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Martine Lappé
Social Sciences Department
California Polytechnic State University, San Luis Obispo (E-mail: mlapp@calpoly.edu)
Robbin Jeffries Hein
California Polytechnic State University, San Luis Obispo
(E-mail: robbinjeffries@ucla.edu)
You Are What Your Mother Endured:
Intergenerational Epigenetics, Early Caregiving,
and the Temporal Embedding of Adversity
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 ex-
periences and their effects on children’s neurodevelopmental and behavioral health.
We nd 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 ndings 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.
[epigenetics, adversity, temporality, intergenerational, maternal care]
Biologizing Adversity
A growing body of social, biomedical, and epidemiological research demonstrates
that inequalities resulting from systemic forms of oppression and inadequate infras-
tructures 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 environ-
mental 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 Dis-
ease Control and Prevention (CDC) Kaiser Adverse Childhood Experiences (ACE)
458
MEDICAL ANTHROPOLOGY QUARTERLY,Vol.35,Issue4,pp.458–475,ISSN0745-
5194, online ISSN 1548-1387. © 2021 by the American Anthropological Association. All rights
reserved. DOI: 10.1111/maq.12683
The Temporal Embedding of Adversity 459
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 anthropol-
ogists 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 recogni-
tion that social experiences of adversity can become “biologically embedded” (Aris-
tizabal et al. 2019; Hertzman 2012). From the late 19th through the mid-20th cen-
tury, 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 exemplied by neurobiologist Michael Meaney
and geneticist Moshe Szyf’s identication 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 ndings
“reinvigorated longstanding questions around the transmission and heritability of
acquired features” (Pickersgill et al. 2013: 433) but in doing so, their work also nat-
uralized heteronormative gender relations (see Franklin 2001; MacCormack and
Strathern 1980) by foregrounding the mother–child dyad as central to the biolo-
gized effects of adversity. This conceptual and methodological transition in studies
of stress helped produce pregnancy and children’s early neurodevelopment as cen-
tral 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 nu-
merous disciplines to study the biological effects of stress, trauma, and adversity,
and to explore their lasting impacts on individual and intergenerational health (Lan-
decker and Panofsky 2013; Mulligan 2016; Yehuda et al. 2009, 2014). Environmen-
tal epigenetics is a broad eld of molecular biological research focused on how ex-
periences and exposures inuence 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 struc-
tural inequalities by reinforcing individual blame, gendered responsibilities, and bi-
ological determinism (Kenney and Müller 2016; Lock 2015; Richardson et al. 2014;
Waggoner and Uller 2015; Warin et al. 2012). Despite these ongoing debates sur-
rounding the eld, epigenetic ndings 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).
460 Medical Anthropology Quarterly
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 histor-
ical 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 identies “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.” Along-
side 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 im-
portance within epigenetic studies (Lappé and Landecker 2015), describe concep-
tual 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 specically consider the gender and temporal dimensions em-
bodied in and produced through epigenetic research by exploring what is made vis-
ible and what is foreclosed, eclipsed, and left out in the production of intergener-
ational 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, fam-
ily, and responsibility are prioritized and produced? How is this knowledge shaping
emergent understandings of health and illness related to stress, trauma, and adver-
sity? 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 embod-
ied, 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 cen-
tral to understanding the intergenerational effects of stress, trauma, and adversity.
We illustrate how this naturalizes maternal care as specically consequential for in-
tergenerational health. While others have also observed the overwhelming focus of
environmental epigenetics on mothers (Kenney and Müller 2016; Richardson et al.
2014; Sharpet al. 2018), here we document how researchers’ use of particular mod-
els 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, reecting what we call the temporal embed-
ding of adversity.
The Temporal Embedding of Adversity 461
Building on the language of “biological embedding,” the concept of temporal
embedding draws attention to how “highly specied constructions of the environ-
ment” 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 specicity of researchers’ conceptualizations there-
fore inuences both how epigenetic knowledge is produced and its translational po-
tential (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 understand-
ings of health and behavior intertwine to shape the practices and consequences of
epigenetic research.
Methods
Our ndings 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 eld notes taken during approximately 200 hours of ob-
servations conducted across three university laboratories and at scientic meetings
in the United States and Canada (Charmaz 2006; Glaser and Strauss 1967). Key
themes found in scientic literature and media also informed our analysis and helped
us triangulate our ndings. 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 Rhein-
berger’s (2007 [2004]) cultural history of heredity across scientic domains. They
write that “before the metaphor of biological heredity could be applied at all, phe-
nomena of organic reproduction had to be recongured discursively as to make
reproduction itself accessible as a phenomenon that extended beyond the produc-
tion 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
reected in the models and measures they use in their studies. Our ndings suggest
that discourse is not merely what is spoken by the researchers we study, but a reec-
tion of their practices as well. In conceptualizing what counts as stress, trauma, and
adversity, and situating their signicance during early life, scientists’ research deci-
sions and discussions help produce early-life adversity as molecularly meaningful in
specic ways. Their conceptualizations render novel scientic models of health and
illness “accessible as phenomenon”in ways that are specically gendered and tempo-
ral. Our ndings therefore point to the production of an “epistemic space” enabled
by environmental epigenetics and within which a temporally specic, 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
462 Medical Anthropology Quarterly
observed postdoctoral researchers, mid-career principal investigators and profes-
sors, clinician–researchers, and full professors. Many researchers we interviewed
and observed embraced an interdisciplinary, “integrated training” approach, believ-
ing 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’ specic 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; Manseld 2017; Pen-
tecost 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
uctuations 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 fel-
low 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
The Temporal Embedding of Adversity 463
those rst 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 specically the “early caregiver
relationship” as transmitting all the “broader contextual things that are going on,”
reected how researchers often conceptualized early-life stress, trauma, and adver-
sity 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 re-
searchers who were longitudinally tracing associations between infant stress in the
mother–child dyad and children’s later brain and behavioral outcomes. They studied
epigenetic modications in amygdala functioning because of their link to memory
and learning, maturation, and separation anxiety (Participant 10, 5-18-17). Dur-
ing 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 de-
velopment, moving from an exclusive focus on early life to specic periods of pre-
adolescence when early adversity may manifest. This is signicant because embod-
iment 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
464 Medical Anthropology Quarterly
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 specic 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-specic
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 inuence
their health.
