Childhood trauma is often described as serious adverse childhood experiences (ACEs).[1] Children may go through a range of experiences that classify as psychological trauma, these might include neglect,[2] abandonment,[2] sexual abuse, and physical abuse,[2] witnessing abuse of a sibling or parent, or having a mentally ill parent. These events have profound psychological, physiological, and sociological impacts and can have negative, lasting effects on health and well-being. Kaiser Permanente and the Centers for Disease Control and Prevention's 1998 study on adverse childhood experiences determined that traumatic experiences during childhood are a root cause of many social, emotional, and cognitive impairments that lead to increased risk of unhealthy self-destructive behaviors,[2] risk of violence or re-victimization, chronic health conditions, low life potential and premature mortality. As the number of adverse experiences increases, the risk of problems from childhood through adulthood also rises.[3] Nearly 30 years of study following the initial study has confirmed this. Many states, health providers, and other groups now routinely screen parents and children for ACEs.
Health outcomes
Traumatic experiences during childhood causes stress that increases an individual's allostatic load and thus affects the immune system, nervous system, and endocrine system.[4][5][6][7] Childhood trauma is often associated with adverse health outcomes including depression, hypertension, autoimmune diseases, lung cancer, and premature mortality.[4][6][8][9] Effects of childhood trauma on brain development includes a negative impact on emotional regulation and impairment of development of social skills.[6] Research has shown that children raised in traumatic or risky family environments tend to have excessive internalizing (e.g., social withdrawal, anxiety) or externalizing (e.g., aggressive behavior), and suicidal behavior.[6][10][11] Recent research has found that physical and sexual abuse are associated with mood and anxiety disorders in adulthood, while personality disorders and schizophrenia are linked with emotional abuse as adults.[12][13]
Psychological impact
Childhood trauma can increase the risk of mental disorders including posttraumatic stress disorder (PTSD), attachment issues, depression, and substance abuse. Sensitive and critical stages of child development can result in altered neurological functioning, adaptive to a malevolent environment but difficult for more benign environments.
In a study done by Stefania Tognin and Maria Calem comparing healthy comparisons (HC) and individuals at clinically high risk for developing psychosis (CHR), 65.6% CHR patients and 23.1% HC experienced some level of childhood trauma. The conclusion of the study shows that there is a correlation between the effects of childhood trauma and the being at high risk for psychosis.[14]
Epigenetics
Childhood trauma can leave epigenetic marks on a child's genes, which chemically modify gene expression by silencing or activating genes.[15] This can alter fundamental biological processes and adversely affect health outcomes throughout life.[15] A 2013 study found that people who had experienced childhood trauma had different neuropathology than people with PTSD from trauma experienced after childhood.[15] Another recent study in rhesus macaques showed that DNA methylation changes related to early-life adversity persisted into adulthood.[16]
The theoretical link between exposure to extreme stress and the development of PTSD provided the rationale for early hypotheses that PTSD-related biological alterations would be similar in direction to those observed acutely in animals exposed to stressors. When subsequent findings indicated that only a minority of trauma-exposed individuals develop PTSD, an alternative hypothesis was generated proposing that PTSD involves a failure of mechanisms involved in recovery and restitution of physiological homeostasis, possibly resulting from individualistic predisposition. Translational studies of PTSD are the use of a developmental neurobiological approach, spanning across the entire course of the illness. Symptom severity in PTSD can wax and wane over several decades. Biological alterations reflecting risk rather than pathophysiology may not account for this phenomenon. On the other hand, even putative risk factors such as glucocorticoid responsiveness and hippocampal volume show changes in response to factors such as environmental exposures, duration of illness, comorbidity, and aging. Thus, it is important to understand whether risk factors influence, or are influenced by, other parameters associated with PTSD (Yehuda, and LeDooux, 2007).[17]
In this sense parental trauma exposure is associated with greater risk for post-traumatic stress disorder (PTSD) and mood and anxiety disorders in offspring since biological alterations associated with PTSD and/or other stress-related disorders have also been observed in offspring of trauma survivors who do not themselves report trauma exposure or psychiatric disorder. Animal models have demonstrated that stress exposure can result in epigenetic alterations in the next generation, and such mechanisms have been hypothesized to underpin vulnerability to symptoms in offspring of trauma survivors. Enduring behavioral responses to stress and epigenetic alterations in adult offspring have been demonstrated to be mediated by changes in gametes in utero effects, variations in early postnatal care, and/or other early life experiences that are influenced by parental exposure (Yehuda, Daskalakis, Bierer, Bader, Klengel, Holsboer, and Binder, 2015).
