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Running head: CULTURAL TRAUMA AND EPIGENETICS
Cultural Trauma and Epigenetic Inheritance
Amy Lehrner and Rachel Yehuda
James J. Peters Bronx Veterans Affairs Hospital, Bronx, NY, USA; Departments of Psychiatry
and Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA
Citation information: Lehrner, A., & Yehuda, R. (n.d.). Cultural trauma and epigenetic
inheritance. Development and Psychopathology, 1-15. doi:10.1017/S0954579418001153
Published online: 28 September 2018. https://doi.org/10.1017/S0954579418001153
This manuscript represents the post-refereed version but not the publisher’s final version.
Corresponding author: Amy Lehrner, PhD. James J. Peters VA Medical Center, 130 W.
Kingsbridge Road (526/OOMH), Bronx, NY 10468; Phone: (718) 584-9000, x3205; Fax: (718)
741-4703; Email: amy.lehrner@va.gov
Acknowledgements: The authors would like to thank Alex Ropes, Migle Staniskyte, and
Emmanuel Ruhamya for assistance with manuscript preparation.
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Abstract
The question of whether and how the effects of cultural trauma can be transmitted
intergenerationally from parents to offspring, or even to later generations, has evoked interest
and controversy in academic and popular forums. Recent methodological advances have spurred
investigations of potential epigenetic mechanisms for this inheritance, representing an exciting
area of emergent research. Epigenetics has been described as the means through which
environmental influences “get under the skin,” directing transcriptional activity and influencing
the expression or suppression of genes. Over the past decade, this complex environment-biology
interface has shown increasing promise as a potential pathway for the intergenerational
transmission of the effects of trauma. This article reviews challenges facing research on cultural
trauma, biological findings in trauma and posttraumatic stress disorder, and putative epigenetic
mechanisms for transmission of trauma effects, including through social, intrauterine and
gametic pathways. Implications for transmission of cultural trauma effects are discussed,
focused on the relevance of cultural narratives and the possibilities of resilience and adaptivity.
Keywords: intergenerational, transgenerational, trauma, posttraumatic stress disorder,
epigenetics
CULTURAL TRAUMA AND EPIGENETICS
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The world breaks every one and afterward many are strong at the broken places.
— Ernest Hemingway, A Farewell to Arms, 1929, p. 249
It has long been recognized that the experiences of parents and ancestors influence future
generations (Harper, 2005). Indeed, many cultural practices and rituals function to transmit
historical knowledge and experience across generations. The Jewish Passover seder gathers
family and friends for a meal during which the biblical story of the escape from bondage in
Egypt is retold and freedom is celebrated. Children are specifically instructed to consider what
the story means to them and about them. When survivors and witnesses to communal trauma,
such as genocide, die off, cultural memory is enshrined and conveyed through memorials,
museums, the arts, and memorialized anniversaries and rituals. Cultural trauma has been defined
as occurring “when members of a collectivity feel they have been subjected to a horrendous
event that leaves indelible marks upon their group consciousness, marking their memories
forever and changing their future identity in fundamental and irrevocable ways” (Alexander,
2004). The shared experience of cultural trauma, targeting a cultural or ethnic group, becomes
part of the story the community tells about the world, about itself, and about its survival (Volkan,
2001). It is hoped that the lessons of the past will be passed on, although the nature of the lesson
may be a matter of disagreement. While the historical events may be in some way fixed, they are
also open to reinterpretation and new meaning for future generations.
In the fields of psychology and psychiatry, both the experience and the developmental
sequelae of trauma have primarily been conceptualized and studied as individual level
phenomena. The Diagnostic and Statistical Manual of Mental Disorders (DSM 5) defines trauma
as “exposure to actual or threatened death, serious injury, or sexual violence” including war,
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physical assault, threatened or actual sexual violence, terrorism, natural or man-made disasters,
and severe accidents (American Psychiatric Association, 2013). Diagnoses such as posttraumatic
stress disorder (PTSD) or depression following trauma are, of course, applied only to individuals.
However, when trauma exposure is communal, it is not clear whether it requires different
conceptual models, and whether the effects will be similar to any other trauma exposure, with
comparable psychological, neuroendocrine, neurological, and molecular correlates. Clearly, the
impact of cultural trauma must be evaluated not only at the individual level, but also at the meso-
level community and macro-level societal levels (Bronfenbrenner, 1977; Bronfenbrenner, 2009).
Consideration of the effects of cultural trauma thus requires an interdisciplinary and multi-level
approach, and indeed, cultural trauma has been approached from anthropological, sociological,
psychological, historical, literary, political, and religious frameworks (Argenti & Schramm,
2009; Danieli, 1998; Doucet & Rovers, 2010; Hooker & Czajkowski, no date; Moon, 2009;
Prager, 2003; Schwab, 2010). The integration of these with biological analyses poses a
significant and important challenge for the interdisciplinary field interested in the
intergenerational effects of trauma.
Recent advances in molecular biology have facilitated investigations of the
intergenerational transmission of trauma related effects through epigenetic mechanisms.
Epigenetics is the study of mechanisms that modify gene expression, thus shaping phenotypic
outcome, but do not alter the underlying DNA sequence (Goldberg, Allis, & Bernstein, 2007).
Epigenetics has been described as the means by which the environment “gets under the skin,”
facilitating or suppressing the expression of genes which are themselves fixed and immutable
(McEwen, 2012). The idea that such adaptations would be passed to the next generation was
once rejected as an example of the failed Lamarckian theory of evolution. However, converging
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evidence, primarily in animal models but also in humans, indicates that subtle adaptations at the
molecular level may not be completely erased in gametes and at conception, but may be
conserved in offspring (Bale, 2014; Yehuda & Lehrner, in press).
This article will review some of the challenges in studying cultural trauma (versus
individual level trauma), as well as research on the biological sequelae of trauma and PTSD and
the intergenerational transmission of biological, psychological and behavioral effects of trauma.
Putative epigenetic mechanisms for such transmission, through social, intrauterine, and gametic
pathways, will be presented. Finally, the interpretations and implications of this body of research
will be discussed, with an emphasis on alternative narratives of cultural specificity, growth and
resilience, and continued plasticity.
Challenges in Studying Cultural Trauma
The experience of cultural trauma has profound consequences for the targeted
community. These consequences may include geographical dispossession, loss of material
possessions, dispersion of family and social networks, financial and educational hardship, and
inadequate access to resources. The material and concrete challenges that ensue following
cultural traumas, such as genocide, slavery, and forced separation of families, reshape the
community and the lives of survivors and future generations. Psychological consequences, such
as distressing nightmares or flashbacks, hypervigilance, profound grief and horror, and
dissociative numbing co-exist with the need to come to terms with the nature of humanity, one’s
place in a community, and what it means to be part of a people, not just an individual entity.
