You Are What Your Mother Endured: Intergenerational Epigenetics, Early Caregiving, and the Temporal Embedding of Adversity

Abstract

Environmental epigenetics has become a site of growing attention related to the intergenerational effects of stress, trauma, and adversity. This article draws on a multi-sited ethnography of epigenetic knowledge production in the United States and Canada to document how scientists conceptualize, model, and measure these experiences and their effects on children’s neurodevelopmental and behavioral health. We find that scientists’ efforts to identify the molecular effects of stress, trauma, and adversity results in a temporal focus on the mother–child dyad during early life. This has the effect of biologizing early childhood adversity, positioning it as a consequence of caregiving, and producing epigenetic findings that often align with individually oriented interventions rather than social and structural change. Our analysis suggests that epigenetic models of stress, trauma, and adversity therefore situate histories of oppression, inequality, and subjugation in discrete and gendered family relations, resulting in the temporal embedding of adversity during early life.

Biologizing Adversity

A growing body of social, biomedical, and epidemiological research demonstrates that inequalities resulting from systemic forms of oppression and inadequate infrastructures of care can become biologically embedded (see Landecker 2016; Wahlberg 2018), a phenomenon that epidemiologist Nancy Krieger refers to as “embodied harm” (Krieger 2005, 2020). In the United States and Canada, the rise of environmental epigenetic research on stress, trauma, and adversity corresponds to broader concerns about environmental harm and growing urgency about the long-term, embodied impacts of early life experiences (Lamoreaux 2016; Müller et al. 2017). Informed by foundational work in animal models and the landmark Centers for Disease Control and Prevention (CDC) Kaiser Adverse Childhood Experiences (ACE) Study that found correlations between ACEs and psychosocial health and chronic disease across the life course, numerous studies now explore the impacts of early life adversity on later mental health and disease (CDC n.d.; Müller and Kenney 2020). Most recently, the COVID-19 pandemic has also laid bare what medical anthropologists and others have documented ethnographically: that social conditions produce not only distinct meanings of health, risk, and disease, they also structure the very conditions for life and death as well (Gibbon et al. 2020).

Awareness of embodied inequality is not new (Kuzawa and Quinn 2009; Kuzawa and Sweet 2009; Lock 2013, 2015; Martin 2010; Meloni et al. 2016), nor is recognition that social experiences of adversity can become “biologically embedded” (Aristizabal et al. 2019; Hertzman 2012). From the late 19th through the mid-20th century, psychosocial stress and its role in health were often understood in relation to large-scale social phenomena brought about by industrialization and the effects of war (Abbott 1990; Beard 1972 [1881]; Kirk 2014; Lazarus 1966; Robinson 2018; Selye 1950, 1974; Viner 1999). By the early 21st century, however, a molecular focus in studies of stress developed. This is exemplified by neurobiologist Michael Meaney and geneticist Moshe Szyf’s identification of an epigenetic mechanism for the effects of “maternal caregiving adversity” on the expression of stress hormones in adult offspring (Meaney et al. 2004). Based on a rodent model of stress, their findings “reinvigorated longstanding questions around the transmission and heritability of acquired features” (Pickersgill et al. 2013: 433) but in doing so, their work also naturalized heteronormative gender relations (see Franklin 2001; MacCormack and Strathern 1980) by foregrounding the mother–child dyad as central to the biologized effects of adversity. This conceptual and methodological transition in studies of stress helped produce pregnancy and children’s early neurodevelopment as central areas of concern in the logics and practices of environmental epigenetic research (Richardson 2013).

