A major research effort in the past two decades has begun to illuminate how experience 'gets under the skin' - that is - the cellular and molecular processes that are associated with adversity and resilience. We selectively review three areas of this research: epigenetics, especially DNA methylation, telomere length, and inflammatory processes, and consider the implications of this work for better understanding the effects of adversity and pathways of recovery. Because infant mental health practitioners focus on children in the earliest years of life, they are well positioned to favorably alter the developmental trajectories of children experiencing or at risk for maladaptation. In addition to helping us develop more individually effective treatments, we consider other ways in which research advances in cell and molecular biology may be especially important to infant mental health practitioners in the future. Better understanding these processes will enhance effectiveness and potentially enlarge the scope of our practice.

Caregiver sensitivity is the extent to which a caregiver notices a child's signal, interprets it correctly, and responds quickly and appropriately. Although originally introduced to developmental science as the key antecedent of attachment security, decades since its conception, hundreds of studies have been conducted examining the predictive significance of caregiver sensitivity to a broad range of developmental outcomes. The literature on caregiver sensitivity and related constructs (e.g., warmth, responsivity, negative parenting) has grown exponentially and is now the focus of several meta-analyses. We conducted an umbrella review - a systematic review of reviews - to examine the extent to which caregiver sensitivity and related constructs are associated with child attachment, socioemotional, and cognitive outcomes. Searches in EMBASE, PsycINFO, and Medline and yielded 2,157 abstracts. Studies were included if they were a meta-analysis of caregiver sensitivity or a related construct, focused on children's developmental outcomes, were available in English, French, or Spanish, and were published between 2010 and 2024. Conducted and reported in accordance with PRISMA guidelines, 17 meta-analyses were identified. Using the metaumbrella package in R, we conducted quantitative analyses which demonstrated that caregiver sensitivity was moderately associated with attachment security (r = .25, k = 253, n = 37,444), cognition (r = .23, k = 44, n = 6,777), language skills (r = .26, k = 54, n = 11,136), and weakly associated with socioemotional problems (r = -.07, k = 135, n = 33,305). Narrative analysis of other meta-analyses on caregiver warmth, responsivity, positive and negative parenting, and child outcomes also showed associations in the expected direction. Our findings demonstrate the critical importance of caregiver sensitivity on children's socioemotional and cognitive development, supporting caregiver sensitivity as an important target for early childhood prevention and intervention programs.

The gut microbiome is increasingly implicated in childhood mental health and may influence positive youth development (PYD). This study aims to characterize PYD transition patterns from childhood to adolescence and explore the predictive value of the gut microbiome. This cohort study used two waves of data from the Chinese Adolescent Cohort study, including children aged 8-11 years at Wave 1, from Sichuan, Guizhou, and Chongqing provinces. PYD was assessed at both time points, and latent transition analysis identified changes over the 3-year follow-up period. Baseline stool samples were analyzed using 16 s rRNA sequencing. A light gradient boosting machine model was developed to link gut microbiota with PYD transition type in a training set (70%, n = 461), and validated with multinominal logistic analysis within a test set (30%, n = 200). Linear regression models were performed to assess dietary modifications on the gut microbiome. Three PYD transition profiles were identified: downgraded (declining to a lower pattern), promoted (advancing to a higher pattern), and stable development type (remaining in the same pattern). Fifteen microbial genera were identified as predictors of PYD transitions, and children with higher abundance of these taxa were more likely to transition to a stable or promoted profile rather than a downgraded profile (odds ratio ranging from 2.03 to 5.45). This predictive model demonstrated excellent performance, with an area under the curve of 0.91 (95% CI: 0.89, 0.93). The microbiome-PYD transition association was more pronounced in children in earlier stages of puberty. Furthermore, a diet high in fruits, vegetables, and soybeans was positively linked with PYD stable or promoted transition type. The gut microbiome presents predictive value in PYD transition from childhood to adolescence. Targeting these microbial taxa may inform future health promotion programs to optimize child development, particularly during the critical pubertal transition.

