Publications

Background: Labour market disengagement among youths has lasting negative economic and social consequences, yet is poorly understood. We compared four types of work-related self-perceptions, as well as vulnerability to mental health and substance abuse problems, among youths not in education, employment or training (NEET) and among their peers. Methods: Participants were from the Environmental Risk (E-Risk) longitudinal study, a nationally representative UK cohort of 2,232 twins born in 1994–1995. We measured commitment to work, job-search effort, professional/technical skills, ‘soft skills (e.g. teamwork, decision-making, communication), optimism about getting ahead, and mental health and substance use disorders at age 18. We also examined childhood mental health. Results: At age 18, 11.6% of participants were NEET. NEET participants reported themselves as committed to work and searching for jobs with greater diligence than their non-NEET peers. However, they reported fewer ‘soft skills (B = ?0.98, p

STUDY OBJECTIVES: People with insomnia complain of cognitive deficits in daily life. Results from empirical studies examining associations between insomnia and cognitive impairment, however, are mixed. Research is needed that compares treatment-seeking and community-based insomnia study samples, measures subjective as well as objective cognitive functioning, and considers participants pre-insomnia cognitive function.\n\nDESIGN AND PARTICIPANTS: We used data from the Dunedin Study, a representative birth cohort of 1,037 individuals, to examine whether insomnia in early midlife was associated with subjective and objective cognitive functioning. We also tested whether individuals with insomnia who reported seeking treatment for their sleep problems (treatment-seekers) showed greater impairment than other individuals with insomnia (non-treatment-seekers). The role of key confounders, including childhood cognitive ability and comorbid health conditions, was evaluated.\n\nMEASUREMENTS: Insomnia was diagnosed at age 38 according to DSM-IV criteria. Objective neuropsychological assessments at age 38 included the WAIS-IV IQ test, the Wechsler Memory Scale, and the Trail-Making Test. Childhood cognitive functioning was assessed using the Wechsler Intelligence Scale for Children-Revised (WISC-R).\n\nRESULTS: A total of 949 cohort members were assessed for insomnia symptoms and other study measures at age 38. Although cohort members with insomnia (n = 186, 19.6%) had greater subjective cognitive impairment than their peers at age 38, they did not exhibit greater objective impairment on formal testing. Treatment-seekers, however, exhibited significant objective impairment compared to non-treatment-seekers. Controlling for comorbidity, daytime impairment, and medications slightly decreased this association. Childhood cognitive deficits antedated the adult cognitive deficits of treatment-seekers.\n\nCONCLUSIONS: Links between insomnia and cognitive impairment may be strongest among individuals who seek clinical treatment. Clinicians should take into account the presence of complex health problems and lower premorbid cognitive function when planning treatment for insomnia patients.

There is evidence that persistent psychiatric disorders lead to age-related disease and premature mortality. Telomere length has emerged as a promising biomarker in studies that test the hypothesis that internalizing psychiatric disorders are associated with accumulating cellular damage. We tested the association between the persistence of internalizing disorders (depression, generalized anxiety disorder and post-traumatic stress disorder) and leukocyte telomere length (LTL) in the prospective longitudinal Dunedin Study (n=1037). Analyses showed that the persistence of internalizing disorders across repeated assessments from ages 11 to 38 years predicted shorter LTL at age 38 years in a dose-response manner, specifically in men ([beta]=-0.137, 95% confidence interval (CI): -0.232, -0.042, P=0.005). This association was not accounted for by alternative explanatory factors, including childhood maltreatment, tobacco smoking, substance dependence, psychiatric medication use, poor physical health or low socioeconomic status. Additional analyses using DNA from blood collected at two time points (ages 26 and 38 years) showed that LTL erosion was accelerated among men who were diagnosed with internalizing disorder in the interim ([beta]=-0.111, 95% CI: -0.184, -0.037, P=0.003). No significant associations were found among women in any analysis, highlighting potential sex differences in internalizing-related telomere biology. These findings point to a potential mechanism linking internalizing disorders to accelerated biological aging in the first half of the life course, particularly in men. Because internalizing disorders are treatable, the findings suggest the hypothesis that treating psychiatric disorders in the first half of the life course may reduce the population burden of age-related disease and extend health expectancy.

Study Objectives: Insomnia is a highly prevalent condition that constitutes a major public health and economic burden. However, little is known about the developmental etiology of adulthood insomnia. Design: We examined whether indicators of psychological vulnerability across multiple developmental periods (psychiatric diagnoses in young adulthood and adolescence, childhood behavioral problems, and familial psychiatric history) predicted subsequent insomnia in adulthood. Setting and Participants: We used data from the ongoing Dunedin Multidisciplinary Health and Development Study, a population-representative birth cohort study of 1,037 children in New Zealand who were followed prospectively from birth (1972-1973) through their fourth decade of life with a 95% retention rate. Measurements: Insomnia was diagnosed at age 38 according to DSM-IV criteria. Psychiatric diagnoses, behavioral problems, and family psychiatric histories were assessed between ages 5 and 38. Results: In cross-sectional analyses, insomnia was highly comorbid with multiple psychiatric disorders. After controlling for this concurrent comorbidity, our results showed that individuals who have family histories of depression or anxiety, and who manifest lifelong depression and anxiety beginning in childhood, are at uniquely high risk for age-38 insomnia. Other disorders did not predict adulthood insomnia. Conclusions: The link between lifelong depression and anxiety symptoms and adulthood insomnia calls for further studies to clarify the neurophysiological systems or behavioral conditioning processes that may underlie this association.

