Canada’s Colonial Genocide of Indigenous Peoples: History
View Latest Version
Please note this is an old version of this entry, which may differ significantly from the current revision.
Contributor:
Kimberly Matheson
,
Ann seymour
,
Jyllenna Landry
,
Katelyn Ventura
,
Emily Arsenault
,
Hymie Anisman
,
Kim Matheson

Indigenous Peoples worldwide, including in Canada and the U.S. have, over generations, experienced assaults on their very survival, along with their culture, land, and ways of life. The Truth and Reconciliation Commission of Canada, established to bring to light the experiences of survivors of the Indian Residential Schools, referred to this program as constituting cultural genocide. While these events all inflicted severe and lasting harm to the survivors, resilience and the perseverance of many aspects of culture may be maintained through intergenerational processes.

  • Indigenous
  • colonization
  • historical trauma
  • epigenetic

1. Historical Trauma: 500 Years of Colonization

Colonization has long been a way for some nations to gain wealth and influence. The African continent has experienced colonization for more than two millennia. The colonization of what was to become the Americas began in the early part of the 16th century, before which Indigenous Peoples had their own kinship and governance structures, ceremonies and belief systems, as well as knowledge developed over many generations regarding a balanced co-dependent relationship with the land. A degree of cooperation initially existed between Indigenous Peoples and the Europeans who arrived, including the sharing of skills and knowledge, as well as trade and military alliances. Thus, at the outset, relationships with Indigenous Peoples were greatly valued—until they were no longer needed and viewed as an encumbrance. As settler populations increased, their desire for land and wealth grew. The colonization of Indigenous Peoples over several centuries was achieved by guns and by old-world bioweapons that comprised the introduction of smallpox, tuberculosis, and influenza that killed more people than settler bullets did. In fact, in what is now Canada, the Indigenous population pre-colonization was estimated to have been between 350,000 and 500,000 (but some estimates have it as high as 2 million), but declined to just 125,000 by 1867.
In addition to the physical appropriation of land was the colonial effort to eliminate the transmission of cultural identity, traditional skills, and connection to the land. Beginning in 1883 (while this was the date of the first federally established church school, similar institutions existed as early as the 1830s, years before Canadian federation) Indian Residential Schools (IRSs) were established in Canada (as were American Indian Boarding Schools in 1862). Children were forcibly removed from their families and were institutionalized in IRSs with the explicit goal of ‘taking the Indian out of the child’. These mandated church-run IRSs endeavoured to save the souls of the ‘savages’ by immersing them in Euro–Christian beliefs and eradicating access to traditional socialization values, language, practices and ways of life. By the 1930s, roughly 75% of First Nations children attended IRSs, as did many Métis and Inuit children. The last of the IRSs was closed in 1996, but by then several generations of children had experienced the mistreatment that abounded in these institutions.
While the treatment of children varied across the different IRSs, they frequently experienced harsh and denigrating conditions [1]. In addition to physical, emotional and sexual abuse and neglect, children were stripped of their identities, made to feel ashamed of themselves and their culture, and denied the use of their language, beliefs, and ways of being. Some IRSs were associated with Indian hospitals where sick children were transferred but, owing to poor isolation procedures, diseases such as tuberculosis were often acquired. Indian hospitals were not intended to administer treatment that incorporated traditional medicines, midwives or holistic strategies; rather, the hospitals’ assimilationist goals were to replace traditional healing with Western biomedical procedures [2]. In the Indian hospitals, which treated Indigenous patients in addition to IRS students, non-consensual sterilization was commonly undertaken (such non-consensual operations were performed on Indigenous women even as recently as 2018). In some IRSs, nutritional experiments were conducted from 1942 to 1952 to determine whether vitamin supplements (riboflavin, thiamine, niacin, and bone meal) would limit the effects of purposefully introduced malnourishment. These experiments continued despite the deteriorating health and increased mortality of children, and the developmental delays that were produced [3]. Indeed, these experiments continued well after the UN Convention on genocide was signed. The consequences for IRS survivors resulted in marked and varied repercussions on health, which has been elucidated in detail in a tragically poignant report [4].
The trauma did not end for children once they were released from the IRSs. They were returned to reserves that had been subjugated into poverty, and where they felt disconnected from their families and communities. There was much discord between community members, often instigated by prior conflicts (bullying) brought about by a need to survive in the IRSs [5]. Moreover, on some reserves, divisions existed between members who had internalized the religious precepts imposed on them at the IRSs, whereas others were intent on maintaining traditional Indigenous ways of life. Thus, where communities had operated as cohesive collectives, the IRS experience fostered divisions and conflicts over fundamental values. Further contributing to dysfunction in some communities, adult survivors frequently experienced shame and guilt owing to their powerlessness in protecting their children or siblings from the IRS experience, resulting in coping behaviors that were self-abusive or abusive of others.
Although the experiences of the children who attended the IRSs and the consequences that emerged are relatively well known, far less attention has been directed toward the Sixties Scoop. During the period from the 1950s to the 1990s, about 20,000 Indigenous children in Canada were removed from their families and communities by child welfare services. Indigenous children whose parents attended IRSs were at greater risk of experiencing childhood adversity in their homes, thus increasing the likelihood of their removal and placement with non-Indigenous foster parents, adoptive parents, and in group homes, often permanently separated from their families and from their cultural identity [6][7].
Even today, despite representing only 7.7% of the Canadian population, Indigenous children represent over half (52.2%) of children aged 14 and younger in foster care, described as the ‘millennial scoop’ [8]. Remarkably, there are currently more Indigenous children in the care of the child welfare system (CWS) than there were in IRSs at any single point in time [1]. In numerous regional jurisdictions in Canada, there remains a policy of putting expecting mothers, disproportionately those who are Indigenous, on ‘birth alerts’, with social workers being present to apprehend a newborn infant immediately following the birth without parental consent. Even in regions where birth alerts are no longer official policy, it has been suggested that the practice continues, largely due to systemic biases within the CWS. There is growing evidence that the overrepresentation of Indigenous children at risk of apprehension by the CWS can be ascribed to social and economic inequities [6][9][10], most of which are linked to the continued legacy of governmental forced assimilation policies [6]. Sadly, experiencing the child welfare system is predictive of poorer mental health outcomes, along with juvenile and adult incarceration in the criminal justice system. In addition to affecting the children taken, these experiences promoted profound mental health consequences in parents [11].
Colonialist actions involving policies such as the IRSs and the Sixties Scoop, along with forced relocations and the restricted movement of Indigenous community members, have contributed to the erosion of the knowledge of the land that was passed down through generations. Treaties were created that were regarded by settlers to represent a surrender of the land by First Nations. The Indian Act restricted First Nations Peoples to reserves and diminished access to the broad resources of their ancestral territories either by limiting practices, physical access, or by developments that destroyed the land, contaminated the water, or eradicated traditional ways of life and livelihoods. As with so many Indigenous populations globally, the land is not perceived as an object to be possessed. Instead, the plants, animals, and waters are viewed as ‘life’ and inter-connected relationships, as ‘members of the larger other-than-human community’ [12]. Thus, the systematic removal of Indigenous Peoples from their lands and the development (desecration) of traditional territories, ranging from clear-cutting to changes to waterways (hydro dams) to fracking and pipelines, to the toxic disposal of pollutants in the air and water systems, all constitute traumatic insults with incumbent consequences [13]. The Canadian determination to establish sovereignty in remote areas (e.g., the Arctic circle) involved the duplicitous relocation of Inuit families to thousands of kilometres from their home territories. Elders have recounted decreased physical, mental, and emotional health after experiencing dispossession from the land [14]. Spiritual impact and loss are felt related to the inability to pass on traditional Indigenous knowledge to younger generations; reduced access to the land preventing its use for ceremonies, traditional practices and sustenance; the reduced ability for water to give and support life; the loss of language that is essential to express their connection with; and lost knowledge of the land [14][15].
Beyond colonial exploitation of the land, environmental racism and climate change are impacting the health and well-being of Indigenous Peoples, especially in the north [16][17]. The most recent report of the Intergovernmental Panel on Climate Change [18] points to climate change as a contemporary manifestation of colonialism. In this regard, colonialism is implicated as both a driver of climate change and in exacerbating the vulnerability of Indigenous communities. When the land is the main source of sustenance, the inability to predict environmental phenomena or the lack of tools to contend with such changes can have particularly devastating effects on well-being at both the individual and community level. Many Indigenous communities have been contending with critical environmental issues, including the toxicity of local bodies of water and exposure to natural and human-made disasters, such as floods and forest fires. When such events force displacement, temporarily or permanently, there is the additional diminishment of the safety and security of displaced populations. Under these conditions, resources (e.g., financial, along with basic needs such as water, food, and clean air) are stretched or no longer accessible, family and community members may be divided or lost, safety and security are undermined, and exposure to potential toxicants and disease are heightened. Warming temperatures, as well as changes in weather patterns and ice stability, have altered access to resources critical to community survival and created barriers to community members’ participation in land-based practices and ways of life, resulting in diminished cultural identity and well-being [16][19]. These effects are occurring even though Indigenous Peoples’ ways of life are least likely to be contributing to the human-made impact on the climate. On the contrary, many of the environmental disasters that have affected the lives and livelihoods of Indigenous Peoples in Canada have, at their roots, industrial developments by corporations with no or minimal Indigenous representation, consultation or benefit.
The built environment of Indigenous communities may further promote severe health issues. Government programs that control the building of homes and infrastructure in fly-in and northern communities apply standards that are not only inappropriate for the climate [20][21], but disregard the cultural and social needs associated with familial and community living. Homes were built with standard designs defined by government agencies (‘Indian Houses Type 1–7’), all with similar floor plans. This strategy undermines traditional family structures and diminishes individuals’ identification with their living spaces [20][21]. The houses in these communities are often built below acceptable quality standards, and without consideration of the high cost of transporting materials to remote communities, thereby limiting the number of new homes and extending the time needed to build.
A failure to include Indigenous perspectives in decision-making continues to severely limit progress for self-determination in housing [21]. The lack of reconciliation in housing policies combined with the substandard construction of homes on-reserve has resulted in statistics that have remained unchanged for decades; in 2006, 44% of on-reserve First Nations homes required major renovations and 36% reported living in overcrowded conditions, and these numbers were still evident in 2016 [22][23]. It has been noted that, ‘The consequence of this crisis is that the home, which for First Nations people has traditionally been a place of pride and identity, instead today exacerbates many social and health problems’ [20] (p. 2). Some of these social problems contribute to intergenerational trauma, including numbing the pain by substance misuse and other related negative coping mechanisms [24].
Colonization as it is recapitulated in current times meets the key criteria of Article II of the UN Convention on Genocide. The intergenerational effects of historic and ongoing systemic racism have had considerable implications for the health and well-being of Indigenous Peoples (Article IIb). Mental health problems are endemic among Indigenous populations; depressive disorders, anxiety, PTSD, and substance use disorders occur at inordinately high levels. In many First Nations and Inuit communities, the occurrence of suicide has been much higher than in the remainder of the Canadian population. The frequency of suicide varies across communities, ranging from 2 to 10 times that of non-Indigenous people, and it is especially disconcerting that over the last two decades suicide has occurred more frequently among young people. This is similarly apparent among American Indians and Alaskan Natives, in whom suicide occurs at 2.5 times the frequency of the population at large.
Understandably, a significant level of distrust between Indigenous Peoples and healthcare professionals exists. Given women’s experiences of forced sterilization, birth alerts, and the removal of children as a result of various policies over generations, the fear of child apprehension is so deeply rooted that some mothers may refuse skin-to-skin contact, breastfeeding, and other bonding strategies because they expect their child to be taken from them (Articles IId, IIe). This learned distrust of healthcare professionals jeopardizes the willingness of expectant mothers to disclose their medical, physical, mental or substance use history. Such mistrust is particularly evident among Indigenous women in fly-in and northern communities. The medical and healthcare services offered in such communities are often limited, forcing expectant mothers to leave the community to deliver in larger, urban, mainstream hospital facilities, and those who experience pregnancy complications are sometimes away from home for extended periods of time. Forced obstetric evacuation is particularly stressful, as due to the nature of medical funding that is applied to Indigenous Peoples, women are typically separated from family and community support for the final weeks of pregnancy, putting a notable strain on the health and wellness of both mother and child. This may contribute to the increased risk of medical intervention during labor, as well as postpartum depression, along with the negative developmental consequences of stress on the fetus, and may even account for why the mortality rate of Indigenous infants is 2–7 times higher than non-Indigenous infants [25]. The loss of the birthing experience and related ceremonies in communities is perceived as a cultural loss and forced evacuation has been long associated with colonial practices.
Just as colonialism continues to influence Indigenous entrance into the world, it also influences death. The built environment hinders the palliative care that reflects the values of Indigenous Peoples. A lack of healthcare access on reserves and inadequate housing that does not allow for proper care necessitates aging individuals leaving their community to access care in a hospital setting [22][26][27]. While the majority of Indigenous people would prefer to pass away at home, many die in urban hospitals where the physical structure of the hospital building or prohibitive administrative policies can prevent end-of-life care that aligns with Indigenous values. In addition, this stage of life is often a time of sharing stories and passing on knowledge, and so death in urban hospitals is another form of systemic racism that further marginalizes Indigenous ways of knowing [22].