Today, the science of environmental epigenetics is used by researchers across numerous disciplines to study the biological effects of stress, trauma, and adversity, and to explore their lasting impacts on individual and intergenerational health (Landecker and Panofsky 2013; Mulligan 2016; Yehuda et al. 2009, 2014). Environmental epigenetics is a broad field of molecular biological research focused on how experiences and exposures influence gene expression without changing DNA sequence (Baedke 2017; Buklijas 2018; Jablonka and Lamb 2014). It has been heralded by some as revolutionary in its emphasis on how experiences get “under the skin” and shape health and development across generations (Aristizabal et al. 2019; Meloni and Testa 2014). This description reinforces broader shifts in understandings of the genome from static and unchanging to reactive and responsive (Keller 2014; Lappé and Landecker 2015). Others argue that epigenetics shifts attention away from structural inequalities by reinforcing individual blame, gendered responsibilities, and biological determinism (Kenney and Müller 2016; Lock 2015; Richardson et al. 2014; Waggoner and Uller 2015; Warin et al. 2012). Despite these ongoing debates surrounding the field, epigenetic findings about the lasting effects of lived experiences now circulate in everything from public health policies to direct-to-consumer tests to demands for environmental reproductive justice, reparations, and calls to address climate change (Davis 2019; Dupras et al 2020; Lappé et al. 2019; Meloni 2015; Park and Kobor 2015; Saldaña-Tejeda and Wade 2019; Warin et al. 2020).

New directions in the environmental epigenetics of stress, trauma, and adversity have also been met by a growing body of anthropological research. These include Conching and Thayer’s (2019: 74) work on the “biological pathways for historical trauma to affect health,” which focuses on epigenetics as an explanation for how “a collective trauma experienced by one generation can negatively impact the well being of future generations,” and Hoke and McDade’s (2015: 187) framework of “biosocial inheritance” that identifies “the process whereby social adversity in one generation is transmitted to the next through reinforcing biological and social mechanisms that impair health, exacerbating social and health disparities.” Alongside these frameworks, others critically examine the practices and consequences of epigenetics, particularly when it comes to the intergenerational effects of early life experiences (Champagne 2010; Mulligan 2016; Sullivan 2013; Warin et al. 2020). These scholars point out how periods of the life course are ascribed different importance within epigenetic studies (Lappé and Landecker 2015), describe conceptual and material instantiations of “the environment” (Agard-Jones 2013; Murphy 2011, 2017), and chart their racialized and gendered dimensions (Chiapperino and Panese 2018; Gkiouleka et al. 2018; Pentecost and Ross 2019; Valdez 2019; Valdez and Deomampo 2019). This work suggests that the discourse of stress, trauma, and adversity appears widely in environmental epigenetic research but, as others in this special issue observe, often serves as a limited placeholder for the social and political contexts that shape lived experiences.

In this article, we specifically consider the gender and temporal dimensions embodied in and produced through epigenetic research by exploring what is made visible and what is foreclosed, eclipsed, and left out in the production of intergenerational epigenetic knowledge related to stress, trauma, and adversity (Lloyd and Müller 2018; Tamashiro et al. 2005). We ask: What values are embedded, enacted, and inscribed onto bodies and lives when scientists attempt to trace lived experiences of adversity intergenerationally? What notions of time, biosocial connection, family, and responsibility are prioritized and produced? How is this knowledge shaping emergent understandings of health and illness related to stress, trauma, and adversity? The answers, as we illustrate below, depend both on the meanings of these concepts, and how scientists model and measure them in their research.

We argue that epigenetic studies produce a relational and temporal accounting of children’s neurodevelopmental and behavioral health that is simultaneously embodied, gendered, and cross-generational (Gibbon and Mathers 2021; Lappé and Jeffries Hein Forthcoming). Drawing on epigenetic scientists’ accounts of their research, we show how our interlocutors emphasize early life and the mother–child dyad as central to understanding the intergenerational effects of stress, trauma, and adversity. We illustrate how this naturalizes maternal care as specifically consequential for intergenerational health. While others have also observed the overwhelming focus of environmental epigenetics on mothers (Kenney and Müller 2016; Richardson et al. 2014; Sharp et al. 2018), here we document how researchers’ use of particular models of early-life stress, trauma, and adversity sustains this gendered focus. This has the effect of embedding broader social, historical, and structural conditions within the mother–child dyad during early life, reflecting what we call the temporal embedding of adversity.

