Psychometric network analysis offers a granular understanding of problem gambling (PG) by modeling individual symptoms within an interconnected system. Identifying central symptoms can help explain symptom co-occurrence and core symptoms relevant for escalating severity.

We estimated undirected cross-sectional and directed cross-lagged network models based on four representative Norwegian population surveys (2013, 2015, 2019, and 2022; age range 16–74) and assessed network stability, accuracy, and generalizability. Cross-sectional samples ranged from n = 3,232 to 6,034 (47–50% women) and cross-lagged samples included n = 3,043 (2013–2015, 50% women) and n = 2,749 (2019–2022, 47% women). PG symptoms were measured with the Problem Gambling Severity Index alongside self-reported gambling expenditure.

Within undirected networks, financial problems showed the strongest strength centrality and these networks showed strong generalizability, including the 2019 and 2022 surveys per Network Comparison Test (p = .65), edge presence (φ = .79), and edge weight (r = .85) correlations. Within directed networks, borrowing money had the strongest association with symptoms at follow-up (out-strength), while guilt at follow-up was most strongly predicted by other symptoms (in-strength). Generalizability between the 2013–2015 and 2019–2022 networks was inconclusive, with low correlation in edge presence (φ = .08) and high correlation in edge weights (r = .74).

Financial problems and borrowing money emerged as the most central PG symptoms in undirected and directed networks, respectively. Following further investigation, these symptoms may act as informative targets for screening, early intervention, and harm-reduction policy.

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder, with symptoms that remit or persist over time. Biological mechanisms underlying symptom change remain poorly understood, though epigenetic processes, like DNA methylation (DNAm), may serve as dynamic biomarkers of clinical outcomes. We examined change in DNAm in children and adolescents with and without ADHD, including differences between remitted and persistent ADHD.

We analyzed 219 saliva samples from 94 participants (aged 9.5–14.5 years) attending two to three waves of NICAP (Neuroimaging of the Children’s Attention Project). DNAm was profiled using the Infinium MethylationEPIC BeadChip. Linear mixed models adjusted for age, sex, medication, batch, and cell-proportion assessed longitudinal change. Comparisons included (1) individuals with versus without ADHD, (2) persistent or remitted ADHD versus without ADHD, and (3) persistent versus remitted ADHD. False discovery rate correction controlled for multiple testing (FDR-adjusted-p < 0.05).

Comparison (1) showed null findings after correction for multiple testing. In contrast to those without ADHD (2), the average DNAm was statistically different at 2 sites in persistent ADHD (FDR-adjusted-p < 0.05) and 3 sites in remitted ADHD (FDR-adjusted-p < 0.03), and methylation of 3 additional CpGs differentially changed in persistent ADHD (FDR-adjusted-p < 0.04). Remitted differed from persistent ADHD (3) at 4 CpGs, including cg21443143 (ZFAT), which showed a decline over time. Gene enrichment links findings to brain structures and function, though these did not survive multiple testing.

Our study identified several epigenetic differences between remitted and persistent ADHD outcomes from typical development, and from each other. Given the early stage of this research, our findings warrant further prospective epigenome-wide studies into these diagnostic trajectories.

Prior research shows that humans adjust their learning rate based on environmental volatility. This adaptation has been shown to be reduced in individuals with high levels of anxious-depression, but past studies have been cross-sectional, making it unclear whether this adaptation is trait-like or responsive to treatment. There are also questions about the basic replicability of this effect with recent studies failing to find robust associations.

In the Precision in Psychiatry study, we examined changes in learning rate adaptation in a points-loss task, following four weeks of treatment in two patient groups receiving either internet-based cognitive behavioral therapy (n = 677) or antidepressants (n = 95), compared to a group of healthy participants (n = 95).

All groups showed increased learning rates in volatile environments at baseline, but against our prediction, learning rate adaptation was not cross-sectionally associated with individual differences in anxious-depression. There was also no evidence that learning rate adaptation changed post-treatment, despite symptom improvements. However, in the antidepressant group, symptom reductions correlated with learning rate adaptation. This finding should be interpreted cautiously as we found that the key outcome measure had poor test–retest reliability.

Overall, our results suggest that associations between learning rate adaptation and anxious-depression, if present, are likely modest, depend on task characteristics, may not be present in treatment-seeking adults, and do not improve following treatment.

Charting developmental abnormalities in future psychotic disorder could help identify pathogenic processes. Head circumference (HC) is a proxy for brain size. Studies of HC and its developmental trajectories in future psychotic disorder cases and across the psychosis spectrum are inconclusive. It is important to determine whether deviations in HC are specific or reflect a general growth disorder.