2. Neurobiological Consequences of Early-Life Trauma

Aside from the psychosocial and environmental factors associated with diminished outcomes emanating from traumatic experiences, numerous biological consequences of chronic and traumatic stressors can contribute to varied psychological and physical illnesses. These, primarily conducted in animal models, have indicated that stressful experiences profoundly affect numerous hormonal processes (e.g., CRH, ACTH, cortisol, estrogen, oxytocin, arginine vasopressin), brain neurotransmitters (e.g., monoamines, GABA, glutamate), neurotrophins (e.g., BDNF, FGF-2, VEGF), brain microglia functioning, and gut microbiota, as well as immune and inflammatory responses that may promote or exacerbate physical and psychological disturbances [28][29][30]. To a considerable extent, many of these effects are moderated by genetic and epigenetic factors, the organism’s previous stressor experiences, and a constellation of psychosocial and environmental variables [31].

Intergenerational Consequences of Prenatal Stressors

Just as Indigenous children are more likely to encounter ACEs than those who are non-Indigenous, as noted earlier, prenatal challenges (stress experienced by pregnant mothers) are more likely to occur among Indigenous women, with implications for the fetus. In animal models, it has become increasingly apparent that prenatal stressful events may have physical and emotional repercussions that appear in offspring. Like the effects of early-life adverse experiences, it was found that stressors experienced by a pregnant dam influenced the neurotrophins that are fundamental for the neurodevelopment and memory processes, and could thereby promote behavioral disturbances [32]. In humans, stressors experienced during pregnancy may profoundly influence the well-being of offspring. The appearance of low birth weight (which is accompanied by the underdevelopment of brain and body functioning) has been apparent in response to diverse stressful experiences, including wartime conditions, domestic violence, and racial discrimination, as well as in the offspring of mothers that experienced PTSD during pregnancy [33]. Moreover, preterm birth is related to cumulative life stressor experiences, including those encountered prior to pregnancy [34]. The precipitation of preterm birth and low birth weight may occur owing to the provocation of numerous hormonal and inflammatory alterations introduced by stressors [35][36].
Individual stressor experiences (e.g., abuse) during pregnancy can have marked effects on the fetus that are manifested as far-reaching postnatal health disturbances. Developmental delays, including emotional and cognitive disturbances associated with variations of limbic and frontotemporal neural networks, have been reported in the offspring of mothers that experience emotional, psychological, physical, or sexual violence during pregnancy [37][38]. Commensurate with these findings, such maternal experiences have been linked to altered hippocampal volume and poor social–emotional development in offspring [39]. Likewise, the stress of exposure to natural disasters could affect pregnant women and lead to offspring displaying poorer cognitive, emotional, and behavioral outcomes [40]. In addition to the psychological disturbances engendered by prenatal stressors, these experiences have been associated with childhood immune-related disorders, such as allergies and asthma, and increased susceptibility to infectious diseases [41]. Stressful events experienced prenatally are similarly accompanied by elevated levels of inflammatory factors [42] that favor the subsequent development of chronic diseases, such as type 2 diabetes, heart disease, and some forms of cancer [28].
It is not simply during pregnancy that maternal stress can affect fetal development. Stressors encountered by women prior to becoming pregnant can affect offspring birth weight [43], fetal brain development, and postnatal psychological disorders [44], which could potentially come about due to the distress related to persistent negative rumination. A prospective analysis similarly revealed that preconception PTSD was associated with elevated negativity when children were 3–5 years old, even after controlling for prenatal and postnatal depressive symptoms or sociodemographic factors [45].