Building on the language of “biological embedding,” the concept of temporal embedding draws attention to how “highly specified constructions of the environment” focused primarily on maternal care join together “biography and milieu” in ways that naturalize and individualize intergenerational health (Niewöhner 2011: 279). The temporal and gendered specificity of researchers’ conceptualizations therefore influences both how epigenetic knowledge is produced and its translational potential (Lappé and Jeffries Hein Forthcoming; Lappé and Landecker 2015; Lloyd et al. 2020). Our analysis illustrates how social values emphasizing the uniqueness of early life, the cultural importance of maternal care, and mechanistic understandings of health and behavior intertwine to shape the practices and consequences of epigenetic research.

Methods

Our findings draw on a four-year multi-sited (Marcus 1998) ethnographic study of epigenetic research related to children’s neurodevelopmental and behavioral health. Using grounded theory, we analyzed transcripts from 40 in-depth interviews with epigenetic scientists and field notes taken during approximately 200 hours of observations conducted across three university laboratories and at scientific meetings in the United States and Canada (Charmaz 2006; Glaser and Strauss 1967). Key themes found in scientific literature and media also informed our analysis and helped us triangulate our findings. Here, we analyze how our interlocutors described their concepts and practices during interviews and ethnographic visits to laboratories.

Our focus on discourse follows an approach outlined in Müller-Wille and Rheinberger’s (2007 [2004]) cultural history of heredity across scientific domains. They write that “before the metaphor of biological heredity could be applied at all, phenomena of organic reproduction had to be reconfigured discursively as to make reproduction itself accessible as a phenomenon that extended beyond the production of individual beings” (2007 [2004]: 4). We trace a similar path by documenting how our interlocutors’ conceptualize stress, trauma, and adversity and how that is reflected in the models and measures they use in their studies. Our findings suggest that discourse is not merely what is spoken by the researchers we study, but a reflection of their practices as well. In conceptualizing what counts as stress, trauma, and adversity, and situating their significance during early life, scientists’ research decisions and discussions help produce early-life adversity as molecularly meaningful in specific ways. Their conceptualizations render novel scientific models of health and illness “accessible as phenomenon”in ways that are specifically gendered and temporal. Our findings therefore point to the production of an “epistemic space” enabled by environmental epigenetics and within which a temporally specific, embodied, and gendered construct of the biology of adversity is made meaningful (Müller-Wille and Rheinberger 2007 [2004]: 4).

The university laboratories we observed were each located in a metropolitan area of the United States or Canada. Labs and interviewees were selected because of their expertise in behavioral or neurodevelopmental epigenetics. Researchers had backgrounds ranging from developmental and clinical psychology, pediatrics, and epidemiology to psychiatry, molecular biology, genetics, and biochemistry. They also varied in their careers and professional status. We interviewed and observed postdoctoral researchers, mid-career principal investigators and professors, clinician–researchers, and full professors. Many researchers we interviewed and observed embraced an interdisciplinary, “integrated training” approach, believing it had the capacity to improve communication across disciplines and positively affect what they “ultimately can do” with their research (Participant 14, 8–8–17). While our interlocutors’ specific motivations for utilizing epigenetics in their studies varied, they all emphasized its potential to bridge lived experiences and molecular understandings of health and behavior. We found that a shared epistemology focused on the unique importance of early life experiences traveled through the labs, conferences, and interviews in our study, shaping understandings of the causes and consequences of stress, trauma, and adversity (Latour and Woolgar 2013).

Sensitive Windows of Development and the Temporal Production of Stress, Trauma, and Adversity

In this section, we highlight researchers’ emphasis on the importance of early life experiences through the notion of “sensitive windows of development” and ideas about plasticity that underlie it (Lappé and Landecker 2015; Mansfield 2017; Pentecost and Ross 2019). Relaying his position on the importance of when an exposure occurs, a U.S.-based neuro-epigeneticist stated,

I think it’s pretty clear based on every piece of literature and also our own work that early periods of neurodevelopment, embryonic development, early postnatal development, are really critical. I mean, you have massive kinds of fluctuations in neurotransmission, you have kind of neural-migration effects, you’ve got a lot of transcriptional plasticity, so these things are obviously very important.

