Associations of hospital-treated infections with subsequent dementia: nationwide 30-year analysis.

Infections, which can prompt neuroinflammation, may be a risk factor for dementia1-5. More information is needed concerning associations across different infections and different dementias, and from longitudinal studies with long follow-ups. This New Zealand-based population register study tested whether infections antedate dementia across three decades. We identified individuals born between 1929 and 1968 and followed them from 1989 to 2019 (n = 1,742,406, baseline age = 21-60 years). Infection diagnoses were ascertained from public hospital records. Dementia diagnoses were ascertained from public hospital, mortality and pharmaceutical records. Relative to individuals without an infection, those with an infection were at increased risk of dementia (hazard ratio 2.93, 95% confidence interval 2.68-3.20). Associations were evident for dementia diagnoses made up to 25-30 years after infection diagnoses. Associations held after accounting for preexisting physical diseases, mental disorders and socioeconomic deprivation. Associations were evident for viral, bacterial, parasitic and other infections, and for Alzheimer's disease and other dementias, including vascular dementia. Preventing infections might reduce the burden of neurodegenerative conditions.

Midlife diseases of despair and cardiometabolic risk: testing shared origins in adolescent psychopathology.

BACKGROUND: Rising midlife mortality in the United States is largely attributable to 'deaths of despair' (deaths from suicide, drug poisonings, and alcohol-related diseases) and deaths from cardiometabolic conditions. Although despair- and cardiometabolic-related mortality are increasing concurrently, it is unclear whether they share common developmental origins. We tested adolescent psychopathology as a potential common origin of midlife diseases of despair and cardiometabolic risk. METHODS: Participants (N = 4578) were from the National Longitudinal Study of Adolescent to Adult Health, a nationally representative cohort followed from adolescence to early midlife. Adolescent psychopathology included depression, anxiety, eating disorders, PTSD, conduct disorder, and ADHD at ages 11-18. Diseases of despair (suicidality, substance misuse, pain, and sleep problems) and cardiometabolic risk (hypertension, hyperlipidemia, high-risk waist circumference, diabetes, and cardiovascular conditions) were multi-modally measured at ages 33-43. RESULTS: At midlife, adolescents who experienced psychopathology exhibited more indicators of despair-related diseases and cardiometabolic risk (IRRs = 1.67 [1.46-1.87] and 1.13 [1.04-1.21], respectively), even after accounting for demographics, adolescent SES, and adolescent cognitive ability. Associations were evident for internalizing and externalizing conditions, and in a dose-response fashion. In mediation analyses, low education explained little of these associations, but early-adult substance use explained 21.5% of psychopathology's association with despair-related diseases. Midlife despair-related diseases and cardiometabolic risk co-occurred within individuals (IRR = 1.12 [1.08-1.16]). Adolescent psychopathology accounted for 8.3% of this co-occurrence, and 16.7% together with adolescent SES and cognitive ability. CONCLUSIONS: Adolescent psychopathology precedes both diseases of despair and cardiometabolic risk. Prevention and treatment of psychopathology may mitigate multiple causes of poor midlife health, reducing premature mortality.

Exposure to community violence as a mechanism linking neighborhood socioeconomic disadvantage and neural responses to reward.

A growing literature links socioeconomic disadvantage and adversity to brain function, including disruptions in reward processing. Less research has examined exposure to community violence (ECV) as a specific adversity related to differences in reward-related brain activation, despite the prevalence of community violence exposure for those living in disadvantaged contexts. The current study tested whether ECV was associated with reward-related ventral striatum (VS) activation after accounting for familial factors associated with differences in reward-related activation (e.g. parenting and family income). Moreover, we tested whether ECV is a mechanism linking socioeconomic disadvantage to reward-related activation in the VS. We utilized data from 444 adolescent twins sampled from birth records and residing in neighborhoods with above-average levels of poverty. ECV was associated with greater reward-related VS activation, and the association remained after accounting for family-level markers of disadvantage. We identified an indirect pathway in which socioeconomic disadvantage predicted greater reward-related activation via greater ECV, over and above family-level adversity. These findings highlight the unique impact of community violence exposure on reward processing and provide a mechanism through which socioeconomic disadvantage may shape brain function.