These challenges undoubtedly shape the lives of survivors and future generations, but it is not
clear whether there are universal effects of cultural traumatic experiences. Indeed, attempting to
CULTURAL TRAUMA AND EPIGENETICS
6
trace the effects of cultural trauma on later generations is fraught with both political implications
and methodological challenges.
Longstanding political and policy debates in many countries hinge on disagreements
about whether historical traumas continue to influence structural inequalities and mental health
problems in those communities. Other discussions include considerations of whether these
histories of cultural trauma warrant some form of reparation (e.g., debates about reparations for
slavery in the United States, for the lost generation in Australian Aboriginal communities, and
for forced family separation in Native American/First Nation communities). These debates have
been recapitulated in the academic literature and public policy discussions aimed at addressing
putative cultural aspects of cycles of poverty (e.g., Leacock, 1971). For example, arguments
about the intergenerational effects of trauma have been used to explain cultural practices and
gaps in achievement, but many deny the continued relevance of historical experiences. This
denial, in turn, is viewed as blaming the victim, and in fact, as resulting in revictimization (e.g.,
Ryan, 1976; Wright, 1993). Scientific inquiry about psychological and biological transmission of
the effects of cultural trauma cannot help but wade into these heated political and cultural
debates.
Psychological and mental health consequences of cultural trauma have also been
considered from both individual and community level perspectives (de Jong, 2006; Steel, Silove,
Phan, & Bauman, 2002). However, while community and cultural level factors may be
investigated as influences on mental health and development, conceptualizations of the mental
health of a community qua community are rare. For example, there are literatures investigating
cultural influences on mental health treatments disparities, or neighborhood effects (e.g., levels
of violence) on individual level mental health indicators (Brach & Fraserirector, 2000; Fowler,
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Tompsett, Braciszewski, Jacques-Tiura, & Baltes, 2009). However, when a trauma is
experienced at the group level, this raises the question of whether mental health and behavioral
consequences can be considered community-wide, and if so, what the implications of this
community-wide effect is for the individual survivor (Chaitin & Steinberg, 2008; de Tubert,
2006). Consideration of community level effects thus complicates research on the developmental
effects of trauma.
Methodologically, there are many challenges to taking a developmental psychopathology
approach to the study of cultural trauma. As a communal event, trauma is experienced by an
entire community across age and developmental stage. This makes it difficult to recruit adequate
samples of survivors at potentially important developmental stages, and creates a confound for
studying children and adolescents in that they are subsequently being raised by adults who are
themselves affected by the event, in a community shaped by the event, etc. Furthermore, it is
difficult to bound what is likely a somewhat chronic and diffused context of trauma, as those
who have fled genocide subsequently face the stressors of being refugees, and are vulnerable to
further traumatization. If cultural trauma influences multiple levels of the individual’s
ecosystem, it is difficult to parse specific influences. There is also the issue of how analysis at
the cultural level might account for individual differences in the response to trauma. If the
traumatic experience is chronic, such as in communities facing years of attempted genocide or
warzone exposure, isolating developmental influences is difficult as survivors are aging
throughout the exposure. And in some cases opportunities to conduct research are only available
years or decades after the trauma, rather than longitudinally following trauma. Prospective
research on trauma at the individual level is notoriously difficult, as it is hard to define a cohort
prior to exposure with adequate power to study traumatic sequelae longitudinally, but
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8
prospective research on communal trauma is difficult to even conceptualize. Finally, in the case
of historical trauma, as described above it is difficult to disentangle the effects of legacies of
trauma from the effects of compounding and ongoing trauma and stress to individuals and
communities that remain under physical threat and are structurally disadvantaged, such as Native
American and First Nation communities, and African American communities in the United
States.
The Holocaust as a Case Study of Cultural Trauma
Research about the effects of cultural trauma cannot help but be part of a larger narrative
about the meaning of the event for survivors and the community. In the case of the Holocaust,
many members of the targeted community felt it was extremely important to demonstrate that the
Nazis had failed in their agenda to destroy the Jewish community, and that living well was the
best revenge. After all, Jews had a long history of surviving oppression, and the Holocaust
provided another instance not only of their victimization, but of their resilience. Indeed, some
research with survivors identified psychological resilience following the Holocaust, with robust
well-being and quality of life and normal adjustment (Dimsdale, 1974; Leon, Butcher, Kleinman,
Goldberg, & Almagor, 1981). However, for others, the traumas they experienced left lasting
psychological scars that impacted their functioning and quality of life, scars that their children
felt, observed, and at times suffered from (Danieli, 1998). Research with survivors documented
these impacts, including psychiatric symptoms, poor adjustment and impaired functioning
(Chodoff, 1963; Dor-Shav, 1978; Eitinger, 1961; Niederland, 1981). Some hypothesized that
survivors may show resilience and normal functioning under regular daily circumstances, but be
more vulnerable and emotionally reactive when faced with intensely stressful or threatening
situations (Van Ijzendoorn, Bakermans-Kranenburg, & Sagi-Schwartz, 2003).
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Interestingly, research that took a developmental approach suggested that understanding
the impact of surviving the Holocaust requires consideration not only of the experience itself, but
also of the developmental stage at the time of the trauma and the ways in which the trauma
exposure may have conferred vulnerability to later stressors. For Holocaust survivors living in
the U.S., as with survivors of other forms of trauma, the presence of PTSD in late life (mean age
= 70) was associated not only with exposure to the trauma of genocide, but also with cumulative
lifetime trauma and more recent stress (Yehuda, Kahana, Schmeidler, & Southwick, 1995).
Symptom profiles also appeared to vary depending on age of exposure (Yehuda, Schmeidler,
Siever, Binder-Brynes, & Elkin, 1997). Thus the impacts of cultural trauma must be considered
in light of the developmental stage of the survivor, and may potentiate the deleterious effects of
later adverse experiences.
Observations of PTSD symptoms and increased vulnerability to PTSD among Holocaust
survivors raised questions of whether these survivors of cultural trauma would demonstrate the
same alterations in neuroendocrine markers observed in combat veterans and civilians with
PTSD. And indeed, Holocaust survivors were found to have signs of heightened sensitivity of
the neuroendocrine stress response, including low urinary cortisol excretion (Yehuda, Bierer,
Andrew, Schmeidler, & Seckl, 2009; Yehuda, Kahana, Binder-Brynes, & Southwick, 1995;
Yehuda, Morris, Labinsky, Zemelman, & Schmeidler, 2007) and increased glucocorticoid
receptor responsiveness (as assessed by the response to the low dose dexamethasone suppression
test) (Yehuda, Halligan, Grossman, Golier, & Wong, 2002), compared to demographically
comparable Jewish controls. Age of exposure to the physical and emotional stressors of the
Holocaust (including nutritional deprivation) has been associated with both psychological
symptom profiles and cortisol metabolism, indicative of trauma’s role in early developmental
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10
programming of the hypothalamic-pituitary-adrenal (HPA) axis and other stress sensitive
pathways (Yehuda et al., 2009).