(Participant 14, 8–8–17)

He continued to explain that in his epigenetic model of the etiology of depression, “early life stress may lead to susceptibility to later life depressive-like phenotypes.” He expressed some ambivalence about later-life models as follows: “I feel like most people who are depressed don’t become depressed necessarily just because they go through a chronic bout of stress later in life. I think oftentimes there are probably more developmental components that lead to that phenotype” (Participant 14, 8–8–17).

In another instance highlighting the importance of early life, a postdoctoral fellow trained in psychology and working in a Canadian lab described her work with “postnatal touch” experiments in a rodent model of early caregiver relationships. She said:

The way I see this early relationship, it’s just the biggest part of your surroundings. Our environments we know are important, but this early caregiver relationship just kind of encompasses everything, because that’s the information the infants or young children get about the world. [It] primarily comes from their caregivers in the beginning. … And this can pick up on all these other broader contextual things that are going on like the status of a family socioeconomically, the culture, the neighborhood. All these things in those first couple years the child isn’t directly so much getting impacted by their broader social context, it’s all communicated through the family.

(Participant 21, 2–15–18)

Her conceptualization of the family, and more specifically the “early caregiver relationship” as transmitting all the “broader contextual things that are going on,” reflected how researchers often conceptualized early-life stress, trauma, and adversity in relation to the mother–child dyad (Richardson 2013; Sharp et al. 2018).

Across other sites and interviews, we found a prominence of the early mother–child dyad, even as the idea of sensitive windows of development extended to later parts of childhood. For example, the notion of “switch points” was relevant to researchers who were longitudinally tracing associations between infant stress in the mother–child dyad and children’s later brain and behavioral outcomes. They studied epigenetic modifications in amygdala functioning because of their link to memory and learning, maturation, and separation anxiety (Participant 10, 5–18–17). During an interview, a U.S.-based postdoctoral fellow provided a fuller explanation of switch points stating:

At 10–11 years old, that seems to be our switch-point age. … It’s almost like a stepwise function for us. We don’t really see this gradual change to adolescence. In many of these behaviors, this 10 to 11 [year] mark seems to be when kids are switching from whatever types of child behaviors and brain responses we’re measuring into these more adolescent-like patterns. We think that’s the switch point, and that means that their critical period is kind of this middle childhood period, so leading up to about 10 years of age.

(Participant 10, 5–18–17)

This research extends the periods of the life course brought to bear on later development, moving from an exclusive focus on early life to specific periods of pre-adolescence when early adversity may manifest. This is significant because embodiment remains a temporally contingent process that is tethered to early caregiving, but in this illustration also extends beyond pregnancy and early childhood. This suggests that sensitive windows of development can be differently conceptualized and modeled in epigenetic studies of child development, but nevertheless remain a central logic that informs all of our interlocutors’ work.

In terms of earlier exposures and experiences, while our interlocutors remained generally focused on “the epigenetics of translating early life experiences into long-lasting outcomes,” there was debate about how to characterize the possibility of ‘prenatal programming’ in particular (Participant 25, 7–13–18; see Barker 1998). A professor of psychology and brain science described this possibility, explaining: “When I think about programming, I think of [it like] you grow up in some type of environment. You can think, ‘I grew up in an abusive environment,’ and there’s great evidence that suggests that those early life stress experiences cause a change in DNA methylation” (Participant 17, 8–23–17).

However, she added that even if DNA methylation “seems pretty stable,” it is not necessarily “stuck” and should not be interpreted as determining future phenotypes (Participant 17, 8–23–17). The principal investigator of a lab studying the epigenetics of maternal caregiving in rodent and human models offered a similar position on the temporal aspects of exposure and biological plasticity. During observations of her lab, she explained:

So it’s a double edged sword, right? So you’re trying to make the statement that the quality of the early life environment is stably altering the epigenome. We’re focused mostly on DNA methylation but the same can be said of other markers. And certainly that’s true. You can see that early life predicts these outcomes that are sustained into adulthood. But we’re also trying to make the case of plasticity. They’ve obviously changed in response to the environment. Why wouldn’t they change again later on or be capable of change? I think there’s some truth to the idea that there are periods in life that are more plastic, changeable, because the brain is still developing, other tissues are still developing. And so when you have a change occurring, then it may be more likely to have sustained effects than a change occurring later on when things are a little bit more canalized.

