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.

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.

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.

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.

Self-harm and eating disorders are often comorbid in clinical samples but their co-occurrence in the general population is unclear. Given that only a small proportion of individuals who self-harm or have disordered eating present to clinical services, and that both self-harm and eating disorders are associated with substantial morbidity and mortality, we aimed to study these behaviours at a population level.

We assessed the co-occurrence of self-harm and disordered eating behaviours in 3384 females and 2326 males from a UK population-based cohort: the Avon Longitudinal Study of Parents and Children (ALSPAC). Participants reported on their self-harm and disordered eating behaviours (fasting, purging, binge-eating and excessive exercise) in the last year via questionnaire at 16 and 24 years. At each age we assessed how many individuals who self-harm also reported disordered eating, and how many individuals with disordered eating also reported self-harm.

We found high comorbidity of self-harm and disordered eating. Almost two-thirds of 16-year-old females, and two-in-five 24-year-old males who self-harmed also reported some form of disordered eating. Young people with disordered eating reported higher levels of self-harm at both ages compared to those without disordered eating.

As self-harm and disordered eating commonly co-occur in young people in the general population, it is important to screen for both sets of difficulties to provide appropriate treatment.

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.

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.

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].

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.

Early puberty is associated with an increased risk of self-harm in adolescent females but results for males are inconsistent. This may be due to the use of subjective measures of pubertal timing, which may be biased. There is also limited evidence for the persistence of pubertal timing effects beyond adolescence, particularly in males. The primary aim of the current study was therefore to examine the association between pubertal timing and self-harm in both sexes during adolescence and young adulthood, using an objective measure of pubertal timing (age at peak height velocity; aPHV). A secondary aim was to examine whether this association differs for self-harm with v. without suicidal intent.

The sample (n = 5369, 47% male) was drawn from the Avon Longitudinal Study of Parents and Children (ALSPAC), a prospective birth cohort study. Mixed-effects growth curve models were used to calculate aPHV. Lifetime history of self-harm was self-reported at age 16 and 21 years, and associated suicidal intent was examined at age 16 years. Associations were estimated using multivariable logistic regression adjusted for a range of confounders. Missing data were imputed using Multiple Imputation by Chained Equations.

Later aPHV was associated with a reduced risk of self-harm at 16 years in both sexes (females: adjusted per-year increase in aPHV OR 0.85; 95% CI 0.75–0.96; males: OR 0.72; 95% CI 0.59–0.88). Associations were similar for self-harm with and without suicidal intent. There was some evidence of an association by age 21 years in females (adjusted per-year increase in aPHV OR 0.91; 95% CI 0.80–1.04), although the findings did not reach conventional levels of significance. There was no evidence of an association by age 21 years in males (adjusted per-year increase in aPHV OR 0.99; 95% CI 0.74–1.31).

Earlier developing adolescents represent a group at increased risk of self-harm. This increased risk attenuates as adolescents transition into adulthood, particularly in males. Future research is needed to identify the modifiable mechanisms underlying the association between pubertal timing and self-harm risk in order to develop interventions to reduce self-harm in adolescence.

We aimed to identify groups of children presenting distinct perinatal adversity profiles and test the association between profiles and later risk of suicide attempt.

Data were from the Québec Longitudinal Study of Child Development (QLSCD, N = 1623), and the Avon Longitudinal Study of Parents and Children (ALSPAC, N = 5734). Exposures to 32 perinatal adversities (e.g. fetal, obstetric, psychosocial, and parental psychopathology) were modeled using latent class analysis, and associations with a self-reported suicide attempt by age 20 were investigated with logistic regression. We investigated to what extent childhood emotional and behavioral problems, victimization, and cognition explained the associations.

