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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.
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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.
This manuscript represents the post-refereed version but not the publishers 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:
Acknowledgements: The authors would like to thank Alex Ropes, Migle Staniskyte, and
Emmanuel Ruhamya for assistance with manuscript preparation.
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,
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,
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
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
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
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,
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
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
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).
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
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.
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,
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
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 (
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
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,
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.
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
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,
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.
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
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
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
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.
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
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
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).
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
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,
the role of genetic factors in epigenetic changes associated with trauma requires further
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
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
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.
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
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
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.
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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.
... There are many ways to measure historical trauma and the historical trauma response [29]; one method may reveal different associations than others. Indeed, historical trauma and the historical trauma response are quite challenging to research as Lehrner et al. (2018) note, "trauma influences multiple levels of the individual's ecosystem" [60]. Further, we do not distinguish temporally distinct phenomenon as embodiment is an ongoing, multidirectional process [61][62][63]. ...
... There are many ways to measure historical trauma and the historical trauma response [29]; one method may reveal different associations than others. Indeed, historical trauma and the historical trauma response are quite challenging to research as Lehrner et al. (2018) note, "trauma influences multiple levels of the individual's ecosystem" [60]. Further, we do not distinguish temporally distinct phenomenon as embodiment is an ongoing, multidirectional process [61][62][63]. ...
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Background Historical trauma experienced by Indigenous peoples of North America is correlated with health disparities and is hypothesized to be associated with DNA methylation. Massive group traumas such as genocide, loss of land and foodways, and forced conversion to Western lifeways may be embodied and affect individuals, families, communities, cultures, and health. This study approaches research with Alaska Native people using a community-engaged approach designed to create mutually-beneficial partnerships, including intentional relationship development, capacity building, and sample and data care. Methods A total of 117 Alaska Native individuals from two regions of Alaska joined the research study. Participants completed surveys on cultural identification, historical trauma (historical loss scale and historical loss associated symptoms scale), and general wellbeing. Participants provided a blood sample which was used to assess DNA methylation with the Illumina Infinium MethylationEPIC array. Results We report an association between historical loss associated symptoms and DNA methylation at five CpG sites, evidencing the embodiment of historical trauma. We further report an association between cultural identification and general wellbeing, complementing evidence from oral narratives and additional studies that multiple aspects of cultural connection may buffer the effects of and/or aid in the healing process from historical trauma. Conclusion A community-engaged approach emphasizes balanced partnerships between communities and researchers. Here, this approach helps better understand embodiment of historical trauma in Alaska Native peoples. This analysis reveals links between the historical trauma response and DNA methylation. Indigenous communities have been stigmatized for public health issues instead caused by systemic inequalities, social disparities, and discrimination, and we argue that the social determinants of health model in Alaska Native peoples must include the vast impact of historical trauma and ongoing colonial violence.
... The word transmission does not automatically imply that it is due to a biological mechanism or something biologically inherited, such as via epigenetic mechanisms. When considering transmission of psychological or physiological trauma effects in FASD, it is important to also carefully consider the influences of social and cultural transmission [67] (discussed in Section 10). ...
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Fetal alcohol spectrum disorder (FASD) results from teratogenic impacts of alcohol consumption during pregnancy. Trauma and prenatal alcohol exposure (PAE) can both cause neurode-velopmental impairment, and it has been proposed that FASD can amplify effects of trauma. Certain PAE and trauma effects are mediated via epigenetic mechanisms. The objective of this review is to present the current evidence for epigenetics in trauma transmission as it relates to FASD, to help bridge a potential knowledge gap for social workers and related health professionals. We include a primer on epigenetic mechanisms and inheritance, followed by a summary of the current biomedical evidence supporting intergenerational and transgenerational epigenetic transmission of trauma, its relevance to FASD, the intersection with social transmission, and finally the application to social work. We propose potential models of transmission, considering where social and epigenetic pathways may intersect and/or compound across generations. Overall, we aim to provide a better understanding of epigenetic-trauma transmission for its application to health professions, in particular which beliefs are (and are not) evidence-based. We discuss the lack of research and challenges of studying epigenetic transmission in humans and identify the need for public health interventions and best practices that are based on the current evidence.
... If the brain mediates all conscious and unconscious experiences-including spiritual experiences-healing, like addictions, it seems to be related to the processes by which the human brain is organized for controlling pleasure and pain [27]. With these thoughts presented herein, we theorize that a healthy spirituality may come more naturally to some individuals, because of the unique interaction of their genes and their environmental induced positive epigenetic impact (possibly via belief in GOD) but negative (bad parenting) that can occur up to three generations without an effect on the DNA [28]. ...