3. Epigenetic Changes Related to Stressful Events

Based on traumatic events, it could induce intergenerational epigenetic changes among survivors of the Holocaust, as well as those experienced by other groups, it has been suggested that similar actions may affect Indigenous Peoples in Canada and elsewhere [46]. However, data are not currently available that assess this possibility. In part, this lack of research is not surprising given the numerous instances in which Indigenous Peoples have been experimented on without consent, lied to about the goals of research [47], and over-researched while at the same time remaining invisible in research [48]. Moreover, there is a concern that genetic research might be used to undermine the responsibility of colonial governments to acknowledge the causal role of history in relation to health inequities. Thus, while understanding how intergenerational trauma and environmental toxicants can influence epigenetic processes, there is currently an absence of mutually beneficial research addressing these issues among Indigenous people in Canada.
Epigenetic research reflects an understanding that social challenges, environmental agents, and even dietary factors can alter the expression of a great number of genes, without altering the genome itself. Through various processes, the functioning of particular genes can be silenced or activated, which can promote multiple phenotypes [49]. Thus, a history of colonial trauma encountered by Indigenous Peoples may have altered gene expression, leading to elevated vulnerability to psychological and physical illnesses. At one time, it had been assumed that epigenetic actions were infrequent, but it is now known that epigenetic changes are exceedingly common, with some becoming fixed (permanent) whereas others are transient. Childhood abuse, for instance, is accompanied by a great many epigenetic marker beyond those evident among individuals who have not experienced early-life abuse [50]. In view of the numerous epigenetic changes that occur, it is difficult to determine the correspondence between specific changes and particular phenotypes. Moreover, finding such relationships does not imply causality.
The majority assessing epigenetic changes has been conducted in animal models, particularly in relation to intergenerational outcomes. Rodents have revealed that stressful events can promote epigenetic changes in genes that code for several hormones, neurotrophins and immune factors, which may favor the occurrence of psychological and physical disturbances [51]. Not unexpectedly, poor diet and nutrition similarly influence the expression of genes that can affect well-being. Specific nutrients (or lack of nutrients) may likewise influence the many bacterial species present within the gut and other parts of the body, and alterations of these ‘microbiota’ can produce epigenetic actions, which then promote the development of psychological disorders. Aside from nutrients, microbiota changes can be influenced by other lifestyle factors, stressors, and environmental toxicants, which can influence gene expression and their consequences.
Like other stressors, poor maternal care of pups during early development may promote epigenetic changes that have been linked to hormonal and neurotrophic processes. This includes neglect experienced by pups during early postnatal development, which can affect the epigenetic processes related to the gene regulation of glucocorticoid functioning, which is linked to elevated stressor reactivity [52]. As well, epigenetic actions stemming from early life adversity have been observed in genes associated with diverse behavioral disturbances. These include genes that influence serotonin processes [53], estrogen receptor functioning in the brain [54], as well as neurotrophin activity in several brain regions [55], all of which can affect normal behavioral functioning and the development of psychiatric disorders. In addition to epigenetic changes being provoked by stressful events during early life, similar actions were provoked in rodents stressed during the juvenile period (the equivalent of adolescence in humans); these rodents subsequently displayed increased reactivity and anxiety. Intense stressors experienced in adulthood likewise promote epigenetic effects that influence neurobiological processes linked to depressive-like features [56][57].
Among humans, epigenetic changes stemming from ACEs may influence health outcomes. The epigenetic changes introduced by childhood stressors are not restricted to those related to brain processes, having been seen in relation to immune cell functioning and inflammatory factors that could potentially contribute to the appearance or progression of varied diseases [58]. Of course, numerous factors, including genes coding for an array of hormones and growth factors, may contribute to later health disturbances as might an array of experiential and environmental influences (e.g., parental behaviors, poverty).

4. Epigenetic Changes Associated with Prenatal Stressor Events

Just as stressors encountered during early life can have long-term ramifications, epidemiological ones have indicated that lifestyles of women during pregnancy (e.g., diet and obesity, tobacco and alcohol use), as well as stressful experiences and exposure to air pollutants, are accompanied by epigenetic changes that could affect offspring [59][60]. Likewise, psychological stressors experienced during pregnancy can elicit epigenetic changes that influence vulnerability to pathology in offspring, and these actions could be transmitted to subsequent generations [61]. A longitudinal analysis conducted among the offspring of women who were pregnant during Hurricane Sandy in 2012 indicated that when they were 3–4 years of age, they exhibited elevated levels of anxiety and aggressive behaviors, together with increased cortisol levels measured in hair samples. These behavioral and hormonal alterations were accompanied by placental mRNA changes that were tied to endocrine and immune processes [62]. It similarly appeared that, in the offspring of women who experienced a severe ice storm while they were pregnant, cognitive disturbances were subsequently apparent that seemed to be mediated by epigenetic changes linked to genes associated with the promotion of diabetes [63]. Indeed, reprogrammed gene expression within the fetus elicited by prenatal stressors resembled those associated with early-life adverse events [64]. These epigenetic effects could involve actions related to diverse biological processes, and particular attention has been devoted to those that influence or reflect stress reactivity (HPA functioning) and emotionality in offspring [65].
While the phenotypic changes associated with prenatal stressors might have been directly related to epigenetic actions stemming from stressful experiences, they could just as well reflect poor rearing conditions and parental distress and anxiety following a traumatic experience. Based on analyses of offspring that were born following in vitro fertilization, wherein they were biologically related or unrelated to their birth mothers, it was concluded that psychological and cognitive disturbances varied as a function of genetic factors, the prenatal environment, and post-natal maternal factors [66]. In effect, the stress experienced by the biological mother may have contributed to epigenetic changes in offspring, even in the absence of prenatal or postnatal stressors.