You Are what Your Mother Endured: Conceptualizing and Measuring the
Intergenerational Effects of Adversity
In this section, we show how scientists use specic 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 rst 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.
Reecting on her research studying maternal and child health, a postdoctoral fel-
low 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
The Temporal Embedding of Adversity 465
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 reections point to a nuanced appreciation for the relationships between peo-
ple’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 nding reinforces
what Niewöhner and Lock (2018) have observed, specically that “situated biolo-
gies” and the broader complexities of human life are often reduced to molecularly
measurable forms and simplied 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 some-
one’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 bio-
logical 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 specic 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 natu-
rally occurring studies of children thought to have been uniquely exposed to early-
life stress, trauma, and adversity. These models provided connections between iso-
lated measures and lived experiences of harm, but also resulted in a focus on discrete
family relations centered around the mother–child dyad. This produced reproduc-
tion 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 sim-
ilar 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 specic 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 specic 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
466 Medical Anthropology Quarterly
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 hu-
mans (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 lab-
oratory.” As Gudsnuk and Champagne (2012: 279) point out in their review of epi-
genetic studies: “Animal models of early-life stress and variation in social experience
across the lifespan have contributed signicantly to our understanding of the envi-
ronmental regulation of the developing brain,” even amid debates about whether
ndings 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 trans-
mission 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 maltreat-
ment, 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
reected 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 em-
bodied in these claims prompted us to develop a parallel phrase to what is commonly
The Temporal Embedding of Adversity 467
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-trafc between epige-
netic studies in rodents and psychological and epidemiological studies in humans.”
They nd that “current research trends work to illustrate rather than interrogate
existing stereotypes about maternal agency and responsibility” (Kenney and Müller
2016: 23). Our ndings illustrate that this “speculative cross-trafc” is foundational
to intergenerational studies of stress, trauma, and adversity as well.
Findings from animal models also informed epigenetic studies focused on natu-
ral experiments, where scientists believed experiences of stress mirrored those ex-
perienced 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 re-
searchers explained that because “there’s no way of designing a maternal separa-
tion 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 af-
forded 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 bet-
ter understand epigenetic mechanisms and how the timing of interventions could
inform offspring resilience. According to a clinical psychologist who conducts neu-
robiological 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 rst 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 rst 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 dened 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 de-
velopment trajectories.”Findings were subsequently correlated with children’s anxi-
ety 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 adop-
tive 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
468 Medical Anthropology Quarterly
on later health, but on research with preterm infants as well. Researchers charac-
terized these populations as experiencing “quasi-experimental, naturally available
conditions” that operated as epistemically consistent with those introduced in ear-
lier 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 environ-
ment, 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 pro-
tective” (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 consid-
ered “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
ndings could help shape policies to improve outcomes for preterm infants.
These examples of extreme conditions allowed scientists to explore the biologi-
cal impacts of early life stressors by creating parallels between lived experiences in
humans and those imposed in animal experiments. Doing so provided researchers
simplied measures in place of the complex dimensions of stress, trauma, and ad-
versity 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 eclips-
ing 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
The Temporal Embedding of Adversity 469
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 respon-
sible 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” (Partici-
pant 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 in-
equalities 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, Indige-
nous, 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 re-
search 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 (Manseld 2012; Valdez 2019).
By showing how scientists conceptualize and mobilize stress, trauma, and adver-
sity in their research, we have highlighted what is made visible and what is often fore-
closed, eclipsed, and left out in the production of epigenetic knowledge. Our ndings
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 ma-
ternal care as specically 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, model-
ing, 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 specically responsible for mitigating them,
even when researchers intend otherwise (Manseld 2017).
Our focus on the temporal embedding of adversity therefore draws attention
to the politics of intergenerational epigenetic research, and how developmental bi-
ology 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 address-
ing 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
470 Medical Anthropology Quarterly
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 sys-
temic 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, xeno-
phobia, sexism, and environmental toxicity have gained global attention, feminist
anthropology and science and technology studies provide an opportunity to criti-
cally 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 be-
tween 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 dimen-
sions of this science also reects that such efforts are possible, as researchers them-
selves already envision stress, trauma, and adversity as more expansive and nuanced
than their models suggest.
Funding
The authors have no conicts of interests to declare. Research for this publication
was supported by NHGRI grant R00HG009154: “Behavioral Epigenetics in Chil-
dren: Exploring the Social and Ethical Implications of Translation.” The content is
solely the responsibility of the authors and does not necessarily represent the ofcial
views of the National Institutes of Health.
Acknowledgments. We thank Katie Ettl, Fionna Fahey, Shanti Herzog, and Devon
Winger for their assistance with research for this article; Sahra Gibbon and Janelle
Lamoreaux for their feedback on previous versions of this manuscript; and the study
participants.
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