Intergenerational Transmission of Trauma Effects
Whereas the intergenerational effects of cultural trauma has long been the subject of
research in disciplines ranging from anthropology to political science (Argenti & Schramm,
2009; Galtung, 1990; Martino, 1980; Mendeloff, 2009; Sullivan, 1986), the psychological and
psychiatric literatures turned to this issue in the wake of converging clinical observations,
demands for clinical services, and social organizations of Holocaust survivor offspring (Danieli,
1985; Solkoff, 1981; Steinitz, 1982). As Holocaust survivors aged, their adult offspring began to
explore the legacy of the Holocaust, not only politically and culturally, but for their own
development and psychological functioning, through literature, film, theater, music, and memoir
(Aarons, 2016; Goldberg, 2015; McGlothlin, 2006; Spiegelman, 2003). A movement of “second
generation” survivors grew, and many felt that through their parents they had also been deeply
and directly affected by the cultural trauma of the Holocaust. This population was relatively
unique in that the entire religious group was targeted, regardless of sex, age, temperament or
other risk factors, the Holocaust ended after the war and so could be chronologically bounded;
and despite the dispersion of survivors they tended to settle in Jewish communities in the U.S.
and Israel and could thus be identified and recruited for study. Furthermore, the second
generation was comprised of adults who were interested in research questions about
intergenerational transmission of trauma effects and of age to consent and participate in such
research. A research literature followed, chasing questions of whether and how a trauma not
directly experienced may have had intergenerational influences, affecting the development of
second and even third generations of offspring.
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11
Research regarding the degree to which Holocaust offspring experienced mental health
problems yielded mixed results, paralleling political and cultural debates about the impact of the
Holocaust on the community. Some found resilience and high levels of functioning, and others
found problems such as depression, anxiety, PTSD, and personality disorders. A large meta-
analysis of 32 samples (n=4,418) indicated that sampling differences in subpopulations of
offspring may explain the divergent findings (Van Ijzendoorn et al., 2003). Among non-clinical
samples, there was no evidence for transmission of effects of trauma to offspring, but among
clinical samples effects of parental trauma were more pronounced.
Although evidence regarding specific mental health and functional outcomes has been
mixed, the experience of feeling affected by parental trauma has been widely described. As with
survivors, some research has suggested that offspring may be more vulnerable should they
experience extreme stress or threat. For example, an important study of Israeli combat soldiers
following the Lebanon war found that those with Holocaust survivor parents were more likely to
develop PTSD (Solomon, Kotler, & Mikulincer, 1988). Furthermore, one epidemiological study
of middle-aged Holocaust offspring found that although offspring, especially those with two
survivor parents, reported higher life satisfaction, quality of life, and optimism and hope
compared with controls, they also experienced more physical health problems, including high
blood pressure and cholesterol, and sleeping problems (Shrira, Palgi, Ben-Ezra, & Shmotkin,
2011; but see Radomislensky and Shemesh, 2007, for epidemiological data that did not find
physical health differences in offspring). These results are consistent with biological findings of
altered HPA axis reactivity among offspring of Holocaust survivors (Yehuda, Schmeidler,
Wainberg, Binder-Brynes, & Duvdevani, 1998), alterations which are strongest for those with
parental PTSD (Yehuda et al., 2000; Yehuda, Blair, Labinsky, & Bierer, 2007; Yehuda,
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12
Halligan, & Bierer, 2002; Yehuda, Teicher, et al., 2007). Taken together, the research literature
and cultural products created by Holocaust survivor offspring suggest that the legacy of cultural
trauma extends beyond the survivors, deeply affecting their offspring. Research on the
intergenerational impact of other genocides, colonization, war, and slavery reflects the
widespread understanding that such traumas resonate across generations and throughout
communities. For example, see discussions relating to First Nation, Native American, Australian
Aboriginal and New Zealand Maori communities (Brave Heart, 1998; Evans-Campbell, 2008;
Gone, 2013; Pihama et al., 2014; Raphael, Swan, & Martinek, 1998), the legacy of slavery
among African Americans (DeGruy, 2017; Eyerman, 2001), and the effects of genocide and war
in Cambodian (Field, Muong, & Sochanvimean, 2013; Münyas, 2008), Armenian (Azarian-
Ceccato, 2010; Esmaeili, 2011; Karenian et al., 2011), Rwandan (Perroud et al., 2014; Roth,
Neuner, & Elbert, 2014), Palestinian (Barron & Abdallah, 2015), Ukrainian (Bezo & Maggi,
2015), Sierra Leonean (Betancourt, McBain, Newnham, & Brennan, 2015) and Croatian
communities (Svob, Brown, Takšić, Katulić, & Žauhar, 2016).
What is Meant by “Transmission”?
The idea that trauma may have intergenerational effects has recently shown broad
cultural resonance, with discussions of the topic in news reports, social media, and
entertainment. A google scholar search for “intergenerational transmission of trauma” yields
approximately 37,000 results; “transgenerational transmission of trauma” yields over 15,000.
This concept is distinct from that of the intergenerational cycle of abuse or violence, which is a
widely researched (but only weakly supported) hypothesis regarding the perpetuation of child
abuse and maltreatment across generations within a family (Widom, 1989). Following reports
that some offspring of traumatized parents reported experiencing their own distress and
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13
psychiatric symptoms, initial investigations into these effects focused on psychodynamic,
parenting, family systems, and learning theory explanations (Abrams, 1999; Barocas & Barocas,
1980; Danieli, 1998). All of these have in common the assumption that the effects of parental
experiences of trauma on their children are mediated by parental symptoms and behaviors.
Similar to the concept of vicarious or secondary traumatization used to describe effects of
combat exposure on soldiers’ children (Rosenheck, 1986), it was thought that offspring were
affected not directly by the trauma, but by the effects of the trauma on the parent’s emotional
state and behavior, which in turn affected their own development, emotional state, and
behavioral repertoire.
The introduction of possible biological mechanisms through which parental trauma might
influence offspring shifted the focus of investigation from psychological and behavioral levels of
analysis to neuroendocrine and molecular levels. But biological findings have raised similar
questions about the origin and nature of intergenerational effects, with significance for the
interpretation of results. In the popular press, such biological findings have been reported to
represent the transmission of the trauma itself across generations (for example, a 2016 magazine
headline stating “Trauma from slavery can actually be passed down through your genes: you can
get PTSD from your ancestors” (https://www.teenvogue.com/story/slavery-trauma-inherited-
genetics). Many reports in the popular press have suggested that memories and trauma are
“inherited” (Yehuda, Lehrner, & Bierer, in press). These interpretations seem to represent a
slippage from a psychological and cognitive level (i.e., the perception and experience of life
threat, the memory of a lived event) to a biological level that treats these as equivalent.