We used data from the Avon Longitudinal Study of Parents and Children (ALSPAC) to chart HC trajectories from birth to 15 years in individuals with operationally-defined psychotic disorder (N = 62), psychotic experiences (PE; N = 339) and controls (N = 3,527). We extracted total intracranial volume (TIV) from MRI data on a subset (N = 347) scanned at age 20.

HC at birth, 7 and 15 years was correlated with TIV at age 20 (r’s = 0.45–0.77). The psychotic disorder group had consistently smaller HC from birth through to adolescence (B = −0.26, p = 0.02). Females with PE had smaller HC across childhood and adolescence (B = −0.27, p = 0.016), while males with PE had consistently larger HC (B = 0.35, p = 0.023). The effects did not change when controlling for maternal and pregnancy-related characteristics but attenuated after controlling for height, except in males with PE.

Deviations in head and hence brain size across the psychosis spectrum likely reflect a more general growth abnormality. Future studies should examine factors regulating growth during early life in relation to psychosis, including sex, to understand underlying mechanisms.

Non-suicidal self-injury (NSSI) is a prevalent behavioural health concern during adolescence and has been consistently linked to emotionally invalidating interpersonal environments.

This study tested whether distress tolerance and negative urgency prospectively explained the link between invalidating environments and adolescent NSSI.

The study used a 2-wave longitudinal design with a 6-month interval; 300 Iranian adolescents (70% female, aged 13–17 years) participated.

Cross-lagged panel modelling showed that invalidating environments at wave 1 predicted higher NSSI at wave 2, when we controlled for baseline NSSI, and were associated with increases in negative urgency. Although both negative urgency and distress tolerance were related to later NSSI, only negative urgency significantly mediated this relationship; distress tolerance and the hypothesised serial pathway did not show significant associations. Sensitivity analyses indicated developmental differences across age groups.

The findings highlight impulsive response under distress as a central mechanism linking environmental invalidation to adolescent NSSI and identify negative urgency as a key intervention target.

Among military veterans, loneliness is common and associated with poorer mental and physical health and functioning. Epidemiological studies have revealed bidirectional, longitudinal associations between loneliness and posttraumatic stress disorder (PTSD). Little is known about loneliness among treatment-seeking veterans, how loneliness impacts PTSD symptom change during treatment, and whether loneliness has differential associations with specific PTSD symptom clusters.

Data were derived from the Veterans Outcome Assessment, an annual, repeated-measures (baseline and 3-month follow-up) telephone survey of patients beginning new episodes of mental health care in the Department of Veterans Affairs. Participants were 1,155 veterans (23% women) entering PTSD specialty care. We tested whether baseline loneliness predicted change in total PTSD symptom severity and according to the five-factor Dysphoric Arousal model of PTSD using hierarchical regressions in which we statistically adjusted for demographics and mental health encounters.

Loneliness decreased between baseline and 3-month follow-up (d = 0.39). Baseline loneliness predicted change in PTSD for the dysphoric arousal and negative alterations in cognitions and mood symptom clusters, with lonelier veterans demonstrating more PTSD change between baseline and follow-up. However, lonelier veterans also had more severe PTSD symptoms at both timepoints. This pattern of results held even after accounting for different types of treatment encounters between timepoints.

While lonelier veterans have more severe PTSD symptoms, they also make greater improvements in symptoms salient to interpersonal functioning over time. Assessment of loneliness should be incorporated into PTSD treatment planning and considered as a treatment target that could be addressed to promote recovery.

Quality of social support is linked to mental health, but less is known about its long-term effects. We aimed to investigate the effects of the quality of social support on affective symptoms from midlife through later life.

Data were used from the MRC National Survey of Health and Development (NSHD), a prospective birth cohort originally consisting of 5,362 people born in 1946. Affective symptoms were measured at ages 53, 60–64, and 69 years using the General Health Questionnaire (GHQ-28), and longitudinal affective symptom trajectories were derived using growth mixture modeling. Quality of social support (positive and negative) was assessed at age 53 years with an adapted version of the Close Persons Questionnaire. Associations of positive and negative social support with affective symptoms at each age and with the longitudinal trajectories were tested using structural equation modeling and the R3 Step approach.

Four distinct affective symptom trajectories were identified: no/low symptoms (83%), low and increasing symptoms (8%), consistently moderate/high symptoms (5%), and moderate/high and decreasing symptoms (4%). In fully adjusted models, negative social support was associated with affective symptoms at all three ages (β: 0.09–0.16, all p-values < .001) and with the ‘consistently moderate/high symptoms’ trajectory (OR = 1.65, 95% CI: 1.36, 2.01, p < .001); no association was found for positive social support.

