Epidemiological evidence shows a concerning rise in youth mental health difficulties over the past three decades. Most evidence, however, comes from countries in Europe or North America, with far less known about changes in other global regions. This study aimed to compare adolescent mental health across two population-based cohorts in the UK, and two population-based cohorts in Pelotas, Brazil.

Four population-based cohorts with identical mental health measures were compared. In Brazil, these included the 1993 Pelotas Birth Cohort and the 2004 Pelotas Birth Cohort. In the UK, cohorts included the Avon Longitudinal Study of Parents and Children, and the Millennium Cohort Study. Mental health was measured in all cohorts using identical, parent-rated scores from the Strengths and Difficulties Questionnaire (SDQ). This was assessed in both countries over approximately the same time periods, when adolescents were aged 11 (2004 vs 2015 in Brazil, and 2003 vs 2012 in the UK), with follow-up analyses focused on outcomes in later adolescence.

Mental health problems were higher in the UK for adolescents born in the early 2000s compared to those born in the early 1990s. In Pelotas, the opposite was found, whereby problems were lower for adolescents born in the early 2000s compared to those born in the early 1990s. Despite these promising reductions in mental health problems in Pelotas over time, SDQ scores remained higher in Pelotas compared to the UK.

Our study represents the first to compare two population-based cohorts in the UK, and two population-based cohorts in Pelotas, Brazil, to understand how mental health problems have changed over time across the two settings. Our findings provide the most up-to-date insight into population-level rates of youth mental health problems in Pelotas, and shed novel insight into how these have changed over the last two decades in comparison to the UK. In doing so, our study provides a tentative first step towards understanding youth mental health over time at a more global scale, and presents a valuable opportunity to examine putative contributors to differences across time.

There is increasing evidence that childhood Attention-Deficit Hyperactivity Disorder (ADHD) elevates the risk of later Bipolar Spectrum Disorder (BD). However, it remains unclear whether different trajectories of ADHD symptoms confer differential risk for BD.

Data from the Avon Longitudinal Study of Parents and Children were available from 7811 children at age 8 years, 7435 at 10, 6798 at 13, and 1217 at 21–23 years. ADHD symptoms were assessed at 8, 10, and 13 years with the Development and Well-Being Assessment. Clinically significant hypomanic symptoms (CSHS) at 21–23 years were assessed using the Hypomania Symptom Checklist (HCL-32). Group trajectories of ADHD and its subtypes were estimated using latent class growth analysis. The prospective associations between different ADHD trajectories and CSHS were tested using logistic regression analysis.

Persistently high, increasing, remitting, and persistently low ADHD symptom trajectories were identified for the three ADHD-related categories. Individuals with persistently high and increasing levels of ADHD symptoms had increased odds of CSHS compared to persistently low class. Sensitivity analyses validated these results. In separate analyses, persistently high levels of hyperactivity and inattentive, and increasing levels of inattentive symptoms were also independently associated with CSHS.

Young people with a longitudinal pattern of high and increasing ADHD symptoms are at higher risk for developing CSHS in young adulthood compared to individuals with low symptom patterns. These two trajectories in childhood and adolescence may represent distinct phenotypic risk profiles for subsequently developing BD and be clinically significant targets for prevention and treatment of BD.

Individuals with borderline intellectual functioning and intellectual disabilities (intellectual impairment) may be at increased risk of psychosis. However, studies have been limited by small and selected samples. Moreover, the role of early life trauma, a key risk factor for psychosis, in the associations is unknown.

Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort, we investigated the associations between intellectual impairment, psychotic disorders, and psychotic experiences, and assessed the mediating role of trauma in childhood. Individuals with intellectual impairment were identified using a multisource measure utilizing indicators from ALSPAC combined with health and administrative records. Psychotic disorder diagnoses were extracted through linkage to primary care records. Psychotic experiences were assessed at ages 18 and 24 using the semi-structured Psychosis-Like Symptoms interview (PLIKSi). Trauma between ages 5 and 11 was assessed with questionnaires and interviews administered to children and parents at multiple ages. Multiple imputation was performed to mitigate bias due to missing data.