Transmission of an effect of trauma at the molecular level is not the same as transmission of an
experience of trauma, whatever that would mean. As biological research on intergenerational
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14
effects of trauma expands, it becomes increasingly important to be clear about what is being
transmitted, and how such transmission might occur.
The Biological Impact of Trauma Survival and PTSD
Research on the biological consequences of trauma exposure emerged from the field of
stress studies, which had identified and characterized the activation of the HPA axis as central to
the acute stress response (Smith & Vale, 2006). Briefly, the perception of threat triggers a
neuroendocrine cascade that is ultimately resolved by the release of glucocorticoids which
returns the organism to homeostasis once the threat has been removed and safety re-established
(De Kloet, Joëls, & Holsboer, 2005). The hypothalamus releases corticotropin-releasing
hormone , which stimulates the pituitary to release adrenocorticotropic hormone .
Adrenocorticotropic hormone travels to the adrenal cortex, activating the adrenal glands to
produce cortisol (a glucocorticoid). As cortisol is released into the system, it acts through
negative feedback on the pituitary and hypothalamus to shut down the cycle. The HPA axis is
also regulated through neuronal, brain, and sympathetic and parasympathetic systems, leading to
a highly adaptive stress response system. Glucocorticoids have wide ranging effects through the
brain and body, influencing memory, inflammatory and immune function, and other disease
processes. The experience of chronic stress, and chronic activation of the stress response system,
has been associated with increased allostatic load and increased rates of morbidity and mortality
(Chrousos, 2009; Juster, McEwen, & Lupien, 2010; McEwen, 1998; McEwen & Wingfield,
2003).
The nature of the stress response system, and its facilitation of emotional, cognitive, and
behavioral responses to promote survival (e.g., fight, flight or freeze), is one of rapid and flexible
response to acute and time limited threat, followed by a return to baseline once the threat is over.
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15
However, some trauma survivors continue to act and feel as if the trauma has not resolved, as if
they have been fundamentally altered by the experience that continues to be ever present instead
of receding into the past. Consistent with this clinical presentation, initial research on the effects
of trauma anticipated signs of an activated HPA axis, as if the survivor was in a state of chronic
stress response. However, the unexpected finding was that trauma survivors with PTSD appeared
to have lower, rather than higher, levels of cortisol (Glover & Poland, 2002; Mason, Giller,
Kosten, Ostroff, & Podd, 1986; Yehuda, Kahana, Binder-Brynes, et al., 1995; Yehuda et al.,
1990; Yehuda, Teicher, Trestman, Levengood, & Siever, 1996), initially indicating, possibly, an
underperforming rather than hyperactive HPA axis. Research with Holocaust survivors, combat
veterans, and civilians exposed to trauma has since consistently identified HPA axis alterations
in association with PTSD (De Kloet et al., 2006; Morris, Compas, & Garber, 2012).
Furthermore, these individuals also demonstrate high glucocorticoid receptor number and
sensitivity (Yehuda, Boisoneau, Mason, & Giller, 1993; Yehuda & Giller Jr, 1995; Yehuda,
Golier, Yang, & Tischler, 2004; Yehuda, Halligan, Grossman, et al., 2002; Yehuda, Lowy,
Southwick, Shaffer, & Giller, 1991; Yehuda, Southwick, et al., 1993), and low glucocorticoid
receptor gene (NR3C1) methylation (Yehuda et al., 2015), contributing to an enhanced negative
feedback sensitivity in the HPA axis. Elevated catecholamine levels (norepinephrine and
epinephrine) (Kosten, Mason, Giller, Ostroff, & Harkness, 1987; Liberzon, Abelson, Flagel, Raz,
& Young, 1999; Yehuda, Siever, et al., 1998; Yehuda, Southwick, Giller, Ma, & Mason, 1992;
Young & Breslau, 2004) in conjunction with suppressed cortisol levels has been hypothesized to
result in a prolonged stress response state, with inadequate levels of cortisol failing to suppress
the HPA axis (Mason, Giller, Kosten, & Harkness, 1988). The organism is thus exposed to
CULTURAL TRAUMA AND EPIGENETICS
16
catecholamines for an extended period, with potential consequences for conditioned learning,
avoidance behavior, memory, and hyperarousal (Yehuda, 2009).
These initially unexpected biological observations are consistent with epidemiological
data that has consistently showed that while the majority of adults worldwide have experienced
at least one traumatic incident, only a minority subsequently develop PTSD (Breslau, 2009;
Galea, Nandi, & Vlahov, 2005; Kessler et al., 2005; Kessler, Sonnega, Bromet, Hughes, &
Nelson, 1995; Sorel, 2010). Taken together, the biological and epidemiological data support the
hypothesis that PTSD is not the predominant reaction to trauma; rather, most people recover
from the experience (Yehuda & McFarlane, 1995). However, the natural recovery process fails
for a minority of survivors, who become stuck in a post-traumatic state that includes alterations
in HPA axis functioning (Yehuda, McFarlane, & Shalev, 1998). This is not to say that all
survivors are not deeply affected by their experiences, but that only a subset develop a lasting,
maladaptive disorder following such an experience.
Biological Findings in Offspring of Trauma Survivors
Given these observations in PTSD, and the fact that the HPA axis is sensitive to
developmental programming (Weaver, 2007), initial biological investigations of offspring
focused on HPA axis parameters. A body of research has grown showing that offspring of
trauma survivors and combat veterans, even offspring without PTSD, have HPA axis alterations
similar to those observed in samples with PTSD, such as lower cortisol levels and higher
glucocorticoid receptor sensitivity (Lehrner et al., 2014; Yahyavi, Zarghami, Naghshvar, &
Danesh, 2015; Yehuda et al., 2000; Yehuda, Blair, et al., 2007; Yehuda, Teicher, et al., 2007).
Although it is methodologically more challenging to establish parental mental health status than
simply exposure to the Holocaust, in studies that have been able to evaluate parental symptoms,
CULTURAL TRAUMA AND EPIGENETICS
17
biological findings in offspring have been specifically associated with parental PTSD (Lehrner et
al., 2014; Yehuda et al., 2014; Yehuda et al.,1998; Yehuda, Teicher, et al., 2007). Importantly,
there have been different patterns observed in association with maternal versus paternal PTSD.
The neuroendocrine patterns in offspring described above appear to be associated with maternal
PTSD (Lehrner et al., 2014; Yehuda et al., 2014; Yehuda, Teicher, et al., 2007).
