed between depression and grandiosity. Largely the same genetic effects influenced depression and paranoia, depression and hallucinations, and depression and cognitive disorganization. Modest overlap in environmental influences also played a role in the associations. Significant bi-directional longitudinal associations were observed between depression and paranoia. Hallucinations and cognitive disorganization during adolescence were found to impact later depression, even after controlling for earlier levels of depression. Our study shows that psychotic experiences and depression, as traits in the community, have a high genetic overlap in mid-adolescence. Future research should test the prediction stemming from our longitudinal results, namely that reducing or ameliorating positive and cognitive psychotic experiences in adolescence would decrease later depressive symptoms

Is digital cognitive behavioural therapy for insomnia effective in treating sub-threshold insomnia: A pilot RCT

Objective/Background: CBT for insomnia (CBT-I) is useful for many. It is currently unknown if those with sub-threshold insomnia also benefit. Here we assessed whether CBT-I is both feasible and acceptable in participants with sub-threshold insomnia. The primary aims were to evaluate participation rates and treatment acceptability, and to establish an effect size for symptom improvement. Patients/Methods: A total of 199 female participants (Mage 20 ± 5 years) took part. Following baseline assessments, participants were randomly allocated to either a 6-week digital CBT-I intervention or a 6-week session control group receiving puzzles. Additional assessments were performed 3-weeks, 6-weeks, and 6-months later. Results: Participation in each survey wave did not differ between the groups (ps > .140), though adherence to weekly tasks was lower in the CBT-I group, p = .02. Treatment acceptability was high (M (SD) = 33.61 (4.82), range 6 – 42). The CBT-I group showed greater improvement in insomnia symptoms at the end of the intervention compared to the control group (p = .013, d = 0.42), with significant variation in outcome (M = 4.69, SD = 5.41). Sub-threshold participants showed a similar pattern of results, whilst those meeting insomnia criteria showed a smaller between-group difference. CBT-I led to improvements in anxiety, paranoia and perceived stress between baseline and end of intervention. Changes in insomnia symptoms were mediated by cognitions about sleep and somatic pre-sleep arousal. Conclusions: CBT-I provides a benefit even in sub-threshold insomnia. CBT-I may be useful as an early preventative intervention to tackle sleep problems before they manifest as chronic insomnia

Sibling Study of Gene-Environment Interplay and Adolescent Development in the UK

The Genesis 12-19 (G1219) Study is an ongoing longitudinal study of a sample of UK twin pairs, non-twin sibling pairs, and their parents. G1219 was initially designed to examine the role of gene-environment interplay in adolescent depression. However, since then data have continued to be collected from both parents and their offspring into young adulthood. This has allowed for longitudinal analyses of depression and has enabled researchers to investigate multiple phenotypes and to ask questions about intermediate mechanisms. The study has primarily focused on emotional development, particularly depression and anxiety, which have been assessed at multiple levels of analysis (symptoms, cognitions, and relevant environmental experiences). G1219 has also included assessment of a broader range of psychological phenotypes ranging from antisocial behaviors and substance use to sleep difficulties, in addition to multiple aspects of the environment. DNA has also been collected. The first wave of data collection began in the year 1999 and the fifth wave of data collection will be complete before the end of 2012. In this article, we describe the sample, data collection, and measures used. We also summarize some of the key findings to date

Anxiety sensitivity in adolescence and young adulthood: the role of stressful life events, 5HTTLPR and their interaction.

Background: Cognitive biases have long been hypothesized to influence the development and maintenance of symptoms of internalizing problems. Anxiety sensitivity represents one such bias and refers to sensitivity to the physical and emotional symptoms of anxiety and the belief that these are harmful. Twin studies indicate a role for both environmental and genetic influences on anxiety sensitivity. However, little work has been done specifying environments or genes involved in this phenotype. In light of this, we looked at the association between stressful life events, the serotonin transporter gene polymorphism (5HTTLPR), and anxiety sensitivity in a longitudinal sample of adolescents. Methods: Stressful life events and anxiety sensitivity were measured in over 1,500 individuals at three time points (mean ages 15, 17, and 20 years). 5HTTLPR was genotyped in 1,109 participants. Results: There was consistent evidence for an association between stressful life events and both anxiety sensitivity and change in anxiety sensitivity over time. Although the effect of independent stressful life events was relatively short lived, dependent stressful life events were associated with anxiety sensitivity over time. There was no evidence for a main effect of 5HTTLPR on anxiety sensitivity. 5HTTLPR genotype did not moderate the effect of stressful life events on anxiety sensitivity. Conclusions: The current study extends previous work by showing that stressful life events, independent of the individual, explained change in cognitions associated with anxiety and depression. This effect does not, however, appear to be moderated by genotype