The transition from adolescence into adulthood is a pivotal phase in a person's life, marking a period of significant social, psychological, and biological changes that can profoundly impact an individual's well-being and developmental trajectory. During this period, adolescents and young adults face increasing environmental demands from academic or occupational responsibilities and social interactions, including the pursuit of romantic partners. These changes are inherently related to stress, which is essential for adolescents and young adults to develop their personality and form an identity. Throughout adolescence into young adulthood, the brain undergoes maturational changes as part of the normal development, and it is possible that deviations from the expected developmental trajectories may contribute to the onset of psychiatric disorders in this age group. This editorial highlights recent work published in the Journal of Child Psychology and Psychiatry that examines important aspects of this developmental period.
Background: Almost one in five (18.8%) UK adolescents are estimated to self-harm and many young people initiate self-harm early (average age 13 years). Prevention of self-harm should be informed by knowledge about risk factors (e.g. socio-demographic indices), characteristics (i.e. motivation for self-harm and help-seeking behaviours), as well as relative aetiological genetic and environmental processes. Previous twin studies evidence both genetic and environmental influences on self-harm. However, to date, there has been no genetically informed research on self-harm aetiology across development, nor studies identifying risk factors for initiating self-harm at a younger age.
Methods: We examined self-harm in the Twins Early Development Study, a birth cohort twin study. Using clustered regression models, we tested associations of socio-demographic factors and victimisation with lifetime self-harm and age of self-harm initiation, both reported at 21. To investigate stability and/or change in genetic and environmental influences on self-harm we interpreted a multivariate Cholesky decomposition across ages ≤16, 21, and 26.
Results: Self-harm was more common in adolescence than early adulthood, and the incidence of self-harm in early adulthood was low (1.4%). The most common motivation for self-harm was 'to get relief from a terrible state of mind' (83.4%). Independent predictors of self-harm and earlier initiation of self-harm were being female, belonging to a gender and/or sexual minority group, and experience of bullying victimisation. Sexual minority status was still significantly associated with self-harm after controlling for familial factors in co-twin control analyses. The Cholesky decomposition showed stability in genetic influences and innovation in non-shared environmental influences on self-harm.
Conclusions: Adolescence should be a key period for self-harm interventions. Women, sexual, and gender minorities, and those experiencing victimisation may need targeted support early in adolescence. Furthermore, it should be acknowledged that different individuals can be at risk at different stages as environmental factors influencing self-harm change across time.
Background: Childhood adversity poses a major transdiagnostic risk for a host of psychiatric disorders. Altered threat-related information processing has been put forward as a potential process underlying the association between childhood adversity and psychiatric disorders, with previous research providing support for decreased discrimination between threat and safety cues, in both children and adults exposed to adversity. This altered threat-safety discrimination has been hypothesized to stem from increased generalization of fear, yet to date, this hypothesis has not been tested in youth.
Methods: Here, we investigate whether childhood adversity is associated with fear generalization during adolescence. 119 adolescents between 12 and 16 years of age (mean = 13.95), of whom 63 exposed to childhood adversity, completed a fear generalization paradigm. Fear conditioning was assessed through trial-by-trial US expectancy ratings and post-experimental ratings of fear, valence and arousal. Additionally, we administered a perceptual discrimination task to assess the potential impact of perceptual discrimination abilities upon fear generalization.
Results: In line with our hypotheses, results showed that childhood adversity is associated with (1) reduced threat-safety differentiation during fear acquisition and (2) increased fear generalization in both boys and girls, albeit to a different extent, as boys showed more generalization towards safety cues while girls showed more generalization towards dangerous cues. Moreover, this overgeneralization of fear could not be attributed to group differences in perceptual discrimination.
Conclusions: Altered fear learning may be an important process through which adversity increases risk for the development of psychopathology. Longitudinal research is essential to elucidate risk and resilience patterns following childhood adversity.