In both cohorts, we identified five profiles: No perinatal risk, Poor fetal growth, Socioeconomic adversity, Delivery complications, Parental mental health problems (ALSPAC only). Compared to children with No perinatal risk, children in the Poor fetal growth (pooled estimate QLSCD-ALSPAC, OR 1.89, 95% CI 1.04–3.44), Socioeconomic adversity (pooled-OR 1.42, 95% CI 1.08–1.85), and Parental mental health problems (OR 1.74, 95% CI 1.27–2.40), but not Delivery complications, profiles were more likely to attempt suicide. The proportion of this effect mediated by the putative mediators was larger for the Socioeconomic adversity profile compared to the others.

Perinatal adversities associated with suicide attempt cluster in distinct profiles. Suicide prevention may begin early in life and requires a multidisciplinary approach targeting a constellation of factors from different domains (psychiatric, obstetric, socioeconomic), rather than a single factor, to effectively reduce suicide vulnerability. The way these factors cluster together also determined the pathways leading to a suicide attempt, which can guide decision-making on personalized suicide prevention strategies.

Previous studies of pubertal timing and self-harm are limited by subjective measures of pubertal timing or by the conflation of self-harm with suicide attempts and ideation. The current study investigates the association between an objective measure of pubertal timing – age at menarche – and self-harm with and without suicidal intent in adolescence and adulthood in females.

Birth cohort study based on 4042 females from the Avon Longitudinal Study of Parents and Children (ALSPAC). Age at menarche was assessed prospectively between ages 8 and 17 years. Lifetime history of self-harm was self-reported at ages 16 and 21 years. Associations between age at menarche and self-harm, both with and without suicidal intent, were examined using multivariable logistic regression.

Later age at menarche was associated with a lower risk of lifetime self-harm at age 16 years (OR per-year increase in age at menarche 0.87; 95% CI 0.80–0.95). Compared with normative timing, early menarche (<11.5 years) was associated with an increased risk of self-harm (OR 1.31, 95% CI 1.04–1.64) and later menarche (>13.8 years) with a reduced risk (OR 0.74, 95% CI 0.58–0.93). The pattern of association was similar at age 21 years (OR per-year increase in age at menarche 0.92, 95% CI 0.85–1.00). There was no strong evidence for a difference in associations with suicidal v. non-suicidal self-harm.

Risk of self-harm is higher in females with early menarche onset. Future research is needed to establish whether this association is causal and to identify potential mechanisms.

To determine rates of parent-reported child awareness of parental depression, examine characteristics of parents, children and families according to child awareness, and explore whether child awareness is associated with child psychopathology. Data were available from 271 families participating in the Early Prediction of Adolescent Depression (EPAD) study, a longitudinal study of offspring of parents with recurrent depression.

Seventy-three per cent of participating children were perceived as being aware of their parent's depression. Older children, and children of parents who experienced more severe depression, were more likely to be aware. Awareness was not associated with child psychopathology.

Considering children in the context of parental depression is important. Child awareness may influence their access to early intervention and prevention programmes. Further research is needed to understand the impact of awareness on the child.

Offspring of mothers with depression are at heightened risk of psychiatric disorder. Many mothers with depression have comorbid psychopathology. How these co-occurring problems affect child outcomes has rarely been considered.

To consider whether the overall burden of co-occurring psychopathology in mothers with recurrent depression predicts new-onset psychopathology in offspring.

Mothers with recurrent depression and their adolescent offspring (9–17 years at baseline) were assessed in 2007 and on two further occasions up to 2011. Mothers completed questionnaires assessing depression severity, anxiety, alcohol problems and antisocial behaviour. Psychiatric disorder in offspring was assessed using the Child and Adolescent Psychiatric Assessment.

The number of co-occurring problems in mothers (0, 1 or 2+) predicted new-onset offspring disorder (odds ratio (OR) = 1.80, 95% CI 1.17–2.77, P = 0.007). Rates varied from 15.7 to 34.8% depending on the number of co-occurring clinical problems. This remained significant after controlling for maternal depression severity (OR = 1.73, 95% CI 1.03–2.89, P = 0.040).

The burden of co-occurring psychopathology among mothers with recurrent depression indexes increased risk of future onset of psychiatric disorder for offspring. This knowledge can be used in targeting preventive measures in children at high risk of psychiatric disorder.