Individuals with a family history of bipolar disorder are at increased risk of developing affective psychopathology. Longitudinal imaging studies in young people with familial risk have been limited, and cortical developmental trajectories in the progression towards illness remain obscure.

To establish high-resolution longitudinal differences in cortical structure that are associated with risk of bipolar disorder.

Using structural magnetic resonance imaging data from 217 unrelated ‘Bipolar Kids and Sibs study’ participants (baseline n = 217, follow-up n = 152), we examined changes over a 2-year period in cortical area, thickness and volume, measured at each vertex across the cortical surface. Groups comprised 105 ‘high-risk’ participants with a first-degree relative with bipolar disorder (female n = 64; age in years: M (mean) = 20.9, s.d. = 5.5) and 112 controls with no familial psychiatric history (females n = 60; age in years: M = 22.4, s.d. = 3.7).

Accelerated thickness and volume reductions over time were observed in ‘high-risk’ individuals across multiple cortical regions, relative to controls, including right lateral orbitofrontal thickness (β = 0.033, P < 0.001) and inferior frontal volume (β = 0.021, P < 0.001). These differences were observed after controlling for age, sex, ancestry, current medication status, lifetime psychiatric diagnoses and measures of gross brain morphology.

Longitudinal group differences suggest the presence of thicker cortex in familial ‘high-risk’ individuals at earlier developmental stages, followed by accelerated thinning towards the typical age of bipolar disorder onset. Future examination of genetic and environmental components of familial risk and the mechanistic nature (pathological or protective) of cortical-trajectory differences over time may facilitate the identification of prodromal biomarkers and opportunities for early clinical intervention.

Depression runs in families, with both genetic and environmental mechanisms contributing to intergenerational continuity, though these mechanisms have often been studied separately. This study examined the interplay between genetic and environmental influences in the intergenerational continuity of depressive symptoms from parents to offspring.

Using data from the Dutch TRAILS cohort (n = 2201), a prospective, genetically informed, multiple-generation study, we examined the association between parents’ self-reported depressive symptoms (reported at mean age of 41 years) and offspring depressive symptoms, self-reported nearly two decades later, in adulthood (mean age: 29 years). We assessed the role of genetic (polygenic scores for depressive symptoms in parents and offspring) and environmental mechanisms (parental warmth during adolescence) in explaining intergenerational continuity of depressive symptoms in separate and combined models.

Parents’ depressive symptoms, offspring genetic predisposition, and parental warmth were associated with an increased risk of depressive symptoms in offspring. In the combined model, parents’ genetic predisposition was linked to their own depressive symptoms, which were linked to lower parental warmth, which, in turn, was linked to higher depressive symptoms in offspring, after accounting for offspring genetic predisposition, sex, age, and socioeconomic status.

Both genetic and environmental mechanisms contribute to the intergenerational continuity of depressive symptoms independently and in interplay. Despite a significant effect, the influence of parental warmth was modest, suggesting limited covariation between this particular parenting measure and depressive symptoms, at least when assessed with large temporal distance.

Previous studies investigating the association between pubertal timing and depression in girls primarily use self-reported age at menarche (AAM). This study examines a range of pubertal timing indicators, including anthropometric and self-reported measures.

Compare associations of multiple indicators of pubertal timing with depressive symptoms and depression in girls and explore whether these associations persist into early adulthood.

The sample comprised 4607 girls from UK-based Avon Longitudinal Study of Parents and Children. Seven measures of pubertal timing were assessed between ages 7 and 17 (age at: peak height velocity (aPHV); peak weight velocity; peak bone mineral content velocity; Tanner pubic hair and breast development stage 3; axillary hair; and AAM). Depressive symptoms were measured at 14, 17, 18 and 24 years using the Short Mood and Feelings Questionnaire. Depression was assessed at 15, 18 and 24 years using the Development and Well-Being Assessment and Clinical Interview Schedule-Revised. Multivariable logistic regression models were adjusted for socioeconomic status and pre-pubertal body mass index.

Later pubertal timing was associated with lower odds of depressive symptoms at age 14 across six measures, including aPHV (adjusted odds ratio (AOR): 0.82; 95% CI 0.72, 0.95) and AAM (AOR: 0.84; 95% CI 0.76, 0.92). Later AAM and Tanner breast stage 3 were associated with lower odds of depression at age 18 (AOR: 0.85; 95% CI 0.75, 0.97 and AOR: 0.83; 95% CI 0.72, 0.95, respectively). Associations attenuated by age 24.

