The alleviating effect of positive youth development (PYD) on psychopathological symptoms (PS) represents the less vulnerability hypothesis, while the damaging effect of PS on PYD represents the competitional hypothesis or the scar hypothesis. This study aims to explore which hypothesis is more dominant and which component of PYD plays the central role across developmental stages and environmental adversity.
Two longitudinal waves of 40,473 Chinese adolescents (48.4% girls, Mage = 12.67 ± 2.28) were analysed via a cross-lagged network panel model.
The results showed that competition indeed exists between the PYD and PS systems, while the alleviating effect of the PYD is greater than the damaging effect of the PS system, but less than the self-loop effect within the PS system. The PYD components with the most alleviating effects are self-esteem, emotion regulation and self-regulation. With adolescents maturing (early, middle and late adolescence), the alleviating effect surpasses the damaging effect and self-loop effect in the PS system. When adversity (low, moderate and high) increases in severity, the alleviating effect also surpasses the damaging effect and self-loop effect in the PS system. In addition, resilience plays a central role in alleviating the PS system only when adversity is high.
Compared with the scar hypothesis, the less vulnerability hypothesis showed a more powerful impact. Early and adversity-aimed interventions aimed at promoting adolescents' positive attributes are the most beneficial. The central PYD components should be treated as core targets in future intervention programs.
Sleep problems and self-harm during adolescence are both highly common and major public health concerns, yet the nature of their relationship remains poorly understood. This study examined the cross-sectional and long-term effects of several sleep phenotypes on self-harm and whether decision-making moderated this relationship.
Data was utilised from the Millennium Cohort Study (n = 10,477, Female = 5,314 [50.72%]) when individuals were approximately 9 months, 14 years and 17 years of age. Sleep variables available were measured at 14 years and included sleep duration on weekdays and weekends, social jetlag, sleep onset latency and night awakenings. Self-harm was measured at 14 and 17 years. The Cambridge Gambling Task assessed rational decision-making at 14 years.
Cross-sectionally, shorter sleep duration on school days (AOR = 0.875; 95% CI = 0.820, 0.933; p < .001), longer sleep onset latency (AOR = 1.005; 95% CI = 1.002, 1.007; p < .001) and more frequent night awakenings (AOR = 1.140; 95% CI = 1.086, 1.197; p < .001) were significantly associated with self-harm at 14, even when controlling for demographic and clinical covariates. Longitudinal results indicated that shorter sleep duration on school days (AOR = 0.926; 95% CI = 0.874–0.982; p = .010), longer sleep onset latency (AOR = 1.003; 95% CI = 1.001–1.005; p = .008) and more frequent night awakenings (AOR = 1.090; 95% CI = 1.043–1.139; p < .001) also had a direct prospective effect on self-harm at 17 when controlling for demographic and clinical factors. Rational decision-making as measured by the Cambridge Gambling Task did not significantly contribute to this relationship.
These findings highlight the prospective association between short sleep duration, increased sleep onset latency, fragmented sleep and self-harm during adolescence. Ensuring adolescents obtain enough good quality, uninterrupted sleep appears critical to prevent engagement with self-harm.
Adolescent self-reported psychotic experiences are associated with mental illness and could help guide prevention strategies. Youth report substantially more experiences than adults. However, with large societal changes like the digital revolution and COVID-19 pandemic, existing questionnaires may no longer accurately capture youth experiences. We aimed to determine the ability of the CAPE-16 questionnaire in capturing psychotic experiences across contexts (biological sex and COVID-19 response) and generations, thereby validating important psychometric aspects of the tool in modern adolescents.
We used data from the Norwegian Mother, Father and Child Study (MoBa), a population-based pregnancy cohort. Adolescents responded to the CAPE-16 questionnaire (n = 18,835). For a comparison between age groups, we included adult men from the parent generation who responded to the CAPE-9 (n = 28,793). We investigated the psychometric properties of CAPE-16 through confirmatory factor analyses, measurement invariance testing across biological sex, response before/during the COVID-19 pandemic, and generations (adolescents and fathers), and examined subscale and item-level associations with subsequent registry-based psychiatric diagnoses (average time between CAPE and last registry update: 3.68 ± 1.34 years).
Out of 18,835 adolescents, 33.2% reported lifetime psychotic experiences. We confirmed a three-factor structure (paranoia, bizarre thoughts, and hallucinations) and good subscale reliability (ω = .86 and .90). CAPE-16 scores were stable across biological sex and pandemic status. CAPE-9 response patterns were non-invariant across adolescents and adult men, with an item related to digital technology particularly prone to bias. CAPE-16 subscales were associated with subsequent psychiatric diagnoses, especially psychotic disorders.
CAPE-16 is a reliable measure of psychotic experiences across sex and a major societal stressor in adolescents. More frequent and distressing experiences increase the risk of subsequent psychiatric diagnoses. Different response patterns between adults and adolescents for items related to digital technology suggest differences in interpretation. Hence, certain items may benefit from revisions.
