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"Harris, Kathleen"
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Genes, gender inequality, and educational attainment
Women’s opportunities have been profoundly altered over the past century by reductions in the social and structural constraints that limit women’s educational attainment. Do social constraints manifest as a suppressing influence on genetic indicators of potential, and if so, did equalizing opportunity mean equalizing the role of genetics? We address this with three cohort studies: the Wisconsin Longitudinal Study (WLS; birth years 1939 to 1940), the Health and Retirement Study, and the National Longitudinal Study of Adolescent Health (Add Health; birth years 1975 to 1982). These studies include a “polygenic score” for educational attainment, providing a novel opportunity to explore this question. We find that within the WLS cohort, the relationship between genetics and educational outcomes is weaker for women than for men. However, as opportunities changed in the 1970s and 1980s, and many middle-aged women went back to school, the relationship between genetic factors and education strengthened for women as they aged. Furthermore, utilizing the HRS and Add Health, we find that as constraints limiting women’s educational attainment declined, gender differences in the relationship between genetics and educational outcomes weakened. We demonstrate that genetic influence must be understood through the lens of historical change, the life course, and social structures like gender.
Journal Article
AN INTEGRATIVE APPROACH TO HEALTH
In this article, I make the case for using an integrative approach to health, broadly defined as social, emotional, mental, and physical well-being; for studying health among the young as an important marker for future health and well-being across the life course; and for understanding health disparities among the young as both causes and consequences of social stratification. An integrative approach bridges biomedical sciences with social and behavioral sciences by understanding the linkages between social, behavioral, psychological, and biological factors in health. It is furthermore vital that integration occur in all steps of the research process: in theory, design, data collection, and analysis. I use the National Longitudinal Study of Adolescent Health, or Add Health, as an example of an integrative approach to health and of the importance of adolescence and the transition to adulthood years for setting health trajectories into adulthood. Evidence is also presented on the linkages between health trajectories during adolescence and the transition to adulthood and social stratification in adulthood.
Journal Article
Childhood Family Instability and Young Adult Health
American children live in a variety of family structures throughout their childhoods. Such instability in family arrangements is common and has important demonstrated implications for short-term child outcomes. However, it is not known whether family instability experienced in childhood has enduring health consequences across the life course. Using demographic, social, and biological data from the National Longitudinal Study of Adolescent to Adult Health, we investigate the family stress model, testing the relationship between parental family instability in childhood and four biological markers of health in young adulthood. This is the first study to examine whether the accumulation of family change in childhood leaves a lasting physiological residue. While family instability is associated with poorer short-term behavioral and socioeconomic outcomes as documented in previous research, we find no evidence of deleterious young adult health consequences. These findings are robust across different measures of physiological health risk and types of family transitions.
Journal Article
Education, Smoking, and Cohort Change
Sociologists interested in the effects of genes on complex social outcomes claim environmental conditions structure when and how genes matter, but they have only studied environmental moderation of genetic effects on single traits at a time (gene-by-environment interactions). In this article, we propose that the social environment can also transform the genetic link between two traits. Taking the relationship between educational attainment and smoking as an exemplary case, we use genome-wide methods to examine whether genetic variants linked to education are also linked to smoking, and whether the strength of this relationship varies across birth cohorts. Results suggest that the genetic relationship between education and smoking is stronger among U.S. adults born between 1974 and 1983 than among those born between 1920 and 1959. These results are supported by replication in additional data from the United Kingdom. Environmental conditions that differ across birth cohorts may result in the bundling of genetic effects on multiple outcomes, as anticipated by classic cohort theory. We introduce genetic correlation-by-environment interaction [(rG)xE] as a sociologically-informed model that will become especially useful as data for more well-powered analyses become available.
Journal Article
Cytokines in Chronic Rhinosinusitis. Role in Eosinophilia and Aspirin-exacerbated Respiratory Disease
Abstract
Rationale
The mechanisms that underlie the pathogenesis of chronic rhinosinusitis without nasal polyps (CRSsNP), chronic rhinosinusitis with nasal polyps (CRSwNP), and aspirin-exacerbated respiratory disease (AERD) are not clear.
Objectives
To first evaluate the inflammatory profiles of CRSsNP and CRSwNP tissues and then to investigate whether clinical differences observed between CRSwNP and AERD are in part secondary to differences in inflammatory mediator expression within nasal polyp (NP) tissues.
Methods
Expression levels of numerous inflammatory mediators were determined by quantitative real-time polymerase chain reaction, ELISA, and multiplex immunoassay.
Measurements and Main Results
CRSwNP NP had increased levels of type 2 mediators, including IL-5 (P < 0.001), IL-13 (P < 0.001), eotaxin-2 (P < 0.001), and monocyte chemoattractant protein (MCP)-4 (P < 0.01), compared with sinonasal tissue from subjects with CRSsNP and control subjects. Expression of IFN-γ messenger RNA or protein was low and not different among the chronic rhinosinusitis subtypes examined. Compared with CRSwNP, AERD NP had elevated protein levels of eosinophil cationic protein (ECP) (P < 0.001), granulocyte–macrophage colony–stimulating factor (GM-CSF) (P < 0.01), and MCP-1 (P = 0.01), as well as decreased gene expression of tissue plasminogen activator (tPA) (P = 0.02). Despite the higher eosinophilia in AERD, there was no associated increase in type 2 mediator protein levels observed.
