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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 and aims: Varenicline and nicotine replacement therapy (NRT) are the most commonly used medications to quit smoking. Given their widespread use, monitoring adverse risks remains important. This study aimed to estimate the neuropsychiatric and cardiovascular risks associated with varenicline and NRT as used in routine UK care. Design Case–cross‐over study. Setting: UK‐based electronic primary care records in the Clinical Practice Research Datalink from 2006 to 2015 linked to hospital and mortality data sets. Participants: Adult smokers (n =282,429) observed during periods when exposed and not exposed to either varenicline or NRT. Measurements Main outcomes included suicide, self‐harm, myocardial infarction (MI), all‐cause death and cause‐specific death [MI, chronic obstructive pulmonary disease (COPD)]. In primary analyses, conditional logistic regression was used to compare the chance of varenicline or NRT exposure during the risk period (90 days prior to the event) with the chance of exposure during an earlier single reference period (91–180 days prior to the event) or multiple 90‐day reference periods to increase statistical power. Findings In the primary analyses, findings were inconclusive for the associations between varenicline and the main outcomes using a single reference period, while NRT was associated with MI [odds ratio (OR) = 1.40, 95% confidence interval (CI) = 1.18–1.67]. Using multiple reference periods, varenicline was associated with an increased risk of self‐harm (OR = 1.32, 95% CI = 1.12–1.56) and suicide (OR = 3.56, 95% CI = 1.32–9.60) but a reduction in all‐cause death (OR = 0.75, 95% CI = 0.61–0.93). NRT was associated with MI (OR = 1.54, 95% CI = 1.36–1.74), self‐harm (OR = 1.30, 95% CI = 1.18–1.44) and deaths from MI (OR = 1.53, 95% CI = 1.11–2.10), COPD (OR = 1.33, 95% CI = 1.14–1.56) and all causes (OR = 1.28, 95% CI = 1.18–1.40) when using multiple reference periods. Conclusions: There appear to be positive associations between (1) nicotine replacement therapy (NRT) and myocardial infarction, death and risk of self‐harm and (2) varenicline and increased risk of self‐harm and suicide, as well as a negative association between varenicline and all‐cause death. The associations may not be causal. They may reflect health changes at the time of smoking cessation (nicotine replacement therapy is prescribed for people with cardiac problems) or be associated with quit attempts (exposure to both medicines was associated with self‐harm). [ABSTRACT FROM AUTHOR]

Background: Adverse childhood experiences (ACEs) such as physical and emotional abuse are strongly associated with self‐harm, but mechanisms underlying this relationship are unclear. Inflammation has been linked to both the experience of ACEs and self‐harm or suicide in prior research. This is the first study to examine whether inflammatory markers mediate the association between exposure to ACEs and self‐harm. Methods: Participants were 4,308 young people from the Avon Longitudinal Study of Parents and Children (ALSPAC), a population‐based birth cohort in the United Kingdom. A structural equation modelling approach was used to fit a mediation model with the number of ACEs experienced between ages 0 and 9 years old (yo), levels of the inflammatory markers interleukin‐6 and C‐reactive protein measured at 9.5 yo, and self‐harm reported at 16 yo. Results: The mean number of ACEs young people experienced was 1.41 (SE 0.03). Higher ACE scores were associated with an increased risk of self‐harm at 16 yo (direct effect relative risk (RR) per additional ACE 1.11, 95% CI 1.05, 1.18, p < 0.001). We did not find evidence of an indirect effect of ACEs on self‐harm via inflammation (RR 1.00, 95% CI 1.00, 1.01, p = 0.38). Conclusions: Young people who have been exposed to ACEs are a group at high risk of self‐harm. The association between ACEs and self‐harm does not appear to be mediated by an inflammatory process in childhood, as indexed by peripheral levels of circulating inflammatory markers measured in childhood. Further research is needed to identify alternative psychological and biological mechanisms underlying this relationship. [ABSTRACT FROM AUTHOR]