Later pubertal timing was associated with reduced odds of depressive symptoms during mid-adolescence, with associations attenuating by adulthood.

Understanding the effect(s) of the COVID-19 pandemic is key for planning for future pandemics.

This study examines change in self-reported mental health difficulties during three months of the pandemic among adolescent (10- to 15-year-olds) participants from the UK Household Longitudinal Study (waves 7, 9 and 11 of the main survey and waves 4, 5 and 8 of the COVID-19 surveys).

We focused on mental health difficulties using the Strengths and Difficulties Questionnaire (SDQ), using repeated cross-sectional and longitudinal analyses to examine data among 6471 adolescents who responded to at least one survey since 2015, and 2,300 who responded to at least one COVID-19 survey during July 2020, November 2020 or March 2021.

Repeated cross-sectional data showed similar mean total SDQ across surveys before and during the pandemic (range during pandemic 11.4 to 11.9; range pre-pandemic 11.1 to 11.8). Longitudinal analyses provided no evidence of mental health change compared with pre-pandemic trends (estimated change mean SDQ (β) = 0.05, 95% CI −0.42 to 0.51; p = 0.85), or differential sociodemographic effects, except greater effects in rural households (β = 0.67, 95% CI −0.08 to 1.41) than urban environments (β = −0.18, 95% CI −0.69 to 0.33). Though subscales generally saw higher scores during the pandemic than before, these were consistent with pre-pandemic trends, excepting a slight improvement in conduct problems (β = −0.26, 95% CI 0.12 to 0.40).

The study offers evidence among a representative sample that mental health difficulties did not, on average, deteriorate for adolescents during three months of the pandemic.

Mental ill-health has a major impact on young people, with pain often co-occurring. We estimated the prevalence and impact of pain in young people with mental ill-health.

Longitudinal data (baseline and three-month follow-up) of 1,107 Australian young people (aged 12–25 years) attending one of five youth mental health services. Multi-level linear mixed models estimated associations between pain characteristics (frequency, intensity, and limitations) and outcomes with false discovery rate (FDR) adjustment. Pain characteristics were baseline-centered to estimate if the baseline score (between-participant effect) and/or change from baseline (within-participant effect) was associated with outcomes.

At baseline, 16% reported serious pain more than 3 days, 51% reported at least moderate pain, and 25% reported pain-related activity limitations in the last week. Between participants, higher serious pain frequency was associated with greater anxiety symptoms (β[95%CI]: 0.90 [0.45, 1.35], FDR-p=0.001), higher pain intensity was associated with greater symptoms of depression (1.50 [0.71, 2.28], FDR-p=0.001), anxiety (1.22 [0.56, 1.89], FDR-p=0.002), and suicidal ideation (3.47 [0.98, 5.96], FDR-p=0.020), and higher pain limitations were associated with greater depressive symptoms (1.13 [0.63, 1.63], FDR-p<0.001). Within participants, increases in pain intensity were associated with increases in tobacco use risk (1.09 [0.48, 1.70], FDR-p=0.002), and increases in pain limitations were associated with increases in depressive symptoms (0.99 [0.54, 1.43], FDR-p<0.001) and decreases in social and occupational functioning (−1.08 [−1.78, −0.38], FDR-p=0.009).

One-in-two young people seeking support for mental ill-health report pain. Youth mental health services should consider integrating pain management.

Ultra-processed food (UPF) consumption varies with socio-economic status (SES) in adults, and evidence suggests that similar patterns exist in adolescents. However, the relationship remains understudied in this critical developmental group. This study aimed to further characterise adolescent UPF consumption and its relationship with SES by exploring dietary patterns within UPF consumption.

Using food-diary data, adolescents’ UPF intake was quantified and categorised. Principal component and clustering analysis were used to identify dietary patterns. Associations of these dietary patterns with socio-demographic characteristics were then analysed.

Pooled data from the rolling, cross-sectional National Diet and Nutrition Survey, waves 1-to-11 (2008–2019).

UK adolescents (11- to18-year-olds) (n 3199).