Survivors of war trauma or childhood maltreatment are at increased risk for trauma-spectrum disorders[18] such as post-traumatic stress disorder (PTSD). In addition, traumatic stress has been associated with alterations in the neuroendocrine and the immune system, enhancing the risk for physical diseases. Traumatic experiences might even affect psychological as well as biological parameters in the next generation, i.e. traumatic stress might have trans generational effects.[18] So currently there is a new field trying to explain how epigenetic processes, which represent a pivotal biological mechanism for dynamic adaptation to environmental challenges, might contribute to the explanation of the long-lasting and intergenerational effects of trauma.[18] In particular, epigenetic alterations in genes regulating the hypothalamus–pituitary–adrenal axis as well as the immune system have been observed in survivors of childhood and adult trauma.[19]
These changes could result in enduring alterations of the stress response as well as the physical health risk. Furthermore, the effects of parental trauma could be transmitted to the next generation by parental distress and the pre- and postnatal environment, as well as by epigenetic marks transmitted via the germline. While epigenetic research has a high potential of advancing our understanding of the consequences of trauma, the findings have to be interpreted with caution, as epigenetics only represent one piece of a complex puzzle of interacting biological and environmental factors.[18]
The mechanism of intergenerational transmission of epigenetic effects at bin 3/site 6 is not known but does not appear to be mediated by childhood adversity, as is the case for bin 2. From a biological perspective, accommodation to multiple environmental influences at distinct and potentially redundant sites on genes central to stress regulation would facilitate maximal stress responsively and adaptation.
Future studies should focus on assessing the effects of trauma at various developmental stages, as well as potential differences in maternal and paternal effects. Additionally, the mechanism of intergenerational transmission of trauma and functional importance of site specificity remain to be explored. Early detection of such epigenetic marks may advance the development of preventive strategies to address the intergenerational sequel of exposure to trauma.
As it has been said Cytosine methylation of glucocorticoid related genes represents an epigenetic modification thought to underlie the developmental programming of hypothalamic-pituitary-adrenal (HPA) axis function.[19] The importance of epigenetic studies offer promise as diagnostic or prognostic markers, but it is not known whether these measures associate with, or predict, clinical state.
Subsequent studies in humans showed that childhood adversity associates with higher methylation of the GR exon 1F promoter (the human ortholog of the rat exon 17 promoter sequence) lower hippocampal GR expression and increased HPA-axis responses to stress. The examination of biological measures in association with PTSD symptom change following an efficacious psychotherapy trial was designed to yield a sample with a variable degree of symptom improvement, with some showing large decreases in symptom severity, and others, minimal or moderate change. An additional advantage of this approach is the ability to modify symptoms without introducing exogenousmedications that might have direct effects on the biological measures of interest. (Yehuda, Daskalakis, Desarnaud, Makotkine, Lehrner, Koch, Flory, Buxbaum, Meaney, and Bierer, 2013; Yahyavi, Zarghami, Marwah, 2014).
Epidemiologic research has clarified risk factors that increase the likelihood of PTSD after exposure to a potentially traumatic event. PTSD is an interaction between a subject, a traumatogenic factor and a social context. With each epidemiological, psychopathological and more particularly neurogenetic study, we will expand on the impact of these interactions on the therapeutic treatment of psycho-traumatized persons (Uuxéméry, 2012).
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