The maximum sample after multiple imputation was 9,407. We found associations between intellectual impairment and psychotic disorders (OR = 4.57; 95%CI: 1.56–13.39). Evidence was weaker in the case of psychotic experiences (OR = 1.63; 95%CI: 0.93–2.84). There was some evidence suggesting a mediating role of trauma in the associations between intellectual impairment and psychotic experiences (OR = 1.09; 95%CI: 1.03–1.15). Complete records analyses yielded comparable estimates.

Intellectual impairment is associated with psychotic disorders and experiences in adulthood. Research into the contribution of trauma could shape intervention strategies for psychotic disorders in this population.

Early pubertal timing is associated with depressive symptoms in girls, but studies in boys are limited and have yielded conflicting results.

N = 4,664 male participants from a UK birth cohort (Avon Longitudinal Study of Parents and Children – ALSPAC). Seven indicators of pubertal timing were measured repeatedly from 7 to 17 years (age at: peak height velocity, peak weight velocity, peak bone mineral content velocity, Tanner stage 3 pubic hair, Tanner stage 3 genitalia, axillary hair, and voice break), categorised into ‘early’, ‘on-time,’ and ‘late’ (mean ± 1 SD). Depressive symptoms (binary variable indicating higher versus lower levels) were assessed at 14 and 18 years, and depression (ICD-10 diagnosis) was assessed at 18 years. Multivariable logistic regression was used to examine associations between each indicator of pubertal timing and depressive symptoms/depression, adjusted for socioeconomic status (SES) and prepubertal body mass index (BMI).

Compared to males with normative pubertal development, the odds of depression at age 18 were higher in those with early age at peak height velocity (OR: 2.06; 95% CI 1.27–3.34), early age at peak weight velocity (OR: 2.10; 95% CI 1.16–3.79), and early age at Tanner genitalia stage 3 (OR: 1.81; 95% CI 1.01–3.26). There was no evidence for associations between pubertal timing and depressive symptoms at age 14 or 18.

We found evidence that males with an earlier pubertal timing had increased odds of depression at age 18. Early maturing boys could be targeted for interventions aimed at preventing depression.

Peripheral inflammatory markers, including serum interleukin 6 (IL-6), are associated with depression, but less is known about how these markers associate with depression at different stages of the life course.

We examined the associations between serum IL-6 levels at baseline and subsequent depression symptom trajectories in two longitudinal cohorts: ALSPAC (age 10–28 years; N = 4,835) and UK Biobank (39–86 years; N = 39,613) using multilevel growth curve modeling. Models were adjusted for sex, BMI, and socioeconomic factors. Depressive symptoms were measured using the Short Moods and Feelings Questionnaire in ALSPAC (max time points = 11) and the Patient Health Questionnaire-2 in UK Biobank (max time points = 8).

Higher baseline IL-6 was associated with worse depression symptom trajectories in both cohorts (largest effect size: 0.046 [ALSPAC, age 16 years]). These associations were stronger in the younger ALSPAC cohort, where additionally higher IL-6 levels at age 9 years was associated with worse depression symptoms trajectories in females compared to males. Weaker sex differences were observed in the older cohort, UK Biobank. However, statistically significant associations (pFDR <0.05) were of smaller effect sizes, typical of large cohort studies.

These findings suggest that systemic inflammation may influence the severity and course of depressive symptoms across the life course, which is apparent regardless of age and differences in measures and number of time points between these large, population-based cohorts.

Markers of inflammation and cannabis exposure are associated with an increased risk of mental disorders. In the current study, we investigated associations between cannabis use and biomarkers of inflammation.

