- Open Access
Mechanisms linking childhood trauma exposure and psychopathology: a transdiagnostic model of risk and resilience
BMC Medicine volume 18, Article number: 96 (2020)
Transdiagnostic processes confer risk for multiple types of psychopathology and explain the co-occurrence of different disorders. For this reason, transdiagnostic processes provide ideal targets for early intervention and treatment. Childhood trauma exposure is associated with elevated risk for virtually all commonly occurring forms of psychopathology. We articulate a transdiagnostic model of the developmental mechanisms that explain the strong links between childhood trauma and psychopathology as well as protective factors that promote resilience against multiple forms of psychopathology.
We present a model of transdiagnostic mechanisms spanning three broad domains: social information processing, emotional processing, and accelerated biological aging. Changes in social information processing that prioritize threat-related information—such as heightened perceptual sensitivity to threat, misclassification of negative and neutral emotions as anger, and attention biases towards threat-related cues—have been consistently observed in children who have experienced trauma. Patterns of emotional processing common in children exposed to trauma include elevated emotional reactivity to threat-related stimuli, low emotional awareness, and difficulties with emotional learning and emotion regulation. More recently, a pattern of accelerated aging across multiple biological metrics, including pubertal development and cellular aging, has been found in trauma-exposed children. Although these changes in social information processing, emotional responding, and the pace of biological aging reflect developmental adaptations that may promote safety and provide other benefits for children raised in dangerous environments, they have been consistently associated with the emergence of multiple forms of internalizing and externalizing psychopathology and explain the link between childhood trauma exposure and transdiagnostic psychopathology. Children with higher levels of social support, particularly from caregivers, are less likely to develop psychopathology following trauma exposure. Caregiver buffering of threat-related processing may be one mechanism explaining this protective effect.
Childhood trauma exposure is a powerful transdiagnostic risk factor associated with elevated risk for multiple forms of psychopathology across development. Changes in threat-related social and emotional processing and accelerated biological aging serve as transdiagnostic mechanisms linking childhood trauma with psychopathology. These transdiagnostic mechanisms represent critical targets for early interventions aimed at preventing the emergence of psychopathology in children who have experienced trauma.
A central tenet of developmental approaches to psychopathology is that the same environmental experience, psychological process, or neurobiological factor may ultimately lead to different developmental outcomes or forms of psychopathology across people, a phenomenon known as multifinality . Increasing recognition of this multifinality has led to the emergence of transdiagnostic models of psychopathology. Transdiagnostic approaches seek to identify core psychological and neurobiological processes that underlie multiple forms of psychopathology . These models afford many benefits over disorder-specific approaches by identifying core mechanisms that might play a role in many different forms of psychopathology, determining whether such factors explain the high rates of comorbidity across disorders, and providing key targets for interventions that could be used to prevent or treat multiple types of psychopathology . Much existing work on transdiagnostic factors has focused on cognitive and affective processes that are associated with vulnerability for multiple forms of psychopathology, such as rumination and other forms of repetitive negative thinking or disruptions in emotion regulation [3,4,5]. Here, we expand this focus to encompass environmental experiences occurring early in development. Specifically, we argue that exposure to trauma in childhood is a particularly powerful transdiagnostic factor that is associated with increased risk for many types of psychopathology. Next, we present a transdiagnostic model that highlights several key mechanisms that appear to explain how childhood trauma ultimately confers risk for multiple forms of psychopathology throughout the life-course (see Fig. 1). We end by reviewing the implications of this transdiagnostic model for screening and early intervention.
Childhood trauma exposure
Traumatic events are experiences that have a high potential for harm, including actual or threatened death, serious injury, or sexual violation . We focus here on traumatic events that involve exposure to interpersonal violence—including experiences of direct victimization as well as witnessing violence occurring to another person, as these types of traumatic events have particularly strong associations with psychopathology [7,8,9].
A majority of children and adolescents in the United States will experience a traumatic event by the time they reach adulthood . A smaller but still substantial proportion of children—about one quarter to one third across studies—have experienced or witnessed interpersonal violence [9,10,11]. Childhood trauma exposure is also a common problem cross-nationally [10, 12, 13].