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It is with a saddened heart that we are dedicating this article to the loving memory of our dear departed friend and associate B. William Downs. Bill was well known in the nutritional space worldwide for his major contributions to the health and welfare of millions around the globe. The founder of Victory Nutrition International (VNI) in conjunction with Kim Downs, as well as so many contributions to scientific literature, to those that knew him personally will forever be touched. Bill was a highly spirited human with a never ending love for caring and helping so many individuals. To know Bill is to walk in the face of a music lover playing drums, trained as a martial artist, and riding through the winds of a Beamer driven by an iconic man driven to victory. Our hearts may be saddened but Bills spirit to those that know him will be forever. In this article we discuss and review some potential futuristic concepts and technological advancements in terms of geneospirituality engineering to help prevent relapse and or even protect against an unwanted predisposition to RDS behaviors. Futuristic development may contribute to an attenuation of both DNA antecedents as well as epigenetic reward system insults leading to unwanted substance and non-substance addictive behaviors.
... Individuals may be haunted for decades by unprocessed trauma that, among other things, can influence how events are experienced, reacted to and remembered (e.g., Shalev et al. 2000;Van der Kolk 2015;Wolynn 2017;Bourke 2005Bourke , 2014Maté and Maté 2022). Children and grandchildren can be affected by behavioural patterns and types of stress markers which follow genetic material through conception (e.g., Yehuda and Lehrner 2018;Lehrner and Yehuda 2018;Mucci 2022). ...
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The article takes its starting point in more than 160 personal narratives from former migrants, their children, and grandchildren. The testimonies have been collected by cultural-history museums in seven European countries – Norway, Denmark, Sweden, Poland, Lithuania, Slovenia and Croatia – and provide a haunting impression of the long-term consequences of war and forced migration for at least three generations. The research aimed at understanding how exactly the Untold and the silence of the first generation – the not-sharing of what they, as time witnesses, experienced – can be sensed by their children and grandchildren and influence their lives, family relations and the surrounding society in a negative way. The findings show that the need for personal and public information by the second and third generations cannot be overestimated and that sharing and getting to know could be a key to more healthy relations between family members and within communities.
... Some studies have shown that paternal or grandparent malnutrition has effects on the phenotypes of the next generations. This has been shown to increase the risk of developing diabetes and heart disease among grandchildren (Lehrner and Yehuda 2018). There are also some clinical studies showing that sperm DNA methylation is affected by fathers with excessive alcohol use (Curley et al. 2011). ...
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Social events that cause stress can cause epigenetic changes on living things. The study of the effects of social events experienced by an individual on epigenetic marks on the genome has created the field of social epigenetics. Social epigenetics examines the effects of psychosocial stress factors such as poverty, war trauma and childhood abuse on epigenetic mechanisms. Epigenetic mechanisms alter chemical markers in the genome structure without changing the DNA sequence. Among these mechanisms, DNA methylation in particular may have different phenotypic effects in response to stressors that may occur in the psychosocial environment. Post-traumatic stress disorder is one of the most significant proofs of the effects of epigenetic expressions altered due to traumatic events on the phenotype. The field of epigenetic inheritance has shown that epigenetic changes triggered by environmental influences can, in some cases, be transmitted through generations. This field provides a better understanding of the basis of many psychological disorders. This review provides an overview of social epigenetics, PTSD, and epigenetic inheritance.
... Research has examined epigenetic changes related to the cumulative stress of historical trauma, which is associated with pervasive health inequities in communities with historically oppressed identities (Brockie et al., 2013;Conching & Thayer, 2019;Heberle et al., 2020;Lehrner & Yehuda, 2018). ...
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Aim: The objective of this integrative review was to critically synthesize the evidence on protective factors in early childhood that buffer the effects of exposure to intimate partner violence (IPV) on young children's health outcomes. Methods: Studies were eligible for inclusion in this review if the article was (a) in English, (b) title or abstract discussed protective factors, buffering, resilience or mitigating factors in early childhood for young children who experienced IPV. Results: A total of 23 articles of 492 manuscripts identified from the search from peer-reviewed journals from 2010 to 2022 were included. Individual-level protective factors for young children exposed to IPV and include emotional self-regulation, child temperament and child self-esteem. Family-level protective factors were maternal physical and mental health; warm, responsive parenting; knowledge of child development; socioeconomic advantage; caregiver employment; and maternal education. Conclusion: The results of this integrative review highlight the critical importance of a dyadic approach to early childhood intervention. Health and legal systems should not only focus solely on pathology of family violence but also conceptualize treatment and courses of action from a strength-based perspective in order to empower victims of IPV, and promote the safety, health and well-being of children. Future research should examine the role of system-level protective factors. Impact: This review adds to the growing body of the evidence of positive relational health as a key social determinant of health for children. This will be foundational to design interventions that shield children from further harm and promote health, flourishing and recovery from violence and trauma.