Potential Epigenetic Mechanisms for Transmission of the Effects of Trauma
With observations of both psychological and biological differences in offspring whose
parents had PTSD compared with controls, the question of potential mechanism(s) for
transmission these effects takes on new relevance. As the field has seen rapid advances in
methods for studying molecular processes, there has been heightened interest and research on
potential epigenetic mechanisms for intergenerational transmission of trauma effects. Epigenetic
marks consist of chemical modifications of chromatin (chromosomal material, including protein,
RNA, and DNA) that are induced by environmental factors. These alterations usually affect
transcriptional activity, leading some to describe epigenetics as the means by which the
environment “turns genes on and off.” Epigenetic mechanisms include DNA methylation,
usually on cytosine residues of CpG islands, modifications of histone proteins, and noncoding
RNA, with functional interactions across these pathways (Goldberg et al., 2007). DNA
methylation suppresses gene transcription and thus silences the gene. These marks are
considered generally stable, but there are “erasers,” such as DNA and histone demethylases, as
well, and some modifications are quite dynamic (Daxinger & Whitelaw, 2012). The field of
epigenetics has generated great interest by offering a mechanism through which the environment
shapes us, representing a rejection of genetic determinism.
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18
The concept of epigenetic transmission or inheritance warrants clarification (see Figure
1). Parental, or intergenerational effects, are those induced by the offspring’s direct exposure to
the trauma, such as in utero exposure, which may affect the embryo or fetus and its developing
germline (Heard & Martienssen, 2014). Transgenerational effects are those observed in
generations not directly exposed to the triggering environment. For this reason, effects are only
considered transgenerational if observed in F3 females (F0 is the exposed mother), because the
F1 female offspring and her F2 germ cells would be exposed to the trauma in utero. F3 would
therefore be the first generation not directly exposed to the trauma. In males, effects observed in
F2 would be considered transgenerational, because spermatogenesis occurs during adolescence
rather than in the fetus, and thus F1germ cells would not be directly exposed to the trauma in
utero (Dias & Ressler, 2014; Heard & Martienssen, 2014).
Epigenetic mechanisms have been associated with parenting and social influences, in
utero transmission, and transmission through gametes (sperm or oocyte) (for review, see Yehuda
& Lehrner, in press). In other words, social interactions such as parenting may shape the
epigenome (the sum of all epigenetic information attached to the genome) of the offspring, a
form of “transmission” in which the social context, rather than parental biology, transfers
information that is biologically encoded in offspring. Myriad forms of social information,
including parent-offspring interactions, social learning, and symbolic cultural communication,
can lead to the transmission of epigenetic variations (Jablonka & Raz, 2009). The intrauterine
environment can also affect the offspring epigenome, through fetoplacental interactions that are
influenced by maternal stress, physical condition and mental state. In this case, the offspring is
directly exposed during gestation to an aspect of the maternal experience, mediated by the
CULTURAL TRAUMA AND EPIGENETICS
19
placenta. These are all forms whereby parental experiences may influence offspring biology
through epigenetic mechanisms, and represent intergenerational epigenetic effects.
Inheritance of epigenetic marks from the parent to the offspring, representing inter- or
transgenerational epigenetic inheritance, requires transmission through the gametes. In
multicellular organisms this occurs when epigenetic marks are conserved through meiosis (cell
division creating gametes), gametogenesis, and early embryogenesis, which involve significant
demethylation and restructuring of chromatin (Heard & Martienssen, 2014; Jablonka & Raz,
2009). Despite these processes, methylation marks are not completely erased, and re-methylation
processes also occur. Furthermore, some RNAs may also be transmitted through the germline
(Jablonka & Raz, 2009).
Transmission of Trauma Effects through Parental Care
In seminal work with rats, Meaney and colleagues demonstrated that variations in
maternal care, operationalized as licking and grooming of pups, altered DNA methylation in the
glucocorticoid receptor gene (NR3C1) in the hippocampus of the offspring (Weaver et al., 2004).
As adults, the rats showed alterations in HPA axis functioning, including altered basal and stress
induced corticosterone levels, higher GR sensitivity, and more hippocampal GR (Meaney,
Aitken, Bodnoff, Iny, & Sapolsky, 1985; Meaney, Aitken, Bodnoff, Iny, Tatarewicz, et al., 1985;
Meaney, Aitken, van Berkel, Bhatnagar, & Sapolsky, 1988). This work demonstrated that
maternal behavior can affect offspring at the level of DNA chemistry in the brain, and that
methylation at identified regions in the GR gene promoter shapes the development of the
glucocorticoid mediated stress response system.
These findings were translated to humans in a study of hippocampal glucocorticoid
receptor in human suicide victims, which found higher methylation at the glucocorticoid receptor
CULTURAL TRAUMA AND EPIGENETICS
20
1F promoter in post-mortem tissue in victims with a history of childhood abuse (McGowan et al.,
2009). Glucocorticoid receptor methylation in white blood cells of healthy children and adults
has also been associated with childhood adversity and negative parenting styles (Tyrka, Price,
Marsit, Walters, & Carpenter, 2012; Tyrka et al., 2015; Tyrka et al., 2016). In adult offspring of
Holocaust survivors, maternal and paternal PTSD had interacting effects on glucocorticoid
receptor methylation in blood, such that offspring with maternal PTSD had lower methylation of
the exon 1F promoter region, but those with paternal PTSD only showed higher levels (Yehuda
et al., 2014). There have been no studies to date of epigenetic effects of community level effects
of cultural trauma, as contextual factors have been measured as mediated through parental
behavior and biology.
Prenatal In utero Trauma Effects on Offspring
The differential effects of parental sex suggest the possibility that the intrauterine
environment or the gametes contribute to transmission of trauma effects. The HPA axis is
developed by 22 weeks of gestation, and is sensitive to developmental programming throughout
gestation. Fetoplacental interactions may buffer, or expose, the developing fetus to maternal
glucocorticoids related to stress, physical adversity or psychiatric symptoms, particularly through
placental 11B-hydroxysteroid dehydrogenase type 2 (11β-HSD2), an enzyme that converts
cortisol to inactive cortisone (Nugent & Bale, 2015). Influences during gestation may include
maternal state, environmental exposures, developmental stage of the fetus, and even the sex of
the fetus (Carpenter, Grecian, & Reynolds, 2015; Oberlander et al., 2008). For example, a
prospective study of infants born to pregnant female survivors of the World Trade Center attacks
found low cortisol levels in association with maternal PTSD, an effect that was strongest for
those exposed in the third trimester (Yehuda et al., 2005). Offspring of mothers with PTSD also
CULTURAL TRAUMA AND EPIGENETICS
21
showed signs of anxiety and disrupted behavior, as well as being rated by their mothers as
having greater distress to novelty. There is also a growing body of work with rodent models
documenting the intergenerational effects of prenatal environmental exposures to biological
toxins and maternal stress (Gapp, von Ziegler, Tweedie-Cullen, & Mansuy, 2014). Taken
together, this literature provides evidence that in utero exposure to maternal trauma may affect
the developing HPA axis of the fetus.