Exposure to childhood trauma is a potent risk factor for multiple forms of psychopathology. Evidence from population-based studies suggests that children who have experienced trauma are about twice as likely to develop a mental disorder compared to those who have never experienced trauma [10, 14]. This elevated risk for the emergence of psychopathology is present not only during childhood but persists throughout adolescence and adulthood [15,16,17]. Exposure to childhood trauma is associated with virtually all commonly occurring forms of psychopathology, including mood, anxiety, substance use, and disruptive behavior disorders, with little meaningful variation in the strength of associations across disorders [14, 16,17,18,19,20]. Childhood trauma is also associated with psychotic experiences [21, 22] and suicidal ideation and attempts [23,24,25,26]. In addition, more than one in six children exposed to trauma develop post-traumatic stress disorder (PTSD) , a diagnosis that occurs only in those who have experienced a traumatic event. Together, these findings demonstrate clearly that childhood trauma is associated with increased risk for psychopathology transdiagnostically.
Several population-based studies have examined whether childhood trauma has stronger associations with some forms of psychopathology than others. These studies have repeatedly shown the associations of child maltreatment—which includes traumatic experiences of abuse as well those involving neglect—with lifetime psychopathology operate largely through a latent factor for internalizing and externalizing psychopathology, with no significant direct effects on specific mental disorders after adjusting for associations with this latent factor [28, 29]. This pattern suggests that exposure to trauma in childhood likely influences the development of psychological and neurobiological processes that confer broad vulnerability to multiple types of psychopathology. In the following sections, we describe three sets of potential mechanisms that appear to underlie the link between childhood trauma and psychopathology transdiagnostically.
Trauma exposure may have a particularly pernicious influence when it happens early in life given the heightened brain plasticity that characterizes childhood and adolescence . This plasticity reflects the ability of the brain to change in response to environmental experiences. Although elevated brain plasticity in early life confers many advantages by allowing children to learn rapidly from experience and adapt to the environment in which they are being raised, it may also have long-term costs for children raised in environments that are dangerous. Specifically, environments characterized by violence and high potential for harm can influence patterns of social, emotional, and neurobiological development in ways that facilitate the rapid detection of potential threats . Although these developmental adaptations may enhance safety in dangerous environments by mobilizing behavioral responses to avoid threats, they also may increase risk for multiple forms of psychopathology. To serve as a transdiagnostic mechanism, a particular process must (a) be influenced by childhood trauma exposure, (b) predict the later emergence of multiple forms of psychopathology, and (c) explain the association between childhood trauma and later psychopathology.
Importantly, the mechanisms we highlight below appear to be relatively specific to experiences of childhood trauma as opposed to adversity more globally. For example, none of these mechanisms have been consistently observed in children who experience forms of adversity involving deprivation (e.g., neglect). Indeed, recent conceptual models argue that different types of adverse early-life environments have distinct influences on cognitive, emotional, and neurobiological development, in ways that reflect plasticity mechanisms that allow children to adapt to the environments in which they are developing [32,33,34]. Below, we outline several fundamental processes that reflect these types of developmental adaptations to threatening early environments but also appear to confer risk for psychopathology transdiagnostically (see Fig. 1).
Social information processing mechanisms
Biases in social information processing—specifically, the perception, identification, and interpretation of social cues—are one set of core mechanisms that contribute to the strong association between childhood trauma and transdiagnostic psychopathology [31, 35]. Across a range of social information processing domains, children who have experienced trauma exhibit biases that prioritize the identification of potentially threatening social cues and are more likely to perceive or classify such cues as threatening [36,37,38].
Children who have experienced trauma can identify expressions of anger or fear with less perceptual information than children who have never experienced trauma; this heightened perceptual sensitivity is specific to threat cues and does not exist for other emotions (e.g., happiness and sadness) [37,38,39]. The magnitude of perceptual sensitivity to threat increases as the severity of trauma increases  and persists into adulthood following trauma exposure in childhood . Similar patterns have been observed using tasks that assess attentional processes involved in orienting towards and disengaging from emotionally salient stimuli. Children who have experienced trauma exhibit faster attentional orienting to angry facial expressions and vocal cues, but not other emotions, suggesting that their attention is more easily captured by threatening stimuli than children who have never experienced trauma [42,43,44]. Once their attention has been captured, children with trauma histories also have more difficulty disengaging from anger cues than children who have not experienced trauma . Finally, trauma-exposed children appear to use more liberal criteria for classifying emotional expressions and social situations as threatening (i.e., involving anger); specifically, they are more likely than children who have never experienced trauma to misclassify other negative emotions like sadness and fear and even neutral facial expressions as anger [37, 38]. Importantly, children who have experienced neglect have difficulty discriminating between different emotions broadly but do not exhibit these types of threat-related biases in perceptual sensitivity or emotion identification .