... However, the least common symptoms among these four regions differed (i.e., hyperarousal for Cambodia and Ethiopia; avoidance behaviors for Algeria and Gaza) [42]. Lastly, growing literature has focused on the biopsychosocial intergenerational transmission of cultural trauma [39,43]. That is, through epigenetic mechanisms, biologic changes in response to a cultural trauma may be transmitted from parents to their progeny. ...
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We reviewed the phenomenology of Post-Traumatic Stress Disorder (PTSD) and Traumatic Brain Injury (TBI), as well as the combined effects of PTSD + TBI comorbidity on functional outcomes. We also provide a series of research and treatment recommendations based on gaps in the literature with an emphasis on culture, interpersonal trauma, and treatment. Rates of PTSD + TBI are remarkably high. This comorbidity is especially common among combat-exposed military populations (with current estimates among Veterans returning from Afghanistan/Iraq at approximately 48%), as well as individuals who experience motor vehicle collisions (estimated base rate = 12%). These conditions often co-occur primarily because the events preceding the brain injury are both physically and psychologically traumatic. In many cases of PTSD + TBI, especially mild TBI, psychological factors largely account for accompanying functional outcomes (e.g., cognitive sequela, somatosensory health, quality of life, occupational functioning, social engagement). Overall, we suggest the importance of integrative teams in the early assessment, conceptualization, and treatment of PTSD + TBI. Psychological interventions and cognitive rehabilitation may synergistically improve psychological and functional outcomes for this patient population.
This chapter addresses something of whether the trauma inherent in legal study and practice might be mitigated by less focus on thinking like a lawyer and more on what an embodied approach to learning could open up.Although law is intended to keep people safe, its privileging of education from the neck up acts to disconnect students and practitioners at a very deep level from their bodies, emotions and feeling states. This disconnection can leave us not feeling safe in our bodies, resulting in processes of the autonomic nervous system, paving the way for chronic stress.As many involved in law in any capacity are impacted at a very visceral level, the chapter explores the role of the autonomic nervous system as a potential catalyst for enhancing emotional regulation, deepening learning and helping us feel safer in our bodies. From a place of safety, our learning and decision-making processes are likely to be more holistic and discerning. Using the lens of Polyvagal Theory, the chapter presents an experimental approach at the Law School of Ulster University, seeking to imbue the undergraduate curriculum, in particular, with somatic, trauma-aware learning, drawing on and intertwining mindfulness, somatic exploration and the new science of safety. The chapter further considers some difficulties and potential attending the embedding of a more embodied, polyvagal-informed approach in mainstream legal education.KeywordsLegal educationAutonomic nervous systemPolyvagal TheoryMindfulnessSafety
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For many Māori students, staying in the main flow of the awa (river) is not easy in New Zealand’s mainstream education system. But with the right support mechanisms and structures in place, it is possible, for a Māori doctoral student to achieve educational success as Māori in higher education. This paper discusses what is entailed in the dual journey of a first in family, Māori doctoral student when completing a doctoral qualification alongside a Māori journey in strengthening connections within te Ao Māori (the Māori world). The narrative shares insights of the researcher’s experiences which led to the development of an Indigenous methodology model called ‘He Pūtauaki Model’. A number of key factors for ensuring her success as a Māori doctoral candidate was the continual support and guidance provided from kaumātua (elders), whānau (family), hapū (sub-tribe) and iwi (tribe), over a four-year period of completing the doctoral journey, and when a Mahitahi approach was adopted by her supervisors and reinforced by other Te Ipukarea Research Institute postgraduate students made a difference for her in overcoming the challenges that an Indigenous Māori doctoral student can face when navigating the awa (structural mechanisms and psychosocial challenges) at Auckland University of Technology (AUT).
Over the last century, anthropological discourse about race changed dramatically. Once a core concept in anthropology, it is now widely accepted as the “myth” coined by Ashley Montagu to denote that race is a social construction with no basis in biology. The social constructivist view of race was long in the making in American anthropology. Typological thinking about human variation persists in science and society and race continues to be important to biological anthropologists in many ways. This chapter explores three of them. First, the race concept is not dead. Second, racial thinking may still influence researchers' understanding of human variation, population relationships, and human evolution. Finally, while social races are not genealogical entities, they have biological dimensions. The race concept is currently alive and well in the general public, providing fodder for neo‐fascists globally, but it has also persisted in biological anthropology until very recently.