Dementia, dementia's risk factors and premorbid brain structure are concentrated in disadvantaged areas: National register and birth-cohort geographic analyses.

INTRODUCTION: Dementia risk may be elevated in socioeconomically disadvantaged neighborhoods. Reasons for this remain unclear, and this elevation has yet to be shown at a national population level. METHODS: We tested whether dementia was more prevalent in disadvantaged neighborhoods across the New Zealand population (N = 1.41 million analytic sample) over a 20-year observation. We then tested whether premorbid dementia risk factors and MRI-measured brain-structure antecedents were more prevalent among midlife residents of disadvantaged neighborhoods in a population-representative NZ-birth-cohort (N = 938 analytic sample). RESULTS: People residing in disadvantaged neighborhoods were at greater risk of dementia (HR per-quintile-disadvantage-increase = 1.09, 95% confidence interval [CI]:1.08-1.10) and, decades before clinical endpoints typically emerge, evidenced elevated dementia-risk scores (CAIDE, LIBRA, Lancet, ANU-ADRI, DunedinARB; ß's 0.31-0.39) and displayed dementia-associated brain structural deficits and cognitive difficulties/decline. DISCUSSION: Disadvantaged neighborhoods have more residents with dementia, and decades before dementia is diagnosed, residents have more dementia-risk factors and brain-structure antecedents. Whether or not neighborhoods causally influence risk, they may offer scalable opportunities for primary dementia prevention.

Peer connectedness and substance use in adolescence: A systematic review and meta-analysis.

OBJECTIVE: Adolescents' relationships with their peers play a pivotal role in their substance-use behaviors. As such, decades of research have examined how substance use relates to adolescents' overall levels of closeness to their peers, here termed peer connectedness, with mixed results. This report sought to determine how the operationalizations of peer connectedness and substance use affect the nature of the relationship between them. METHOD: We used a systematic review strategy to find a comprehensive set of studies investigating the relationship between peer connectedness and substance use. Three-level meta-analytic regression was used to empirically test whether the operationalization of these variables moderates effect sizes across studies. RESULTS: We found 147 studies, of which 128 were analyzed using multilevel meta-analytic regression models. Operationalizations of peer connectedness varied widely, encompassing sociometric and self-report measures. Of these measures, sociometric indices specifically pertaining to popularity were most strongly predictive of substance use. Less consistent relationships were observed between substance use and sociometric measures of friendship, as well as with self-report measures. CONCLUSIONS: Being perceived as popular by one's peers is positively related to substance use among adolescents. This relationship is stronger and more consistent than those between substance use and other peer-connectedness variables, underscoring the necessity of operationalizing these constructs specifically and clearly. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Suicides, drug poisonings, and alcohol-related deaths cluster with health and social disadvantage in 4.1 million citizens from two nations.

BACKGROUND: Deaths from suicides, drug poisonings, and alcohol-related diseases ('deaths of despair') are well-documented among working-age Americans, and have been hypothesized to be largely specific to the U.S. However, support for this assertion-and associated policies to reduce premature mortality-requires tests concerning these deaths in other industrialized countries, with different institutional contexts. We tested whether the concentration and accumulation of health and social disadvantage forecasts deaths of despair, in New Zealand and Denmark. METHODS: We used nationwide administrative data. Our observation period was 10 years (NZ = July 2006-June 2016, Denmark = January 2007-December 2016). We identified all NZ-born and Danish-born individuals aged 25-64 in the last observation year (NZ = 1 555 902, Denmark = 2 541 758). We ascertained measures of disadvantage (public-hospital stays for physical- and mental-health difficulties, social-welfare benefit-use, and criminal convictions) across the first nine years. We ascertained deaths from suicide, drugs, alcohol, and all other causes in the last year. RESULTS: Deaths of despair clustered within a population segment that disproportionately experienced multiple disadvantages. In both countries, individuals in the top 5% of the population in multiple health- and social-service sectors were at elevated risk for deaths from suicide, drugs, and alcohol, and deaths from other causes. Associations were evident across sex and age. CONCLUSIONS: Deaths of despair are a marker of inequalities in countries beyond the U.S. with robust social-safety nets, nationwide healthcare, and strong pharmaceutical regulations. These deaths cluster within a highly disadvantaged population segment identifiable within health- and social-service systems.