These social information processing biases extend beyond facial and vocal expressions to the interpretation of a broader range of social situations. When presented with ambiguous social situations, children who have experienced trauma are less attentive to relevant social cues and more likely to assume that others have hostile intentions—a pattern known as hostile attribution bias [36, 46,47,48]. Trauma-exposed children are also more likely to generate aggressive responses to these ambiguous social situations and perceive aggression to be a more effective response than children who have never experienced trauma [36, 46,47,48].
Together, these social information processing biases prioritize threat-related information in ways that may help children identify early signals of danger in the environment—this rapid and over-identification of threat may help to promote safety in environments where danger is routinely encountered. However, these developmental adaptations following childhood trauma also appear to increase risk for psychopathology transdiagnostically [31, 49]. Perceptual and attentional biases to threat cues are associated with anxiety [50,51,52,53], depression [53, 54], PTSD [55,56,57], psychosis [58,59,60], and the general psychopathology factor (i.e., p-factor) . Hostile attribution bias, in contrast, is associated with risk for externalizing problems [36, 46, 53] and has also been observed consistently in people with psychosis [62, 63]. Moreover, across many studies, these social information processing biases have been shown to explain the association between childhood trauma and the later emergence of transdiagnostic psychopathology [36, 44, 64].
Emotional processing mechanisms
A second set of well-established transdiagnostic mechanisms linking childhood trauma with psychopathology involve altered patterns of emotional processing, including heightened emotional reactivity, low emotional awareness, and difficulties with emotion regulation. Consistent with biases in social information processing, youth exposed to trauma exhibit a pattern of emotional responding characterized by increased vigilance and magnified emotional responses to potential threats in the environment. One of the most consistently observed emotional patterns among children with trauma exposure is heightened emotional reactivity, such that salient negative cues in the environment (e.g., angry or fearful faces; social situations depicting people experiencing negative emotions) elicit greater emotional responses in children with trauma histories as compared to children who have never encountered trauma [31, 65]. This heightened emotional reactivity has been observed in studies utilizing behavioral tasks, self-report measures, and experience sampling (i.e., ecological momentary assessment) methods [61, 66,67,68] as well as neurobiological responses, including greater activation in the amygdala and anterior insula, brain regions that encode emotional salience, to negative relative to neutral stimuli [69,70,71,72,73]. These patterns have been observed inconsistently in children exposed to other forms of adversity, particularly those involving deprivation .
In addition to elevated emotional reactivity, childhood trauma exposure also appears to alter patterns of learning about threat in the environment. Young children exposed to trauma exhibit an earlier emergence of aversive learning—as indexed by the ability to generate a conditioned fear response to a previously neutral cue that predicts an aversive stimulus—than children without such exposure . However, by adolescence, trauma-exposed youth exhibit difficulty discriminating between cues that predict threat and safety. For example, during aversive learning, trauma-exposed youth showed less differentiated physiological response between conditioned fear cues and unconditioned safety cues compared to youth without trauma histories . This pattern may reflect a failure to encode the relevant perceptual features of stimuli that predict threat, and contribute to greater generalization of fear responses. The developmental shift from earlier emergence of fear learning to difficulty discriminating between cues that predict threat versus safety may occur when children are raised in environments where violence is experienced chronically and unpredictably—ultimately, making it difficult to learn the most relevant cues for predicting the presence of danger.
Trauma-exposed youth also exhibit a number of difficulties in identifying and regulating their emotions. Childhood trauma is associated with poor emotional awareness—a reduced ability to identify and differentiate one’s own emotions . This tendency for low emotional awareness may contribute to difficulties with emotion regulation, which have also been consistently observed among children exposed to trauma. For example, children exposed to trauma are more likely to report using maladaptive emotion regulation strategies like rumination, expressive suppression, and impulsive responses to distress; greater use of maladaptive emotion regulation strategies has also been observed in studies using behavioral paradigms and caregiver report [31, 61, 67, 77,78,79]. When asked to use effective emotion regulation strategies like cognitive reappraisal to dampen emotional reactivity, youth exposed to trauma recruit the prefrontal cortex (PFC) to a greater degree than those without trauma histories , a pattern that emerges across the transition to adolescence . This pattern suggests that using explicit emotion regulation strategies like cognitive reappraisal might be more difficult or require greater cognitive resources for children who have experienced trauma—potentially as a result of the heightened emotional reactivity common in these youth. These difficulties with emotion regulation have generally not been observed among children exposed to neglect .
