WP 2018-389

Recent research has found, in some groups of Americans, dramatic increases in deaths due to drug overdose and suicide and an overall stagnation of trends toward increased longevity. This study examines the link between mortality of older working age (45 to 64) adults and local economic downturns in the U.S. to evaluate the role of economic shifts in various causes of death and their related mortality trends. Specifically, we estimate regression models to test the hypotheses that the longevity effects of poor economic prospects are reflected through (1) increased suicide, drug overdose, and other “deaths of despair” and (2) other causes of death linked to exposure to economic and social stress such as heart and cerebrovascular disease. To avoid the problem of endogeneity of local economic conditions to mortality conditions, we measure the local economic shock of lost employment with predicted employment based on baseline industrial composition and national trends in employment by industry. We find evidence consistent with prior research that among non-Hispanic white adults, midlife mortality has increased since 1990, particularly among those with low educational attainment. We also find that “deaths of despair” are important contributors to that trend. However, we find that while distress in local, area economies does predict increased mortality for chronic disease, it predicts decreased mortality from suicides, opioids, and other substance abuse. This finding suggests caution in the application of the construct of despair in explaining recent mortality patterns.Social Security Adminstration, Award number RRC08098401-10, R-UM18-07https://deepblue.lib.umich.edu/bitstream/2027.42/148126/1/wp389.pdfDescription of wp389.pdf : Working pape

A "missing" family of classical orthogonal polynomials

We study a family of "classical" orthogonal polynomials which satisfy (apart from a 3-term recurrence relation) an eigenvalue problem with a differential operator of Dunkl-type. These polynomials can be obtained from the little $q$-Jacobi polynomials in the limit $q=-1$. We also show that these polynomials provide a nontrivial realization of the Askey-Wilson algebra for $q=-1$.Comment: 20 page

CMV matrices in random matrix theory and integrable systems: a survey

We present a survey of recent results concerning a remarkable class of unitary matrices, the CMV matrices. We are particularly interested in the role they play in the theory of random matrices and integrable systems. Throughout the paper we also emphasize the analogies and connections to Jacobi matrices.Comment: Based on a talk given at the Short Program on Random Matrices, Random Processes and Integrable Systems, CRM, Universite de Montreal, 200

Jedi public health: Co-creating an identity-safe culture to promote health equity

© 2016 The Authors. The extent to which socially-assigned and culturally mediated social identity affects health depends on contingencies of social identity that vary across and within populations in day-to-day life. These contingencies are structurally rooted and health damaging inasmuch as they activate physiological stress responses. They also have adverse effects on cognition and emotion, undermining self-confidence and diminishing academic performance. This impact reduces opportunities for social mobility, while ensuring those who "beat the odds" pay a physical price for their positive efforts. Recent applications of social identity theory toward closing racial, ethnic, and gender academic achievement gaps through changing features of educational settings, rather than individual students, have proved fruitful. We sought to integrate this evidence with growing social epidemiological evidence that structurally-rooted biopsychosocial processes have population health effects. We explicate an emergent framework, Jedi Public Health (JPH). JPH focuses on changing features of settings in everyday life, rather than individuals, to promote population health equity, a high priority, yet, elusive national public health objective. We call for an expansion and, in some ways, a re-orienting of efforts to eliminate population health inequity. Policies and interventions to remove and replace discrediting cues in everyday settings hold promise for disrupting the repeated physiological stress process activation that fuels population health inequities with potentially wide application.National Institute on Aging (Grant # R01 AG032632)National Institute on Aging (Grant # T32 AG00221

America’s Declining Well-Being, Health, and Life Expectancy: Not Just a White Problem

Although recent declines in life expectancy among non-Hispanic Whites, coined “deaths of despair,” grabbed the headlines of most major media outlets, this is neither a recent problem nor is it confined to Whites. The decline in America’s health has been described in the public health literature for decades and has long been hypothesized to be attributable to an array of worsening psychosocial problems that are not specific to Whites. To test some of the dominant hypotheses, we show how various measures of despair have been increasing in the United States since 1980 and how these trends relate to changes in health and longevity. We show that mortality increases among Whites caused by the opioid epidemic come on the heels of the crack and HIV syndemic among Blacks. Both occurred on top of already higher mortality rates among all Americans relative to people in other nations, and both occurred among declines in measures of well-being. We believe that the attention given to Whites is distracting researchers and policymakers from much more serious, longer-term structural problems that affect all Americans

Vulnerability as a Function of Individual and Group Resources in Cumulative Risk Assessment

BACKGROUND: The field of risk assessment has focused on protecting the health of individual people or populations of wildlife from single risks, mostly from chemical exposure. The U.S. Environmental Protection Agency recently began to address multiple risks to communities in the “Framework for Cumulative Risk Assessment” [EPA/630/P02/001F. Washington DC:Risk Assessment Forum, U.S. Environmental Protection Agency (2003)]. Simultaneously, several reports concluded that some individuals and groups are more vulnerable to environmental risks than the general population. However, vulnerability has received little specific attention in the risk assessment literature. OBJECTIVE: Our objective is to examine the issue of vulnerability in cumulative risk assessment and present a conceptual framework rather than a comprehensive review of the literature. In this article we consider similarities between ecologic and human communities and the factors that make communities vulnerable to environmental risks. DISCUSSION: The literature provides substantial evidence on single environmental factors and simple conditions that increase vulnerability or reduce resilience for humans and ecologic systems. This observation is especially true for individual people and populations of wildlife. Little research directly addresses the topic of vulnerability in cumulative risk situations, especially at the community level. The community level of organization has not been adequately considered as an end point in either human or ecologic risk assessment. Furthermore, current information on human risk does not completely explain the level of response in cumulative risk conditions. Ecologic risk situations are similarly more complex and unpredictable for cases of cumulative risk. CONCLUSIONS: Psychosocial conditions and responses are the principal missing element for humans. We propose a model for including psychologic and social factors as an integral component of cumulative risk assessment

Is telomere length socially patterned? Evidence from the West of Scotland Twenty-07 study

Lower socioeconomic status (SES) is strongly associated with an increased risk of morbidity and premature mortality, but it is not known if the same is true for telomere length, a marker often used to assess biological ageing. The West of Scotland Twenty-07 Study was used to investigate this and consists of three cohorts aged approximately 35 (N = 775), 55 (N = 866) and 75 years (N = 544) at the time of telomere length measurement. Four sets of measurements of SES were investigated: those collected contemporaneously with telomere length assessment, educational markers, SES in childhood and SES over the preceding twenty years. We found mixed evidence for an association between SES and telomere length. In 35-year-olds, many of the education and childhood SES measures were associated with telomere length, i.e. those in poorer circumstances had shorter telomeres, as was intergenerational social mobility, but not accumulated disadvantage. A crude estimate showed that, at the same chronological age, social renters, for example, were nine years (biologically) older than home owners. No consistent associations were apparent in those aged 55 or 75. There is evidence of an association between SES and telomere length, but only in younger adults and most strongly using education and childhood SES measures. These results may reflect that childhood is a sensitive period for telomere attrition. The cohort differences are possibly the result of survival bias suppressing the SES-telomere association; cohort effects with regard different experiences of SES; or telomere possibly being a less effective marker of biological ageing at older ages