Disordered gambling in a longitudinal birth cohort: from childhood precursors to adult life outcomes.

BACKGROUND: Despite its introduction into the diagnostic nomenclature over four decades ago, there remain large knowledge gaps about disordered gambling. The primary aims of the present study were to document the long-term course, childhood precursors, and adult life outcomes associated with disordered gambling. METHODS: Participants enrolled in the population-representative Dunedin Study were prospectively followed from birth through age 45. Disordered gambling was assessed six times from age 18; composite measures of childhood social class, general intelligence, and low self-control were based on assessments obtained from birth through age 15; adult socioeconomic, financial, and legal outcomes were obtained through age 45. Lifetime disordered gambling was predicted from the three childhood precursors and the adult outcomes were predicted from lifetime disordered gambling. RESULTS: Past-year disordered gambling usually occurred at only a single time point and recurrence was relatively uncommon. Lower childhood social class, general intelligence, and self-control significantly predicted lifetime disordered gambling in adulthood. In turn, lifetime disordered gambling in adulthood significantly predicted occupational, educational, and financial problems in adulthood (ds = 0.23-0.41). These associations were markedly reduced and sometimes rendered nonsignificant after adjusting for childhood precursors (ds = 0.04-0.32). CONCLUSIONS: Socioeconomic, financial, and legal outcomes in adulthood are not merely consequences of disordered gambling, but also are predicted from childhood precursors. Deflecting the trajectories of young people at risk for developing disordered gambling may help to ameliorate not just the development of later disordered gambling, but also other associated adverse outcomes.

Preparedness for healthy ageing and polysubstance use in long-term cannabis users: a population-representative longitudinal study.

BACKGROUND: Cannabis is often characterised as a young person's drug. However, people who began consuming cannabis in the 1970s and 1980s are no longer young and some have consumed it for many years. This study tested the preregistered hypothesis that long-term cannabis users show accelerated biological ageing in midlife and poorer health preparedness, financial preparedness, and social preparedness for old age. METHODS: In this longitudinal study, participants comprised a population-representative cohort of 1037 individuals born in Dunedin, New Zealand, between April, 1972, and March, 1973, and followed to age 45 years. Cannabis, tobacco, and alcohol use and dependence were assessed at ages 18 years, 21 years, 26 years, 32 years, 38 years, and 45 years. Biological ageing and health, financial, and social preparedness for old age were assessed at age 45 years. Long-term cannabis users were compared using independent samples t tests with five groups: lifelong cannabis non-users, long-term tobacco users, long-term alcohol users, midlife recreational cannabis users, and cannabis quitters. In addition, regression analyses tested dose-response associations for continuously measured persistence of cannabis dependence from age 18 years to 45 years, with associations adjusted for sex, childhood socioeconomic status, childhood IQ, low childhood self-control, family substance dependence history, and persistence of alcohol, tobacco, and other illicit drug dependence. FINDINGS: Of 997 cohort members still alive at age 45 years, 938 (94%) were assessed at age 45 years. Long-term cannabis users showed statistically significant accelerated biological ageing and were less equipped to manage a range of later-life health, financial, and social demands than non-users. Standardised mean differences between long-term cannabis users and non-users were large: 0·70 (95% CI 0·46 to 0·94; p<0·0001) for biological ageing, -0·72 (-0·96 to -0·49, p<0·0001) for health preparedness, -1·08 (-1·31 to -0·85; p<0·0001) for financial preparedness, and -0·59 (-0·84 to -0·34, p<0·0001) for social preparedness. Long-term cannabis users did not fare better than long-term tobacco or alcohol users. Tests of dose-response associations suggested that cannabis associations could not be explained by the socioeconomic origins, childhood IQ, childhood self-control, and family substance-dependence history of long-term cannabis users. Statistical adjustment for long-term tobacco, alcohol, and other illicit drug dependence suggested that long-term cannabis users' tendency toward polysubstance dependence accounted for their accelerated biological ageing and poor financial and health preparedness, although not for their poor social preparedness (ß -0·10, 95% CI -0·18 to -0·02; p=0·017). INTERPRETATION: Long-term cannabis users are underprepared for the demands of old age. Although long-term cannabis use appears detrimental, the greatest challenge to healthy ageing is not use of any specific substance, but rather the long-term polysubstance use that characterises many long-term cannabis users. Substance-use interventions should include practical strategies for improving health and building financial and social capital for healthy longevity. FUNDING: The National Institute on Aging and the UK Medical Research Council. The Dunedin Research Unit is supported by the New Zealand Health Research Council and the New Zealand Ministry of Business, Innovation and Employment.