Beyond these explicit (i.e., intentional) emotion regulation strategies, differences in automatic or implicit forms of emotion regulation have also been observed following childhood trauma. Children exposed to trauma exhibit poor adaptation to emotional conflict [82, 83]—a behavioral process that reflects coupling between the medial prefrontal cortex (mPFC) and amygdala . Activity in the mPFC is associated with dampened amygdala activity in numerous forms of implicit emotion regulation. Consistent with these behavioral patterns, children exposed to trauma also exhibit reduced functional coupling of the amygdala and mPFC in studies of resting-state functional connectivity [84, 85], suggesting that childhood trauma may alter the function of this emotional processing circuit.
These patterns of emotional processing that are common in trauma-exposed children are strongly associated with multiple forms psychopathology. Elevated emotional reactivity is associated with psychopathology transdiagnostically across numerous studies [61, 67, 68, 86]. Recent evidence suggests that low emotional awareness is also associated with the general psychopathology (i.e., p-factor) and mediates the association between childhood trauma and the p-factor . Similarly, disruptions in emotion regulation are associated with virtually all types of psychopathology and predict the onset of internalizing and externalizing problems [87,88,89,90] as well as account for comorbidity between disorders [5, 91, 92]. Indeed, elevated emotional reactivity, difficulties with emotion regulation, and reduced functional coupling between the mPFC and amygdala—a neural pattern associated with poor implicit emotion regulation—have all been shown to mediate the link between childhood trauma exposure and transdiagnostic psychopathology [61, 67, 68, 84, 86], including the p-factor .
Accelerated biological aging
A final mechanism through which childhood trauma may confer risk for transdiagnostic psychopathology is accelerated biological aging, whereby exposure to threatening early-life environments might actually alter the pace of development. Life History Theory postulates that experiences in early life can program an individual’s developmental trajectory and pace of aging to respond most effectively to the current environment and environmental demands they are likely to encounter in the future [93,94,95]. For instance, in a comfortable and predictable environment, a slow and protracted developmental trajectory may be optimal, as it allows for maximal parental investment prior to offspring independence. However, in a harsh or unpredictable environment, a faster pace of development in which children reach adult-like capabilities at an earlier age may be favored in order to maximize reproduction prior to potential mortality.
Two key indicators of accelerated aging in development include pubertal timing and cellular aging. The timing and pace of pubertal development is most commonly measured by age of menarche in females [96, 97] and measures of pubertal stage controlling for chronological age [98, 99]. Cellular aging is most commonly measured by leukocyte telomere length [100, 101] and DNA methylation (DNAm) age [102, 103]. These metrics can be used to evaluate whether the pace of aging at the reproductive or cellular level is occurring faster than what would be expected given an individual’s chronological age.
Numerous studies have found that childhood trauma is associated with earlier pubertal timing [98, 104,105,106]. A smaller but increasing number of studies have also observed accelerated cellular aging following childhood trauma, including shorter telomere length [107, 108], and advanced DNAm age relative to chronological age [104, 109]. In a recent meta-analysis—including 43 studies of pubertal timing with 114,450 participants and 11 studies of cellular aging with 1560 participants—we found that the association between ELA and accelerated biological development was specific to adversities involving exposure to trauma. Specifically, children exposed to trauma exhibited accelerated biological aging in measures of pubertal development and cellular aging, but children exposed to deprivation (e.g., neglect) and low socioeconomic status did not exhibit this pattern of accelerated aging . These results support dimensional models of adversity arguing that different forms of early-life adversity have unique influences on cognitive, emotional, and neurobiological development [32,33,34].
Accelerated biological aging is associated with multiple forms of psychopathology. Earlier pubertal timing is associated with elevated levels of risk-taking behavior, delinquency and substance abuse problems [111, 112], depression and anxiety disorders [113, 114], and the p-factor  and is considered a transdiagnostic risk factor for psychopathology [116, 117]. Accelerated cellular aging is associated with depression [104, 118], anxiety , PTSD , psychosis [121,122,123], and the p-factor , suggesting that it may also be a transdiagnostic risk factor. These patterns of accelerated biological aging—including earlier pubertal timing  and accelerated cellular aging as indexed by DNAm age —have been shown to mediate the association of trauma exposure with multiple forms of psychopathology. These findings provide strong evidence for accelerated biological aging as a transdiagnostic risk factor for psychopathology following childhood trauma. However, the biological mechanisms through which trauma exposure in childhood actually accelerates reproductive development and cellular aging are not well understood. Characterizing these mechanisms is an important goal for future research.