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This paper reviews the research evidence concerning the intergenerational transmission of trauma effects and the possible role of epigenetic mechanisms in this transmission. Two broad categories of epigenetically mediated effects are highlighted. The first involves developmentally programmed effects. These can result from the influence of the offspring's early environmental exposures, including postnatal maternal care as well as in utero exposure reflecting maternal stress during pregnancy. The second includes epigenetic changes associated with a preconception trauma in parents that may affect the germline, and impact fetoplacental interactions. Several factors, such as sex‐specific epigenetic effects following trauma exposure and parental developmental stage at the time of exposure, explain different effects of maternal and paternal trauma. The most compelling work to date has been done in animal models, where the opportunity for controlled designs enables clear interpretations of transmissible effects. Given the paucity of human studies and the methodological challenges in conducting such studies, it is not possible to attribute intergenerational effects in humans to a single set of biological or other determinants at this time. Elucidating the role of epigenetic mechanisms in intergenerational effects through prospective, multi‐generational studies may ultimately yield a cogent understanding of how individual, cultural and societal experiences permeate our biology.
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There has been great interest in the possibility that effects of trauma might be passed from parent to offspring through epigenetic mechanisms. This topic has stimulated discussion and controversy in the scientific literature, the popular press, and culture at large. This article describes the initial observations that have led to recent examinations of epigenetic mechanisms in association with effects of parental trauma exposure on offspring. Epigenetic research in animals has provided models for how such effects might be transmitted. However, the attribution of any specific epigenetic mechanisms in human studies of offspring of trauma survivors is premature at this time. The article describes some of the ways in which initial epigenetic findings in the offspring of trauma survivors have been represented in the popular media. Reports have ranged from overly simplistic and sensationalistic claims to global dismissals. The authors discuss the importance of clarity in language when describing epigenetic findings for lay audiences, the need to emphasize the limitations as well as the promise of research on intergenerational transmission of trauma effects, and the importance of countering popular interpretations that imply a reductionist biological determinism. Scientists have an obligation to assist in translating important research findings and nascent avenues of research to the public. It is important to recognize the ways in which this research may unintentionally be received as supporting a narrative of permanent and significant damage in offspring, rather than contributing to discussions of potential resilience, adaptability, and mutability in biological systems affected by stress.
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Although it is assumed that epigenetic mechanisms, such as changes in DNA methylation (DNAm), underlie the relationship between adverse intrauterine conditions and adult metabolic health, evidence from human studies remains scarce. Therefore, we evaluated whether DNAm in whole blood mediated the association between prenatal famine exposure and metabolic health in 422 individuals exposed to famine in utero and 463 (sibling) controls. We implemented a two-step analysis, namely, a genome-wide exploration across 342, 596 cytosine-phosphate-guanine dinucleotides (CpGs) for potential mediators of the association between prenatal famine exposure and adult body mass index (BMI), serum triglycerides (TG), or glucose concentrations, which was followed by formalmediation analysis.DNAm mediated the association of prenatal famine exposure with adult BMI and TG but not with glucose. DNAm at PIM3 (cg09349128), a gene involved in energy metabolism, mediated 13.4% [95% confidence interval (CI), 5 to 28%] of the association between famine exposure and BMI. DNAm at six CpGs, including TXNIP (cg19693031), influencing b cell function, and ABCG1 (cg07397296), affecting lipid metabolism, together mediated 80% (95% CI, 38.5 to 100%) of the association between famine exposure and TG. Analyses restricted to those exposed to famine during early gestation identified additional CpGs mediating the relationship with TG near PFKFB3 (glycolysis) and METTL8 (adipogenesis). DNAm at the CpGs involved was associated with gene expression in an external data set and correlated with DNAm levels in fat depots in additional postmortem data. Our data are consistent with the hypothesis that epigenetic mechanisms mediate the influence of transient adverse environmental factors in early life on long-termmetabolic health. The specific mechanism awaits elucidation.