The developmental origins of health and disease field (DOHD) investigates fetal origins
of myriad adult disorders, based on findings of the influence of prenatal and even pre-conception
factors of myriad health outcomes, including psychiatric and medical conditions (Gillman,
2005). Epidemiological studies of intergenerational effects of two large scale famines have
documented health and disease outcomes in offspring over multiple generations. Supporting the
hypothesis that there are developmentally sensitive windows during gestation, both phenotypic
outcomes and epigenetic marks were observed in adults exposed to famine at conception and
during the first half of gestation, but not in those exposed in the third trimester or postnatal
period (Heijmans et al., 2008; Ravelli, Stein, & Susser, 1976). DNA methylation mediated the
association of prenatal famine exposure and adult metabolic health, with additional CPG sites
identified among those exposed early in gestation (Tobi et al., 2018). Exposure to famine during
pregnancy was associated with neonatal adiposity and poorer health in offspring of the exposed
female fetus, providing the first human evidence that starvation during pregnancy can affect
health outcomes in grandchildren (Painter et al., 2008). This literature supports hypotheses that
aversive environmental stimuli or deprivation during pregnancy may have effects on health
outcomes over two generations, and that these effects may be partly mediated by epigenetic
alterations in the offspring.
CULTURAL TRAUMA AND EPIGENETICS
22
Regarding trauma exposure specifically, there is evidence that prenatal exposure to
violence has effects on offspring methylation, although these studies are not powered to analyze
gestational age of exposure. Higher methylation of the glucocorticoid receptor gene has been
observed in adolescent offspring of mothers who experienced prenatal intimate partner violence
(Radtke et al., 2011), newborns of women exposed to severe prenatal stress, particularly warzone
stressors, in the Democratic Republic of Congo (Mulligan, D'Errico, Stees, & Hughes, 2012),
and young adult offspring of Tutsi widows exposed to the Rwandan genocide during the second
and third trimesters of pregnancy (Perroud et al., 2014). These observations are directionally
different than those observed in older Holocaust offspring, raising questions of whether pre-
conception exposure, age of offspring, prior maternal trauma exposure or concurrent psychiatric
symptoms influence the degree and directionality of DNA methylation. It is unclear whether and
to what degree the influence of prenatal stress and trauma exposure on fetal development is
mediated through maternal psychiatric symptoms or subjective distress, which may affect
intrauterine signals during gestation. Furthermore, HPA axis sensitization may lead to changes in
functioning over time as the system attempts to adapt or becomes exhausted. For example,
among individuals with PTSD, higher basal cortisol has been observed proximally to trauma
exposure, but lower HPA axis activity observed related to more distal trauma exposure (Morris
et al., 2012).
Transmission of the Effects of Trauma through Gametes
The foregoing describes the transmission of effects of trauma as mediated by social
processes (e.g., parental behavior) or in utero influences. Trauma that occurred prior to
conception may also affect offspring through alterations in parental germ cells that are conserved
during fertilization and embryogenesis. As noted above, initial understanding of DNA
CULTURAL TRAUMA AND EPIGENETICS
23
methylation, based on animal research, was that epigenetic marks were erased during
comprehensive reprogramming in games and in the early embryo (Daxinger & Whitelaw, 2012).
However, since the late 1980s evidence has accrued that parental epigenetic states can be
transmitted through the gametes and maintained across more than one generation (Daxinger &
Whitelaw, 2012).
There are no studies to date of trauma induced epigenetic marks in oocytes, which
although present since birth are sensitive to environmental influences, particularly during
childhood (Cortessis et al., 2012; Faulk & Dolinoy, 2011). Interestingly, the age of maternal
Holocaust exposure was associated with cortisol levels and metabolism in offspring,
independently of maternal PTSD, with the strongest effect for women who were children during
the war, suggesting a possible gametic effect (Bader et al., 2014). There is data from animal
models showing that methylation status in dams can affect offspring phenotype, suggesting that
epigenetic marks may survive oogenesis and affect the epigenetic state of offspring (Jaenisch &
Bird, 2003)
There is a growing literature on transmission of environmental effects through sperm,
which is more easily isolated from confounding influences than oocytes. Spermatogenesis begins
at puberty and continues throughout the lifespan (Desai, Ludgin, Sharma, Anirudh, & Agarwal,
2017). There are no known investigations of transgenerational effects of trauma through human
sperm, but there are observational studies linking environmental exposures in men, including diet
and famine, smoking, alcohol consumption, toxins, and stress, with both biological and
behavioral outcomes in offspring, in some cases with demonstrated epigenetic marks in paternal
sperm (Anway, Cupp, Uzumcu, & Skinner, 2005; Friedler, 1996; Schagdarsurengin & Steger,
2016; Yehuda & Lehrner, in press). For example, studies have shown that adult offspring of
CULTURAL TRAUMA AND EPIGENETICS
24
fathers exposed to famine had higher body mass index and obesity rates (Veenendaal et al.,
2013). Observations of paternal transmission in humans have been extended to three generations.
Parental and grandparental diet and food availability prior to puberty has been linked with
different sex specific risk and protective factors in children and grandchildren (Kaati, Bygren,
Pembrey, & Sjöström, 2007). Smoking, alcohol, dependence, and opioid dependence have all
been linked with changes in DNA methylation and chromatin in sperm (Chorbov, Todorov,
Lynskey, & Cicero, 2011; Hamad, Shelko, Kartarius, Montenarh, & Hammadeh, 2014; Ouko et
al., 2009). In at least one study, paternal smoking effects on offspring were limited to cases of
pre-pubertal smoking in fathers (Pembrey et al., 2006).
This body of epidemiological and associational research provides support for the
hypothesis that trauma effects could be transmitted through gametes in humans. However, the
majority of this work has been conducted in animals for methodological reasons, such as the
ability to control other environmental stimuli, including in utero or early developmental effects.
A body of experimental research with rodents has documented effects of paternal stress or
environmental insults, using a variety of paradigms across developmental stages, on offspring
behavior, neurology and sperm (Bale, 2014; Franklin et al., 2010; Yehuda & Lehrner, in press),
although not all stressors have been shown to affect offspring through sperm (Dietz et al., 2011).