Polygenic Liability to Depression Is Associated With Multiple Medical Conditions in the Electronic Health Record: Phenome-wide Association Study of 46,782 Individuals.

BACKGROUND: Major depressive disorder (MDD) is a leading cause of disease-associated disability, with much of the increased burden due to psychiatric and medical comorbidity. This comorbidity partly reflects common genetic influences across conditions. Integrating molecular-genetic tools with health records enables tests of association with the broad range of physiological and clinical phenotypes. However, standard phenome-wide association studies analyze associations with individual genetic variants. For polygenic traits such as MDD, aggregate measures of genetic risk may yield greater insight into associations across the clinical phenome. METHODS: We tested for associations between a genome-wide polygenic risk score for MDD and medical and psychiatric traits in a phenome-wide association study of 46,782 unrelated, European-ancestry participants from the Michigan Genomics Initiative. RESULTS: The MDD polygenic risk score was associated with 211 traits from 15 medical and psychiatric disease categories at the phenome-wide significance threshold. After excluding patients with depression, continued associations were observed with respiratory, digestive, neurological, and genitourinary conditions; neoplasms; and mental disorders. Associations with tobacco use disorder, respiratory conditions, and genitourinary conditions persisted after accounting for genetic overlap between depression and other psychiatric traits. Temporal analyses of time-at-first-diagnosis indicated that depression disproportionately preceded chronic pain and substance-related disorders, while asthma disproportionately preceded depression. CONCLUSIONS: The present results can inform the biological links between depression and both mental and systemic diseases. Although MDD polygenic risk scores cannot currently forecast health outcomes with precision at the individual level, as molecular-genetic discoveries for depression increase, these tools may augment risk prediction for medical and psychiatric conditions.

Longitudinal Associations of Mental Disorders With Dementia: 30-Year Analysis of 1.7 Million New Zealand Citizens.