5. Transgenerational Transmission through Epigenetic Changes

While not diminishing the functional consequences of maternal and psychosocial factors, it has been clear in animals that trauma-related epigenetic actions can affect the well-being of offspring across generations. The epigenetic changes brought about by stressors and other environmental exposures can be transmitted from parents to offspring if these alterations occur in germline cells (i.e., sperm or ova) and may occur across several generations, even if further stressors or other experience-dependent changes are not encountered [67][68]. Among other factors, exposure to stressors during pregnancy may promote sex-dependent transgenerational effects on anxiety-like behaviors, together with epigenetic changes within genes that code for or influence glucocorticoid receptor functioning and neurotrophins within particular brain regions [69][70].
Some of the transgenerational effects of the stressors discovered primarily occurred in males, whereas others were more evident in females. Sex-dependent effects have been assumed to be related to maternal influences, as mothers are the primary caregivers in most rodent species. Several ones, however, have suggested that epigenetic outcomes can occur through paternal transmission. Specifically, maternal separation from their male offspring resulted in the pups subsequently exhibiting depressive-like behaviors and increased reactivity to stressors as adults. In the offspring of these males, epigenetically related behavioral and neuroendocrine disturbances were evident, even though they had not come into contact with their male parent [71][72]. It was similarly reported that the impact of exposure to a stressor over 6 weeks prior to breeding led to paternal epigenetic effects [73]. Consistent for animals, the paternal transmission of epigenetic changes stemming from ACEs in humans was linked to attention problems apparent in their offspring [74]. The early-life stressful experiences of a male parent were similarly associated with altered brain development in neonates, even after controlling for multiple maternal factors [75].
It was similarly demonstrated that early-life paternal challenges that comprised a series of different stressors could engender behavioral disturbances that were evident up to the fourth generation of offspring [76]. Effects such as these have been attributed to epigenetic actions that are especially notable among stress-reactive mice, pointing to the fundamental importance of individual difference factors in predicting the transmission of stressor effects over generations. As well, the intergenerational effects of stressors are determined by the characteristics of the stressor experienced (e.g., social versus asocial stressors; acute versus chronic stressors) and the age of the animal at the time of stressor exposure [77].
Predictably, far fewer have assessed the intergenerational and transgenerational effects of stressful experiences in humans. The length of time for each generation to come to the age of having children has limited the research regarding the intergenerational effects of trauma. Even when it were conducted to assess the transmission of stressor effects across generations, it was uncertain whether the effects observed were related to the trauma experiences, given that they were assessed retrospectively. Moreover, most complex psychological and physical disorders are mediated by multiple genes whose actions can be moderated by numerous psychosocial and experiential factors, making attributions to epigenetic changes and intergenerational outcomes tenuous. Nonetheless, an array of factors related to stressors have been identified that are subject to epigenetic changes, some of which might be relevant to intergenerational outcomes.
Epigenetic changes in genes associated with glucocorticoid functioning have been observed in relation to aging, as well as stressor experiences [78], and it has been found that aging and stressor actions are synergistically linked in affecting pathology and inflammatory processes [79]. Adverse childhood events are similarly tied to epigenetic changes that are associated with brain changes relevant to both executive functioning and adult depression [80]. Moreover, among individuals with a history of childhood abuse and neglect who had died by suicide, epigenetic changes were present within the genes of the glucocorticoid receptors within the hippocampus [81].
The intergenerational effects of traumatic events have been examined more extensively among survivors of the Holocaust than among other groups. The survivors frequently displayed elevated glucocorticoid functioning in response to stressors [82][83][84], and such effects were frequently apparent in the adult offspring of Holocaust survivors. These behavioral and hormonal alterations were, in many instances, accompanied by epigenetic changes in both the survivors and their children [85], varying in relation to whether one or both parents had been survivors, as well as whether one or both parents had developed PTSD [86]. These data imply neither causal nor direct connections between particular epigenetic effects and any specific phenotypic changes, especially as the latter may be mediated by parental mental health problems and disturbed parenting styles [87]. Importantly, offspring might not ordinarily present with disturbed day-to-day behaviors, but the actions of epigenetic changes might be most evident upon encounters with further adverse events [88].
As alluded to earlier, the intergenerational epigenetic changes associated with stressors were not unique to Holocaust survivors. Many women who experienced extreme abuse (sexual violence, torture) during the Kosovo war developed PTSD during pregnancy, and epigenetic changes were detected in their children, including those that coded for a glucocorticoid receptor and a serotonin receptor, as well as a neurotrophin [89]. Paralleling these findings, the children of pregnant women who developed PTSD during the 1994 Tutsi genocide subsequently displayed increased epigenetic changes tied to glucocorticoid receptor levels relative to those apparent in women that had not been exposed to the trauma [90]. The presence of an epigenetic marker related to the oxytocin receptor has also been associated with changes in discrete brain regions related to altered empathy in mothers [91], and could affect parent–offspring interactions.
Epigenetic changes do not only occur as a result of psychosocial stressors. Environmental toxicants and drugs consumed during pregnancy may promote teratogenic effects in a developing fetus, and epigenetic variations can similarly be engendered in the fetus by environmental challenges. Endocrine-disrupting compounds, such as phthalates and bisphenol-A, as well as pesticides and dioxins, can promote epigenetic changes that are transmitted to the next generation of rodents, thereby increasing health risk [92]. Pesticides and fungicides can similarly promote epigenetic changes that increase vulnerability to viral challenges, and these actions can be transmitted transgenerationally [93][94]. Paternal intergenerational effects have been implicated with epigenetic changes associated with nutrients consumed and with deficiencies in folic acid [95]. Likewise, epigenetically transmitted actions related to paternal diet (high fat or low protein) are associated with risk of disease in offspring [96]. Given that stressors can affect nutrient intake, it can reasonably be expected that intergenerational effects can be transmitted indirectly by a male parent.
Lasting epigenetic changes have been reported among individuals that were born during severe famine conditions. Near the end of the Second World War, towns in the western parts of the Netherlands that had been occupied by Nazi forces were prevented from obtaining food or fuel, leading to misery and starvation. Children born during this period, referred to as the Dutch Hunger Winter, subsequently presented with elevated heart disease and the risk of type 2 diabetes. Psychiatric disturbances such as schizophrenia and depression occurred more often, and poor cognitive performance was apparent in later life [97]. The experience of the Dutch Hunger Winter was associated with genetic changes that influenced birth weight and subsequent LDL cholesterol levels [98]. Moreover, analyses conducted decades after this famine indicated that individuals who had prenatally experienced this condition expressed epigenetic changes related to factors that may have disposed individuals to type 2 diabetes [99][100].
Data collected in a different context are consistent with those obtained from ones of the Dutch Winter hunger. Specifically, among children born during the Great Chinese famine (1959–1961) the risk for adult type 2 diabetes was elevated and this outcome could have been transmitted across generations [101] (Li, 2017). Likewise, early-life differences in famine conditions within two regions of China revealed differences in epigenetic changes associated with neurotrophins, together with changes in cholesterol levels [102]. The intergenerational impact of the Holodomor genocide of 1932–1933, when Ukraine experienced a famine created by policies created by Stalin, is another situation in point [103]. The constellation of behaviors associated with famine (or food insecurity) has been described as living in ‘survival mode’, including horror, fear, mistrust, sadness, shame, anger, stress and anxiety, decreased self-worth, stockpiling of food, reverence for food, overemphasis on food and overeating, inability to discard unneeded items, indifference towards others, social hostility, and risky health behaviors. However, the imposition of such conditions and their implications have not been addressed in relation to Indigenous Peoples, despite the high levels of food insecurity in many Indigenous communities.
In view of the multiple epigenetic changes that have been associated with distressing events and with diverse psychological problems, as well as the influence of numerous psychosocial factors, it is premature to point to a single epigenetic alteration as being responsible for pathological outcomes stemming from adverse events. Many epigenetic actions have been identified among individuals who experienced stressful events during early life [57]. The involvement of these epigenetic changes in the intergenerational effect of stressors remains to be fully evaluated, but the findings are certainly in line with the view that actions other than, or in addition to, those associated with glucocorticoids may contribute to the persistent actions of early-life adversity. More extensive prospective analyses concerning the emergence of pathological conditions, together with whole epigenome analyses, could point to clusters of epigenetic markers relevant to the concatenation of factors that link generations of historical trauma exposure to illness occurrence.
Being subjected to collective trauma has long-term intergenerational consequences that are instigated through multiple psychosocial and neurobiological mechanisms. Nonetheless, resilience in the aftermath of such challenges does occur. Resilience is fostered when the survivors of natural events are able to express and anticipate collective solidarity and cohesion, and act cooperatively to draw on collective social support resources [104]. Processes that ground people in an identity, self-affirmation, belonging, and safety [105], and are further imbued with spirituality can serve to promote continuity of relationships across generations [106]. In effect, intergenerational resilience can be derived from the symbiotic relationship to the land, encompassing physical and non-physical elements, such as the social, emotional and spiritual aspects that provide the foundation of identity, social connectedness, and a sense of community and belonging [107][108].
With so many factors playing into the compromised well-being of Indigenous Peoples, multiple issues need to be addressed concurrently to bring about meaningful change. The challenges that Indigenous Peoples continue to encounter, ranging from community infrastructure (housing, clean water) to food security and quality, along with access to appropriate health services, need to be addressed now. Rather than applying singular or isolated solutions emanating from Western mental health frameworks, what is needed is to enable Indigenous Peoples to identify and implement culturally relevant strategies that reflect the connections between individuals and their social, cultural and environmental contexts. Indigenous Peoples are reclaiming their inherent rights to self-determination and reconnecting to their cultural roots, including renewing land-based values, skills, and spiritual connections among the next generation of young people. Indigenous understandings of wellness are inherently holistic, with resilience emanating from the adaptive balance of protective and risk factors over time and space [109]. This may provide the perspective needed to counter the centuries of genocidal actions targeted against them.

