There is an unprecedented societal focus on young people’s mental health, including efforts to expand access to child and adolescent mental health services (CAMHS). There has, however, been a lack of research to date to investigate adult mental health outcomes of young people who attend CAMHS.

We linked Finland’s healthcare registries for all individuals born between 1987 and 1992. We investigated mental disorder diagnoses recorded in specialist adult mental health services (AMHS) and both inpatient and outpatient service use by age 29 (December 31, 2016) for former CAMHS patients.

Before the end of their 20s, more than half (52.4%, n = 21,183) of all CAMHS patients had gone on to attend AMHS. The most prevalent recorded adult psychiatric diagnoses received by former CAMHS patients were depressive disorders (30%, n = 11,768), non-phobic anxiety disorders (21%, n = 7,910), alcohol use disorders (9.5%, n = 3,427), personality disorders (9.3%, n = 3,366), and schizophrenia-spectrum disorders (7.6%, n = 2,945). In the total population, more than half of all AMHS appointments (53.1%, k = 714,239/1,345,060) were for former CAMHS patients. More than half of all inpatient psychiatry bed days were for former CAMHS patients (53.1%, k = 1,192,991/2,245,247).

While there is a strong focus on intervening in childhood and adolescence to reduce the burden of mental illness, these findings suggest that young people who receive childhood intervention very frequently continue to require specialist psychiatric interventions in adulthood, including taking up a majority of both outpatient and inpatient service use. These findings highlight the need for a greater focus on research to alter the long-term trajectories of CAMHS patients.

Emotional neglect means that the child’s emotional and developmental needs are not fulfilled by the parents or other caregivers. Adverse childhood events (ACEs) are a risk factor for mental health problems and impaired parenting skills. The objective here was to examine whether parents’ ACEs increase the child’s risk of experiencing emotional neglect.

The participants in the present study were members of the Northern Finland Birth Cohort 1986 (NFBC1986). Emotional neglect experiences were measured in 190 members of this cohort by means of the Trauma and Distress Scale (TADS), and ACEs in both parents were measured with a specific questionnaire. A linear regression model was used to examine the association between parents’ ACEs and the children’s emotional neglect scores.

The children’s mean emotional neglect score was 8.11 on a scale from 5 to 25. There was no significant difference between males (mean 8.01) and females (mean 8.19). Only father’s ACEs were associated with child’s emotional neglect score. In the linear regression model, the children’s emotional neglect scores increased by 0.3 points for father’s ACE.

Our findings suggest that father’s ACEs may increase the child’s risk of experiencing emotional neglect. It seems that childhood adversities are transferred from parents to children, but larger samples would be needed to confirm these findings.

People with severe mental illness (SMI) have an elevated risk of obesity but the causes and mechanisms are unclear. We explored the familial association between parental SMI and body mass index (BMI) in middle-aged offspring. Our objective was to determine if the offspring of either parent with SMI have an increased risk for obesity.

The Northern Finland Birth Cohort 1966 is a cohort study of offspring with expected date of birth in 1966. The data include originally 12 068 mothers and 12 231 children from the provinces of Lapland and Oulu in Finland. The final study sample included 5050 middle-aged offspring. Parental SMI was used as exposure in the study. BMI measured at the age of 46 years was used as a primary outcome.

Risk for obesity was elevated in the offspring of mothers with SMI [overweight: adjusted odds ratio (OR) 1.93 (1.29–2.90), obese class I: 1.97 (1.20–3.25), obese classes II–III: 2.98 (1.67–5.33)]. For the offspring of either parent with SMI, statistically significant results were found in obese class I and obese classes II–III [overweight: adjusted OR 1.21 (0.94–1.54), obese class I: 1.52 (1.03–1.08), obese classes II–III: 1.53 (1.01–2.32)].

We found an elevated risk of obesity in the middle-aged offspring of either parent with SMI, especially in the offspring of mothers with SMI. Thus, there might be a common familial pathway leading to the co-occurrence of obesity and SMI.

Studies on the transmission of suicide risk have focused on parental history of suicide attempts (SAs), overlooking when the attempt happened. This study examined how the offspring's risk of attempting or dying by suicide varied by the timing of a first parental SA and the sex of the parent who attempted suicide.

Participants were 59 469 members of the 1987 Finnish Birth Cohort. The Finnish Hospital Discharge and Cause of Death Registers were the sources for parental and offspring SAs and offspring suicide. Timing of parental SA was coded as before (pre-pregnancy and pregnancy) and after the child's birth [infant/toddler years (0–2 years), childhood (3–11 years), adolescence (12–17 years), and young adulthood (18–26 years)].