IMPORTANCE: Mental disorders are an underappreciated category of modifiable risk factors for dementia. Developing an evidence base about the link between mental disorders and dementia risk requires studies that use large, representative samples, consider the full range of psychiatric conditions, ascertain mental disorders from early life, use long follow-ups, and distinguish between Alzheimer disease and related dementias. OBJECTIVE: To test whether mental disorders antedate dementia across 3 decades of observation. DESIGN, SETTING, AND PARTICIPANTS: This population-based administrative register study of mental disorders and Alzheimer disease and related dementias included all individuals born in New Zealand between 1928 and 1967 who resided in the country for any time during the 30-year observation period between July 1988 and June 2018. Data were from the New Zealand Integrated Data Infrastructure, a collection of whole-of-population administrative data sources linked at the individual level. Data were analyzed from October 2020 to November 2021. EXPOSURES: Diagnoses of mental disorders were ascertained from public-hospital records. MAIN OUTCOMES AND MEASURES: Diagnoses of dementia were ascertained from public-hospital records, mortality records, and pharmaceutical records. RESULTS: Of 1 711 386 included individuals, 866 301 (50.6%) were male, and individuals were aged 21 to 60 years at baseline. Relative to individuals without a mental disorder, those with a mental disorder were at increased risk of developing subsequent dementia (relative risk [RR], 4.24; 95% CI, 4.07-4.42; hazard ratio, 6.49; 95% CI, 6.25-6.73). Among individuals with dementia, those with a mental disorder developed dementia a mean of 5.60 years (95% CI, 5.31-5.90) earlier than those without a mental disorder. Associations held across sex and age and after accounting for preexisting chronic physical diseases and socioeconomic deprivation. Associations were present across different types of mental disorders and self-harm behavior (RRs ranged from 2.93 [95% CI, 2.66-3.21] for neurotic disorders to 6.20 [95% CI, 5.67-6.78] for psychotic disorders), and were evident for Alzheimer disease (RR, 2.76; 95% CI, 2.45-3.11) and all other dementias (RR, 5.85; 95% CI, 5.58-6.13). CONCLUSIONS AND RELEVANCE: In this study, mental disorders were associated with the onset of dementia in the population. Ameliorating mental disorders in early life might also ameliorate neurodegenerative conditions and extend quality of life in old age.

Use of Population-Level Administrative Data in Developmental Science.

Population-level administrative data-data on individuals' interactions with administrative systems (e.g., health, criminal justice, and education)-have substantially advanced our understanding of life-course development. In this review, we focus on five areas where research using these data has made significant contributions to developmental science: (a) understanding small or difficult-to-study populations, (b) evaluating intergenerational and family influences, (c) enabling estimation of causal effects through natural experiments and regional comparisons, (d) identifying individuals at risk for negative developmental outcomes, and (e) assessing neighborhood and environmental influences. Further advances will be made by linking prospective surveys to administrative data to expand the range of developmental questions that can be tested; supporting efforts to establish new linked administrative data resources, including in developing countries; and conducting cross-national comparisons to test findings' generalizability. New administrative data initiatives should involve consultation with population subgroups including vulnerable groups, efforts to obtain social license, and strong ethical oversight and governance arrangements.

Vital personality scores and healthy aging: Life-course associations and familial transmission.

OBJECTIVES: Personality traits are linked with healthy aging, but it is not clear how these associations come to manifest across the life-course and across generations. To study this question, we tested a series of hypotheses about (a) personality-trait prediction of markers of healthy aging across the life-course, (b) developmental origins, stability and change of links between personality and healthy aging across time, and (c) intergenerational transmission of links between personality and healthy aging. For our analyses we used a measure that aggregates the contributions of Big 5 personality traits to healthy aging: a "vital personality" score. METHODS: Data came from two population-based longitudinal cohort studies, one based in New Zealand and the other in the UK, comprising over 6000 study members across two generations, and spanning an age range from birth to late life. RESULTS: Our analyses revealed three main findings: first, individuals with higher vital personality scores engaged in fewer health-risk behaviors, aged slower, and lived longer. Second, individuals' vital personality scores were preceded by differences in early-life temperament and were relatively stable across adulthood, but also increased from young adulthood to midlife. Third, individuals with higher vital personality scores had children with similarly vital partners, promoted healthier behaviors in their children, and had children who grew up to have more vital personality scores themselves, for genetic and environmental reasons. CONCLUSION: Our study shows how the health benefits associated with personality accrue throughout the life-course and across generations.

Nationwide evidence that education disrupts the intergenerational transmission of disadvantage.