Utilizing a sample of 914 participants from the Avon Longitudinal Study of Parents and Children, we investigated whether interleukin-6 (IL-6), tumor necrosis factor α (TNFα), C-reactive protein (CRP), and soluble urokinase plasminogen activator receptor (suPAR) measured at age 24 were associated with past year daily cannabis use, less frequent cannabis use, and no past year cannabis use. We adjusted for a number of covariates including sociodemographic measures, body mass index, childhood trauma, and tobacco smoking. We found evidence of a strong association between daily or near daily cannabis use and suPAR.

We did not find any associations between less frequent cannabis use and suPAR. We did not find evidence of an association between IL-6, TNFα or CRP, and cannabis use.

Our finding that frequent cannabis use is strongly associated with suPAR, a biomarker of systemic chronic inflammation implicated in neurodevelopmental and neurodegenerative processes is novel. These findings may provide valuable insights into biological mechanisms by which cannabis affects the brain and impacts the risk of serious mental disorders.

Suicide is one of the major causes of premature death in patients diagnosed with a schizophrenia-spectrum psychotic disorder. However, associations between psychotic-like experiences in youth and suicidality in later life remain under-researched.

We aimed to investigate any associations between early experiences of thought interference and auditory-verbal hallucinations (AVHs) with first-rank symptoms of schizophrenia and suicidal thoughts and behaviours in adulthood.

This study used data from the Avon Longitudinal Study of Parents and Children (ALSPAC). We calculated combined thought interference score at ages 11 years 8 months, 13 years 1 month, 14 years 1 month and 16 years 6 months. We also assessed AVHs at the same age points. For outcome variables, we used specific variables measuring delusions of control, AVHs and suicidality at 24 years of age. We carried out logistic regressions and mediation analyses to assess the relationships among these variables.

Thought interference and AVHs at all ages throughout childhood and adolescence were associated with suicidal thoughts and behaviours, and also with clinically more significant symptoms of delusions of control and AVHs at age 24. Substance use-induced psychotic-like experiences mediated a large proportion of the relationship between early psychotic-like experiences and suicidality in later life.

Thought interference and AVHs in childhood and adolescence are associated with first-rank symptoms and suicidality in adulthood. Mental health interventions in children and adolescents need to take into account the impact of specific psychotic-like experiences and allow for the early detection of thought interference and AVH-related symptoms.

Identifying children and/or adolescents who are at highest risk for developing chronic depression is of utmost importance, so that we can develop more effective and targeted interventions to attenuate the risk trajectory of depression. To address this, the objective of this study was to identify young people with persistent depressive symptoms across adolescence and young adulthood and examine the prospective associations between factors and persistent depressive symptoms in young people.

We used data from 6711 participants in the Avon Longitudinal Study of Parents and Children. Depressive symptoms were assessed at 12.5, 13.5, 16, 17.5, 21 and 22 years with the Short Mood and Feelings Questionnaire, and we further examined the influence of multiple biological, psychological and social factors in explaining chronic depressive symptoms.

Using latent class growth analysis, we identified four trajectories of depressive symptoms: persistent high, persistent low, persistent moderate and increasing high. After applying several logistic regression models, we found that loneliness and feeling less connected at school were the most relevant factors for chronic course of depressive symptoms.

Our findings contribute with the identification of those children who are at highest risk for developing chronic depressive symptoms.

Depression is a common mental health disorder that often starts during adolescence, with potentially important future consequences including ‘Not in Education, Employment or Training’ (NEET) status.

We took a structured life course modeling approach to examine how depressive symptoms during adolescence might be associated with later NEET status, using a high-quality longitudinal data resource. We considered four plausible life course models: (1) an early adolescent sensitive period model where depressive symptoms in early adolescence are more associated with later NEET status relative to exposure at other stages; (2) a mid adolescent sensitive period model where depressive symptoms during the transition from compulsory education to adult life might be more deleterious regarding NEET status; (3) a late adolescent sensitive period model, meaning that depressive symptoms around the time when most adults have completed their education and started their careers are the most strongly associated with NEET status; and (4) an accumulation of risk model which highlights the importance of chronicity of symptoms.

