By Arline T. Geronimus, Sc.D.
Professor, Health Behavior and Health Education, School of Public Health
Research Professor, Population Studies Center, Institute for Social Research
University of Michigan
My monozygotic twins—now young men—never engaged in parallel play with each other. Parallel play is a type of toddler-to-preschool play where, even though two or more children are in the same room or even the same sandbox, they each remain absorbed in their own personal activity and do not interact. Yet before they could walk or talk, my sons delighted in playing together, cooperating on projects, and putting on musical performances that they would end by bowing in unison, each one’s arm around the other’s waist. They scaled higher heights, literally, than playing alone. We found them lying on the tops of our highest kitchen cabinets, giggling together, when they were 2. Even strapped into their stroller, they enacted perfectly synchronized and complexly coordinated routines we called “stroller surfing,” which were at once wonderful and hair-raising to watch and noticeably enchanting to passersby.
My sons were then—and they remain to this day—among the most engaged, charismatic, sociable, and creative people I have known. Most likely being twins had something—maybe even a lot—to do with this. While causality is hard to prove, I often think that their continuing creativity and ability to work things out owes much to having been able to play interactively from the beginning. Maybe it was a twin thing, but it set in motion positive recursive processes.
As part of the NIMHD visioning process on life course approaches to causes of health disparities, we began with members in parallel play. We all agreed that life course approaches are critical to understanding the development and perpetuation of social inequities in health, but we came with strong ideas based on our own scholarly histories on what a life course approach was and why it mattered. Our first instinct was to turn to parallel play rather than do the harder, more creative work of integrating our different perspectives, evidence bases, and scholarly commitments. Working together over several months and iterations to produce one analytic essay on the etiology of health disparities through a life course lens, we set the stage for a more integrated theoretical and scientific approach.1
We established that our different perspectives on the life course could be categorized as developmental and structural. The developmental life course approach is theorized in the developmental origins of health and disease (DOHaD) hypothesis. It focuses attention on the role of critical and sensitive developmental stages in shaping later life health. Gene–environment interactions during fetal, infant, early childhood, and adolescent development produce the biological architecture that at a minimum heavily influences and perhaps even programs later life health. The rationale is that heightened plasticity in these early periods enables environmental exposures or deficiencies to more profoundly affect development than at other times, with enduring effects. Mechanistically, adverse uterine or childhood environments activate epigenetic modifications during these highly plastic periods that remain consequential across the life span.2
The structural life course approach can be encapsulated by the theory of weathering3, a cumulative stress perspective grounded in social research. It proposes that different social identity groups— identified by race, ethnicity, religion, sexual orientation, gender, socioeconomic position, place, immigrant status, et cetera—have different lived experiences that are structured in part by history, policies, power dynamics, and dominant cultural frameworks. These frameworks influence the distribution, cadence, and intensity of life course demands and stressors across various social groups, as well as the coping resources these groups have available. Mechanistically, the structural perspective focuses on the health effects of physiological stress processes that are chronically activated in marginalized groups and the persistent high-effort coping this requires of them, especially in the young adult through middle ages, when family leadership roles are assumed. The resultant stress-mediated wear and tear on important body systems and cellular integrity precipitate accelerated aging, the dysregulation of body systems by midlife, and the early onset of chronic diseases of aging.4
Although they have different emphases and draw on different scientific frames and skills, these two perspectives are not mutually exclusive. For some overlapping and some different reasons, each perspective is hard to prove.5 In parallel play, advocates of each perspective make a case for causal evidence of that perspective, yet neither case is subject to constructive cross-examination by the other, and neither benefits from the skills and knowledge the other may have to fill in gaps.
Moreover, refinements of theory, empirical tests, and translation of findings to promote heath equity will surely benefit from the deep integration of both perspectives, including interdisciplinary work across the biomedical and social sciences—and even the humanities to discern important historical, policy, and ethnographic influences on lived experience that shape health across the life course.5
But scientists with different backgrounds, skill sets, and perspectives continue to parallel play. And worse, power dynamics apply to favor biomedical research, inasmuch as substantially more resources are awarded to elucidating the developmental compared with the structural perspective. Meanwhile, population health inequities persist and, in some areas, have grown. We in the scientific community could take a note from my 2-year-old sons. Engaging in interactive play can lead to more creative, enchanting, and productive synergies than continuing to parallel play in the same sandbox.
- Jones, N. L., Gilman, S. E., Cheng, T. L., Drury, S. S., Hill, C. V., & Geronimus, A. T. (2019). Life course approaches to advance the understanding of the causes of health disparities. American Journal of Public Health, 109(S1), S48–S55. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6356123/
- Gluckman, P. D., Hanson, M. A., Cooper, C., & Thornburg, K. L. (2008). Effect of in utero and early-life conditions on adult health and disease. New England Journal of Medicine, 359(1), 61–73. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3923653/
- Geronimus, T., Pearson, J. A., Linnenbringer, E. P., Schulz, A. J., Reyes, A., Epel, E. S., . . . Blackburn, E. H. (2015). Race/Ethnicity, poverty, urban stressors and telomere length in a Detroit community-based sample. Journal of Health and Social Behavior, 56(2), 199–224. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4621968/
- Geronimus, T. (2013). Deep integration: Letting the epigenome out of the bottle without losing sight of the structural origins of population health and disease. American Journal of Public Health, 103(S1), S56–S63. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3786760/