IMPORTANCE Suicidal behavior has increased since the onset of the global recession, a trend that may have long-term health and social implications. OBJECTIVE To test whether suicide attempts among young people signal increased risk for later poor health and social functioning above and beyond a preexisting psychiatric disorder. DESIGN We followed up a cohort of young people and assessed multiple aspects of their health and social functioning as they approached midlife. Outcomes among individuals who had self-reported a suicide attempt up through age 24 years (young suicide attempters) were compared with those who reported no attempt through age 24 years (nonattempters). Psychiatric history and social class were controlled for. SETTING AND PARTICIPANTS The population-representative Dunedin Multidisciplinary Health and Development Study, which involved 1037 birth cohort members comprising 91 young suicide attempters and 946 nonattempters, 95%of whom were followed up to age 38 years. MAIN OUTCOMES AND MEASURES Outcomes were selected to represent significant individual and societal costs: mental health, physical health, harm toward others, and need for support. RESULTS As adults approaching midlife, young suicide attempters were significantly more likely to have persistent mental health problems (eg, depression, substance dependence, and additional suicide attempts) compared with nonattempters. They were also more likely to have physical health problems (eg, metabolic syndrome and elevated inflammation). They engaged in more violence (eg, violent crime and intimate partner abuse) and needed more social support (eg, long-term welfare receipt and unemployment). Furthermore, they reported being lonelier and less satisfied with their lives. These associations remained after adjustment for youth psychiatric diagnoses and social class. CONCLUSIONS AND RELEVANCE Many young suicide attempters remain vulnerable to costly health and social problems into midlife. As rates of suicidal behavior rise with the continuing global recession, additional suicide prevention efforts and long-term monitoring and after-care services are needed.

Cross-sectional studies have found that obesity is associated with low intellectual ability and neuroimaging abnormalities in adolescence and adulthood. Some have interpreted these associations to suggest that obesity causes intellectual decline in the first half of the life course. We analyzed data from a prospective longitudinal study to test whether becoming obese was associated with intellectual decline from childhood to midlife. We used data from the ongoing Dunedin Multidisciplinary Health and Development Study, a population-representative birth cohort study of 1,037 children in New Zealand who were followed prospectively from birth (1972-1973) through their fourth decade of life with a 95% retention rate. Intelligence quotient (IQ) was measured in childhood and adulthood. Anthropometric measurements were taken at birth and at 12 subsequent in-person assessments. As expected, cohort members who became obese had lower adulthood IQ scores. However, obese cohort members exhibited no excess decline in IQ. Instead, these cohort members had lower IQ scores since childhood. This pattern remained consistent when we accounted for children s birth weights and growth during the first years of life, as well as for childhood-onset obesity. Lower IQ scores among children who later developed obesity were present as early as 3 years of age. We observed no evidence that obesity contributed to a decline in IQ, even among obese individuals who displayed evidence of the metabolic syndrome and/or elevated systemic inflammation.

Evolutionary theory, when coupled with research from epidemiology, demography, and population endocrinology, suggests that contracting economies affect the fitness and health of human populations via natural selection in utero. We know, for example, that fetal death increases more among males than females when the economy unexpectedly contracts; that unexpected economic contraction predicts low secondary sex ratios; and that males from low sex ratio birth cohorts live, on average, longer than those from high sex ratio cohorts. We also know that low levels of human chorionic gonadotropin (i.e., hCG) measured in the serum of pregnant women predict fetal death. We do not, however, know whether male survivors of conception cohorts subjected to contracting economies exhibit, as theory predicts, higher hCG than those from other cohorts. We show, in 71 monthly conception cohorts including nearly two million California births, that they do. We thereby add to the literature suggesting that the economy, a phenomenon over which we collectively exercise at least some control, affects population health. Our findings imply that the effect arises via natural selection - a mechanism we largely ignore when attempting to explain, or alter, how collective choice affects our biology.

Objectives: Antagonists in the debate over whether the maternal stress response during pregnancy damages or culls fetuses have invoked the theory of selection in utero to support opposing positions. We describe how these opposing arguments arise from the same theory and offer a novel test to discriminate between them. Our test, rooted in reports from population endocrinology that human chorionic gonadotropin (hCG) signals fetal fitness, contributes not only to the debate over the fetal origins of illness, but also to the more basic literature concerned with whether and how natural selection in utero affects contemporary human populations. Methods: We linked maternal serum hCG measurements from prenatal screening tests with data from the California Department of Public Health birth registry for the years 2001-2007. We used time series analysis to test the association between the number of live-born male singletons and median hCG concentration among males in monthly gestational cohorts. Results: Among the 1.56 million gestations in our analysis, we find that median hCG levels among male survivors of monthly conception cohorts rise as the number of male survivors falls. Results: Elevated median hCG among relatively small male birth cohorts supports the theory of selection in utero and suggests that the maternal stress response culls cohorts in gestation by raising the fitness criterion for survival to birth. © 2012 Wiley Periodicals, Inc.