Our analysis sample included participants with full information on NEET status (N = 3951), and the results supported the accumulation of risk model, showing that the odds of NEET increase by 1.015 (95% CI 1.012–1.019) for an increase of 1 unit in depression at any age between 11 and 24 years.

Given the adverse implications of NEET status, our results emphasize the importance of supporting mental health during adolescence and early adulthood, as well as considering specific needs of young people with re-occurring depressed mood.

Emotional problems, especially anxiety, have become increasingly common in recent generations. Few population-based studies have examined trajectories of emotional problems from early childhood to late adolescence or investigated differences in psychiatric and functional outcomes.

Using the Avon Longitudinal Study of Parents and Children (ALSPAC, n = 8286, 50.4% male), we modeled latent class growth trajectories of emotional problems, using the parent-reported Strength and Difficulties Questionnaire emotional scale (SDQ-E) on seven occasions (4–17 years). Psychiatric outcomes in young adulthood (21–25 years) were major depressive disorder (MDD), generalized anxiety disorder (GAD), and self-harm. Functional outcomes were exam attainment, educational/occupational status, and social relationship quality.

We identified four classes of emotional problems: low (67.0%), decreasing (18.4%), increasing (8.9%), and persistent (5.7%) problems. Compared to those in the low class, individuals with decreasing emotional problems were not at elevated risk of any poor adult outcome. Individuals in the increasing and persistent classes had a greater risk of adult MDD (RR: 1.59 95% CI 1.13–2.26 and RR: 2.25 95% CI 1.49–3.41) and self-harm (RR: 2.37 95% CI 1.91–2.94 and RR: 1.87 95% CI 1.41–2.48), and of impairment in functional domains. Childhood sleep difficulties, irritability, conduct and neurodevelopmental problems, and family adversity were associated with a persistent course of emotional problems.

Childhood emotional problems were common, but those whose symptoms improved over time were not at increased risk for adverse adult outcomes. In contrast, individuals with persistent or adolescent-increasing emotional problems had a higher risk of mental ill-health and social impairment in young adulthood which was especially pronounced for those with persistent emotional problems.

Maternal anxiety, depression, and stress during and after pregnancy are negatively associated with child cognitive development. However, the contribution of positive maternal experiences, such as social support, to child cognitive development has received less attention. Furthermore, how maternal experience of social support during specific developmental periods impacts child cognitive development is largely unknown.

Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC; n = 5784) and the Prediction and Prevention of Preeclampsia and Intrauterine Growth Restriction study (PREDO; n = 420), we investigated the associations between maternal perceived social support during and after pregnancy and child's general cognitive ability at 8 years of age, assessed with the Wechsler Intelligence Scale for Children (WISC). Bayesian relevant life course modeling was used to investigate timing effects of maternal social support on child cognitive ability.

In both cohorts, higher maternal perceived social support during pregnancy was associated with higher performance on the WISC, independent of sociodemographic factors and concurrent maternal symptoms of depression and anxiety. In ALSPAC, pregnancy emerged as a sensitive period for the effects of perceived social support on child cognitive ability, with a stronger effect of social support during pregnancy than after pregnancy on child cognitive ability.

Our findings, supported from two prospective longitudinal cohorts, suggest a distinct role of maternal perceived social support during pregnancy for cognitive development in children. Our study suggests that interventions aimed at increasing maternal social support during pregnancy may be an important strategy for promoting maternal and child well-being.

Girls who experience an earlier onset of menarche than their peers are at increased risk of depressive symptoms in mid-adolescence, but it is unclear if this association persists into adulthood. This study examines whether longitudinal patterns of depressive symptoms from adolescence to adulthood vary according to timing of menarche.

About 4,864 female participants in the UK Avon Longitudinal Study of Parents and Children provided data on age at onset of menarche (assessed in repeated questionnaires from 8 to 17 years) and depressive symptoms across nine time points (13 to 26 years) using the Short Mood and Feelings Questionnaire. We compared patterns of depressive symptoms in girls with ‘early’ (<11.5 years), ‘normative’ (11.5 to 13.5 years) and ‘late’ (≥13.5 years) menarche using a linear spline multilevel growth curve model adjusted for indicators of socioeconomic position, father absence and body mass index.

