Embodiment, Plasticity, Biosociality, and Epigenetics: The Politics of a Vulnerable Body for Toxic Times
Maurizio Meloni
The complex links between social structures and biological bodies are increasingly recognized. The field of epigenetics offers scientific evidence about the “biological embedding” of social experience - how environmental factors can be inscribed on the biological body. However, the social implications of epigenetics for race, class, and gender inequalities have to be addressed carefully.
While ideas of embodiment are far from new and go back in the West to the Hippocratic treatise on Airs, Waters, and Places in the 5th/4th century BCE, modern biomedical views, and genetics in particular, have traditionally sidelined this ecological line of thought. Biomedical thought in the 20th century has mostly foregrounded internal factors, such as genes, as the root of health trajectories. Significantly, this line of thought has tended to clearly separate biological from social factors, postulating the latter intervene at some secondary time to alter or interact with the capacity of the first. The last three decades have witnessed a significant questioning of this approach. As reviewed in Impressionable Biologies (Meloni, 2019), a wealth of evidence has emerged on the complex pathways that link social experience to biology, health and disease risk, opening up questions on the separation of biological and social factors.
At the level of the individual body, data from neuroimmunolog-ical research and neuroscience have highlighted the dependence of neuroendocrine and immune functions on social and psychological processes. The emphasis has been on how socio-economic status and social structures - such as the qualities of neighborhoods and communities, or social isolation - may have a profound impact on brain development and functioning and patterns of morbidity and mortality (Cacioppo & Patrick, 2008). Moving from the individual body to what Stuckler and Basu (2013) call the “body economic,” an increasing number of studies now focus on the way in which austerity policies and inequalities are literally killing factors. As Krieger argued in Epidemiology and People’s Health (2011), these recent works can be better appreciated within the context of a longer tradition of social epidemiology research on how inequality, discrimination, and racism literally harm health, producing different population patterns of disease distribution.
Epigenetics and Embodiment: Deepening the Agenda
A framework rooted in biological embedding-to use Clyde Hertzman’s term - posits that the biological body bears the inscriptions of its lived experience and its social and material contexts, and these contexts are constituted by the socially modulated biographies of the body, past and present (toxic exposures, dietary factors, financial and educational capital, social networks). Epigenetics has raised hope and expectations that it could provide this debate on how environmental factors get under the skin and are inscribed on the biological body with crucial, and so far missing, molecular evidence. Epigenetics describes changes to the chemical structure of DNA triggered by environmental cues. These changes alter gene and phenotypic expression of an organism without change to DNA base-pair sequences.
Coined by British embryologist and polymath C. H. Waddington (1905 1975) in the 1940s, epigenetics was originally meant as a neologism from epigenesis (not “on the top of” or “above genes” as in today’s folk etymology) to define in a broader nonmolecular sense an interdisciplinary study of all the “causal interactions between genes and their products which bring the phenotype into being” (Waddington, 1942, cited in Meloni, 2019). Since the early 2000s, epigenetics has turned into a burgeoning subbranch of molecular biology where the developmental complexity that links genes and environments to phenotypes is investigated at the molecular level. DNA methylation is the most recognized and studied of these molecular mechanisms of epigenetic mutation. The term refers to the addition of a methyl group to a DNA base, resulting in inhibition of gene transcription. It is often dependent on nutritional or wider extra-cellular factors, giving a wider dynamism to genetic functioning.
Michael Meaney’s experiments on the transmission of poor maternal care in rats well illustrate this dynamism of the genome via methylation changes, where wider social signals regulate the organism physiology. Certain behavioral exposures (low licking/ grooming by the mother rat, or dam) shape changes in methylation patterns in offspring that alter genetic expression and hence long-term neurochemical responses in the brain. This modifies the physiology of the pups, who, as adults, will reproduce the inducing behavior and consequently modify their environmental niche, thus shaping the biological life also of a next generation. Importantly, cross-fostering pups to high licking/grooming dams reversed the methylation pattern (Weaver et al., 2004, cited in Meloni, 2016).