Social support as a transdiagnostic protective factor
Children who have experienced trauma often struggle to form and maintain healthy relationships [77, 125, 126]. As such, cultivating social support—a well-established protective factor against the emergence of psychopathology following stressors [127,128,129]—may be particularly important in this population. Indeed, meta-analysis suggests that children with high levels of social support are less likely to develop trauma-related psychopathology transdiagnostically . In studies that have conceptualized social support broadly, youth who perceive greater social support or engage in more support-seeking behavior following exposure to stress exhibit lower levels of both internalizing and externalizing psychopathology than those who do not [131,132,133,134,135]. Critically, perceived social support is a protective factor that buffers against the onset and progression of psychopathology following trauma exposure [136,137,138].
Caregiver support is a particularly important form of social support that may protect against the emergence of psychopathology following childhood trauma. Recent evidence suggests that the presence of a supportive caregiver can buffer against the elevated threat-related processing that is common in children who have experienced trauma. The presence of a supportive caregiver is associated with lower amygdala reactivity, greater functional coupling of the mPFC and amygdala during threat processing, and enhanced discrimination of threat and safety cues during aversive learning [139, 140]. Thus, caregiver buffering of threat-related processing may be one particularly important pathway through which support can mitigate risk for psychopathology in children who have experienced trauma. Future work should examine whether interventions that promote caregiver support and broader social support-seeking behaviors may have potential for reducing vulnerability to psychopathology among children exposed to trauma.
Understanding the mechanisms that contribute to multiple forms of psychopathology can facilitate identification of the most important targets for intervention. In contrast to disorder-specific approaches that have historically been common, altering these transdiagnostic mechanisms through intervention provides the opportunity to more broadly reduce psychopathology risk. The clear advantages of such an approach have led to the emergence of transdiagnostic treatments for both children and adults [141, 142].
With regard to childhood trauma, the transdiagnostic mechanisms reviewed here—particularly in the domains of social information and emotional processing—reflect characteristics that could be targeted with early interventions aimed at preventing the onset of psychopathology. Elsewhere, we articulate how these social and emotional processing mechanisms could be targeted with existing evidence-based intervention techniques to prevent child and adolescent psychopathology . Although specific techniques that could reduce the accelerated pace of biological aging following childhood trauma are less well understood, mindfulness interventions have shown promise for slowing the pace of biological aging in adults . Moreover, early pubertal maturation is a readily observable feature that could allow medical practitioners to identify youth who may require additional assessment for childhood trauma exposure and early intervention within the context of routine primary care visits. Determining if early interventions targeting these mechanisms have the potential to reduce risk for psychopathology, and whether the effectiveness of such approaches vary for children in different stages of development, is a critical question for future research.
Transdiagnostic processes confer risk for multiple types of psychopathology, explain comorbidity of different disorders, and provide targets for early intervention and treatment. Childhood trauma exposure is a powerful transdiagnostic factor that is associated with elevated risk for virtually all commonly occurring forms of psychopathology. Children who experience trauma exhibit consistent changes in social information processing in ways that involve the prioritization and over-identification of threat in the environment; patterns of emotional processing characterized by elevated emotional reactivity, low emotional awareness, and difficulties with emotional learning and emotion regulation; and accelerated biological aging across metrics of pubertal development and cellular aging. Together, these patterns reflect developmental adaptations to an early environment characterized by danger that may provide short-term benefits. However, these changes in social information processing, emotional responding, and the pace of biological aging are also consistently associated with elevated risk for the emergence of multiple forms of internalizing and externalizing psychopathology and explain the link between childhood trauma exposure and transdiagnostic psychopathology. As such, these mechanisms represent critical targets for early interventions aimed at preventing the emergence of psychopathology in children who have experienced trauma.
Availability of data and materials
Cicchetti D, Rogosch FA. No title. Dev Psychopathol 1996;8(4):597–600.
Nolen-Hoeksema S, Watkins ER. A heuristic for developing transdiagnostic models of psychopathology. Perspect Psychol Sci. 2011;6(6):589–609 Available from: http://pps.sagepub.com/cgi/alerts. [cited 2019 Dec 13].
Ehring T, Watkins ER. Repetitive negative thinking as a transdiagnostic process. Int J Cogn Ther. 2008;1(3):192–205.
Aldao A, Nolen-Hoeksema S. Specificity of cognitive emotion regulation strategies: a transdiagnostic examination. Behav Res Ther. 2010;48(10):974–83.
McLaughlin KA, Nolen-Hoeksema S. Rumination as a transdiagnostic factor in depression and anxiety. Behav Res Ther. 2011;49(3):186–93.