Background: Atypical reward processing is implicated in a range of psychiatric disorders associated with childhood maltreatment and may represent a latent vulnerability mechanism. In this longitudinal study, we investigated the impact of maltreatment on behavioural and neural indices of reward learning in volatile environments and examined associations with future psychopathology assessed 18 months later.
Methods: Thirty-seven children and adolescents with documented histories of maltreatment (MT group) and a carefully matched group of 32 non-maltreated individuals (NMT group) aged 10-16 were presented with a probabilistic reinforcement learning task featuring a phase of stable and a phase of volatile reward contingencies. Brain activation and connectivity were assessed simultaneously using functional magnetic resonance imaging (fMRI). Computational models were used to extract individual estimates of learning rates and temperature, and neural signals in prespecified regions of interest were analysed during volatile and stable environments. In regression analyses, behavioural measures and neural signals at baseline were used to predict psychological symptoms at follow-up.
Results: The MT group showed lower behavioural exploration, which predicted decreased internalising symptoms at follow-up. The MT group had lower activation in the orbitofrontal cortex (OFC) during outcome delivery in volatile relative to stable contexts. OFC connectivity with an area in the mid-cingulate cortex was also lower during outcome processing, which predicted higher general psychopathology at follow-up.
Conclusions: These findings are consistent with the notion that low exploratory behaviour following childhood maltreatment is potentially a protective adaptation against internalising symptoms, while disrupted neural processing of reward learning in volatile environments may index latent vulnerability to mental illness.
Contemporary research on developing theory of mind emphasizes its cognitive and neurobiological foundations, but studies of its relational origins have potential for opening new terrain in this expansive literature. The study by Kochanska and colleagues shows this in several ways. First, it offers a model for constructing theoretically guided causal models built on longitudinal research enlisting multiple predictors of developing theory of mind that can be examined in concert. Second, the findings invite deeper consideration of the processes by which theory of mind emerges by unpacking the relational predictors highlighted in this and other studies. In particular, examining the characteristics of early conversation focused on the child's experiences and mental states and studying the coordination of subjective states in parent-child interaction are each warranted avenues. Third, enlisting fathers and mothers into this inquiry broadens the range of relational partners contributing to young children's developing understanding of the mind.
Background: More than half of the current US population was exposed to adverse lead levels in childhood as a result of lead's past use in gasoline. The total contribution of childhood lead exposures to US-population mental health and personality has yet to be evaluated.
Methods: We combined serial, cross-sectional blood-lead level (BLL) data from National Health and Nutrition Examination Surveys (NHANES) with historic leaded-gasoline data to estimate US childhood BLLs from 1940 to 2015 and calculate population mental-health symptom elevations from known lead-psychopathology associations. We utilized five outcomes: (1) General Psychopathology "points", reflecting an individual's liability to overall mental disorder, scaled to match IQ scores (M = 100, SD = 15); (2) Symptoms of Internalizing disorders (anxiety and depression) and Attention-deficit/Hyperactivity Disorder (AD/HD), both z-scored (M = 0, SD = 1); and (3) Differences in the personality traits of Neuroticism and Conscientiousness (M = 0, SD = 1).
Results: Assuming that published lead-psychopathology associations are causal and not purely correlational: We estimate that by 2015, the US population had gained 602-million General Psychopathology factor points because of exposure arising from leaded gasoline, reflecting a 0.13-standard-deviation increase in overall liability to mental illness in the population and an estimated 151 million excess mental disorders attributable to lead exposure. Investigation of specific disorder-domain symptoms identified a 0.64-standard-deviation increase in population-level Internalizing symptoms and a 0.42-standard-deviation increase in AD/HD symptoms. Population-level Neuroticism increased by 0.14 standard deviations and Conscientiousness decreased by 0.20 standard deviations. Lead-associated mental health and personality differences were most pronounced for cohorts born from 1966 through 1986 (Generation X).
Conclusions: A significant burden of mental illness symptomatology and disadvantageous personality differences can be attributed to US children's exposure to lead over the past 75 years. Lead's potential contribution to psychiatry, medicine, and children's health may be larger than previously assumed.