(Participant 3, 9–20–16)

It was through these characterizations of epigenetics and sensitive windows of development that scientists focused on “how stressors become, for lack of a better word, biologically embedded”primarily during pregnancy and early childhood, even as they recognized the possibility of plasticity during other periods of the life course (Participant 38). The collective focus on specific periods of development therefore had the effect of not only producing early life as critical for child health, but also emphasizing the importance of epigenetics as a means of providing timing-specific mechanisms connecting environmental stressors and their embodied consequences. This was striking to us in part because of the extensive experiences that individuals have throughout their lives and the social conditions that would inevitably influence their health.

You Are what Your Mother Endured: Conceptualizing and Measuring the Intergenerational Effects of Adversity

In this section, we show how scientists use specific models and measures anchored in epigenetics, psychology, developmental biology, developmental origins of health and disease (DOHaD) (see Barker et al. 2010), and animal modeling to study stress, trauma, and adversity as distinct and measurable phenomena. We first highlight scientists’ struggles to conceptualize stress, trauma, and adversity. We then illustrate how epigenetic research at our sites invoked a transmission model of stress from one generation to another in both animal and human studies.

Reflecting on her research studying maternal and child health, a postdoctoral fellow in psychiatry explained that she had been “questioning a lot of assumptions and just wondering what is really going on” in studies of stress, trauma, and adversity. She explained:

I wasn’t really happy with the way it’s [trauma is] constructed as a problem. I’d like to do more research that tries to get into, not just that exposure getting to the fetus, but what’s really going on in people’s lives. The work I’m doing now is allowing me to look at things differently—we can use the word “exposures” if you’re talking about the fetus—but it’s also just life and women’s mental health and experiences in a bigger sense. … I’m trying to look at trauma, women who are survivors of either current intimate partner violence or past childhood experiences of adversity, and how that might impact her now and her pregnancy and into the future, [and] her own experience of parenting. I guess that is getting into the generational effects of trauma. I kind of wanted to think about the bigger picture, both for mom, and her mom, and for her children.

(Participant 9, 5–16–17)

Her reflections point to a nuanced appreciation for the relationships between people’s lived experiences, the embodied effects they may have across generations, and how to study them. Other researchers shared similarly layered conceptualizations of stress, trauma, and adversity, but noted that these understandings were inconsistent with what they could assess with epigenetic research alone. This finding reinforces what Niewöhner and Lock (2018) have observed, specifically that “situated biologies” and the broader complexities of human life are often reduced to molecularly measurable forms and simplified through the tools and technologies of epigenetics.

One assistant professor of neuroscience explained: “Stress is one of those things that it’s kind of subjective. It kind of depends on a lot of things going on in someone’s life, and their situation, and their social support” (Participant 22, 3–14–18). For her and others, it was precisely this subjectivity that demanded “some kind of biological measure of stress … [that] would really enable modeling these events, that would make things much easier” for epigenetic researchers (Participant 22, 3–14–18). At another lab, a postdoctoral fellow similarly explained that because adversity is “obviously a huge, broad umbrella term,” it required more specific measures and mechanisms (Participant 10, 5–18–17).

In practice, however, the molecularized approaches intended to capture complex social phenomena often diminished more robust understandings of how adversity “gets under the skin.” Despite and because of this, we found that scientists utilized particular methods in their work, including experimental animal studies and naturally occurring studies of children thought to have been uniquely exposed to early-life stress, trauma, and adversity. These models provided connections between isolated measures and lived experiences of harm, but also resulted in a focus on discrete family relations centered around the mother–child dyad. This produced reproduction and care as central domains of intervention into the intergenerational effects of stress, trauma, and adversity.