Early, compared with normative, menarche was associated with higher levels of depressive symptoms at age 14 (imputed adjusted estimated difference = 0.94, 95% confidence interval [CI] = 0.44, 1.45), but the association attenuated at 24 years (0.24 [−0.72, 1.19]). Late menarche, compared with normative, was associated with a lower level of depressive symptoms at age 14 (−0.69 [−1.10, −0.29]), but this association also attenuated at 24 years (−0.15 [−0.92, 0.62]).

This study did not find a persistent effect of early menarche, compared to normative, on depressive symptoms. However, our findings are consistent with the level of depressive symptoms increasing at the onset of menarche irrespective of timing. The late onset girls ‘catch up’ with their peers who experience menarche earlier in terms of depressive symptoms. Future studies should continue to assess the impact of timing of menarche further into adulthood.

Religious/spiritual beliefs and behaviours (RSBB) have been associated with health outcomes, with diet a potential mediator of this relationship. We therefore explored whether RSBB were associated with differences in diet.

Dietary patterns and nutrient intakes were derived from food frequency questionnaire completed by pregnant women in 1991–1992 (mean age = 28·3 years, range = 15–46) and by the mothers and partners 4 years post-partum (mothers mean age = 32·3, range = 19–49; partners mean age = 34·5, range = 18–74). RSBB exposures measured in pregnancy included religious belief, affiliation and attendance. We first explored whether RSBBs were associated with dietary patterns in confounder-adjusted linear regression models. If associations were found, we examined whether RSBB were associated with nutrient intake (linear regression) and following nutrient intake guidelines (logistic regression).

Prospective birth cohort study in Southwest England (Avon Longitudinal Study of Parents and Children; ALSPAC).

13 689 enrolled mothers and their associated partners.

In pregnant women, RSBB were associated with higher ‘traditional’ (i.e. ‘meat and two veg’) and lower ‘vegetarian’ dietary pattern scores. Religious attendance and non-Christian religious affiliation were associated with higher ‘health-conscious’ dietary pattern scores. Religious attendance was associated with increased micronutrient intake and following recommended micronutrient intake guidelines, with weaker effects for religious belief and affiliation. Comparable patterns were observed for mothers and partners 4 years post-partum, although associations between RSBB and nutrient intakes were weaker for partners.

RSBBs are associated with broad dietary patterns and nutrient intake in this cohort. If these reflect causal relationships, diet may potentially mediate the pathway between RSBB and health.

Bereaved youth are at greater risk for adverse mental health outcomes, yet less is known about how social context shapes health for bereaved children. Ecosocial theory is employed to conceptualize bereavement in the context of sociodemographic factors.

This longitudinal study used data from the Avon Longitudinal Study of Parents and Children. Of the 15,454 pregnancies enrolled, 5050 youth were still enrolled at age 16.5 and completed self-report questionnaires on life events and emotional/behavioral symptoms.

Sociodemographic precursors associated with parent, sibling, or close friend bereavement included maternal smoking, parental education levels, and financial difficulties. The significant yet small main effect of higher cognitive ability, assessed at age 8, on reduced emotional/behavioral symptoms at age 16.5 (β = −0.01, SE = 0.00, p < 0.001) did not interact with bereavement. Bereavement of a parent, sibling, or close friend was associated with a 0.19 point higher emotional/behavioral symptom log score compared to non-bereaved youth (95% CI: 0.10–0.28), across emotional, conduct, and hyperactivity subscales.

Descriptive findings suggest sociodemographic precursors are associated with bereavement. While there was an association between the bereavement of a parent, sibling, or close friend and elevated emotional/behavioral symptoms, cognitive ability did not moderate that effect.