American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 5th edition (DSM-5). Washington, D.C.: American Psychiatric Press; 2013.
Koenen KC, Ratanatharathorn A, Ng L, McLaughlin KA, Bromet EJ, Stein DJ, et al. Posttraumatic stress disorder in the World Mental Health Surveys. Psychol Med. 2017;47:2260–74.
Walsh K, McLaughlin KA, Hamilton A, Keyes KM. Trauma exposure, incident psychiatric disorders, and disorder transitions in a longitudinal population representative sample. J Psychiatr Res. 2017;92:212–8.
McLaughlin KA, Koenen KC, Hill ED, Petukhova M, Sampson NA, Zaslavsky AM, et al. Trauma exposure and posttraumatic stress disorder in a national sample of adolescents. J Am Acad Child Adolesc Psychiatry. 2013;52(8):815–830.e14. https://doi.org/10.1016/j.jaac.2013.05.011 [cited 2019 Dec 13].
Lewis SJ, Arseneault L, Caspi A, Fisher HL, Matthews T, Moffitt TE, et al. The epidemiology of trauma and post-traumatic stress disorder in a representative cohort of young people in England and Wales. Lancet Psychiatry. 2019;6(3):247–56.
Finkelhor D, Ormrod R, Turner H, Hamby SL. The victimization of children and youth: a comprehensive, national survey. Child Maltreatment. 2005;10:5–25.
Perkonigg A, Kessler RC, Storz S, Wittchen H-U. Traumatic events and post-traumatic stress disorder in the community: prevalence,risk factors and comorbidity. Acta Psychiatr Scand. 2000;101(1):46–59. https://doi.org/10.1034/j.1600-0447.2000.101001046.x [cited 2019 Dec 13].
Borges G, Benjet C, Medina-Mora ME, Orozco R, Molnar BE, Nock MK. Traumatic events and suicide-related outcomes among Mexico City adolescents. J Child Psychol Psychiatry. 2008;49(6):654–66. https://doi.org/10.1111/j.1469-7610.2007.01868.x [cited 2019 Dec 13].
McLaughlin KA, Green JG, Gruber MJ, Sampson NA, Zaslavsky AM, Kessler RC. Childhood adversities and first onset of psychiatric disorders in a national sample of US adolescents. Arch Gen Psychiatry. 2012;69(11):1151 Available from: http://archpsyc.jamanetwork.com/article.aspx?doi=10.1001/archgenpsychiatry.2011.2277.
McLaughlin KA, Conron KJ, Koenen KC, Gilman SE. Childhood adversity, adult stressful life events, and risk of past-year psychiatric disorder: a test of the stress sensitization hypothesis in a population-based sample of adults. Psychol Med. 2010;40(10):1647–58.
Green JG, McLaughlin KA, Berglund PA, Gruber MJ, Sampson NA, Zaslavsky AM, et al. Childhood adversities and adult psychiatric disorders in the national comorbidity survey replication I: associations with first onset of DSM-IV disorders. Arch Gen Psychiatry. 2010;67(2):113–23 Available from: http://archpsyc.jamanetwork.com/article.aspx?doi=10.1001/archgenpsychiatry.2009.187.
Kessler RC, McLaughlin KA, Green JG, Gruber MJ, Sampson NA, Zaslavsky AM, et al. Childhood adversities and adult psychopathology in the WHO world mental health surveys. Br J Psychiatry. 2010;197(5):378–85 Available from: https://www.cambridge.org/core/product/identifier/S0007125000253506/type/journal_article. [cited 2019 Dec 13].
Dube SR, Felitti VJ, Dong M, Chapman DP, Giles WH, Anda RF. Childhood abuse, neglect, and household dysfunction and the risk of illicit drug use: the adverse childhood experiences study. Pediatrics. 2003;111(3):564–72.
Chapman DP, Whitfield CL, Felitti VJ, Dube SR, Edwards VJ, Anda RF. Adverse childhood experiences and the risk of depressive disorders in adulthood. J Affect Disord. 2004;82(2):217–25.
Weich S, Patterson J, Shaw R, Stewart-Brown S. Family relationships in childhood and common psychiatric disorders in later life: systematic review of prospective studies. Br J Psychiatry. 2009;194:392–8.
McGrath JJ, McLaughlin KA, Saha S, Aguilar-Gaxiola S, Al-Hamzawi A, Alonso J, et al. The association between childhood adversities and subsequent first onset of psychotic experiences: a cross-national analysis of 23 998 respondents from 17 countries. Psychol Med. 2017;47(7):1230–45.