Primary to this process were models of early life stress in rodents that were similar to those used in the research by Michael Meaney and Moshe Szyf noted earlier. These models involve mother mice or rats (dams) and their offspring (pups) and entail specific protocols to produce experiences of adversity for offspring (Lappé 2018; Meaney 2001; Szyf et al. 2005; Weaver et al. 2004). Research in this area is characterized as “caregiving adversity or deprivation” because it involves periods of forced separation between dams and pups and specific changes to living conditions that lead to forms of “extreme stress” (Tata 2012). Scientists explained that these experiences have been shown to affect the “bonding interaction between mother and infant”and are thought to affect DNA methylation in the brain derived neurotrophic factor gene (BDNF) (Participant 29, 9–5–18). BDNF, we were told, is important for neurodevelopment and plasticity, and methylation changes to BDNF are associated with poor behavioral outcomes in animal models and psychiatric disorders in humans (Participant 17, 8–23–17).

In her analysis of the paradox of care in epigenetic research, Lappé (2018: 705) notes that “mouse models have been used over the past several decades in attempts to observe the biological effects that separation has in the controlled space of the laboratory.” As Gudsnuk and Champagne (2012: 279) point out in their review of epigenetic studies: “Animal models of early-life stress and variation in social experience across the lifespan have contributed significantly to our understanding of the environmental regulation of the developing brain,” even amid debates about whether findings in rodents can effectively translate to human contexts. Animal models are therefore a cornerstone of epigenetic studies of stress, trauma, and adversity and have been central to understandings of early intervention and intergenerational and transgenerational inheritance.

Today, the prominence of these models in epigenetic studies preserves the mother–child dyad as uniquely meaningful in studies of “behavioral transmission of traits across generations”(Participant 3, 9–20–16). A professor of psychology in the United States described how experimental work with developmental animal models in her lab has expanded to incorporate “preconception, prenatal, postnatal [periods]” of the life course (Participant 3, 9–20–16). She described a model of behavioral transmission between generations as follows:

Behavioral transmission is when an environmental exposure is affecting the neural systems that regulate social reproductive behavior. And by doing so, they shape the environmental context of the next generation. So if a mother bestows very low levels of maternal care towards her offspring, that may not necessarily affect the germline, the gametes, but it’ll affect the brain. And the brain will affect the behavior of those offspring when they’re adults and caring for their own offspring. And so that kind of transmission involves using the brain as a vector of inheritance, rather than the germline.

(Participant 3, 9–20–16)

Like many scientists in our study, she hoped to better characterize “what the construct is that’s important in these stresses.” Finding “nicer parallels” between rodents and humans, she said, can help improve predictions for children at greater risk for poor neurodevelopmental outcomes. “Extreme stressors including maltreatment, abuse, and neglect” are indeed hypothesized as having the potential for an epigenetic “spill over [to] be inherited or transmitted to future generations,” as one researcher explained to us (Participant 2, 8–26–16). Another scientist put it bluntly that when adult female pups have been subjected to the “caregiver maltreatment condition, [they] become basically crappy moms” (Participant 17, 8–23–17). This idea of mothers as particularly vulnerable to and shaped by early life adversity was reflected in many of our interlocutors’ studies and points to a sense of anticipatory motherhood that is central to many intergenerational models of stress, trauma, and adversity (Adams et al. 2009; Waggoner 2017). The overtones of determinism embodied in these claims prompted us to develop a parallel phrase to what is commonly expressed in nutritional epigenetics; rather than “you are what your mother ate,” here we found studies reinforced the idea that “you are what your mother endured.”

In their analysis of epigenetic research in rodents, feminist STS scholars Kenney and Müller (2016: 23) highlight how these experiments “come to support claims about human motherhood through a dense speculative cross-traffic between epigenetic studies in rodents and psychological and epidemiological studies in humans.” They find that “current research trends work to illustrate rather than interrogate existing stereotypes about maternal agency and responsibility” (Kenney and Müller 2016: 23). Our findings illustrate that this “speculative cross-traffic” is foundational to intergenerational studies of stress, trauma, and adversity as well.

