Session sponsored by Wiley – Publisher of Developmental Psychobiology
Chairs:
Jessica F. Sperber, Session Chair, Teachers College, Columbia University, New York, United States
Dr. Kimberly G. Noble, MD, PhD, Session Co-Chair and Discussant, Professor of Neuroscience and Education, Director, Developmental Psychology Program, Teachers College, Columbia University
Symposium Presenters:
Jessica F. Sperber, Teachers College, Columbia University, New York, United States
Abby deSteiguer, MSc, MA, University of Texas at Austin, Austin, United States
Yayouk Willems, PhD, Max Planck Research Group Biosocial – Biology, Social Disparities, and Development; Max Planck Institute for Human Development, Berlin, Germany
Matthew Zipple, PhD, Cornell University, Department of Neurobiology and Behavior, Ithaca, United States
Symposium Description:
The experience of low social status is robustly associated with deleterious physical, cognitive, and behavioral outcomes across the lifespan. Recent work has identified epigenetic signatures that are sensitive to both early experiences of inequality as well as the associated health outcomes of socioeconomic disadvantage. Understanding how these biomarkers respond to social environments and their emergence over the life course will enable researchers to examine in real-time the long-term effects of social inequality on developmental trajectories of health and well-being.
To begin, Jessica Sperber will examine the extent to which biomarkers of social status are detectable at the beginning of postnatal life by discussing a pre-registered analysis of the link between prenatal socioeconomic status and epigenetic aging in newborns. Next, Abby deSteiguer will present a novel DNA methylation biomarker of socioeconomic position developed in saliva samples from a longitudinal study of children. Next, Dr. Yayouk Willems will present pre-registered findings of the first randomized control trial of poverty reduction in the United States. These results reveal the extent to which a DNA methylation index of biological aging in children is causally related to changes in socioeconomic status. Finally, Dr. Matthew Zipple will present experimental work in rodents demonstrating the impact of early life contingencies on social status, as well as the downstream epigenetic differences in physiological functioning of experiencing a low social position among genetically identical mice. Dr. Kimberly Noble will subsequently lead a discussion around the social determinants of health, biological mediators of socioeconomic disadvantage, and the implications of the works presented for the field at large.
This symposium encompasses 4 areas of research – correlational, measure development, causal designs, and animal models – to integrate the study of socioeconomic disparities on human health and well-being. Furthermore, this symposium will showcase four early career researchers in predoctoral and postdoctoral positions, conducting innovative research. This international group of promising young scholars will showcase novel and multimodal methods of research with a particular focus on reducing social disparities and improving developmental trajectories for the most under-resourced communities.
Presentations:
ASSOCIATIONS AMONG SOCIOECONOMIC STATUS AND ACCELERATED AGING IN NEWBORN INFANTS
Presenter: Jessica F. Sperber, Teachers College, Columbia University, New York, United States
Additional Authors: Emma R. Hart1, Sonya V. Troller-Renfree1, Tyler W. Watts1, Melissa Miller2, Ariel Bellatin2, Jerrold Meyer3, Amanda M. Dettmer4, Frances A. Champagne2, Kimberly G. Noble1
Affiliations:
1 Teachers College, Columbia University
2 University of Texas at Austin
3 University of Massachusetts-Amherst
4 Yale Child Study Center, Yale School of Medicine
Abstract
Numerous studies find that early life exposure to socioeconomic disadvantage is associated with epigenetic indicators of accelerated biological aging during later childhood and adolescence. However, it is unknown when these associations first emerge during development. The present study investigates the associations among maternal socioeconomic status during pregnancy and indicators of biological aging in newborn infants. In this pre-registered investigation, we hypothesized that lower prenatal socioeconomic status (SES) would be associated with accelerated aging in infants.
A socioeconomic and racially diverse sample of participants were recruited from New York City during the last 5 weeks of pregnancy (n=209). At the prenatal visit, mothers reported their years of formal education as well as their annual household income and household size to calculate family income-to-needs ratio. At 1-month postpartum, a saliva sample was collected from infants to assess epigenetic aging. Sample were analyzed for concentration of DNA methylation using EPIC 850k Beadchip Arrays. This data was used to calculate several different estimates of epigenetic age (Horvath, PedBE, PhenoAge, GrimAge, and DunedinPACE).
We observed small, nonsignificant associations between prenatal socioeconomic factors (family income, maternal education) and multiple measures of epigenetic aging. These associations were unchanged after adjusting for demographic characteristics. Overall, we did not detect a robust association between prenatal socioeconomic status and infant epigenetic aging. Findings will be discussed in the context of previous studies on biological aging and socioeconomic disparities in later childhood. Furthermore, we consider the validity of assessing epigenetic aging during infancy using algorithms developed in adult samples.