Callous-unemotional (CU) traits identify youth with more severe and chronic trajectories of conduct problems. However, the etiology of CU traits may be heterogeneous, undermining the search for effective treatments. The level of co-occurring anxiety has been used to identify "primary" (lower anxiety) versus "secondary" (higher anxiety) variants of CU traits. The primary variant has been hypothesized to emerge from strong genetic influence and secondary variants as an adaptation to adversity, such as exposure to childhood maltreatment. However, little research has tested this hypothesis directly. We examined whether anxiety moderates the etiology of CU traits to determine whether this phenotypic feature can help distinguish CU traits with stronger genetic or environmental risk. In two population-based twin cohorts (initial sample: N = 1,196, aged 6-11, oversampled for exposure to neighborhood disadvantage; follow-up sample: N = 13,486, age 7), we used genotype-by-environment interaction twin modeling to examine if parent-reported child anxiety moderated the etiology of concurrent parent-reported child CU traits. Anxiety moderated the etiology of CU traits across both samples, such that nonshared environmental influences increased as anxiety increased. Additionally, in the larger sample, genetic influences decreased with increasing anxiety. These findings support theories suggesting that co-occurring anxiety may distinguish CU traits with different origins: CU traits with higher anxiety appear more influenced by nonshared environmental factors-potentially including adversity-and may show weaker genetic influence. Assessing for co-occurring child anxiety is likely important for diagnosing and personalizing treatments among children with CU traits.

Early life vitamin D levels may be associated with autism spectrum disorder (ASD) and related traits, but causality is unknown. We examine whether higher-than-standard vitamin D3 supplementation during the first 2 years, as well as higher pregnancy and childhood 25-hydroxyvitamin D (25(OH)D) levels and their trajectories, are associated with lower ASD trait scores at ages 6-8 years in a non-clinical cohort. This secondary analysis of the double-blind randomized clinical trial vitamin D intervention in infants (VIDI) comprised 366 Finnish children aged 6-8 years, 177 of whom were randomized to receive 400-IU and 189 to receive 1,200-IU daily oral vitamin D3 supplementation between ages 2 weeks and 2 years. ASD-related traits were assessed at mean age 7.2 years (SD 0.4) using the parent-reported Autism Spectrum Screening Questionnaire (ASSQ). Predictor variables were supplementation group, 25(OH)D concentrations measured during pregnancy and at ages 1 and 2 years, as well as 25(OH)D trajectories (high vs. low) derived from these time points. None of the predictor variables of interest were associated with the outcome in the full sample. After sex stratification, among boys, 25(OH)D concentrations at 1 and 2 years were inversely associated with ASSQ scores (mean difference -0.2 of normalized SD score (95% CI -0.3 to -0.1, p = .003) and -0.2 (95% CI -0.3 to -0.05, p = .01) per 10 ng/mL 25(OH)D) after adjustment for age, breastfeeding, parental education, maternal depressive symptoms, and season of 25(OH)D assessment as was belonging to the higher 25(OH)D trajectory, -0.45 SD (95% CI -0.79 to -0.10, p = .01). We found no indication that higher-than-normal vitamin D3 supplementation between ages 0 and 2 years decreases ASD-related trait scores at ages 6-8 years. Sex-stratified analysis suggested an inverse association, among boys, between early life 25(OH)D concentrations and ASD-related traits, warranting further studies on potential causal direction and sex specificity of associations.

Unblocking the translational path between science and practice is a major priority for the field of child psychology and psychiatry. I have recently argued that key to this, going forward, will be our ability to come up with new framings of old challenges that allow us to develop new theories, hypotheses, methods and interpretations. I called this creative seeking-out of different perspectives, paradigm flipping. In this editorial, I argue that incorporating young people with neurodevelopmental and mental health conditions into the heart of our science, as co-investigators and not just advisors, can promote effective paradigm flipping in a way that can invigorate our science. I illustrate this by highlighting a recent programme of research, Regulating Emotion and Strengthening Adolescent Resilience (RE-STAR), which demonstrated not only that such a radical participatory approach is possible but that it can change the way we do science in demonstrably positive ways.

Early oral language interventions boost children's language skills, yet we know strikingly little about whether these gains endure. The handful of long-term follow-up studies available suggest that even high-quality language interventions show substantial fade-out. This gap in our evidence base has real consequences for families and for policy, especially as demand for language support continues to rise. We suggest that long-term impact might depend on three levels: characteristics of the intervention (e.g. breadth, instructional approach, and fidelity), features of the learning environment (e.g. classroom ethos, continuity of support, and language resources available) and child-specific factors (e.g. children's cognitive profiles). We call on funders and researchers to prioritise the routine capture of long-term outcomes and to invest in identifying the mechanisms and tools that could drive sustained improvement (e.g. regular booster sessions). We feel this is a critical priority for future research, as it would help us design support that genuinely shifts developmental trajectories.