Findings from animal models also informed epigenetic studies focused on natural experiments, where scientists believed experiences of stress mirrored those experienced by rodents. For example, one way that researchers sought to understand the impacts of maternal separation on humans was to study children who were orphaned and severely neglected in large-scale facilities outside the United States and later adopted. This represented “an extreme experience of adversity,” and researchers explained that because “there’s no way of designing a maternal separation experiment in humans, they are the only way to even consider what impact that might have on a human” (Participant 9, 5–16–17). These groups therefore afforded researchers the ability to test the biological plasticity of traits in a way that resembled the experimental cross-fostering of rodent pups in animal studies to better understand epigenetic mechanisms and how the timing of interventions could inform offspring resilience. According to a clinical psychologist who conducts neurobiological research in both rodents and humans:

We had rats that were exposed to maternal separation, so I took them away from their parents for three hours of the day for the first two weeks of their life. Now, the thing you’ll notice about that model … is that it’s actually … something akin to, [adopted children’s] previous institutionalization. It is that stressful experience [and] is limited to this early life period. In the rat one, we’ll ask questions about critical periods, so if you’re stressed just in these first two weeks of life, what impact does that have on your fear behaviors across time? I picked that because I was very interested in this data from children who’d been stressed early in life.

(Participant 10, 5–18–17)

This scientist defined early experiences of “caregiver adversity” as “the lack of a stable and consistent caregiver,” an environment she said can shape phenotypes across both “the child and grandchild generation.” In her work with children, early caregiver adversity was analyzed in connection with the expression and/or inhibition of fear responses over time, and these were then linked to children’s “accelerated development trajectories.” Findings were subsequently correlated with children’s anxiety as a long-term cost, we were told, of early adversity (Participant 10, 5–18–17). Yet researchers also emphasized that the positive outcomes for children raised by adoptive parents following institutionalization suggest that supportive interventions can ameliorate the effects of adverse early experiences in critical ways.

Elsewhere, scientists we interviewed and observed relied not only on studies with orphaned children to trace the epigenetic effects of stress, trauma, and adversity on later health, but on research with preterm infants as well. Researchers characterized these populations as experiencing “quasi-experimental, naturally available conditions” that operated as epistemically consistent with those introduced in earlier animal models of stress (Participant 29, 9–5–18). A psychologist working in a clinical setting described studies of preterm infants as offering insights into possible long-term effects of early adversity. Citing the research by Meaney noted earlier, she explained:

We thought that the preterm infant is the exact and elite population in human subjects that is really close to the experience of Michael Meaney’s mice and rats. Because they are very early separated from their mother … put through stressful conditions and so, we asked ourselves, we wondered … “are they experiencing the same epigenetic changes that we see in Michael Meaney’s animals?”

(Participant 29, 9–5–18)

She went on to describe preterm infants as “fragile” and the “physical environment, the painful stimulations, [and] the maternal separation” involved in a neonatal intensive care unit (NICU) setting as stressful for newborns in ways that were similar to those experienced by pups in animal studies (Participant 29, 9–5–18). In her view, being able to provide biological clues about the effects of stress on patterns of DNA methylation could suggest ways to enhance environments to be “epigenetically protective” (Participant 29, 9–5–18). Among these were “sustaining early contact with the mother [and] sustaining the physical and emotional bonding” while infants are in the NICU. And while she noted that this practice of “parental presence” is considered “standard of care” in the United States and Canada, in her country of origin she explained that it was not. It was within this context that she believed that epigenetic findings could help shape policies to improve outcomes for preterm infants.

These examples of extreme conditions allowed scientists to explore the biological impacts of early life stressors by creating parallels between lived experiences in humans and those imposed in animal experiments. Doing so provided researchers simplified measures in place of the complex dimensions of stress, trauma, and adversity at play for humans (Tamashiro et al. 2005). The result was an emphasis on early life and the family, most centrally in the form of caregiving and the mother–child dyad, even as researchers actively acknowledged the critical importance of the broader systems that shape these relationships. The use of these particular models therefore situated stress, trauma, and adversity as primarily consequential during early life and as a result of detrimental caregiving, neglect, or abuse, largely eclipsing the larger social and historical contexts that shape such experiences.