DNA-METHYLATION PATTERNS OF SOCIOECONOMIC STATUS AND POVERTY IN CHILDREN’S SALIVA
Presenter: Abby deSteiguer, MSc, MA, University of Texas at Austin, Austin, United States
Additional Authors: Wu, Q.2, Smith, T.3, Goode, J.3, Tucker-Drob1,4, E.M., Mitchell, C.3,5, Harden1,4, K.P., Raffington, L.2
Affiliations:
1Department of Psychology, University of Texas at Austin, Austin, TX, USA
2Max Planck Institute for Human Development; Max Planck Research Group Biosocial – Biology, Social Disparities, and Development, Berlin, Germany
3Survey Research Center of the Institute for Social Research, University of Michigan, Ann
Arbor, Michigan, USA
4Population Research Center, The University of Texas at Austin, Austin, TX, USA
5Population Studies Center, University of Michigan, Ann Arbor, Michigan, USA
Abstract
Early life socioeconomic contexts and poverty are associated with a range of developmental processes including cognitive and pubertal development, as well as physical and mental health in later life. Epigenome-wide analysis of DNA-methylation (DNAm) in children may help identify biosocial pathways that link early life socioeconomic contexts and poverty to lifespan development and health. We leverage two large, sociodemographically diverse cohorts of children and adolescents to identify epigenetic markers of childhood socioeconomic status (SES) and poverty. First, we perform a meta-analyzed epigenome-wide association study to identify biological pathways associated with SES and poverty in US children from the Texas Twin Project and the Future of Families Child Wellbeing Study. Second, we use elastic net models to develop methylation profile scores (MPSs) of childhood socioeconomic status and poverty in those cohorts. Third, using the multi-generational Framingham Heart Study, we probe whether these DNAm scores, when calculated in adulthood, are associated with adults’ childhood socioeconomic contexts. We compare our genome-wide DNAm results to discoveries from previous studies of DNAm associations with socioeconomic status, and our novel MPSs of SES and poverty to existing epigenetic clocks that index biological aging (DunedinPACE, GrimAge, PhenoAge).
EFFECTS OF A CASH TRANSFER RANDOMIZED CONTROLLED TRIAL ON CHILD EPIGENETIC INDICATORS OF BIOLOGICAL AGING AND COGNITION
Presenter: Yayouk Willems, Ph.D.+ , Max Planck Research Group Biosocial – Biology, Social Disparities, and Development; Max Planck Institute for Human Development, Berlin, Germany
Additional Authors: Raffington, L. 1, Sperber, J. F. 2+, Costanzo, M. A.3, Zarandooz, S.Z. 1, Notterman, D.A. 4, Mitchell, C. 5,6, Tucker-Drob, E. M.7,8, Gennetian, L. A.9, Fox, N. A.10, Yoshikawa, H. 11, Greg J. Duncan12, Magnuson, K.3, Troller-Renfree, S.V.2, Binder, E.B. 13, Harden, K. P. 7,8, Noble, K.G.2
Affiliations:
1 Max Planck Research Group Biosocial – Biology, Social Disparities, and Development; Max Planck Institute for Human Development
2 Teachers College, Columbia University
3 Institute for Research on Poverty, University of Wisconsin–Madison
4Department of Molecular Biology, Princeton University
5 Survey Research Center, University of Michigan
6Population Studies Center, University of Michigan
7 Department of Psychology, University of Texas at Austin
8 Population Research Center, University of Texas at Austin
9 Sanford School of Public Policy, Duke University
10 Department of Human Development and Quantitative Methodology, University of Maryland
11Global TIES for Children Center, New York University
12School of Education, University of California
13 Department Genes and Environments; Max Planck Institute for Psychiatry
+ These authors contributed equally
Abstract
Children who grow up in poverty show, on average, poorer cognitive performance, educational attainment, and mental and physical health throughout life, extending into old age. Epigenetic changes, which regulate gene activity, have been proposed as a molecular mechanism by which early childhood environments are biologically embedded to affect lifelong health and cognition. Previous correlational studies of cohorts of children and adolescents have found that children growing up in environments characterized by socioeconomic disadvantage show evidence of epigenetic (DNA methylation) profile scores that – in adults – are associated with faster biological aging and lower cognitive performance. However, DNA methylation profile scores have yet to be integrated into experimental designs capable of testing causal hypotheses about the impact of childhood environments.
Here we report results from our clinical trial preregistration (ClinicalTrials.gov identifier NCT03593356) examining whether cash transfers to low-income mothers for the first 4 years of the child’s life cause differences in the child’s methylation profile scores of the pace of biological aging (DunedinPACE) and cognitive performance (Epigenetic-g). Additionally, we report results from our preregistered analysis plan (https://osf.io/8grhj) probing whether there is an interaction between treatment group and these methylation profile scores in the association with developmental traits (body mass index, health, nutrition, language and cognition, and neural activity). Our results evaluate whether saliva epigenetic profiling can detect early economic influences on children’s genome.
THE IMPORTANCE OF COMPETITION AND EARLY LIFE LUCK FOR THE DEVELOPMENT OF INDIVIDUALITY, INEQUALITY, AND HEALTH DEFICITS IN GENETICALLY IDENTICAL, FREE-LIVING MICE
Presenter: Matthew Zipple, Ph.D., Cornell University, Department of Neurobiology and Behavior, Ithaca, United States
Additional Authors: Daniel Chang Kuo1,2, Xinmiao Meng1,3, Tess M Reichard1, Kwynn Guess1, Caleb C Vogt1, Andrew H Moeller1,4, Michael J Sheehan1
Affiliations:
1Cornell University, Department of Neurobiology and Behavior, Ithaca NY
2University of California Berkeley, Department of Integrative Biology, Berkeley CA
3Yale University, School of Public Health, New Haven CT
4Princeton University, Department of Ecology and Evolutionary Biology, Princeton NJ
Abstract
Contingency (or ‘luck’) plays an important role in shaping individuals’ development. When individuals live within larger societies social experiences may cause the importance of early contingencies to be magnified or dampened. Here we test the hypothesis that competition magnifies the importance of early contingency by comparing the developmental trajectories of genetically identical, free-living lab mice who either experienced high levels of territorial competition (males) or did not (females). We show that male territoriality results in a competitive feedback loop that magnifies the importance of early contingency and pushes individuals onto divergent, self-reinforcing life trajectories. By early adulthood, genetically identical males who all started life with equal opportunities display strikingly unequal life outcomes. Using bulk RNA sequencing data, we also show that low social status affects expression of 20% of all genes in the liver, including markers of increased immune activity and oxidative stress. Our results have implications for understanding the role of luck, competition, and merit on life outcomes as well as the constraints of reducing inequality by equalizing opportunity.