The recent recession and lingering high unemployment will likely lead to a burst of research studying the health effects of economic decline. We aim to inform that work by summarizing empirical research concerned with those effects. 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.

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BackgroundThe theory of fundamental causes explains why health disparities persist over time, even as risk factors, mechanisms, and diseases change. Using an intersectional framework, we evaluated multifactorial discrimination as a fundamental cause of mental health disparities.MethodsUsing baseline data from the Project STRIDE: Stress, Identity, and Mental Health study, we examined the health effects of discrimination among individuals who self-identified as lesbian, gay, or bisexual. We used logistic and linear regression to assess whether multifactorial discrimination met the four criteria designating a fundamental cause, namely that the cause: 1) influences multiple health outcomes, 2) affects multiple risk factors, 3) involves access to resources that can be leveraged to reduce consequences of disease, and 4) reproduces itself in varied contexts through changing mechanisms.ResultsMultifactorial discrimination predicted high depression scores, psychological well-being, and substance use disorder diagnosis. Discrimination was positively associated with risk factors for high depression scores: chronic strain and total number of stressful life events. Discrimination was associated with significantly lower levels of mastery and self-esteem, protective factors for depressive symptomatology. Even after controlling for risk factors, discrimination remained a significant predictor for high depression scores. Among subjects with low depression scores, multifactorial discrimination also predicted anxiety and aggregate mental health scores.ConclusionsMultifactorial discrimination should be considered a fundamental cause of mental health inequities and may be an important cause of broad health disparities among populations with intersecting social identities.

Inflammatory cytokine levels predict a wide range of human diseases, including depression, cardiovascular disease, type 2 diabetes, autoimmune disease, general morbidity, and mortality. Stress and social experiences throughout the lifecourse have been associated with inflammatory processes. We conducted studies in humans and laboratory rats to examine the effect of early life experience and adult social position in predicting IL-6 levels. Human participants reported family homeownership during their childhood and current subjective social status. Interleukin-6 (IL-6) was measured from oral mucosal transudate. Rats were housed in groups of three, matched for quality of maternal care received. Social status was assessed via competition for resources, and plasma IL-6 was assessed in adulthood. In both humans and rats, we identified an interaction effect; early social experience moderated the effect of adult social status on IL-6 levels. Rats that experienced low levels of maternal care and people with low childhood socioeconomic status represented both the highest and lowest levels of IL-6 in adulthood, depending on their social status as young adults. The predicted interaction held for non-Hispanic people, but did not occur among Hispanic individuals. Adversity early in life may not have a monotonically negative effect on adult health, but may alter biological sensitivity to later social experiences.

Most research describing the biological response to unemployment appears appropriately motivated by clinical or public health concerns and focuses on death, disease, and medical care. We argue that expanding the work to include other outcomes could contribute to basic science. As an example, we use the response to mass layoffs to discriminate between two explanations of low ratios of male to female live births in stressed populations. One explanation asserts that ambient stressors reduce the ratio of males to females conceived. The other argues that the maternal stress response selects against males in utero. We show that selection in utero better explains the observed data. We conclude that human adaptation to the economic environment deserves scrutiny from a wider array of scientists than it now receives.

We find support for the hypothesis that changes in the monthly odds of a twin among live-born males predict subsequent and opposite changes in the odds of a twin among live-born females. The hypothesis arises from the long standing argument that natural selection has conserved mechanisms by which pregnant women in stressed populations spontaneously abort fetuses least likely to yield grandchildren. Previous attempts to empirically test this argument focus almost entirely on males. We contribute to the literature by showing that, consistent with the logic of natural selection, maternal adaptations to environmental changes likely have effects on the survival of both male and female conceptuses and fetuses.

Our findings contribute to the evidence supporting selection in utero. They also suggest that research into the association between maternal stress and adverse birth outcomes should acknowledge the possibility that fetal loss may affect findings and their interpretation. Strengths of our analyses include the large number and size of our birth cohorts and our control for autocorrelation. Weaknesses include that we, like nearly all researchers in the field, have no direct measure of fetal loss.

Much literature argues that natural selection has conserved mechanisms by which stressed females cull frail males in utero. This argument implies that males from low sex ratio birth cohorts should, on average, live longer than those from high sex ratio cohorts. Research reports such associations but these tests use completed lifespan as the outcome and, therefore, must end with cohorts born in 1913 because too many males survive from more contemporary cohorts to determine average lifespan. The empirical literature does not, therefore, address whether selection affects male mortality in contemporary cohorts. We apply time-series methods to monthly cohorts born in California between 1989 and 2003 to measure the association between the ratio of male to female live births and infant mortality, controlling for all forms of autocorrelation that induce spurious correlations. Consistent with theories of selection in utero, we find a positive correlation between cohort sex ratio and male infant mortality. The results suggest that natural selection conserved the stress mechanism in females to end the gestation of relatively less fit males and that this mechanism manifests itself in contemporary human societies.