Early temperament has been shown to predict socioemotional outcomes, but its neural correlates are not yet fully understood. In the current study, we investigated the relationship between early temperament and neuronal network functional connectivity (FC), and how these factors contribute to the risk of psychopathology. Using a longitudinal cohort followed from infancy to age 7 (N = 749 collected at infancy), we assessed temperament through two approaches: data-driven profiles extracted from parent-reported questionnaires collected from infancy to age 3 and lab-based assessments of behavioral inhibition (BI) at age 3. Symptoms of psychopathology were measured at age 7 with the parent-reported Child Behavior Checklist (CBCL). Resting-state EEG data collected at ages 3, 5, and 7, along with source-space connectivity methods, were used to examine FC within brain networks. Children with an emotionally and behaviorally dysregulated (EBD) profile, an identified risk factor for psychopathology, exhibited reduced FC in the frontoparietal network compared to their emotionally and behaviorally regulated (EBR) peers. BI at age 3 was also negatively correlated with FC in the ventral attention network at age 3 and the frontoparietal network at age 7. Additionally, frontoparietal FC moderated the relationship between early temperament and later attention-deficit symptoms: EBD children showed higher levels of attention problems than their EBR peers, but only when frontoparietal FC was low. These findings underscore the importance of network connectivity in understanding early temperament and its socioemotional outcomes. Specifically, they highlight the role of attention and control networks in the development of psychopathology, suggesting potential targets for early interventions aimed at at-risk children.

Reward learning is thought to undergo refinement in adolescence, but little is known about how computational components of reinforcement learning develop. Given that adolescence is a sensitive period for reward system plasticity with associated vulnerability for depression, it is important to understand developmental trajectories of different reinforcement learning parameters in normative development and in youth at risk for depression. Youth aged 9-17 years completed the Play-or-Pass Iowa Gambling Task (PoP-IGT) across five timepoints. We calculated task metrics using a traditional scoring approach - yielding summary scores for good deck play, bad deck play, and net play - and a computational modeling approach - yielding parameters for reward learning rate, punishment learning rate, go bias, and sensitivity to win/loss frequency ignoring outcome magnitude. We examined normative developmental trajectories for each traditional and computational performance metric using multilevel models. Further, we examined whether maternal history of depression was associated with individual differences in these trajectories. As hypothesized, youth showed a significant age-related increase in net play (p = 0.003), a measure of overall good performance. Exploratory analyses found that youth showed significant developmental change in reward-specific learning parameters including age-related increases in win/loss frequency sensitivity (FDR = 0.016) and age-related decreases in reward learning rate (FDR < 0.001). In line with hypotheses, youth at high risk for depression showed lower reward learning rates in early adolescence (p = 0.041). The observed developmental changes in traditional and computational metrics are largely consistent with the optimization of learning from rewards across adolescence. Further, the observed developmental changes in specifically reward-related computational parameters are consistent with heightened adolescent reward system plasticity. Additionally, there was support for our hypothesis that maternal history of depression may exert a unique effect on learning from rewards specifically, but further research across additional reward learning tasks is needed.

Reward sensitivity plays a crucial role in shaping emotional and behavioural responses, yet its internal structure and dynamic interplay with depression remain underexplored. This study systematically examined the network structure of reward sensitivity and its associations with depression using a network analysis framework. Based on two waves of data (T1: N = 1,136, Mage = 14.33, 52.46% female; T2: N = 1,083, Mage = 14.32, 52.82% female), we constructed multiple cross-sectional and bridge networks, as well as a cross-lagged panel network model (CLPN). (1) Cross-sectional network analysis reveals that positive feedback serves as the core node in the depression group, while hobbies dominate in the healthy group; (2) bridging network analysis identifies hobbies and positive affect as key bridging nodes linking reward sensitivity and depression; (3) CLPN analysis demonstrates that greater engagement in hobbies at baseline significantly predicts lower levels of depression 6 months later. This study provided a novel network perspective on the structural and temporal characteristics of reward sensitivity in depression. The findings underscored the importance of targeting specific reward types in intervention strategies and personalised mental health approaches.