Conclusion: Structural Harm, Lived Experiences, and Reimagining the Biology of Adversity

Our analysis above shows that epigenetic research on the lasting effects of early life stress, trauma, and adversity raises profound questions about not only how and when to address these burdens, but the scales at which they are studied within and across generations. Scientists we observed and interviewed expressed hope that their research could alleviate the outcomes of early-life adversity. Despite the discrete measures and models they utilized, many pointed to larger questions of stewardship and intergenerational responsibility as motivating their work. One scientist asked: “Are the actions we [take] and the things we expose ourselves to … are we responsible for subsequent generations” (Participant 24, 4–5–18)? Others told us that “it’s a no brainer” to act on existing research to support families “as early as possible,” emphasizing “the importance of starting to provide support to pregnant women, particularly with regard to reducing stress and increasing social support” (Participant 5, 3–10–17). These sentiments echo broader ideas about the critical connections between structural harms and lived experiences that the science of environmental epigenetics has promised to address (Yates-Doerr 2020).

Yet the notion that growing epigenetic evidence will help alleviate large scale inequalities is complicated not only by the models and measures epigenetic studies rely on, but the broader cultural contexts that shape its translation as well. The studies we followed were produced and disseminated within the United States and Canada, where pregnant people’s rights and well-being are often actively undermined and the burdens of child wellbeing individualized and gendered, especially for Black, Indigenous, and People of Color (Benjamin 2018; Dow and Lamoreaux 2020; D. Roberts 1997; E. F. S. Roberts 2017). It is in this sociopolitical context that epigenetic research on the effects of early life stress, trauma, and adversity is both necessary and problematic as it can provide critical evidence of the need for social support and structural change, and is also weaponized and racialized against the very people most affected by these forces (Mansfield 2012; Valdez 2019).

By showing how scientists conceptualize and mobilize stress, trauma, and adversity in their research, we have highlighted what is made visible and what is often foreclosed, eclipsed, and left out in the production of epigenetic knowledge. Our findings point to the temporal embedding of adversity during early life and the centrality of the mother–child dyad in this practice. The concept of temporal embedding and its experimental forms thus illustrate how scientists’ attempts to study the molecular effects of adversity often biologize complex experiences and position pregnancy and early childhood as primary sites of attention. This focus on early life naturalizes maternal care as specifically consequential for later health, reproducing a limited sense of kinship, and reinforcing the use of models and measures that rely on, rather than challenge, it. As a result, the intersecting processes of temporal embedding, modeling, and measurement focus attention on reproduction and care as key sites of study and intergenerational intervention. In doing so, they embed histories of oppression, inequality, and subjugation in mother–child relationships, individualizing structural harms and often situating women as specifically responsible for mitigating them, even when researchers intend otherwise (Mansfield 2017).

Our focus on the temporal embedding of adversity therefore draws attention to the politics of intergenerational epigenetic research, and how developmental biology and social values intertwine to shape this science (see Lappé and Jeffries Hein Forthcoming). These conceptual models and empirical investigations bring attention to the possibilities and limitations of epigenetics as a means of addressing social harms. This matters not only for understanding epigenetics and related health interventions as we have described here, but in the context of far-reaching changes that have engulfed our world. Recently, the unequal effects of COVID-19 in Black, Brown, and Indigenous communities, the failures of governments to ensure healthcare and economic support in the face of the pandemic, and calls for police abolition and accountability after the murders of numerous Black people, make abundantly clear what anthropologists and advocates have long known: that systemic racism and oppression shape not only who experiences stress, trauma, and adversity, but their embodied effects as well (McEwen and McEwen 2017; Krieger 2012; Shonkoff et al. 2021).

At a moment when the intersections of these concerns with climate change, xenophobia, sexism, and environmental toxicity have gained global attention, feminist anthropology and science and technology studies provide an opportunity to critically examine how stress, trauma, and adversity are conceptualized, modeled, and measured in epigenetic research. Here, we have critiqued epigenetics in ways that we hope will help reimagine it. By pointing to the epistemic and ontological divides between epigenetics and the lived experiences it aims to address, our analysis suggests the need to bring more complex social and historical contexts to bear in epigenetic research (see Roberts and Sanz 2018). Exploring the temporal and gendered dimensions of this science also reflects that such efforts are possible, as researchers themselves already envision stress, trauma, and adversity as more expansive and nuanced than their models suggest.