JCPP advances最新文献

Background

In their recent paper, Del Giudice and Haltigan argue that attachment in childhood and attachment representations in adulthood are influenced by the cognitive capabilities of children and parents, that would causally link parents' attachment states of mind to children's attachment.

In the current pre-registered study, we empirically explored the idea of an association between attachment and cognition using phenotypic child IQ and parent and child IQ-related polygenic scores as predictors of children's attachment behavior and attachment representations.

Methods

We used data from the Leiden Consortium on Individual Development study (L-CID, n = 992), a two-cohort longitudinal twin study, in which attachment representations were measured in parents and their 9-year-old children using the Attachment Script Assessment (ASA). Polygenic scores of IQ were computed for parents and their children using PRSice-2 and phenotypic child IQ was measured as well. We split the twin sample in two groups randomly to prevent non-independence of data and conducted structural equation models.

Results

Neither parental nor child polygenic scores of IQ predicted representations of attachment. In one cohort, phenotypically measured IQ predicted attachment.

Conclusions

This preliminary study did not find convincing support for a role of IQ in the intergenerational transmission of attachment.

Background

Behavioral parenting programs are a primary strategy used to reduce children's conduct problems. Although behavior problems in siblings may co-occur, behavioral parenting program trials typically report outcomes for one child per family (the index child), with potential program effects on any non-targeted sibling largely neglected. This study examined co-occurring patterns of index child and non-targeted sibling conduct problems, and how parental participation in the Incredible Years (IY) program changes these patterns.

Methods

We used individual participant data pooled across three randomized trials of the IY parenting program in England, Wales, and Ireland, with data for the index child and one non-targeted sibling (N = 240 families, 480 children; index child: M age = 4.73, SD = 1.44, range 2–9 years, 62% male; non-targeted sibling: M age = 5.94 years, SD = 3.15, range 6 months−15 years, 49% male). We used latent transition analysis to identify latent classes at both baseline and posttest based on families' combinations of index child and non-targeted sibling conduct problems.

Results

We identified two classes with distinct patterns of co-occurring sibling dyad conduct problems: one with moderate clinical levels of index child conduct problems and non-clinical levels for the non-targeted sibling; and one with severe clinical levels for both children. In terms of the effects of IY, most intervention families maintained their patterns of sibling dyad conduct problems, but with lower levels across classes. Most intervention families reported improvements predominantly for the index child. However, a minority of families with severe baseline levels of conduct problems in both children moved to a class with non-clinical levels for both children.

Conclusions

For most families, IY had limited effects on non-targeted sibling disruptive behavior. However, IY may reduce co-occurring sibling conduct problems for a small number of families with initially severe levels in both children.

Background

Adverse experiences – such as abuse and neglect – occurring during childhood and adolescence have been found to predict poorer mental and cognitive health. Social adversities, including bullying and social exclusion, are likely to be particularly salient during adolescence. However, our understanding of how social adversities co-occur in adolescence and how they predict cognitive functioning is limited.

Methods

We used latent profile analysis to investigate adolescents' experiences of social adversities and regressions to identify their relationship to cognition later in development. Data was analysed from UKHLS (N = 493, aged 14–16 years, preregistered analysis) and ALSPAC (N = 14,856, aged 12–22 years, replication analysis).

Results

Adolescents clustered into four profiles in both cohorts: low adversity, peer difficulties, sibling bullying and poly-adversity. We found that 17%–22% of participants fell into the poly-adversity profile and reported experiencing several social adversities. In ALSPAC, but not UKHLS, cognitive functioning differed between social adversity profiles (working memory: F(3, 3773) = 8.07, p < 0.001; fluid reasoning: F(3, 5258) = 3.36, p = 0.018; verbal fluency: F(3, 5261) = 6.24, p < 0.001). After controlling for sex, adolescents in the low adversity profile scored significantly higher on the working memory task than those in the sibling bullying profile and the poly-adversity profile, but effect sizes were small.

Conclusion

These findings have implications for understanding adolescents' social experiences. To understand individual differences in lifespan outcomes, it is essential to capture a broad spectrum of social interactions, including peer and sibling difficulties, bullying, exclusion, and school issues.

Background

Autism and attention-deficit/hyperactivity disorder (ADHD) overlap to a considerable degree and have been associated with mental health difficulties, yet there is limited research on this relationship. Young adulthood is a time of heightened risk for mental health problems in general. The risk may be greater for individuals with these conditions, for whom societal demands tied to this transitional time may heighten the impact of internalising behaviours. Elucidating the relationships between neurodevelopmental differences and vulnerability to psychopathology may inform future adaptations for specialised support.