Janssen I, Krabbendam L, Bak M, Hanssen M, Vollebergh W, Graaf R, et al. Childhood abuse as a risk factor for psychotic experiences. Acta Psychiatr Scand. 2004;109(1):38–45. doi: https://doi.org/10.1046/j.0001-690X.2003.00217.x. [cited 2019 Dec 13].
Bruffaerts R, Demyttenaere K, Borges G, Haro JM, Chiu WT, Hwang I, et al. Childhood adversities as risk factors for onset and persistence of suicidal behaviour. Br J Psychiatry. 2010;197(1):20–7.
Afifi TO, Enns MW, Cox BJ, Asmundson GJG, Stein MB, Sareen J. Population attributable fractions of psychiatric disorders and suicide ideation and attempts associated with adverse childhood experiences. Am J Public Health. 2008;98(5):946–52 Available from: http://www.ncbi.nlm.nih.gov/pubmed/18381992. [cited 2019 Dec 13].
Dube SR, Anda RF, Felitti VJ, Chapman DP, Williamson DF, Giles WH. Childhood abuse, household dysfunction, and the risk of attempted suicide throughout the life span: findings from the Adverse Childhood Experiences Study. JAMA. 2001;286(24):3089–96.
Molnar BE, Berkman LF, Buka SL. Psychopathology, childhood sexual abuse and other childhood adversities: relative links to subsequent suicidal behaviour in the US. Psychol Med. 2001;31(6):965–77.
Alisic E, Zalta AK, Van Wesel F, Larsen SE, Hafstad GS, Hassanpour K, et al. Rates of post-traumatic stress disorder in trauma-exposed children and adolescents: meta-analysis. Br J Psychiatry. 2014;204:335–40.
Keyes KM, Eaton NR, Krueger RF, McLaughlin KA, Wall MM, Grant BF, et al. Childhood maltreatment and the structure of common psychiatric disorders. Br J Psychiatry. 2012;200(2):107–15.
Caspi A, Houts RM, Belsky DW, Goldman-Mellor SJ, Harrington H, Israel S, et al. The p factor: one general psychopathology factor in the structure of psychiatric disorders? Clin Psychol Sci. 2014;2(2):119–37.
Kolb B, Gibb R. Searching for the principles of brain plasticity and behavior. Cortex. 2014;58:251–60.
McLaughlin KA, Lambert HK. Child trauma exposure and psychopathology: mechanisms of risk and resilience. Curr Opin Psychol. 2017;14:29–34 Available from: http://www.sciencedirect.com/science/article/pii/S2352250X16301361.
McLaughlin KA, Sheridan MA, Lambert HK, KA. M, MA. S, HK. L. Childhood adversity and neural development: deprivation and threat as distinct dimensions of early experience. Neurosci Biobehav Rev 2014 47(PG-578-91):578–591.
McLaughlin KA, Sheridan MA. Beyond cumulative risk: a dimensional approach to childhood adversity. Curr Dir Psychol Sci. 2016;25(4):239–45 Available from: http://cdp.sagepub.com/lookup/doi/10.1177/0963721416655883.
Sheridan MA, McLaughlin KA. Dimensions of early experience and neural development: deprivation and threat. Trends Cogn Sci. 2014;18(11):580–5 Available from: https://www.sciencedirect.com/science/article/pii/S1364661314002022.
Lau JYF, Waters AM. Annual Research Review: An expanded account of information-processing mechanisms in risk for child and adolescent anxiety and depression. J Child Psychol Psychiatry. 2017;58(4):387–407. https://doi.org/10.1111/jcpp.12653.
Dodge KA, Pettit GS, Bates JE, Valente E. Social information-processing patterns partially mediate the effect of early physical abuse on later conduct problems. J Abnorm Psychol. 1995;104(4):632–43 Available from: https://psycnet.apa.org/record/1996-93514-001.
Pollak SD, Cicchetti D, Hornung K, Reed A. Recognizing emotion in faces: developmental effects of child abuse and neglect. Dev Psychol. 2000;36(5):679–88 Available from: http://doi.apa.org/getdoi.cfm?doi=10.1037/0012-16126.96.36.1999.
Pollak SD, Kistler DJ. Early experience is associated with the development of categorical representations for facial expressions of emotion. Proc Natl Acad Sci. 2002;99(13):9072–6 Available from: http://www.pnas.org/content/99/13/9072.