Full-text available
Although it is assumed that epigenetic mechanisms, such as changes in DNA methylation (DNAm), underlie the relationship between adverse intrauterine conditions and adult metabolic health, evidence from human studies remains scarce. Therefore, we evaluated whether DNAm in whole blood mediated the association between prenatal famine exposure and metabolic health in 422 individuals exposed to famine in utero and 463 (sibling) controls. We implemented a two-step analysis, namely, a genome-wide exploration across 342,596 cytosine-phosphate-guanine dinucleotides (CpGs) for potential mediators of the association between prenatal famine exposure and adult body mass index (BMI), serum triglycerides (TG), or glucose concentrations, which was followed by formal mediation analysis. DNAm mediated the association of prenatal famine exposure with adult BMI and TG but not with glucose. DNAm at PIM3 (cg09349128), a gene involved in energy metabolism, mediated 13.4% [95% confidence interval (CI), 5 to 28%] of the association between famine exposure and BMI. DNAm at six CpGs, including TXNIP (cg19693031), influencing β cell function, and ABCG1 (cg07397296), affecting lipid metabolism, together mediated 80% (95% CI, 38.5 to 100%) of the association between famine exposure and TG. Analyses restricted to those exposed to famine during early gestation identified additional CpGs mediating the relationship with TG near PFKFB3 (glycolysis) and METTL8 (adipogenesis). DNAm at the CpGs involved was associated with gene expression in an external data set and correlated with DNAm levels in fat depots in additional postmortem data. Our data are consistent with the hypothesis that epigenetic mechanisms mediate the influence of transient adverse environmental factors in early life on long-term metabolic health. The specific mechanism awaits elucidation.
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This article explores the relevance of historical trauma theory for Māori research. In exploring the impact of historical trauma upon Māori it has become clear that the terminology associated with historical trauma theory is considered controversial in Aotearoa New Zealand. As such, this article provides an overview of key definitions relevant to historical trauma and explores these in relation to recent reporting related to the use of the terms “holocaust” and “genocide” in the context of colonization in Aotearoa New Zealand. It is argued that in order to engage fully with the impacts of colonization on Māori wellbeing we must articulate fully the impact of historical trauma events and the contribution of those events to the negative health disparities experienced by many of our whānau (extended family), hapū (sub-tribes) and iwi (tribes).
H. Keilson (1979) coined the term “sequential traumatization” for the accumulation of traumatic stresses confronting the Holocaust survivors before, during, and after the war. A central question is whether survivors were able to raise their children without transmitting the traumas of their past. Through a series of meta‐analyses on 32 samples involving 4,418 participatns, we tested the hypothesis of secondary traumatization in Holocaust survivor families. In the set of adequately designed nonclinical studies, no evidence for the influence of the parents' traumatic Holocaust experiences on their children was found. Secondary traumatization emerged only in studies on clinical participants, who were stressed for other reasons. A stress‐diathesis model is used to interpret the absence of secondary traumatization in nonclinical offspring of Holocaust survivors.
In this book, Ron Eyerman explores the formation of the African-American identity through the theory of cultural trauma. The trauma in question is slavery, not as an institution or as personal experience, but as collective memory: a pervasive remembrance that grounded a people's sense of itself. Combining a broad narrative sweep with more detailed studies of important events and individuals, Eyerman reaches from Emancipation through the Harlem Renaissance, the Depression, the New Deal and the Second World War to the Civil Rights movement and beyond. He offers insights into the intellectual and generational conflicts of identity-formation which have a truly universal significance, as well as providing a compelling account of the birth of African-American identity. Anyone interested in questions of assimilation, multiculturalism and postcolonialism will find this book indispensable.
In this extraordinary new text, an international array of scholars explore the enduring legacy of such social shocks as war, genocide, slavery, tyranny, crime, and disease. Among the cases addressed are - instances of genocide in Turkey, Cambodia, and Russia - the plight of the families of Holocaust survivors, atomic bomb survivors in Japan, and even the children of Nazis - the long-term effects associated with the Vietnam War and the war in Yugoslavia - and the psychology arising from the legacy of slavery in America.
This article develops a conceptual model of cultural competency’s potential to reduce racial and ethnic health disparities, using the cultural competency and disparities literature to lay the foundation for the model and inform assessments of its validity. The authors identify nine major cultural competency techniques: interpreter services, recruitment and retention policies, training, coordinating with traditional healers, use of community health workers, culturally competent health promotion, including family/community members, immersion into another culture, and administrative and organizational accommodations. The conceptual model shows how these techniques could theoretically improve the ability of health systems and their clinicians to deliver appropriate services to diverse populations, thereby improving outcomes and reducing disparities. The authors conclude that while there is substantial research evidence to suggest that cultural competency should in fact work, health systems have little evidence about which cultural competency techniques are effective and less evidence on when and how to implement them properly.