The categorical diagnostic approach in the DSM-5 for Neurodevelopmental Disorders often reveals significant limitations, as high rates of comorbidity are common across conditions such as ADHD, autism spectrum disorder, and developmental coordination disorder. This co-occurrence aligns with a neuroconstructive dimensional perspective of neurodevelopment, which emphasizes the interconnectedness of cognitive, motor, and social impairments evolving throughout development. This perspective challenges modular and categorical views of neurodevelopmental phenotypic manifestations. Envisioning the DSM-6, a proposed dimensional Alternative Model for Neurodevelopmental Disorders (AMND) could integrate functioning severity and pathological traits, drawing inspiration from DSM-5 innovations, such as the Autism Spectrum Disorder severity levels. Such a model could facilitate nuanced profiling of individual strengths, needs, and developmental risks, accommodating both categorical and dimensional diagnostic approaches. This framework could also improve early identification of vulnerabilities to severe mental illnesses and clarify the developmental antecedents of adult-onset psychiatric conditions, offering pragmatic insights for clinical interventions and prognosis.
Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder in school-age children. Abnormal sensory–motor integration, such as concurrent visuomotor selection, is a prominent feature of ADHD. However, underlying pathophysiological substrates of impaired sensory–motor integration in childhood ADHD remain unclear. Identifying neural markers of cognitive impairment in children with ADHD is vital for the early assisted diagnosis and the selection of intervention targets.
We collected electroencephalography (EEG) signals from 70 children with ADHD and 65 matched typically developing (TD) children while performing a visual search task. Oscillation-based multivariate pattern decoding was used to investigate visuomotor coordination during spatial attention.
Compared with TD children, children with ADHD showed impairments in accuracy, response time, and response time variability. Multivariate machine learning revealed that the ADHD group showed deficits in alpha (visual-related) and beta (motor-related) power-based decoding accuracy, indicating the impaired sensory orienting and motor preparation. Importantly, children with ADHD exhibited a delay between alpha and beta decoding, suggesting a deficit of concurrent visuomotor coordination. However, this visuomotor asynchrony was absent in TD children. Furthermore, the degree of visuomotor asynchrony between alpha and beta decoding was predictive of behavioral impairments and symptom severity in children with ADHD.
These observations reveal that impaired concurrent visuomotor coordination might be a potential neural marker of impaired sensory–motor integration in children with ADHD, further advancing the understanding of cognitive deficits, and providing potential research directions for the early diagnosis and optimization of intervention in neurodevelopmental disorders.
It has long been hypothesized that increasing heritability with age of cognitive and educational performance is partly attributable to evocative gene–environment correlation. However, this hypothesis has not been widely tested.
We addressed this gap by examining whether children's education polygenic scores (PGSedu) were associated with maternal self-reported positive and literacy-focused parenting when children were 5 years old, and if evoked parenting differences mediated genetic effects on children's educational outcomes (mother-reported at 6–8 years of age), while controlling for parental PGSedu. We also investigated whether maternal reports of children's language at 5 years old were associated with parenting and mediated genetic effects on educational performance. These questions were addressed in a sample of 83,627 parent-offspring trios from the Norwegian Mother, Father and Child Cohort Study, a longitudinal population-based pregnancy cohort.
Children's PGSedu were significantly associated with maternal literacy-focused (β = .03, 95% CI [0.01, 0.05], p = .021) but not positive parenting (β = 0.01, 95% CI [−0.02, 0.05], p = .410), and literacy-focused parenting significantly mediated the effects of children's PGSedu on their educational performance (β = 0.01, 95% CI [1 × 10−3, 0.01], p = .023). Children's language was associated with maternal parenting and mediated the effects of children's PGSedu on their educational performance (β = 0.01, 95% CI [3 × 10−3, 0.02], p = .002).
These findings support our hypotheses and suggest early language and parenting may be mechanisms implicated in the pathways from children's genetics to their educational outcomes.
Lower parental income is associated with more psychiatric disorders among offspring, but it is unclear if this association reflects effects of parental income (social causation) or shared risk factors (social selection). Prior research finds contradictory results, which may be due to age differences between the studied offspring.
Here, we studied psychiatric disorders in the entire Norwegian population aged 10 to 40 years between 2006 and 2018 (N = 2,468,503). By linking tax registries to administrative health registries, we described prevalence rates by age, sex, and parental income rank. Next, we grouped observations into age groups (adolescence, ages 10–20 years; early adulthood, 21–30 years; adulthood, 30–40 years) and applied kinship-based models with extended families of twins and siblings to decompose the parent–offspring correlation into phenotypic transmission, passive genetic transmission, and passive environmental transmission.
We found that lower parental income rank was associated with higher prevalence of nearly all psychiatric disorders, except for eating disorders, for both men and women at all ages from 10 to 40 years. Comparing the top with the bottom paternal income quartile, the prevalence ratio of any psychiatric disorder was 0.47 among 10-year-olds and decreased to 0.72 among 40-year-olds. The parent–offspring correlation was −.15 in adolescence, −.10 in early adulthood, and −.06 in adulthood. The kinship-based models indicated that phenotypic transmission could account for 39% of the parent–offspring correlation among adolescents (p < .001), but with no significant contribution in early adulthood (p = .181) or adulthood (p = .737). Passive genetic and environmental transmission contributed to the parent–offspring correlation in all age groups (all p's < .001).
Our findings are consistent with a significant role of social causation during adolescence, while social selection could fully explain the parent–offspring correlation in adulthood.
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