Epigenetic mechanisms may include DNA methylation, oxidative damage to sperm DNA,
histone modifications, and changes in small noncoding RNAs, including microRNA (Heard &
Martienssen, 2014; Yehuda & Lehrner, in press). Overall, this body of research suggests that
stress to males across the lifespan can lead to phenotypic and biological changes in offspring
mediated by epigenetic changes in sperm (Rodgers, Morgan, Bronson, Revello, & Bale, 2013).
CULTURAL TRAUMA AND EPIGENETICS
25
Permanence Versus Plasticity of the Epigenome
Because epigenetic marks are relatively stable (versus transient hormonal responses to
stress, for example), trauma induced changes and their transmission have often been considered
permanent. However, given that epigenetic processes represent a fundamental biological
mechanism of plasticity and adaptability, this assumption bears examination. Over generations,
such changes may lead to more extreme phenotypes or more reliable transmission if the
environmental contexts endure, or conversely, may fade away over generations if the contexts
change (Jablonka & Raz, 2009). These questions are more easily pursued with animals, as the
shorter lifespan facilitates study of transgenerational effects, and breeding and environmental
influences can be controlled.
A new line of research has emerged investigating possibilities for preventing the
transmission of trauma induced epigenetic effects. Mansuy and colleagues found that
environmental enrichment (including sensory, motor and cognitive stimuli) after weaning in
male mice prevented behavioral and biological effects associated with early stress in male
offspring (Gapp et al., 2016). Specifically, hippocampal DNA methylation and glucocorticoid
receptor gene expression levels associated with paternal stress were reversed in the adult
offspring. Stressed males exposed to enriched environment and their offspring performed
similarly to controls in response to stressful challenges in adulthood, whereas without
enrichment fathers and offspring showed behavioral effects of early paternal stress.
Furthermore, offspring of fathers exposed to enrichment after early stress failed to show
alterations in glucocorticoid receptor expression and DNA methylation associated with early
stress exposure, indicating a normalization of gene expression following enrichment. The
researchers analyzed sperm to isolate the mechanism of this transmission, and found that DNA
CULTURAL TRAUMA AND EPIGENETICS
26
methylation was altered in sperm cells of stressed males, but that these effects were no longer
found in sperm of fathers raised in the enriched environment. It is of interest to note, however,
that the behavioral alterations of offspring associated with paternal early life stress conferred
resilience to aversive conditions and more active coping in responding to aversive stimuli (Gapp
et al., 2016).
Implications of Potential Epigenetic Transmission of Trauma Effects
As research on intergenerational inheritance of environmentally induced epigenetic
marks grows, a landscape of post-Lamarckian, non-Mendelian heritability unfolds to great, if
sometimes overstated, excitement (Goldberg et al., 2007; Lim & Brunet, 2013; Miller, 2010;
Yehuda, Lehrner, & Bierer, in press). There has been much excitement about the possibility that
what happens to individuals, societies, and cultures, can have longlasting effects on the way
genes function. However, the study of epigenetic influences of environmental stimuli, especially
in early life, has been primarily conducted in animals. It remains to be seen if these observations
will be reliably observed in humans. If so, it will be important to determine whether epigenetic
marks in blood cells have functional significance. Furthermore, epigenetic research on
behavioral or psychiatric indicators in humans has relied almost exclusively on peripheral
samples such as blood rather than brain tissue. Because methylation patterns are tissue specific,
it is not clear whether and to what extent methylation patterns observed in peripheral tissue
reflect activity in the brain or other tissue of interest. While there is some support from rats that
there may be overlapping patterns of gene expression related to stress across both blood and
brain, with convergent glucocorticoid signaling pathways, this has not yet been examined with
respect to methylation patterns (Daskalakis, Cohen, Cai, Buxbaum, & Yehuda, 2014). Finally,
CULTURAL TRAUMA AND EPIGENETICS
27
the role of genetic factors in epigenetic changes associated with trauma requires further
investigation.
When the environmental context is traumatic – when it involves genocide, violence, and
oppression – it may be natural to assume that any adaptations to such contexts must be harmful,
as it is difficult to conceptualize benefits from such traumas. Interpretations of biological
transmission tend to fall under the (usually unspecified) cumulative stress model, in which the
impact of early life adversity and maternal stress is assumed to confer vulnerability to later
insults. And indeed, there is a strong body of literature in animals documenting such effects in
response to maternal stressors (Daskalakis, Oitzl, Schächinger, Champagne, & de Kloet, 2012).
But from a biological perspective, changes in response to environmental stimuli are not
inherently “good” or “bad.” It may make evolutionary sense for parents to pass on adaptations to
threat to their offspring; whether these adaptations serve offspring depends on the environmental
contexts the organism encounters across its lifespan.
Epigenetic mechanisms facilitate adaptive response and flexibility to environmental
perturbations with possible evolutionary significance (Jablonka & Raz, 2009). Indeed, heritable
epigenetic changes in response to traumatic environments would be evolutionarily advantageous,
preparing offspring for events that are unpredictable but intense and potentially recurring,
especially when the offspring is born into more favorable conditions (Harper, 2005) These
epigenetic accommodations to external stimuli are relatively stable, rather than transient, but they
are not permanent and are sensitive to subsequent remodeling. They are part of a dynamic system
that continues to evolve, maximizing the organism’s ability to thrive. It is teleological to argue
that the existence of such mechanisms necessarily indicates adaptivity, but the intergenerational
conservation of information relevant to environmental contexts is certainly likely to generate a
CULTURAL TRAUMA AND EPIGENETICS
28
wider range of phenotypes, thus expanding the community’s ability to adapt and respond to
changing environments. The intergenerational transmission of effects of trauma is not
synonymous with permanent damage in offspring, it just implies change as a result of
environmental exposure
It has been argued that inheritance of trauma effects may be detrimental in the case of an
environmental mismatch, where the offspring is primed for threat but the sociocultural context
has changed (Santarelli et al., 2014; Schmidt, 2011). This is consistent with epidemiological
research indicating that offspring conceived during famine but raised in contexts of food
abundance demonstrate poorer health outcomes. There is also the possibility that inherited
effects remain dormant in the absence of a relevant environmental trigger. In this case, offspring
may not show phenotypic similarity with the parent (such as psychiatric or behavioral
indicators), but may have increased vulnerability or reactivity when confronted with relevant
stimuli. Jablonka and colleagues (2009) have termed this “epigenetic recall,” similar to a
memory trace that requires re-induction for memory reconstruction. This possibility is consistent
with research on Holocaust offspring showing healthy functioning in general, but poor responses
to severe stressors (Van Ijzendoorn et al., 2003).