Three UPF dietary patterns were identified: (i) the ‘Restrictive’ pattern, which included the lowest total consumption of UPF (95 % CI: 33·1, 34·9 % g/d), but elevated consumption of UPF often perceived as healthy, was associated with adolescents of a higher SES; (ii) the ‘Permissive’ pattern included 61·6 % g/d (95 % CI: 60·3, 63·0 % g/d) total UPF, dominated by ‘ready-to-eat,’ low nutrient-density UPF, and was associated with adolescents of a lower SES and (iii) the ‘Traditional’ pattern had moderate consumption of total UPF (95 % CI: 47·6, 50·9 % g/d) with higher intake of UPF used in home-cooking and had less distinct associations with SES.

Results suggest that SES impacts both the amount and type of UPF consumed by adolescents in the UK, underscoring the importance of this factor when designing interventions. Distinct dietary patterns within adolescents’ high UPF diets have potential behavioural, nutritional and health implications.

Executive functioning (EF) impairments are widely known to represent transdiagnostic risk factors of psychopathology. However, a recent alternative account has been proposed, according to which EF impairments emerge as consequences of psychopathology.

Using a longitudinal cross-lagged panel network analysis approach, we tested these competing theoretical accounts at different stages during adolescence. We used data from the Brazilian High-Risk Cohort Study for the Development of Childhood Psychiatric Disorders, in which 61% of individuals at wave 1 were selected due to their high risk for psychopathology. Participants were assessed across three assessment waves during early (wave 1: n = 1,992, mean age = 10.20 years) and middle adolescence (wave 2: n = 1,633, mean age = 13.48 years; wave 3: n = 1,439, mean age = 18.20 years). We examined associations between working memory, inhibitory control, and broad-band measures of psychopathology.

During early adolescence, lower inhibitory control was a risk factor for externalizing problems that, in turn, predicted lower working memory capacity. During middle adolescence, bidirectional associations became more prominent: inhibitory control and working memory functioned as both risk factors and consequences. Externalizing problems both predicted and were predicted by poor inhibitory control. Internalizing and externalizing symptoms showed bidirectional associations over time. Externalizing problems predicted more internalizing symptoms, whereas internalizing symptoms predicted fewer externalizing problems during middle adolescence.

Our results corroborate dynamic theories that describe executive dysfunctions as precursors and consequences of psychopathology in middle adolescence.

This study aims to examine the different aspects of socio-economic status (SES) patterns in mental health from adolescence into adulthood by investigating the mean, prevalence, cumulative incidence and trajectories of several mental health measures, including depressive symptoms, mental disorder diagnosis and medication use. The different aspects of SES are investigated through the measures of subjective social status (SSS) in school, SSS in society, income and parental educational level.

Individuals born in 1989 were followed from 2004 to 2021 with surveys at ages 15, 18, 21, 28 and 32 years, supplied with yearly register data. The mean level of depressive symptoms, yearly prevalence of medication use and cumulative incidence of mental disorder diagnosis were calculated for each SES group (low, middle and high) across each measure. Group-Based Trajectory Modelling (GBTM) was used to identify depressive symptom trajectories and logistic regressions were used to analyse the relative odds ratios (ROR) of membership to the different trajectory groups by characteristics.

Individuals with low SES at age 15 years across all SES measures showed higher mean depressive symptoms, prevalence of medication use and cumulative incidence of mental disorder diagnosis through adolescence and adulthood (age 15–32 years). Four depressive symptom trajectories were identified: low stable, moderate stable, decreasing and increasing trajectories. Being female, receiving medication or a mental disorder diagnosis in early adulthood and during the study period, having low SSS in school, parents not living together, being bullied, lacking support from teachers or classmates, lower levels of parents’ support or higher school pressure resulted in higher RORs of membership to the other trajectory groups compared to the low stable trajectory, while having high SSS in society resulted in a lower ROR.

This is the first study to detect the role of social support in relation to depressive symptom trajectories. While individuals with low social status consistently experienced more negative mental health outcomes than those with middle and high social status in the study period (age 15–32 years), low SSS showed the strongest associations. This indicates that SSS may capture vulnerable individuals not identified by traditional SES. Being female, having low SES, low social support, and other mental health outcomes were associated with higher odds of being in trajectories with more depressive symptoms. Preventive initiatives should therefore target individuals with such characteristics. It is worth exploring whether adolescents with increasing depressive symptoms could benefit from increased social support.