Despite overall improvements in health and living standards in the Western world, health and social disadvantages persist across generations. Using nationwide administrative databases linked for 2.1 million Danish citizens, we leveraged a three-generation approach to test whether multiple, different health and social disadvantages-poor physical health, poor mental health, social welfare dependency, criminal offending, and Child Protective Services involvement-were transmitted within families and whether education disrupted these statistical associations. Health and social disadvantages concentrated, aggregated, and accumulated within a small, high-need segment of families: Adults who relied disproportionately on multiple, different health and social services tended to have parents who relied disproportionately on multiple, different health and social services and tended to have children who evidenced risk for disadvantage at an early age, through appearance in protective services records. Intra- and intergenerational comparisons were consistent with the possibility that education disrupted this transmission. Within families, siblings who obtained more education were at a reduced risk for later-life disadvantage compared with their cosiblings who obtained less education, despite shared family background. Supporting the education potential of the most vulnerable citizens might mitigate the multigenerational transmission of multiple disadvantages and reduce health and social disparities.

Disparities in the pace of biological aging among midlife adults of the same chronological age have implications for future frailty risk and policy.

Some humans age faster than others. Variation in biological aging can be measured in midlife, but the implications of this variation are poorly understood. We tested associations between midlife biological aging and indicators of future frailty-risk in the Dunedin cohort of 1037 infants born the same year and followed to age 45. Participants' Pace of Aging was quantified by tracking declining function in 19 biomarkers indexing the cardiovascular, metabolic, renal, immune, dental, and pulmonary systems across ages 26, 32, 38, and 45 years. At age 45 in 2019, participants with faster Pace of Aging had more cognitive difficulties, signs of advanced brain aging, diminished sensory-motor functions, older appearance, and more pessimistic perceptions of aging. People who are aging more rapidly than same-age peers in midlife may prematurely need supports to sustain independence that are usually reserved for older adults. Chronological age does not adequately identify need for such supports.

Association of History of Psychopathology With Accelerated Aging at Midlife.

Importance: Individuals with mental disorders are at an elevated risk of developing chronic age-related physical diseases. However, it is not clear whether psychopathology is also associated with processes of accelerated aging that precede the onset of age-related disease. Objective: To test the hypothesis that a history of psychopathology is associated with indicators of accelerated aging at midlife. Design, Setting, and Participants: This prospective cohort study was based on the Dunedin Multidisciplinary Health and Development Study, a population-representative birth cohort of 1037 individuals born between April 1, 1972, and March 31, 1973, in Dunedin, New Zealand. Members were followed up to age 45 years (until April 2019). Data were analyzed from January 6 to December 7, 2020. Exposures: Mental disorders were assessed in 6 diagnostic assessments from ages 18 to 45 years and transformed through confirmatory factor analysis into continuous measures of general psychopathology (p-factor) and dimensions of internalizing, externalizing, and thought disorders (all standardized to a mean [SD] of 100 [15]). Main Outcomes and Measures: Signs of aging (biological pace of aging; declines in sensory, motor, and cognitive functioning; and facial age) were assessed up to age 45 years using previously validated measures including biomarkers, clinical tests, and self-reports. Results: Of the original 1037 cohort participants, 997 were still alive at age 45 years, of whom 938 (94%) were assessed (474 men [50.5%]). Participants who had experienced more psychopathology exhibited a faster pace of biological aging (ß, 0.27; 95% CI, 0.21-0.33; P < .01); experienced more difficulties with hearing (ß, 0.18; 95% CI, 0.12-0.24; P < .01), vision (ß, 0.08; 95% CI, 0.01-0.14; P < .05), balance (ß, 0.20; 95% CI, 0.14-0.26; P < .01), and motor functioning (ß, 0.19; 95% CI, 0.12-0.25; P < .01); experienced more cognitive difficulties (ß, 0.24; 95% CI, 0.18-0.31; P < .01); and were rated as looking older (ß, 0.20; 95% CI, 0.14-0.26; P < .01). Associations persisted after controlling for sex, childhood health indicators, maltreatment, and socioeconomic status and after taking into account being overweight, smoking, use of antipsychotic medication, and the presence of physical disease. Tests of diagnostic specificity revealed that associations were generalizable across externalizing, internalizing, and thought disorders. Conclusions and Relevance: In this cohort study, a history of psychopathology was associated with accelerated aging at midlife, years before the typical onset of age-related diseases. This link is not specific to any particular disorder family but generalizes across disorders. Prevention of psychopathology and monitoring of individuals with mental disorders for signs of accelerated aging may have the potential to reduce health inequalities and extend healthy lives.