Previous research has examined the role of parental religious belief in offspring mental health, but has revealed inconsistent results, and suffered from a number of limitations. The aim of this study is to examine the prospective relationship between maternal religiosity and offspring mental health and psychosocial outcomes.

We used latent classes of religious belief (Highly religious, Moderately religious, Agnostic, Atheist) in mothers from the Avon Longitudinal Study of Parents and Children from 1990, and examined their association with parent-reported mental health outcomes and self-reported psychosocial outcomes in their children at age 7–8 (n = 6079 for mental health outcomes and n = 5235 for psychosocial outcomes). We used inverse probability weighted multivariable logistic regression analysis adjusted for maternal mental health, adverse childhood experience, and socioeconomic variables.

There was evidence for a greater risk of internalising problems among the offspring of the Highly religious and Moderately religious classes [e.g. for depression; OR 1.40. 95% CI (1.07–1.85), OR 1.48, 95% CI (1.17–1.87)], and greater risk of externalising problems in the offspring of the Atheist class [e.g. for ADHD; OR 1.41, 95% CI (1.08–1.85)], compared to the offspring of the Agnostic class.

These novel findings provide evidence associations between maternal religiosity and offspring mental health differ when examined using a person-centred approach, compared to the previously used variable-centred approaches. Our findings also suggest that differences may exist in the relationship between religious (non)belief and mental health variables when comparing the UK and US.

The aetiology of dual harm (co-occurring self-harm and violence towards others) is poorly understood because most studies have investigated self-harm and violence separately. We aimed to examine childhood risk factors for self-harm, violence, and dual harm, including the transition from engaging in single harm to dual harm.

Data from the Avon Longitudinal Study of Parents and Children, a UK-based birth cohort study, were used to estimate prevalence of self-reported engagement in self-harm, violence, and dual harm at ages 16 and 22 years. Risk ratios were calculated to indicate associations across various self-reported childhood risk factors and risks of single and dual harm, including the transition from single harm at age 16 years to dual harm at age 22.

At age 16 years, 18.1% of the 4176 cohort members had harmed themselves, 21.1% had engaged in violence towards others and 3.7% reported dual harm. At age 22 the equivalent prevalence estimates increased to 24.2, 25.8 and 6.8%, respectively. Depression and other mental health difficulties, drug and alcohol use, witnessing self-harm and being a victim of, or witnessing, violence were associated with higher risks of transitioning from self-harm or violence at age 16 to dual harm by age 22.

Prevalence of dual harm doubled from age 16 to 22 years, highlighting the importance of early identification and intervention during this high-risk period. Several childhood psychosocial risk factors associated specifically with dual harm at age 16 and with the transition to dual harm by age 22 have been identified.

Mother and father depression symptoms often co-occur, and together can have a substantial impact on child emotional well-being. Little is understood about symptom-level mechanisms underlying the co-occurrence of depression symptoms within families.

The objective was to use network analysis to examine depression symptoms in mothers and fathers after having a baby, and emotional symptoms in children in early adolescence.

We examined data from 4492 mother–father–child trios taken from a prospective, population-based cohort in the UK. Symptoms were examined using two unregularised partial correlation network models. The initial model was used to examine the pattern of associations, i.e. the overall network structure, for mother and father depression symptoms, and then to identify bridge symptoms that reinforce depression symptoms between parents during offspring infancy. The second model examined associations between the parent symptom network, including bridge symptoms, with later child emotional difficulties.

The study included 4492 mother–father–child trios; 2204 (49.1%) children were female. Bridge symptoms reinforcing mother and father depression symptoms were feeling guilty and self-harm ideation. For mothers, the bridge symptom of feeling guilty, and symptoms of anhedonia, panic and sadness were highly connected with child emotional difficulties. For fathers, the symptom of feeling overwhelmed associated with child emotional difficulties. Guilt and anhedonia in fathers appeared to indirectly associate with child emotional difficulties through the same symptom in mothers.

Our findings suggest that specific symptom cascades are central for co-occurring depression in parents and increased vulnerability in children, providing potential therapeutic targets.