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Evidence on how different types of social media use contribute to digital stress in early adolescence is lacking. In-depth interviews were conducted with 24 13-14-year-olds. Interviews were transcribed verbatim, coded and thematically analysed. Themes were generated based on digital stressors specific to passive social media use (time-wasting and digital guilt, and exposure to harmful content); private social media communication (expectations of availability and unsolicited contact by strangers); and social media broadcasting (expectations of perfection and sexualisation, fear of negative evaluation and risks to privacy). Several digital stressors appeared pervasive in everyday social media use. Bolstering social and emotional resources offline and encouraging effective implementation of privacy settings may improve resilience against several sources of digital stress.

Background: Adverse childhood experiences (ACEs) are well‐established risk factors for self‐harm and depression. However, despite their high comorbidity, there has been little focus on the impact of developmental timing and the duration of exposure to ACEs on co‐occurring self‐harm and depression. Methods: Data were utilised from over 22,000 children and adolescents participating in three UK cohorts, followed up longitudinally for 14–18 years: the Avon Longitudinal Study of Parents and Children (ALSPAC), the Millennium Cohort Study (MCS) and the Environmental Risk (E‐Risk) Longitudinal Twin Study. Multinomial logistic regression models estimated associations between each ACE type and a four‐category outcome: no self‐harm or depression, self‐harm alone, depression alone and self‐harm with co‐occurring depression. A structured life course modelling approach was used to examine whether the accumulation (duration) of exposure to each ACE, or a critical period (timing of ACEs) had the strongest effects on self‐harm and depression in adolescence. Results: The majority of ACEs were associated with co‐occurring self‐harm and depression, with consistent findings across cohorts. The importance of timing and duration of ACEs differed across ACEs and across cohorts. For parental mental health problems, longer duration of exposure was strongly associated with co‐occurring self‐harm and depression in both ALSPAC (adjusted OR: 1.18, 95% CI: 1.10–1.25) and MCS (1.18, 1.11–1.26) cohorts. For other ACEs in ALSPAC, exposure in middle childhood was most strongly associated with co‐occurring self‐harm and depression, and ACE occurrence in early childhood and adolescence was more important in the MCS. Conclusions: Efforts to mitigate the impact of ACEs should start in early life with continued support throughout childhood, to prevent long‐term exposure to ACEs contributing to risk of self‐harm and depression in adolescence. [ABSTRACT FROM AUTHOR]

Background: The aetiology of dual harm (co-occurring self-harm and violence towards others) is poorly understood because most studies have investigated self-harm and violence separately. We aimed to examine childhood risk factors for self-harm, violence, and dual harm, including the transition from engaging in single harm to dual harm. Methods: Data from the Avon Longitudinal Study of Parents and Children, a UK-based birth cohort study, were used to estimate prevalence of self-reported engagement in self-harm, violence, and dual harm at ages 16 and 22 years. Risk ratios were calculated to indicate associations across various self-reported childhood risk factors and risks of single and dual harm, including the transition from single harm at age 16 years to dual harm at age 22. Results: At age 16 years, 18.1% of the 4176 cohort members had harmed themselves, 21.1% had engaged in violence towards others and 3.7% reported dual harm. At age 22 the equivalent prevalence estimates increased to 24.2, 25.8 and 6.8%, respectively. Depression and other mental health difficulties, drug and alcohol use, witnessing self-harm and being a victim of, or witnessing, violence were associated with higher risks of transitioning from self-harm or violence at age 16 to dual harm by age 22. Conclusions: Prevalence of dual harm doubled from age 16 to 22 years, highlighting the importance of early identification and intervention during this high-risk period. Several childhood psychosocial risk factors associated specifically with dual harm at age 16 and with the transition to dual harm by age 22 have been identified. [ABSTRACT FROM AUTHOR]

Background: Emotional dysregulation may be a risk factor for disordered eating and self‐harm in young people, but few prospective studies have assessed these associations long‐term, or considered potential mediators. We examined prospective relationships between childhood emotional dysregulation and disordered eating and self‐harm in adolescence; and social cognition, emotional recognition, and being bullied as mediators. Methods: We analysed Avon Longitudinal Study of Parents and Children data on 3,453 males and 3,481 females. We examined associations between emotional dysregulation at 7 years and any disordered eating and any self‐harm at 16 years with probit regression models. We also assessed whether social cognition (7 years), emotional recognition (8 years) and bullying victimisation (11 years) mediated these relationships. Results: Emotional dysregulation at age 7 years was associated with disordered eating [fully adjusted probit B (95% CI) = 0.082 (0.029, 0.134)] and self‐harm [fully adjusted probit B (95% CI) = 0.093 (0.036, 0.150)] at age 16 years. There was no evidence of sex interactions or difference in effects between self‐harm and disordered eating. Mediation models found social cognition was a key pathway to disordered eating (females 51.2%; males 27.0% of total effect) and self‐harm (females 15.7%; males 10.8% of total effect). Bullying victimisation was an important pathway to disordered eating (females 17.1%; males 10.0% of total effect), but only to self‐harm in females (15.7% of total effect). Indirect effects were stronger for disordered eating than self‐harm. Conclusions: In males and females, emotional dysregulation in early childhood is associated with disordered eating and self‐harm in adolescence and may be a useful target for prevention and treatment. Mediating pathways appeared to differ by sex and outcome, but social cognition was a key mediating pathway for both disordered eating and self‐harm. [ABSTRACT FROM AUTHOR]

Background: The occurrence of early childhood adversity is strongly linked to later self-harm, but there is poor understanding of how this distal risk factor might influence later behaviours. One possible mechanism is through an earlier onset of puberty in children exposed to adversity, since early puberty is associated with an increased risk of adolescent self-harm. We investigated whether early pubertal timing mediates the association between childhood adversity and later self-harm. Methods: Participants were 6698 young people from a UK population-based birth cohort (ALSPAC). We measured exposure to nine types of adversity from 0 to 9 years old, and self-harm when participants were aged 16 and 21 years. Pubertal timing measures were age at peak height velocity (aPHV – males and females) and age at menarche (AAM). We used generalised structural equation modelling for analyses. Results: For every additional type of adversity; participants had an average 12–14% increased risk of self-harm by 16. Relative risk (RR) estimates were stronger for direct effects when outcomes were self-harm with suicidal intent. There was no evidence that earlier pubertal timing mediated the association between adversity and self-harm [indirect effect RR 1.00, 95% confidence interval (CI) 1.00–1.00 for aPHV and RR 1.00, 95% CI 1.00–1.01 for AAM]. Conclusions: A cumulative measure of exposure to multiple types of adversity does not confer an increased risk of self-harm via early pubertal timing, however both childhood adversity and early puberty are risk factors for later self-harm. Research identifying mechanisms underlying the link between childhood adversity and later self-harm is needed to inform interventions. [ABSTRACT FROM AUTHOR]