In the multivariate models, having a parent who attempted suicide increased the offspring's risk of attempting suicide (odds ratio (OR) = 1.77, 95% confidence interval (CI) 1.39–2.25), but not of dying by suicide. Compared to unexposed offspring, those exposed after child's birth were at higher risk of attempting suicide (OR = 1.90, 95% CI 1.46–2.47), specifically when the parent attempted during offspring's childhood, adolescence, and young adulthood. A first maternal SA increased offspring's risk of attempting suicide regardless of the timing.

The impact of a parental SA on offspring's risk of attempting suicide differed depending on the timing and sex of the parent who attempted suicide, suggesting that the transmission of suicide risk may occur through genetic as well as environmental factors. Our findings call for an intergenerational approach in suicide risk assessment.

Psychoses, especially schizophrenia, are often preceded by cognitive deficits and psychosis risk states. Altered metabolic profiles have been found in schizophrenia. However, the associations between metabolic profiles and poorer cognitive performance and psychosis risk in the population remain to be determined.

Detailed molecular profiles were measured for up to 8976 individuals from two general population-based prospective birth cohorts: the Northern Finland Birth Cohort 1986 (NFBC 1986) and the Avon Longitudinal Study of Parents and Children (ALSPAC). A high-throughput nuclear magnetic resonance spectroscopy platform was used to quantify 70 metabolic measures at age 15–16 years in the NFBC 1986 and at ages 15 and 17 years in ALSPAC. Psychosis risk was assessed using the PROD-screen questionnaire at age 15–16 years in the NFBC 1986 or the psychotic-like symptoms assessment at age 17 years in ALSPAC. Cognitive measures included academic performance at age 16 years in both cohorts and general intelligence and executive function in ALSPAC. Logistic regression measured cross-sectional and longitudinal associations between metabolic measures and psychosis risk and cognitive performance, controlling for important covariates.

Seven metabolic measures, primarily fatty acid (FA) measures, showed cross-sectional associations with general cognitive performance, four across both cohorts (low density lipoprotein diameter, monounsaturated FA ratio, omega-3 ratio and docosahexaenoic acid ratio), even after controlling for important mental and physical health covariates. Psychosis risk showed minimal metabolic associations.

FA ratios may be important in marking risk for cognitive deficits in adolescence. Further research is needed to clarify whether these biomarkers could be causal and thereby possible targets for intervention.

Although schizotypal traits, such as anhedonia and aberrant perceptions, may increase the risk for schizophrenia-spectrum disorders, little is known about early-life characteristics that predict more pronounced schizotypal traits.

To examine whether birth size or several other early-life factors that have been previously linked with schizophrenia predict schizotypal traits in adulthood.

Participants of the Northern Finland 1966 Birth Cohort Study (n = 4976) completed a questionnaire on positive and negative schizotypal traits at the age of 31 years.

Lower placental weight, lower birth weight and smaller head circumference at 12 months predicted elevated positive schizotypal traits in women after adjusting for several confounders (P<0.02). Moreover, higher gestational age, lower childhood family socioeconomic status, undesirability of pregnancy, winter/autumn birth, higher birth order and maternal smoking during pregnancy predicted some augmented schizotypal traits in women, some in men and some in both genders.

The results point to similarities in the aetiology of schitzotypal traits and schizophrenia-spectrum disorders.

Subtle motor, emotional, cognitive and behavioural abnormalities are often present in apparently healthy individuals who later develop schizophrenia, suggesting that some aspects of causation are established before overt psychosis.

To outline the development of schizophrenia.

We drew on evidence from The Northern Finland 1966 Birth Cohort supplemented by selected findings from other relevant literature.

The main known risk factors in development of schizophrenia are genetic causes, pregnancy and delivery complications, slow neuromotor development, and deviant cognitive and academic performance. However, their effect size and predictive power are small.

No powerful risk factor, premorbid sign or risk indicator has been identified that is useful for the prediction of schizophrenia in the general population.

The aim was to give estimates of the incidence of different mental disorders from a Finnish prospective epidemiological follow-up study, the UKKI Study.

The original probability sample consisted of 1000 persons, aged 15–64 years. The baseline survey took place in 1969–71, and follow-up surveys were conducted 5 and 16 years after the baseline survey. The research methods included a personal psychiatric interview and data collection from different registers. The diagnostic system was based on the ICD–8 classification.

The estimated annual incidence of all mental disorders was close to 15 per 1000 both between baseline and the 5-year follow-up as well as between the 5-year and the 16-year follow-up. During the entire 16-year follow-up period the annual incidence of all disorders was 14 per 1000 in men and 17 per 1000 in women. The annual incidence of neurotic disorders was 10 per 1000 in men and 14 per 1000 in women, and that of psychotic disorders 2 per 1000.

In the literature, there are huge differences in the results concerning incidence of mental disorders. The results of the present study were rather close to those of the Swedish Lundby Study, but nowhere near the results of the American ECA Study.