This entry is adapted from the peer-reviewed paper 10.3390/ijerph19116455

References

  1. Truth and Reconciliation Commission of Canada. Honouring the Truth, Reconciling for the Future; Truth and Reconciliation Commission of Canada: Ottawa, ON, Canada, 2015.
  2. Lux, M. Indian Hospitals in Canada. The Canadian Encyclopedia. 2018. Available online: https://www.thecanadianencyclopedia.ca/en/article/indian-hospitals-in-canada (accessed on 1 April 2022).
  3. Mosby, I. Administering Colonial Science: Nutrition Research and Human Biomedical Experimentation in Aboriginal Communities and Residential Schools, 1942–1952. Hist. Soc./Soc. Hist. 2013, 46, 145–172.
  4. Niessen, S. Shattering the Silence: The Hidden History of Indian Residential Schools in Saskatechewan. Available online: https://www2.uregina.ca/education/saskindianresidentialschools/ (accessed on 1 February 2022).
  5. Matheson, K.; Bombay, A.; Haslam, S.A.; Anisman, H. Indigenous identity transformations: The pivotal role of student-to-student abuse in Indian Residential Schools. Transcult. Psychiatry 2016, 53, 551–573.
  6. Bombay, A.; Mcquaid, R.; Young, J.; Sinha, V.; Currie, V.; Anisman, H.; Matheson, K. Familial Attendance at Indian Residential School and Subsequent Involvement in the Child Welfare System Among Indigenous Adults Born During the Sixties Scoop Era. First Peoples Child Fam. Rev. Interdiscip. J. Honouring Voices Perspect. Knowl. First Peoples 2020, 15, 62.
  7. Stevenson, A. Intimate Integration: A History of the Sixties Scoop and the Colonization of Indigenous Kinship; University of Toronto Press: Toronto, ON, Canada, 2020.
  8. Statistics Canada. Aboriginal Peoples in Canada: Key Results from the 2016 Census. Available online: https://www150.statcan.gc.ca/n1/daily-quotidien/171025/dq171025a-eng.htm (accessed on 1 April 2022).
  9. Barker, B.; Sedgemore, K.; Tourangeau, M.; Lagimodiere, L.; Milloy, J.; Dong, H.; Hayashi, K.; Shoveller, J.; Kerr, T.; DeBeck, K. Intergenerational Trauma: The Relationship Between Residential Schools and the Child Welfare System Among Young People Who Use Drugs in Vancouver, Canada. J. Adolesc. Health 2019, 65, 248–254.
  10. Caldwell, J.; Sinha, V. (Re) Conceptualizing Neglect: Considering the Overrepresentation of Indigenous Children in Child Welfare Systems in Canada. Child. Ind. Res. 2020, 13, 481–512.
  11. Kenny, K.S. Mental Health Harm to Mothers When a Child Is Taken by Child Protective Services: Health Equity Considerations. Can. J. Psychiatry 2018, 63, 304–307.
  12. Brave Heart, M.Y.; DeBruyn, L.M. The American Indian Holocaust: Healing Historical Unresolved Grief. Am. Indian Alsk. Nativ. Ment. Health Res. 1998, 8, 56–78.
  13. Johnson-Jennings, M.; Walters, K.; Billiot, S. Returning to Our Roots: Tribal Health and Wellness through Land-Based Healing. Genealogy 2020, 4, 91.
  14. Tobias, J.K.; Richmond, C.A.M. “That Land Means Everything to Us as Anishinaabe….”: Environmental Dispossession and Resilience on the North Shore of Lake Superior. Health Place 2014, 29, 26–33.
  15. McGregor, H.E. Exploring Ethnohistory and Indigenous Scholarship: What Is the Relevance to Educational Historians? Hist. Educ. 2014, 43, 431–449.
  16. Cunsolo Willox, A.; Harper, S.L.; Ford, J.D.; Landman, K.; Houle, K.; Edge, V.L. Rigolet Inuit Community Government “From This Place and of This Place:” Climate Change, Sense of Place, and Health in Nunatsiavut, Canada. Soc. Sci. Med. 2012, 75, 538–547.
  17. Sarkar, A.; Hanrahan, M.; Hudson, A. Water Insecurity in Canadian Indigenous Communities: Some Inconvenient Truths. Rural Remote Health 2015, 15, 3354.
  18. Intergovernmental Panel on Climate Change (IPCC). Sixth Assessment Report. 2021. Available online: https://www.ipcc.ch/assessment-report/ar6/ (accessed on 1 April 2022).
  19. Willox, A.C.; Harper, S.; Ford, J.; Edge, V.; Landman, K.; Houle, K.; Blake, S.; Wolfrey, C. Climate Change and Mental Health: An Exploratory Case Study from Rigolet, Nunatsiavut, Canada. Clim. Chang. 2013, 121, 255–270.
  20. MacTavish, T.; Marceau, M.-O.; Optis, M.; Shaw, K.; Stephenson, P.; Wild, P. A Participatory Process for the Design of Housing for a First Nations Community. J. Hous. Built Environ. 2012, 27, 207–224.
  21. McCartney, S.; Herskovits, J.; Hintelmann, L. Developing Occupant-Based Understandings of Crowding: A Study of Residential Self-Assessment in Eabametoong First Nation. J. Hous. Built Environ. 2021, 36, 645–662.
  22. Anderson, M.; Woticky, G. The End of Life Is an Auspicious Opportunity for Healing. Int. J. Indig. Health 2018, 13, 48–60.
  23. Gionet, L. First Nations People: Selected Findings of the 2006 Census. Available online: https://www150.statcan.gc.ca/n1/pub/11-008-x/2009001/article/10864-eng.htm#a10 (accessed on 1 April 2022).
  24. Madden, B.; Thomas, R.; Green, J. A de/colonizing theory of truth and reconciliation education. First Peoples Child Fam. Rev. 2019, 49, 284–312.
  25. Lawford, K. COVID-19 Death Highlights Dangers of Birth Evacuation Policy in Indigenous Communities. Healthy Debate 2021. Available online: https://healthydebate.ca/2021/02/topic/birth-evacuation-indigenous/ (accessed on 1 April 2022).
  26. King, M.; Smith, A.; Gracey, M. Indigenous Health Part 2: The Underlying Causes of the Health Gap. Lancet 2009, 374, 76–85.
  27. Snyder, M.; Wilson, K. “Too Much Moving…There’s Always a Reason”: Understanding Urban Aboriginal Peoples’ Experiences of Mobility and Its Impact on Holistic Health. Health Place 2015, 34, 181–189.
  28. Anisman, H.; Kusnecov, A. Cancer: How Lifestyles May Impact Disease Development, Progression and Treatment; Elsevier: London, UK, 2022.
  29. Cryan, J.F.; O’Riordan, K.J.; Cowan, C.S.M.; Sandhu, K.V.; Bastiaanssen, T.F.S.; Boehme, M.; Codagnone, M.G.; Cussotto, S.; Fulling, C.; Golubeva, A.V.; et al. The microbiota-gut-brain axis. Physiol. Rev. 2019, 99, 1877–2013.
