Importance ADHD is now recognized to occur in adulthood and is associated with a range of negative outcomes. However, less is known about the prospective course of ADHD into adulthood, the risk factors for its persistence past childhood, and the possibility of its emergence in young adulthood in non-clinical populations. Objective To investigate childhood risk factors and young adult functioning of individuals with persistent, remitted and late-onset ADHD. Design, Setting and Participants The study sample is the Environmental Risk (E-Risk) Longitudinal Twin Study, a UK nationally-representative birth cohort of 2,232 twins born in England and Wales in 1994–1995. Main Outcome Measures ADHD diagnoses were assessed in childhood at ages 5, 7, 10, and 12 and in young adulthood at age 18. Childhood predictors included pre/perinatal factors, child clinical characteristics and aspects of the family environment. Age-18 outcomes included ADHD symptoms and associated impairment, overall functioning and other mental health disorders. Results Among individuals with childhood ADHD (n=247), 21.1% met diagnostic criteria for the disorder at age 18. Persistence was associated with higher levels of symptoms and lower IQ in childhood. Persistent individuals had more functional impairment and higher rates of other mental health disorders at age 18 compared to those who remitted. Among individuals with adult ADHD (n=162), 67.9% did not meet criteria for ADHD at any assessment at or prior to age 12. In childhood, individuals with late-onset ADHD showed fewer behavior problems and higher IQ compared to the persistent group; at age 18, they showed comparable ADHD symptoms and impairment and similarly elevated rates of mental health disorders compared to the persistent group. Conclusion and Relevance In this general population cohort, the persistence of ADHD was largely driven by childhood ADHD severity and poorer neuropsychological functioning. Additionally, we identified heterogeneity in the adult ADHD population such that this group consisted of a large late-onset ADHD group with no childhood diagnosis and minimal neuropsychological impairment, and a smaller group with persistent ADHD and associated neuropsychological impairment. Our findings call into question the conceptualization of adult ADHD as a childhood-onset neurodevelopmental disorder.

IMPORTANCE Mental health professionals typically encounter patients at 1 point in patients' lives.This cross-sectional window understandably fosters focus on the current presenting diagnosis.Research programs, treatment protocols, specialist clinics, and specialist journals are oriented to presenting diagnoses, on the assumption that diagnosis informs about causes and prognosis. This study tests an alternative hypothesis: people with mental disorders experience many different kinds of disorders across diagnostic families, when followed for 4 decades. OBJECTIVETo describe mental disorder life histories across the first half of the life course. DESIGN, SETTING, AND PARTICIPANTS This cohort study involved participants born in New Zealand from 1972 to 1973 who were enrolled in the population-representative Dunedin Study. Participants were observed from birth to age 45 years (until April 2019). Data were analyzed from May 2019 to January 2020. MAIN OUTCOMES AND MEASURES Diagnosed impairing disorders were assessed 9 times from ages 11 to 45 years. Brain function was assessed through neurocognitive examinations conducted at age 3 years, neuropsychological testing during childhood and adulthood, and midlife neuroimaging-based brain age. RESULTSOf 1037 original participants (535 male [51.6%]), 1013 had mental health data available.The proportions of participants meeting the criteria for a mental disorder were as follows: 35% (346 of 975) at ages 11 to 15 years, 50% (473 of 941) at age 18 years, 51% (489 of 961) at age 21 years, 48% (472 of 977) at age 26 years, 46% (444 of 969) at age 32 years, 45% (429 of 955) at age 38 years, and 44% (407 of 927) at age 45 years. The onset of the disorder occurred by adolescence for 59% of participants (600 of 1013), eventually affecting 86% of the cohort (869 of 1013) by midlife. By age 45 years, 85% of participants (737 of 869) with a disorder had accumulated comorbid diagnoses.

PurposeTo investigate the association between social isolation and loneliness, how they relate to depression, and whether these associations are explained by genetic influences.MethodsWe used data from the age-18 wave of the Environmental Risk Longitudinal Twin Study, a birth cohort of 1116 same-sex twin pairs born in England and Wales in 1994 and 1995. Participants reported on their levels of social isolation, loneliness and depressive symptoms. We conducted regression analyses to test the differential associations of isolation and loneliness with depression. Using the twin study design, we estimated the proportion of variance in each construct and their covariance that was accounted for by genetic and environmental factors.ResultsSocial isolation and loneliness were moderately correlated (r = 0.39), reflecting the separateness of these constructs, and both were associated with depression. When entered simultaneously in a regression analysis, loneliness was more robustly associated with depression. We observed similar degrees of genetic influence on social isolation (40 %) and loneliness (38 %), and a smaller genetic influence on depressive symptoms (29 %), with the remaining variance accounted for by the non-shared environment. Genetic correlations of 0.65 between isolation and loneliness and 0.63 between loneliness and depression indicated a strong role of genetic influences in the co-occurrence of these phenotypes.ConclusionsSocially isolated young adults do not necessarily experience loneliness. However, those who are lonely are often depressed, partly because the same genes influence loneliness and depression. Interventions should not only aim at increasing social connections but also focus on subjective feelings of loneliness.

SignificanceGenome-wide association study (GWAS) discoveries about educational attainment have raised questions about the meaning of the genetics of success. These discoveries could offer clues about biological mechanisms or, because children inherit genetics and social class from parents, education-linked genetics could be spurious correlates of socially transmitted advantages. To distinguish between these hypotheses, we studied social mobility in five cohorts from three countries. We found that people with more education-linked genetics were more successful compared with parents and siblings. We also found mothers’ education-linked genetics predicted their children’s attainment over and above the children’s own genetics, indicating an environmentally mediated genetic effect. Findings reject pure social-transmission explanations of education GWAS discoveries. Instead, genetics influences attainment directly through social mobility and indirectly through family environments.