Conclusions
CRSwNP was characterized by a predominant type 2 inflammatory environment, whereas CRSsNP did not reflect a classic type 1 milieu, as has been suggested previously. AERD can be distinguished from CRSwNP by elevated ECP levels, but this enhanced eosinophilia is not associated with elevations in traditional type 2 inflammatory mediators associated with eosinophil proliferation and recruitment. However, other factors, including GM-CSF, MCP-1, and tPA, may be important contributors to AERD pathogenesis.
Journal Article
Social relationships and physiological determinants of longevity across the human life span
Two decades of research indicate causal associations between social relationships and mortality, but important questions remain as to how social relationships affect health, when effects emerge, and how long they last. Drawing on data from four nationally representative longitudinal samples of the US population, we implemented an innovative life course design to assess the prospective association of both structural and functional dimensions of social relationships (social integration, social support, and social strain) with objectively measured biomarkers of physical health (C-reactive protein, systolic and diastolic blood pressure, waist circumference, and body mass index) within each life stage, including adolescence and young, middle, and late adulthood, and compare such associations across life stages. We found that a higher degree of social integration was associated with lower risk of physiological dysregulation in a dose–response manner in both early and later life. Conversely, lack of social connections was associated with vastly elevated risk in specific life stages. For example, social isolation increased the risk of inflammation by the same magnitude as physical inactivity in adolescence, and the effect of social isolation on hypertension exceeded that of clinical risk factors such as diabetes in old age. Analyses of multiple dimensions of social relationships within multiple samples across the life course produced consistent and robust associations with health. Physiological impacts of structural and functional dimensions of social relationships emerge uniquely in adolescence and midlife and persist into old age.
Journal Article
The Biosocial Approach to Human Development, Behavior, and Health Across the Life Course
Social and biological phenomena are widely recognized as determinants of human development, health, and socioeconomic attainments across the life course, but our understanding of the underlying pathways and processes remains limited. To address this gap, we define the \"biosocial approach\" as one that conceptualizes the biological and social as mutually constituting, and that draws on models and methods from the biomedical and social/behavioral sciences. By bringing biology into the social sciences, we can illuminate mechanisms through which socioeconomic, psychosocial, and other contextual factors shape human development and health. Human biology is a social biology, and biological measures can therefore identify aspects of social contexts that are harmful, as well as beneficial, with respect to well-being. By bringing social science concepts and study designs to biology and biomedicine, we encourage an epistemological shift that foregrounds social/contextual factors as important determinants of human biology and health. The biosocial approach also underscores the importance of the life course, as assessments of both biological and social features throughout human development over time, and across generations, are needed to achieve a full understanding of social and physical well-being. We conclude with a brief review of the papers in the volume, which showcase the value of a biosocial approach to understanding the pathways linking social stratification, biology, and health across the life course.
Journal Article
Partner Gender Differences in Prestige of Clients Served at the Largest U.S. Audit Firms
Despite tremendous investment to promote gender equity, U.S. public accounting firms continue to be gendered organizations. Our archival study examines gender equity within the partnership of these large firms for a one-year period. We find female partners are clustered in lower prestige client types including investment funds, benefit plans, and single audits, rather than higher prestige public company clients. Second, we consider whether there is gender bias in prestige of client served by female partners who lead public company audits. In these tests of those individuals who have already achieved the partnership and lead public company audits, we find no evidence of bias. This research contributes to the understanding of gender bias in U.S. public accounting firms and helps inform the societal narrative on where women continue to be marginalized even when they have achieved the highest levels in an organization.
Journal Article
Patterns and Life Course Determinants of Black–White Disparities in Biological Age Acceleration: A Decomposition Analysis
Despite the prominence of the weathering hypothesis as a mechanism underlying racialized inequities in morbidity and mortality, the life course social and economic determinants of Black–White disparities in biological aging remain inadequately understood. This study uses data from the Health and Retirement Study (
= 6,782), multivariable regression, and Kitagawa–Blinder–Oaxaca decomposition to assess Black–White disparities across three measures of biological aging: PhenoAge, Klemera–Doubal biological age, and homeostatic dysregulation. It also examines the contributions of racial differences in life course socioeconomic and stress
and
to those exposures to Black–White disparities in biological aging. Across the outcomes, Black individuals exhibited accelerated biological aging relative to White individuals. Decomposition analyses showed that racial differences in life course socioeconomic exposures accounted for roughly 27% to 55% of the racial disparities across the biological aging measures, and racial disparities in psychosocial stress exposure explained 7% to 11%. We found less evidence that heterogeneity in the associations between social exposures and biological aging by race contributed substantially to Black–White disparities in biological aging. Our findings offer new evidence of the role of life course social exposures in generating disparities in biological aging, with implications for understanding age patterns of morbidity and mortality risks.
Journal Article