Longitudinal Associations of Mental Disorders With Physical Diseases and Mortality Among 2.3 Million New Zealand Citizens.

Importance: Excess risk of physical disease and mortality has been observed among individuals with psychiatric conditions, suggesting that ameliorating mental disorders might also be associated with ameliorating the later onset of physical disability and early mortality. However, the temporal association between mental disorders and physical diseases remains unclear, as many studies have relied on retrospective recall, used cross-sectional designs or prospective designs with limited follow-up periods, or given inadequate consideration to preexisting physical illnesses. Objective: To examine whether mental disorders are associated with subsequent physical diseases and mortality across 3 decades of observation. Design, Setting, and Participants: This population-based cohort study used data from the New Zealand Integrated Data Infrastructure, a collection of nationwide administrative data sources linked at the individual level, to identify mental disorders, physical diseases, and deaths recorded between July 1, 1988, and June 30, 2018, in the population of New Zealand. All individuals born in New Zealand between January 1, 1928, and December 31, 1978, who resided in the country at any time during the 30-year observation period were included in the analysis. Data were analyzed from July 2019 to November 2020. Exposures: Nationwide administrative records of mental disorder diagnoses made in public hospitals. Main Outcomes and Measures: Chronic physical disease diagnoses made in public hospitals, deaths, and health care use. Results: The study population comprised 2 349 897 individuals (1 191 981 men [50.7%]; age range at baseline, 10-60 years). Individuals with a mental disorder developed subsequent physical diseases at younger ages (hazard ratio [HR], 2.33; 95% CI, 2.30-2.36) and died at younger ages (HR, 3.80; 95% CI, 3.72-3.89) than those without a mental disorder. These associations remained across sex and age and after accounting for preexisting physical diseases. Associations were observed across different types of mental disorders and self-harm behavior (relative risks, 1.78-2.43; P < .001 for all comparisons). Mental disorders were associated with the onset of physical diseases and the accumulation of physical disease diagnoses (incidence rate ratio [IRR], 2.00; 95% CI, 1.98-2.03), a higher number of hospitalizations (IRR, 2.43; 95% CI, 2.39-2.48), longer hospital stays for treatment (IRR, 2.70; 95% CI, 2.62-2.79), and higher associated health care costs (b = 0.115; 95% CI, 0.112-0.118). Conclusions and Relevance: In this study, mental disorders were likely to begin and peak in young adulthood, and they antedated physical diseases and early mortality in the population. These findings suggest that ameliorating mental disorders may have implications for improving the length and quality of life and for reducing the health care costs associated with physical diseases.

Childhood self-control forecasts the pace of midlife aging and preparedness for old age.

The ability to control one's own emotions, thoughts, and behaviors in early life predicts a range of positive outcomes in later life, including longevity. Does it also predict how well people age? We studied the association between self-control and midlife aging in a population-representative cohort of children followed from birth to age 45 y, the Dunedin Study. We measured children's self-control across their first decade of life using a multi-occasion/multi-informant strategy. We measured their pace of aging and aging preparedness in midlife using measures derived from biological and physiological assessments, structural brain-imaging scans, observer ratings, self-reports, informant reports, and administrative records. As adults, children with better self-control aged more slowly in their bodies and showed fewer signs of aging in their brains. By midlife, these children were also better equipped to manage a range of later-life health, financial, and social demands. Associations with children's self-control could be separated from their social class origins and intelligence, indicating that self-control might be an active ingredient in healthy aging. Children also shifted naturally in their level of self-control across adult life, suggesting the possibility that self-control may be a malleable target for intervention. Furthermore, individuals' self-control in adulthood was associated with their aging outcomes after accounting for their self-control in childhood, indicating that midlife might offer another window of opportunity to promote healthy aging.