Support for the hypothesis that the potential adaptiveness or harmfulness of early trauma
depends on subsequent environmental demands comes from the animal work that initially
identified effects of maternal care on offspring DNA methylation. As adults, the offspring of
low licking and grooming mothers showed deficits in neural plasticity and memory under
baseline conditions (Champagne et al., 2008). But under stressful or high corticosterone (the
animal homologue of cortisol) conditions, the animals displayed enhanced plasticity and
memory, whereas animals who received high licking and grooming demonstrated the opposite
CULTURAL TRAUMA AND EPIGENETICS
29
results. A match/mismatch hypothesis has been proposed to explain how early life experiences,
and by extension, inheritance of biological alterations associated with parental experience, may
confer either vulnerability or enhanced coping and plasticity depending on later life contexts
(Daskalakis et al., 2012).
Conclusions and Future Directions
There is a general consensus that parental and communal trauma affect development, but
how this happens and what it means remain open questions. The emergence of epigenetics as a
potential biological mechanism for transmission of parental experiences has thrust these
questions to the forefront of many academic and popular culture forums. The effects of parental
trauma may influence male and female gametes prior to conception, fetal development in utero,
and postnatal parenting and family environment, all of which may shape offspring biology and
phenotype. It is strange, however, that the possibility of conservation and transmission of
learning related to trauma from parent to offspring is most commonly assumed to convey
vulnerability and damage. Transmission of cultural memory through rituals, symbols and
practices serves to transmit learning and meaning, to allow future generations to understand the
world and to respond adaptively. Few argue that such memory is damaging, poses a threat to
healthy development, or requires preventive interventions (although see Linden and Rutkowski,
2013, for an argument in favor of “beneficial forgetting”). In many traditions, transmission of
memory of important cultural events aims to convey a sense of identity, to forewarn and forearm
future generations against threat, and to celebrate resilience and perseverance. It is interesting
that the possibility that such memory might also be conserved at a molecular level, shaping
expression of the genome, frequently becomes mired in a narrative of damage.
CULTURAL TRAUMA AND EPIGENETICS
30
The cultural narrative about what is being transmitted and what it means profoundly
shapes the nature of the experience of offspring of trauma survivors (Mohatt, Thompson, Thai, &
Tebes, 2014). Western conceptions of mental health and wellness, and definitions of “normalcy,”
are culture bound, and reflect expectations of safety, trust, optimism, and happiness, among other
things. To be affected by experiences that undermine these expectations can be interpreted as
“maladaptive” or reflecting mental illness, and the sociocultural conditions that gave rise to such
experiences and that may continue to shape experiences of later generations can be ignored. Yet
these assumptions are widely unexamined in relation to discussions of the effect of cultural
trauma on development and future generations.
Gone and Kirmayer (2010) provide an instructive example from O’Nell’s (1996)
anthropological work among the Salish Indians of Montana regarding the meaning ascribed to
feeling the intergenerational effects of centuries of conquest, racism and oppression among.
Although members of this community described aspects of depression such as feeling bereaved,
aggrieved, and worthless, only feeling worthless was associated with suicide, whereas feeling
bereaved as understood as appropriate given the losses of the community over the previous
century. Feeling bereaved was respected as a sign of maturity among elderly members, who
were seen to grieve appropriately for the many losses experienced by the community (Gone &
Kirmayer, 2010). In this case, whereas one interpretation might be that intergenerational
transmission puts members of this community at risk for depression, the lived narrative is one
that values the experience of those who continue to bear a mantle of grief over the community’s
history of trauma.
The concept of being strengthened by adversity, and even trauma, has deep roots in
Western paradigms as well. Indeed, the idea that good can come from suffering is embedded in
CULTURAL TRAUMA AND EPIGENETICS
31
Judeo-Christian theology. More recently, the field of psychology has expanded the study of
trauma to include not only posttraumatic maladjustment, but also posttraumatic growth (Calhoun
& Tedeschi, 2014), defined as psychological change following challenging or traumatic events
which may manifest as an “increased appreciation for life in general, more meaningful
interpersonal relationships, an increased sense of personal strength, changed priorities, and a
richer existential and spiritual life” (Tedeschi & Calhoun, 2004). One hypothesized mechanism
for this growth is the development of a trauma narrative that acknowledges the reality of the
trauma, allows the individual to let go of beliefs or schemas that are inconsistent with this reality,
and generates new worldviews that allow for continued movement towards values and goals.
The development of acceptance, of facing existential questions about life, and the perspective
that comes with posttraumatic growth has also been framed as the development of wisdom
(Linden, Baumann, Lieberei, Lorenz, & Rotter, 2011). Although the concept of posttraumatic
growth has been primarily applied to individuals, in their seminal paper delineating the concept,
Tedeschi and Calhoun (2004) address the application of posttraumatic growth to communities
and societies that have experienced shared and widespread trauma. They suggest that such
experiences can be recognized as “turning points” and form the basis of shared social narratives
that can transform the community’s sense of identity, principles and values, and understanding of
the world.
The introduction of epigenetics into the conversation about the intergenerational
transmission of trauma effects has the potential to highlight the phenotypic diversity, potential
adaptiveness, and divergent possibilities inherent in epigenetic inheritance. Too often the
discussion in effect becomes a mirror of the old nature versus nurture debate. On the one hand,
the possibility of epigenetic transmission appears to reject genetic determinism in favor of the
CULTURAL TRAUMA AND EPIGENETICS
32
power of environmental influences. On the other hand, it often reifies a kind of environmental
determinism, implying that the experiences of parents determine the biology and therefore
available repertoire of offspring. Evidence that cultural trauma in past generations may leave
traces in the epigenome may serve to validate offspring experiences or to imply a legacy of
damage. As with the experience of trauma itself, the narrative we tell about its meaning has
much power in determining the consequences.
CULTURAL TRAUMA AND EPIGENETICS
33
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Figure 1. Intergenerational transmission of biological effects of trauma
There are multiple potential pathways for the biological transmission of trauma effects across
generations. Preconception trauma exposure (F0) may affect the epigenetic status of maternal
oocytes or paternal sperm; this may be developmentally dependent, particularly in females.
These effects may be conserved and manifest during embryogenesis, resulting in inheritance of
those effects by offspring. In the case of mothers exposed to trauma during pregnancy, the fetus
(F1) and its developing germline may be affected in utero. In the case of an exposure during
prengancy, the future offspring of the fetus (F2) will have been directly exposed to the
grandmaternal (F0) stress, and as a result only the third generation (F3) can be considered to
evidence transgenerational transmission that was not an effect of direct exposure. In the case of
paternal exposure, F2 can be considered to reflect a true transgenerational effects. Effects of
parental trauma exposure may also be transmitted through parenting, family environment, and
parental behaviors. The experience and transmission of trauma effects are embedded within a
larger cultural context that includes narratives, beliefs, and practices. The effects of trauma are
also felt and transmitted within a sociostructural context that includes access to resources,
relative safety of the neighborhood, and the larger political environment.