  30. Hare, B.D.; Ghosal, S.; Duman, R.S. Rapid Acting Antidepressants in Chronic Stress Models: Molecular and Cellular Mechanisms. Chronic Stress 2017, 1, 2470547017697317.
  31. Anisman, H.; Merali, Z.; Hayley, S. Sensitization Associated with Stressors and Cytokine Treatments. Brain Behav. Immun. 2003, 17, 86–93.
  32. Badihian, N.; Daniali, S.S.; Kelishadi, R. Transcriptional and Epigenetic Changes of Brain Derived Neurotrophic Factor Following Prenatal Stress: A Systematic Review of Animal Studies. Neurosci. Biobehav. Rev. 2020, 117, 211–231.
  33. Seng, J.S.; Low, L.K.; Sperlich, M.; Ronis, D.L.; Liberzon, I. Post-Traumatic Stress Disorder, Child Abuse History, Birthweight and Gestational Age: A Prospective Cohort Study. BJOG 2011, 118, 1329–1339.
  34. Shapiro, G.D.; Fraser, W.D.; Frasch, M.G.; Séguin, J.R. Psychosocial Stress in Pregnancy and Preterm Birth: Associations and Mechanisms. J. Perinat. Med. 2013, 41, 631–645.
  35. Menon, R.; Behnia, F.; Polettini, J.; Richardson, L.S. Novel Pathways of Inflammation in Human Fetal Membranes Associated with Preterm Birth and Preterm Pre-Labor Rupture of the Membranes. Semin. Immunopathol. 2020, 42, 431–450.
  36. Pawelec, M.; Pałczyński, B.; Krzemieniewska, J.; Karmowski, M.; Koryś, J.; Lątkowski, K.; Karmowski, A. Initiation of Preterm Labor. Adv. Clin. Exp. Med. 2013, 22, 283–288.
  37. Lautarescu, A.; Craig, M.C.; Glover, V. Prenatal Stress: Effects on Fetal and Child Brain Development. Int. Rev. Neurobiol. 2020, 150, 17–40.
  38. Toso, K.; de Cock, P.; Leavey, G. Maternal Exposure to Violence and Offspring Neurodevelopment: A Systematic Review. Paediatr. Perinat. Epidemiol. 2020, 34, 190–203.
  39. Moog, N.K.; Nolvi, S.; Kleih, T.S.; Styner, M.; Gilmore, J.H.; Rasmussen, J.M.; Heim, C.M.; Entringer, S.; Wadhwa, P.D.; Buss, C. Prospective Association of Maternal Psychosocial Stress in Pregnancy with Newborn Hippocampal Volume and Implications for Infant Social-Emotional Development. Neurobiol. Stress 2021, 15, 100368.
  40. Lafortune, S.; Laplante, D.P.; Elgbeili, G.; Li, X.; Lebel, S.; Dagenais, C.; King, S. Effect of Natural Disaster-Related Prenatal Maternal Stress on Child Development and Health: A Meta-Analytic Review. Int. J. Environ. Res. Public Health 2021, 18, 8332.
  41. Robinson, M.; Carter, K.W.; Pennell, C.E.; Jacoby, P.; Moore, H.C.; Zubrick, S.R.; Burgner, D. Maternal Prenatal Stress Exposure and Sex-Specific Risk of Severe Infection in Offspring. PLoS ONE 2021, 16, e0245747.
  42. Pedersen, J.M.; Mortensen, E.L.; Christensen, D.S.; Rozing, M.; Brunsgaard, H.; Meincke, R.H.; Petersen, G.L.; Lund, R. Prenatal and early postnatal stress and later life inflammation. Psychoneuroendo 2018, 88, 158–166.
  43. Harris, M.L.; Hure, A.J.; Holliday, E.; Chojenta, C.; Anderson, A.E.; Loxton, D. Association between Preconception Maternal Stress and Offspring Birth Weight: Findings from an Australian Longitudinal Data Linkage Study. BMJ Open 2021, 11, e041502.
  44. Braun, K.; Bock, J.; Wainstock, T.; Matas, E.; Gaisler-Salomon, I.; Fegert, J.; Ziegenhain, U.; Segal, M. Experience-Induced Transgenerational (Re-)Programming of Neuronal Structure and Functions: Impact of Stress Prior and during Pregnancy. Neurosci. Biobehav. Rev. 2020, 117, 281–296.
  45. Swales, D.A.; Davis, E.P.; Mahrer, N.E.; Guardino, C.M.; Shalowitz, M.U.; Ramey, S.L.; Dunkel Schetter, C. Preconception Maternal Posttraumatic Stress and Child Negative Affectivity: Prospectively Evaluating the Intergenerational Impact of Trauma. Dev. Psychopathol. 2022, 1–11.
  46. Bombay, A.; Matheson, K.; Anisman, H. The Intergenerational Effects of Indian Residential Schools: Implications for the Concept of Historical Trauma. Transcult. Psychiatry 2014, 51, 320–338.
  47. Yancey, A.K.; Ortega, A.N.; Kumanyika, S.K. Effective Recruitment and Retention of Minority Research Participants. Annu. Rev. Public Health 2006, 27, 1–28.
  48. Tuck, E. Suspending Damage: A Letter to Communities. Harv. Educ. Rev. 2009, 79, 409–428.
  49. Meaney, M.J.; Szyf, M. Maternal Care as a Model for Experience-Dependent Chromatin Plasticity? Trends Neurosci. 2005, 28, 456–463.
  50. Suderman, M.; Borghol, N.; Pappas, J.; Pereira, S.; Pembrey, M.; Hertzman, C.; Power, C.; Szyf, M. Childhood Abuse Is Associated with Methylation of Multiple Loci in Adult DNA. BMC Med. Genom. 2014, 7, 13.
  51. Nilsson, E.E.; Sadler-Riggleman, I.; Skinner, M.K. Environmentally Induced Epigenetic Transgenerational Inheritance of Disease. Environ. Epigenet. 2018, 4, dvy016.
  52. Szyf, M. The Epigenetics of Perinatal Stress. Dialogues Clin. Neurosci. 2019, 21, 369–378.
  53. Soga, T.; Teo, C.H.; Parhar, I. Genetic and Epigenetic Consequence of Early-Life Social Stress on Depression: Role of Serotonin-Associated Genes. Front. Genet. 2020, 11, 601868.
  54. Champagne, F.A.; Curley, J.P. Epigenetic Mechanisms Mediating the Long-Term Effects of Maternal Care on Development. Neurosci. Biobehav. Rev. 2009, 33, 593–600.
  55. Miao, Z.; Wang, Y.; Sun, Z. The Relationships between Stress, Mental Disorders, and Epigenetic Regulation of BDNF. Int. J. Mol. Sci. 2020, 21, 1375.
  56. Hunter, R.G.; McEwen, B.S. Stress and Anxiety across the Lifespan: Structural Plasticity and Epigenetic Regulation. Epigenomics 2013, 5, 177–194.
  57. Park, C.; Rosenblat, J.D.; Brietzke, E.; Pan, Z.; Lee, Y.; Cao, B.; Zuckerman, H.; Kalantarova, A.; McIntyre, R.S. Stress, Epigenetics and Depression: A Systematic Review. Neurosci. Biobehav. Rev. 2019, 102, 139–152.
  58. Vogelstein, B.; Papadopoulos, N.; Velculescu, V.E.; Zhou, S.; Diaz, L.A.; Kinzler, K.W. Cancer Genome Landscapes. Science 2013, 339, 1546–1558.
  59. Barua, S.; Junaid, M.A. Lifestyle, Pregnancy and Epigenetic Effects. Epigenomics 2015, 7, 85–102.