Methods

This study explored whether autistic and ADHD traits and their interaction were associated with symptoms of depression and anxiety as well as meeting diagnostic criteria for internalising disorders in a sample of 556 young-adult twins (mean age 22 years 5 months, 52% female), controlling for sex, age, cognitive ability, and parental socioeconomic status. Four participant groups were created based on traits assessed in young adulthood: high autistic traits, high ADHD traits, high autistic and ADHD traits, and low ADHD and autistic traits.

Results

High autistic and ADHD traits were independently associated with higher self-reported depression and anxiety symptoms and likelihood of meeting diagnostic thresholds for an anxiety or low mood disorder. While co-occurrence of autism and ADHD exhibited the greatest risk for mental health challenges, no evidence was found for interaction effects between these traits at stringent corrected thresholds. Females with high levels of autistic traits exhibited particularly high risk for concomitant psychopathology.

Conclusions

Our findings suggest that those with high levels of autistic and/or ADHD traits may require individualised care strategies, in light of the complex interplay between traits of neurodivergence and mental health outcomes. Future research may explore the efficacy of psychoeducation and specific adaptations to established therapeutic interventions needed to optimise outcomes for adults with these conditions.

Background

Although the childhood prevalence of ADHD is higher in males than in females, some studies suggest that females report more severe impairment related to ADHD symptoms than males. The reason for this gender paradox is poorly understood. Here we explored sex differences in self-reported ADHD symptoms among adolescents and adults with and without an ADHD diagnosis across clinical and population-based Norwegian cohorts.

Methods

We analysed population-based data from the Norwegian Mother, Father, and Child Cohort Study (MoBa) (N = 90,816; 62% females, mean age 33.4 years), the youth@hordaland study (y@h) (N = 10,257; 53% females, mean age 17.4 years), and the ADHD in Norwegian Adults (ANA) project (N = 1677; 55% females, mean age 29.0 years). The Adult ADHD Self-Report Scale Screener (ASRS-6) was used as an outcome measure to define symptom severity of ADHD. Linear regression analyses were used to explore sex differences in ASRS-6 scores between individuals with and without a self-reported ADHD diagnosis (∆). Age-adjusted, unstandardized regression coefficients (b) with 95% confidence intervals (CI) were reported.

Results

Participants with ADHD reported higher ASRS-6 scores than those without ADHD across all three cohorts. The ASRS-6 scores were highest in the youngest participants, particularly in females from the y@h cohort. The difference in ASRS-6 scores between those with and without an ADHD diagnosis was larger among females than males within all cohorts, at a statistically significant level both in y@h and ANA (MoBa: ∆females: b = 4.6 (95%CI 3.8; 5.4); ∆males: b = 4.2 (3.5; 5.0); y@h: ∆females: b = 5.1 (4.0; 6.2); ∆males: b = 3.2 (2.1; 4.2); ANA: ∆females: b = 8.6 (8.1; 9.2); ∆males: b = 6.5 (5.9; 7.2).

Conclusions

In both population-based and clinical cohorts, representing different age groups and study designs, we found a larger mean difference in reported ADHD symptoms between adolescents and adults with and without ADHD among females than males, suggesting barriers for females related to referral, assessment, and/or diagnosis of ADHD.

Background

Sleep deficiency is common among youth exposed to adverse childhood experiences (ACEs) and may contribute towards persistent/recurrent pain (PRP). This study tested the hypotheses that sleep deficiency mediates the effect of ACEs on PRP and moderates the effect of ACEs on PRP exerted through anxiety and depression symptoms.

Methods

We used 4 years of Adolescent Brain Cognitive Development Study® data to test our hypotheses. Annual assessments of sleep duration and quality (from the Sleep Disturbances Scale for Children), pain, anxiety, and depression (from the Child Behavior Checklist) were used to derive our measures. Structural equation modeling and sleep subgroup comparisons estimated effects of early childhood ACEs (measured with parent/youth surveys) on PRP (defined as pain reported for 3 or 4 years) via sleep duration and quality, accounting for effects of anxiety/depression symptoms. Results are presented as standardized adjusted odds ratios with 95% confidence intervals (adj. OR [95% CI]).

Results

Data from 7912 youth were included, nearly one third of whom (n = 2527) were classified with PRP by age 12–13. The effect of early childhood ACEs on adolescent PRP was mediated, in part, through insufficient sleep duration (adj. OR 1.01 [95% CI 1.01, 1.02]) and higher sleep quality (adj. OR 0.99 [ 95% CI 0.97, 0.99]). The direct effect of ACEs on PRP was significant only for the subgroup of youth with both insufficient duration and low quality sleep (adj. OR 1.43 [95% CI 1.05, 1.95]). Mediation effects of depression and anxiety were supported across all sleep subgroups with one exception, and sleep did not moderate these associations.

Conclusion

Sleep deficiency may underlie the effect of early ACEs on PRP, though anxiety and depression are likely important to these pathways regardless of sleep. Further investigation into the potentially mechanistic role of sleep deficiency in ACEs/pain associations is warranted.