Results highlight the importance of negative social support as a potential modifiable factor in prevention and intervention initiatives for affective symptoms among adults from midlife to later life.

Although adverse childhood experiences (ACEs) have been related to poorer lifespan health, their association with DNA methylation-based indicators of biological aging during adolescence remains incompletely understood, particularly across intersecting social positions. To address this gap, we used an intersectional race–sex approach to identify ACE patterns and examine their associations with biological aging in adolescence.

Participants (n = 1,655) were drawn from the Future of Families and Child Wellbeing Study, a racially diverse urban U.S. birth cohort. ACEs were measured prospectively from ages 3 to 9 and modeled using latent class analysis with measurement invariance testing across six intersecting race–sex groups. Biological aging was assessed using saliva-derived DNA methylation measures at ages 9 and 15, and for change from age 9 to 15 using PhenoAge, GrimAge, and DunedinPACE.

Two ACE classes emerged within each racial/ethnic group. Among Black participants, females showed higher PhenoAge estimates than males across classes at ages 9 and 15 and for longitudinal change. Among White participants, females in the Single-Parent Poverty & Maternal Substance Use class showed higher PhenoAge estimates at age 9 than females in the Maternal Substance Use class, although this difference was not observed at age 15 or for longitudinal change. Findings for GrimAge and DunedinPACE were less consistent.

Prospectively measured ACE configurations showed selective associations with adolescent DNA methylation–based aging measures, most consistently for PhenoAge. Findings support intersectional, person-centered approaches to identifying heterogeneity in early biological risk and underscore the need for caution in interpreting clock-specific findings in youth.

Few studies have examined whether infant dietary diversity is prospectively associated with malnutrition risk in young children. We sought to assess whether dietary diversity and animal-source food (ASF) consumption were associated with malnutrition and body composition among children younger than 2 years at high risk of malnutrition.

Longitudinal cohort of HIV-exposed uninfected (HEU) or HIV-unexposed children with repeated measures of weight, length, circumferences and skinfold thicknesses from age 9 to 23 months from which WHO z-scores were calculated. FFQ assessed infants’ dietary diversity, flesh foods and egg intake. Cox proportional hazards were used to examine whether minimum dietary diversity (MDD, dietary diversity scores ≥ 5) and consumption of ASF were associated with malnutrition, defined as z-score < −2.

Western Kenya

Infants (n 232; 48 % female; 49 % HEU; growth z-scores above −2 at 9 months).

At 9 months, 42 % of infants met MDD, and mean z-scores were above −1 sd. Meeting MDD at 9 months was associated with a lower risk of stunting from 9 to 23 months (HR 0·51; 95 % CI: 0·33, 0·80) but not wasting or underweight. MDD at 9 months was associated with 86 % (95 % CI 0·11, 0·51) lower risk of low subscapular skinfolds; similar trends were observed for flesh foods.

In a cohort of Kenyan infants, MDD at 9 months was associated with reduced risk of stunting through the second year of life. Flesh food intake was associated with lower risk of low trunk adiposity. Improving dietary diversity during infancy may protect against early-life stunting.

Adverse childhood experiences (ACEs) are associated with increased risk of psychotic-like experiences (PLEs), but the relationship between specific adversities and the persistence of PLEs in young people remains unclear. We examined associations between distinct ACEs and the persistence of PLEs until 24 years old.

Using longitudinal data from participants in the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort with at least one PLE datapoint, we used group-based trajectory modeling to estimate longitudinal trajectories of PLEs from age 12–24. We examined their associations with bullying victimization, maltreatment, parental mental health problems, parental substance abuse, parental separation, and parental intimate partner violence prior to first PLE experiences.

Among 4,448 participants, a three-group trajectory model provided the best fit, revealing low, increasing and persistent PLE groups from ages 12–24. In fully adjusted multinomial logistic regression models, those exposed to bullying were more likely to belong to either the increasing (relative risk ratio [RRR]: 1.83, 95%CIs: 1.26–2.66) or high (RRR: 1.78, 95%CIs: 1.07–2.93) PLEs group than the low PLE group; those exposed to maltreatment were more likely to be in the increasing PLE group (RRR: 1.47, 95%CIs: 1.03–2.10). No other ACEs were associated with PLE trajectories.

Bullying was associated with persistent PLEs up to 24 years old, independent of other forms of childhood adversity, with timing-specific effects of maltreatment on increasing symptoms emerging later in adolescence. Findings provide further evidence for the importance of prioritizing bullying and maltreatment reduction as public health targets.