  60. Ladd-Acosta, C.; Feinberg, J.I.; Brown, S.C.; Lurmann, F.W.; Croen, L.A.; Hertz-Picciotto, I.; Newschaffer, C.J.; Feinberg, A.P.; Fallin, M.D.; Volk, H.E. Epigenetic Marks of Prenatal Air Pollution Exposure Found in Multiple Tissues Relevant for Child Health. Environ. Int. 2019, 126, 363–376.
  61. Cao-Lei, L.; de Rooij, S.R.; King, S.; Matthews, S.G.; Metz, G.A.S.; Roseboom, T.J.; Szyf, M. Prenatal Stress and Epigenetics. Neurosci. Biobehav. Rev. 2020, 117, 198–210.
  62. Nomura, Y.; Rompala, G.; Pritchett, L.; Aushev, V.; Chen, J.; Hurd, Y.L. Natural disaster stress during pregnancy is linked to reprogramming of the placenta transcriptome in relation to anxiety and stress hormones in young offspring. Mol. Psychiatry 2021, 26, 6520–6530.
  63. Cao-Lei, L.; Dancause, K.N.; Elgbeili, G.; Laplante, D.P.; Szyf, M.; King, S. DNA Methylation Mediates the Effect of Maternal Cognitive Appraisal of a Disaster in Pregnancy on the Child’s C-Peptide Secretion in Adolescence: Project Ice Storm. PLoS ONE 2018, 13, e0192199.
  64. Martins, J.; Czamara, D.; Sauer, S.; Rex-Haffner, M.; Dittrich, K.; Dörr, P.; de Punder, K.; Overfeld, J.; Knop, A.; Dammering, F.; et al. Childhood Adversity Correlates with Stable Changes in DNA Methylation Trajectories in Children and Converges with Epigenetic Signatures of Prenatal Stress. Neurobiol. Stress 2021, 15, 100336.
  65. Bale, T.L. The Placenta and Neurodevelopment: Sex Differences in Prenatal Vulnerability. Dialogues Clin. Neurosci. 2016, 18, 459–464.
  66. Rice, M.L.; Smolik, F.; Perpich, D.; Thompson, T.; Rytting, N.; Blossom, M. Mean Length of Utterance Levels in 6-Month Intervals for Children 3 to 9 Years with and without Language Impairments. J. Speech Lang. Hear. Res. 2010, 53, 333–349.
  67. Cavalli, G.; Heard, E. Advances in Epigenetics Link Genetics to the Environment and Disease. Nature 2019, 571, 489–499.
  68. Nishi, M. Effects of Early-Life Stress on the Brain and Behaviors: Implications of Early Maternal Separation in Rodents. Int. J. Mol. Sci. 2020, 21, 7212.
  69. Grundwald, N.J.; Brunton, P.J. Prenatal Stress Programs Neuroendocrine Stress Responses and Affective Behaviors in Second Generation Rats in a Sex-Dependent Manner. Psychoneuroendocrinology 2015, 62, 204–216.
  70. Pallarés, M.E.; Monteleone, M.C.; Pastor, V.; Grillo Balboa, J.; Alzamendi, A.; Brocco, M.A.; Antonelli, M.C. Early-Life Stress Reprograms Stress-Coping Abilities in Male and Female Juvenile Rats. Mol. Neurobiol. 2021, 58, 5837–5856.
  71. Franklin, T.B.; Russig, H.; Weiss, I.C.; Gräff, J.; Linder, N.; Michalon, A.; Vizi, S.; Mansuy, I.M. Epigenetic Transmission of the Impact of Early Stress across Generations. Biol. Psychiatry 2010, 68, 408–415.
  72. Gapp, K.; Bohacek, J. Epigenetic Germline Inheritance in Mammals: Looking to the Past to Understand the Future. Genes Brain Behav. 2018, 17, e12407.
  73. Rodgers, A.B.; Morgan, C.P.; Bronson, S.L.; Revello, S.; Bale, T.L. Paternal Stress Exposure Alters Sperm MicroRNA Content and Reprograms Offspring HPA Stress Axis Regulation. J. Neurosci. 2013, 33, 9003–9012.
  74. Merrill, S.; Moore, S.; Gladish, N.; Giesbrecht, G.; Dewey, D.; Konwar, C.; MacIssac, J.; Kobor, M.; Letourneau, N. Paternal Adverse Childhood Experiences: Associations with Infant DNA Methylation. Dev. Psychobiol. 2021, 63, e22174.
  75. Karlsson, H.; Merisaari, H.; Karlsson, L.; Scheinin, N.M.; Parkkola, R.; Saunavaara, J.; Lähdesmäki, T.; Lehtola, S.J.; Keskinen, M.; Pelto, J.; et al. Association of Cumulative Paternal Early Life Stress With White Matter Maturation in Newborns. JAMA Netw. Open 2020, 3, e2024832.
  76. Van Steenwyk, G.; Roszkowski, M.; Manuella, F.; Franklin, T.B.; Mansuy, I.M. Transgenerational Inheritance of Behavioral and Metabolic Effects of Paternal Exposure to Traumatic Stress in Early Postnatal Life: Evidence in the 4th Generation. Environ. Epigenet. 2018, 4, dvy023.
  77. Cunningham, A.M.; Walker, D.M.; Nestler, E.J. Paternal Transgenerational Epigenetic Mechanisms Mediating Stress Phenotypes of Offspring. Eur. J. Neurosci. 2021, 53, 271–280.
  78. Sabbagh, J.J.; O’Leary, J.C.; Blair, L.J.; Klengel, T.; Nordhues, B.A.; Fontaine, S.N.; Binder, E.B.; Dickey, C.A. Age-Associated Epigenetic Upregulation of the FKBP5 Gene Selectively Impairs Stress Resiliency. PLoS ONE 2014, 9, e107241.
  79. Zannas, A.S.; Jia, M.; Hafner, K.; Baumert, J.; Wiechmann, T.; Pape, J.C.; Arloth, J.; Ködel, M.; Martinelli, S.; Roitman, M.; et al. Epigenetic Upregulation of FKBP5 by Aging and Stress Contributes to NF-ΚB-Driven Inflammation and Cardiovascular Risk. Proc. Natl. Acad. Sci. USA 2019, 116, 11370–11379.
  80. Tozzi, L.; Farrell, C.; Booij, L.; Doolin, K.; Nemoda, Z.; Szyf, M.; Pomares, F.B.; Chiarella, J.; O’Keane, V.; Frodl, T. Epigenetic Changes of FKBP5 as a Link Connecting Genetic and Environmental Risk Factors with Structural and Functional Brain Changes in Major Depression. Neuropsychopharmacology 2018, 43, 1138–1145.
  81. McGowan, P.O.; Sasaki, A.; D’Alessio, A.C.; Dymov, S.; Labonté, B.; Szyf, M.; Turecki, G.; Meaney, M.J. Epigenetic Regulation of the Glucocorticoid Receptor in Human Brain Associates with Childhood Abuse. Nat. Neurosci. 2009, 12, 342–348.
  82. Yehuda, R.; Bierer, L.M.; Andrew, R.; Schmeidler, J.; Seckl, J.R. Enduring Effects of Severe Developmental Adversity, Including Nutritional Deprivation, on Cortisol Metabolism in Aging Holocaust Survivors. J. Psychiatry Res. 2009, 43, 877–883.
  83. Yehuda, R.; Halligan, S.L.; Grossman, R.; Golier, J.A.; Wong, C. The Cortisol and Glucocorticoid Receptor Response to Low Dose Dexamethasone Administration in Aging Combat Veterans and Holocaust Survivors with and without Posttraumatic Stress Disorder. Biol. Psychiatry 2002, 52, 393–403.
  84. Yehuda, R.; Morris, A.; Labinsky, E.; Zemelman, S.; Schmeidler, J. Ten-Year Follow-up Study of Cortisol Levels in Aging Holocaust Survivors with and without PTSD. J. Trauma Stress 2007, 20, 757–761.
