Publications

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.

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.

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.

Early-life stress (ELS) is associated with substantially increased lifetime risk for recurrent psychological problems, with evidence indicating that dysregulation of the physiological stress reactivity system may be partly responsible. However, some ELS-exposed people remain psychologically resilient. Although two distinct patterns of hypothalamic-pituitary-adrenal axis (HPA) stress reactivity have been observed in ELS-exposed samples (hyper- and hypo-reactive), the hypothesis that these patterns may be associated with long-term history of psychological problems has not been explored. We used healthy Whitehall II study subjects (n= 543) who participated in the 2008 Heart Scan Study (HSS) to assess salivary cortisol responses to a cognitive stressor, ELS exposure, and other psychosocial factors. Mean age of the sample at the HSS was 63 years. HSS data were linked to nearly 20 years of participants Whitehall data, including repeated measures of psychological distress (GHQ-28). Piecewise growth curve analyses revealed that ELS-exposed persons with a history of recurrent psychological distress in adulthood had significantly blunted cortisol reactivity compared to non-ELS-exposed participants, while ELS-exposed persons with little or no history of distress had significantly elevated baseline cortisol, prolonged responses, and greater total cortisol production. Our findings indicate that for ELS-exposed individuals, different trajectories in psychological health over their adult lifetimes predict different cortisol reactivity patterns. These findings have important implications for our understanding of ELS-related mental health risk and treatment of these disorders. ?? 2012 Elsevier Ltd.

Political pronouncements and policy statements include much conjecture concerning the health and behavioral effects of economic decline. We both summarize empirical research concerned with those effects and suggest questions for future research priorities. We separate the studies into groups defined by questions asked, mechanisms invoked, and outcomes studied. We conclude that although much research shows that undesirable job and financial experiences increase the risk of psychological and behavioral disorder, many other suspected associations remain poorly studied or unsupported. The intuition that mortality increases when the economy declines, for example, appears wrong. We note that the research informs public health programming by identifying risk factors, such as job loss, made more frequent by economic decline. The promise that the research would identify health costs and benefits of economic policy choices, however, remains unfulfilled and will likely remain so without stronger theory and greater methodological agreement.

Background: Theory and empirical evidence suggest that economic contraction predicts increased incidence of psychological disorder. The extent to which this relation can be causally attributed to the economic experiences of individuals remains uncertain. Methods: We critically examine literature concerning the impact of economic contraction, measured at the individual or ecological level, on four mental health outcomes (depression, suicide, substance abuse, and antisocial behavior) from the past two decades. Studies at the individual level use job loss, transition to inadequate employment, or welfare as the independent variable. Studies at the ecological level primarily use the unemployment rate. Results: In the studies that best establish causality, research indicates a moderate but significant adverse effect of job loss on individual depression symptoms, but the net population effect remains speculative. For suicide and antisocial behavior, individual- and ecological-level studies converge to suggest a moderate positive association with economic contraction. Although some research on substance abuse suggests procyclical effects, the majority indicate that job loss significantly increases the risk of heavy drinking and symptoms of alcohol abuse. For all outcomes, various characteristics of the population or the specific economic exposure studied can modify the overall association. Conclusions: The studies reviewed suggest that adverse economic transitions predict increased mental health problems, particularly depression, suicide, and substance abuse. The strength of the association, particularly when measuring the response of populations to contracting economies remains unclear. © 2010 M.E. Sharpe, Inc. All rights reserved.

BACKGROUND: Theory suggests that natural selection conserved reactivity in part because highly reactive women spontaneously abort less fit conceptuses, particularly small males. Other literature argues that high reactivity manifests clinically as anxiety disorders. If true, births to women diagnosed with anxiety disorders should exhibit a low secondary sex ratio (i.e. ratio of male to female births). We explored whether births to women diagnosed with anxiety disorders exhibit a lower sex ratio than births to women diagnosed with other psychiatric disorders, or to women without mental health diagnoses. METHODS: We performed a case-control comparison of the secondary sex ratios among groups of women categorized by mental health diagnosis using birth records linked to data from California County Mental Health system records. We compared sex ratios among 5994 deliveries to mothers diagnosed with anxiety disorders, 23 443 deliveries to mothers diagnosed with other psychiatric disorders and 1 099 198 comparison births. RESULTS: Although comparison births exhibited a higher sex ratio than births to women diagnosed with anxiety disorders or with other diagnoses, differences were not statistically significant. Births to African American women diagnosed with anxiety disorders, however, exhibited sex ratios significantly lower than comparison births among African Americans (OR = 0.89, P = 0.038) or births to African American women with other mental health diagnoses (OR = 0.88, P = 0.042). CONCLUSIONS: We found that infants born to African American women diagnosed with anxiety disorders exhibited a significantly lower secondary sex ratio than reference groups. We urge confirmatory tests of our findings and discuss implications of the reactivity/anxiety hypothesis for psychiatry, obstetrics and public health.