Although epigenetics is often described as the fifth letter of the linear genetic code, it is better understood as an environmentally driven change to chromatin, the macromolecule into which DNA fibers are folded, comprising chromosomes (see Meloni, 2019, for more detail). In a nutshell and at the cost of simplification, DNA is structurally constrained by chromatin architecture and this architecture can be remodeled partly in response to environmental inputs. Chromatin strands can be transcriptionally “open,” and thus potentially expressed, or “closed,” and thus silenced by wider cellular and extra-cellular signals. The flexible rearrangement of chromatin structure enables the dynamic interplay between gene functions and the environment, and more broadly organism and milieu over the lifespan. As a regulator of the chromatin system, epigenetics constitutes a significant opportunity to reconceptualize embodiment in a way that includes genetics factors. However, the so-called post-genomic genome is no longer seen in the driving seat of biological processes. Rather, it has to be understood as embedded into a context-dependent regulative framework, described as highly sensitive and responsive to environmental influences, plastic to social effects and cues. It has become a biosocial genome, to use Muller and colleagues’ (2017) term. This line of investigation highly complicates the neat distinction between biological and social factors, calling increasingly for a “biology of social causes” and a “sociology of biological effects.” It is at this level that the debates on biosocial models of health and disease or biological plasticity have attracted increasing interest and may become an important platform for cross-disciplinary collaborations across the social/natural science divide.
Epigenetics in Toxic Times: A Politics of Vulnerable Bodies
The reassuring fiction of a DNA segregated from experiential factors, which translates into reassuring disciplinary boundaries between nature-oriented and culture-oriented disciplines, may be a luxury we cannot afford anymore given the ubiquitous toxicity of life in the Anthropocene. Epigenetic changes are likely to be studied as an archive or a biomarker of toxic exposures that, especially in crucial key windows of development (in utero, early life, adolescence, pregnancy), may materialize as a morbid alteration to present and future health trajectories. A small but growing body of literature has also highlighted the potential multigenerational effects of poisoned exposures, either to stress, famine, or social exploitation and violence.
The policy implications of these emerging findings, however, present a number of ethical and social dilemmas that need to be addressed carefully. Care is particularly important because there is a long (albeit often forgotten) history of eugenic and racist policies based on the belief that heredity is not fixed at birth but influenced by the environment and hence bad environments result in damaged people (Meloni, 2016). For instance, if the effects of a future parent’s diet on offspring’s wellbeing are validated by epigenetic findings, how does this change notions of responsibility and risk, normality and pathology? If the genome can be damaged by smoking or optimized through exercise, will we not - as White and Wastell (2016) suggest - monitor individual lifestyles more carefully than ever? In this way, aren’t lifestyle and behavioral structures increasingly burdened with biomedical implications and hence normative demands? What about recent popular and scientific claims that people are “poisoned” or “marked for life” by bad environments? Will this lead to claims about social justice and reparation or an identification of vulnerable groups as “at greater risk” and hence open to new types of regulation, policy and medical surveillance?
The recent epigenetic and developmentalist argument that racial differences in health are not the product of a set of inherited genes but the biological embedding of common exposures to racialized structures and social gradients of stress (Kuzawa & Sweet, 2009, cited in Meloni, 2016) may legitimize the notion that there is, after all, a biological meaning to race. Moreover, if people embody their toxic environments in this linear way, and if some of these effects may travel across a certain number of generations, what are policymakers supposed to do with this notion? Offer compensation or reparation for what has occurred in the past and still haunt the biology of contemporary generations? Or instead, as it occurred in past eugenics arguments, use this notion to claim that certain groups are too damaged (not by faulty genes but by toxic histories) to deserve a substantial financial or educational investment for their future? And what about the gender inequality of epigenetic effects, given that women embody their surrounding environments in a more direct way, especially during pregnancy? Might they not be increasingly encouraged by developmental models to plan the health of their offspring well before conception - and to be expected to do so by others - which is a burden not equally borne by men? Finally, what sort of embodiment is epigenetics promoting? One where people are just seen as the passive receivers, not this time of DNA signals but of environmental exposures? How can ideas of agency and vitality be rescued in this model?
These dilemmas do not mean that research in epigenetics will necessarily be hijacked into racialist or sexist political agendas. However, they should sound a warning that views of embodiment and ecologies of the body are not necessarily simplistically aligned with politically progressive views.
For Sources and Further Reading
Cacioppo, J., & Patrick, B. (2008). Loneliness: Human nature and the need for social connection. New York: Norton & Company.
Krieger, N. (2011). Epidemiology and people's health: Theory and context. New York: Oxford University Press.
Meloni, M. (2016). Political biology: Science and social values in human heredity from eugenics to epigenetics. London: Palgrave.
Meloni, M. (2019). Impressionable biologies: From the archaeology of plasticity to the sociology of epigenetics. New York: Routledge.
Müller, R., Hanson, C., Hanson, M., Penkier, M., Samaras, G., Chiappe-rino, L., ... Villa, P. (2017). The biosocial genome? EMBO Reports, 18, 1677-1682.
Stuckler, D., & Basu, S. (2013) The body economic: Why austerity kills. London: Allen Lane.
White, S. J., & Wastell, D. G. (2016). Epigenetics prematurely born(e): Social work and the malleable gene. British Journal of Social Work. 47(4), 2256-2272.