A polygenic score for age-at-first-birth predicts disinhibition.

BACKGROUND: A recent genome-wide association study identified molecular-genetic associations with age-at-first-birth. However, the meaning of these genetic discoveries is unclear. Drawing on evidence linking early pregnancy with disinhibitory behavior, we tested the hypothesis that genetic discoveries for age-at-first-birth predict disinhibition. METHODS: We included participants with genotype data from the two-decade-long Environmental Risk (E-Risk) Study (N = 1,999) and the four-decade-long Dunedin Study (N = 918). We calculated a genome-wide polygenic score for age-at-first-birth and tested whether it was associated with a range of disinhibitory outcomes across the life course, including low childhood self-control; risk for externalizing psychopathology; officially recorded criminal offending; substance dependence; informant reports of disinhibitory problems; and number of lifetime sexual partners. We further tested whether associations were attributable to accelerated pubertal maturation. RESULTS: In both cohorts, the age-at-first-birth polygenic score predicted low childhood self-control, externalizing psychopathology, officially recorded criminal offending, substance dependence, and number of sexual partners. Associations were modest, but robust across replication. Childhood disinhibition partly mediated associations between the polygenic score and reproductive behaviors. In contrast, associations were not attributable to accelerated pubertal timing. CONCLUSIONS: Genomic discoveries for age-at-first-birth are about more than reproductive biology: They provide insight into the disinhibitory traits and behaviors that accompany early parenthood. Age-at-first-birth is a useful proxy phenotype for researchers interested in disinhibition. Further, interventions that improve self-regulation abilities may benefit young parents and their children.

Clustering of health, crime and social-welfare inequality in 4 million citizens from two nations.

Health and social scientists have documented the hospital revolving-door problem, the concentration of crime, and long-term welfare dependence. Have these distinct fields identified the same citizens? Using administrative databases linked to 1.7 million New Zealanders, we quantified and monetized inequality in distributions of health and social problems and tested whether they aggregate within individuals. Marked inequality was observed: Gini coefficients equalled 0.96 for criminal convictions, 0.91 for public-hospital nights, 0.86 for welfare benefits, 0.74 for prescription-drug fills and 0.54 for injury-insurance claims. Marked aggregation was uncovered: a small population segment accounted for a disproportionate share of use-events and costs across multiple sectors. These findings were replicated in 2.3 million Danes. We then integrated the New Zealand databases with the four-decade-long Dunedin Study. The high-need/high-cost population segment experienced early-life factors that reduce workforce readiness, including low education and poor mental health. In midlife they reported low life satisfaction. Investing in young people's education and training potential could reduce health and social inequalities and enhance population wellbeing.

Using DNA From Mothers and Children to Study Parental Investment in Children's Educational Attainment.

This study tested implications of new genetic discoveries for understanding the association between parental investment and children's educational attainment. A novel design matched genetic data from 860 British mothers and their children with home-visit measures of parenting: the E-Risk Study. Three findings emerged. First, both mothers' and children's education-associated genetics, summarized in a genome-wide polygenic score, were associated with parenting-a gene-environment correlation. Second, accounting for genetic influences slightly reduced associations between parenting and children's attainment-indicating some genetic confounding. Third, mothers' genetics were associated with children's attainment over and above children's own genetics, via cognitively stimulating parenting-an environmentally mediated effect. Findings imply that, when interpreting parents' effects on children, environmentalists must consider genetic transmission, but geneticists must also consider environmental transmission.