  85. Yehuda, R.; Daskalakis, N.P.; Bierer, L.M.; Bader, H.N.; Klengel, T.; Holsboer, F.; Binder, E.B. Holocaust Exposure Induced Intergenerational Effects on FKBP5 Methylation. Biol. Psychiatry 2016, 80, 372–380.
  86. Yehuda, R.; Daskalakis, N.P.; Lehrner, A.; Desarnaud, F.; Bader, H.N.; Makotkine, I.; Flory, J.D.; Bierer, L.M.; Meaney, M.J. Influences of Maternal and Paternal PTSD on Epigenetic Regulation of the Glucocorticoid Receptor Gene in Holocaust Survivor Offspring. Am. J. Psychiatry 2014, 171, 872–880.
  87. Dashorst, P.; Mooren, T.M.; Kleber, R.J.; de Jong, P.J.; Huntjens, R.J.C. Intergenerational Consequences of the Holocaust on Offspring Mental Health: A Systematic Review of Associated Factors and Mechanisms. Eur. J. Psychotraumatol. 2019, 10, 1654065.
  88. Van IJzendoorn, M.H.; Bakermans-Kranenburg, M.J.; Sagi-Schwartz, A. Are Children of Holocaust Survivors Less Well-Adapted? A Meta-Analytic Investigation of Secondary Traumatization. J. Trauma Stress 2003, 16, 459–469.
  89. Hjort, L.; Rushiti, F.; Wang, S.-J.; Fransquet, P.; Krasniqi, S.P.; Çarkaxhiu, S.I.; Arifaj, D.; Xhemaili, V.D.; Salihu, M.; A Leku, N.; et al. Intergenerational Effects of Maternal Post-Traumatic Stress Disorder on Offspring Epigenetic Patterns and Cortisol Levels. Epigenomics 2021, 13, 967–980.
  90. Perroud, N.; Rutembesa, E.; Paoloni-Giacobino, A.; Mutabaruka, J.; Mutesa, L.; Stenz, L.; Malafosse, A.; Karege, F. The Tutsi Genocide and Transgenerational Transmission of Maternal Stress: Epigenetics and Biology of the HPA Axis. World J. Biol. Psychiatry 2014, 15, 334–345.
  91. Hiraoka, D.; Nishitani, S.; Shimada, K.; Kasaba, R.; Fujisawa, T.X.; Tomoda, A. Epigenetic Modification of the Oxytocin Gene Is Associated with Gray Matter Volume and Trait Empathy in Mothers. Psychoneuroendocrinology 2021, 123, 105026.
  92. Van Cauwenbergh, O.; Di Serafino, A.; Tytgat, J.; Soubry, A. Transgenerational Epigenetic Effects from Male Exposure to Endocrine-Disrupting Compounds: A Systematic Review on Research in Mammals. Clin. Epigenet. 2020, 12, 65.
  93. Manikkam, M.; Haque, M.M.; Guerrero-Bosagna, C.; Nilsson, E.E.; Skinner, M.K. Pesticide Methoxychlor Promotes the Epigenetic Transgenerational Inheritance of Adult-Onset Disease through the Female Germline. PLoS ONE 2014, 9, e102091.
  94. Post, C.M.; Boule, L.A.; Burke, C.G.; O’Dell, C.T.; Winans, B.; Lawrence, B.P. The ancestral environment shapes antiviral CD8+ T cell responses across generations. iScience 2019, 20, 168–183.
  95. Ly, L.; Chan, D.; Aarabi, M.; Landry, M.; Behan, N.A.; MacFarlane, A.J.; Trasler, J. Intergenerational Impact of Paternal Lifetime Exposures to Both Folic Acid Deficiency and Supplementation on Reproductive Outcomes and Imprinted Gene Methylation. Mol. Hum. Reprod. 2017, 23, 461–477.
  96. Klastrup, L.K.; Bak, S.T.; Nielsen, A.L. The Influence of Paternal Diet on SncRNA-Mediated Epigenetic Inheritance. Mol. Genet. Genom. 2019, 294, 1–11.
  97. Roseboom, T.J.; Painter, R.C.; van Abeelen, A.F.M.; Veenendaal, M.V.E.; de Rooij, S.R. Hungry in the Womb: What Are the Consequences? Lessons from the Dutch Famine. Maturitas 2011, 70, 141–145.
  98. Tobi, E.W.; Goeman, J.J.; Monajemi, R.; Gu, H.; Putter, H.; Zhang, Y.; Slieker, R.C.; Stok, A.P.; Thijssen, P.E.; Müller, F.; et al. DNA methylation signatures link prenatal famine exposure to growth and metabolism. Nat. Commun. 2014, 5, 5592.
  99. Heijmans, B.T.; Tobi, E.W.; Stein, A.D.; Putter, H.; Blauw, G.J.; Susser, E.S.; Slagboom, P.E.; Lumey, L.H. Persistent Epigenetic Differences Associated with Prenatal Exposure to Famine in Humans. Proc. Natl. Acad. Sci. USA 2008, 105, 17046–17049.
  100. Yohannes, S. Dermatoglyphic Meta-Analysis Indicates Early Epigenetic Outcomes and Possible Implications on Genomic Zygosity in Type-2 Diabetes. F1000Research 2015, 4, 617.
  101. Li, J.; Liu, S.; Li, S.; Feng, R.; Na, L.; Chu, X.; Wu, X.; Niu, Y.; Sun, Z.; Han, T.; et al. Prenatal Exposure to Famine and the Development of Hyperglycemia and Type 2 Diabetes in Adulthood across Consecutive Generations: A Population-Based Cohort Study of Families in Suihua, China. Am. J. Clin. Nutr. 2017, 105, 221–227.
  102. Shen, L.; Li, C.; Wang, Z.; Zhang, R.; Shen, Y.; Miles, T.; Wei, J.; Zou, Z. Early-Life Exposure to Severe Famine Is Associated with Higher Methylation Level in the IGF2 Gene and Higher Total Cholesterol in Late Adulthood: The Genomic Research of the Chinese Famine (GRECF) Study. Clin. Epigenet. 2019, 11, 88.
  103. Bezo, B.; Maggi, S. Living in “Survival Mode”: Intergenerational Transmission of Trauma from the Holodomor Genocide of 1932–1933 in Ukraine. Soc. Sci. Med. 2015, 134, 87–94.
  104. Drury, J.; Carter, H.; Cocking, C.; Ntontis, E.; Tekin Guven, S.; Amlôt, R. Facilitating Collective Psychosocial Resilience in the Public in Emergencies: Twelve Recommendations Based on the Social Identity Approach. Front. Public Health 2019, 7, 141.
  105. Hopkins, N.; Dixon, J. Space, Place, and Identity: Issues for Political Psychology. Political Psychol. 2006, 27, 173–185.
  106. Gone, J.P.; Kirmayer, L.J. Advancing Indigenous Mental Health Research: Ethical, Conceptual and Methodological Challenges. Transcult. Psychiatry 2020, 57, 235–249.
  107. Graham, J.; Haidt, J.; Nosek, B.A. Liberals and Conservatives Rely on Different Sets of Moral Foundations. J. Pers. Soc. Psychol. 2009, 96, 1029–1046.
  108. Qazimi, S. Sense of Place and Place Identity. Eur. J. Soc. Sci. Educ. Res. 2014, 1, 306–310.
  109. Hansen, J.; Antsanen, R. Elders’ Teachings about Resilience and Its Implications for Education in Dene and Cree Communities. Int. Indig. Policy J. 2016, 7, 2.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
This entry is offline, you can click here to edit this entry!
Video Production Service
Feedback