Pollak SD, Sinha P. Effects of early experience on children’s recognition of facial displays of emotion. Dev Psychol. 2002;38(5):784–91 Available from: http://doi.apa.org/getdoi.cfm?doi=10.1037/0012-16188.8.131.524.
Pollak SD, Messner M, Kistler DJ, Cohn JF. Development of perceptual expertise in emotion recognition. Cognition. 2009;110(2):242–7 Available from: http://www.sciencedirect.com/science/article/pii/S0010027708002175.
Gibb BE, Schofield CA, Coles ME. Reported history of childhood abuse and young adults’ information-processing biases for facial displays of emotion. Child Maltreat. 2009;14(2):148–56. https://doi.org/10.1177/1077559508326358.
Pollak SD, Klorman R, Thatcher JE, Cicchetti D. P3b reflects maltreated children’s reactions to facial displays of emotion. Psychophysiology. 2001;38(2):267–74 Available from: http://onlinelibrary.wiley.com/doi/abs/10.1111/1469-8986.3820267.
Shackman JE, Pollak SD. Impact of physical maltreatment on the regulation of negative affect and aggression. Dev Psychopathol. 2014;26(4pt1):1021–33 Available from: https://www.cambridge.org/core/journals/development-and-psychopathology/article/impact-of-physical-maltreatment-on-the-regulation-of-negative-affect-and-aggression/360FA4CEFA2207FE9444264C55CDDD61.
Shackman JE, Shackman AJ, Pollak SD. Physical abuse amplifies attention to threat and increases anxiety in children. Emotion. 2007;7(4):838–52. https://doi.org/10.1037/1528-35184.108.40.2068.
Pollak SD, Tolley-Schell SA. Selective attention to facial emotion in physically abused children. J Abnorm Psychol. 2003;112(3):323–38 Available from: http://ezp-prod1.hul.harvard.edu/login?url=http://search.ebscohost.com/login.aspx?direct=true&db=pdh&AN=2003-05990-002&site=ehost-live&scope=site.
Dodge KA, Bates JE, Pettit GS. Mechanisms in the cycle of violence. Science. 1990;250(4988):1678–83 Available from: http://science.sciencemag.org/content/250/4988/1678.
Keil V, Price JM. Social information-processing patterns of maltreated children in two social domains. J Appl Dev Psychol. 2009;30(1):43–52 Available from: http://www.sciencedirect.com/science/article/pii/S0193397308001159.
Price JM, Glad K. Hostile attributional tendencies in maltreated children. J Abnorm Child Psychol. 2003;31(3):329–43. https://doi.org/10.1023/A:1023237731683.
Pollak SD. Experience-dependent affective learning and risk for psychopathology in children. Ann N Y Acad Sci. 2003;1008:102–11.
Briggs-Gowan MJ, Pollak SD, Grasso D, Voss J, Mian ND, Zobel E, et al. Attention bias and anxiety in young children exposed to family violence. J Child Psychol Psychiatry Allied Discip. 2015;56(11):1194–201 Available from: http://onlinelibrary.wiley.com/doi/abs/10.1111/jcpp.12397.
Dudeney J, Sharpe L, Hunt C. Attentional bias towards threatening stimuli in children with anxiety: a meta-analysis. Clin Psychol Rev. 2015;40:66–75 Available from: http://www.sciencedirect.com/science/article/pii/S027273581500077X.
Mathews A, MacLeod C. Induced processing biases have causal effects on anxiety. Cogn Emot. 2002;16(3):331–54. https://doi.org/10.1080/02699930143000518.
Reid SC, Salmon K, Lovibond PF. Cognitive biases in childhood anxiety, depression, and aggression: are they pervasive or specific? Cognit Ther Res. 2006;30(5):531–49. https://doi.org/10.1007/s10608-006-9077-y.
Platt B, Waters AM, Schulte-Koerne G, Engelmann L, Salemink E. A review of cognitive biases in youth depression: attention, interpretation and memory. Cogn Emot. 2017;31(3):462–83 Available from: https://www.tandfonline.com/doi/full/10.1080/02699931.2015.1127215.
Briggs-Gowan MJ, Grasso D, Bar-Haim Y, Voss J, McCarthy KJ, Pine DS, et al. Attention bias in the developmental unfolding of post-traumatic stress symptoms in young children at risk. J Child Psychol Psychiatry. 2016;57(9):1083–91. https://doi.org/10.1111/jcpp.12577.
Masten CL, Guyer AE, Hodgdon HB, McClure EB, Charney DS, Ernst M, et al. Recognition of facial emotions among maltreated children with high rates of post-traumatic stress disorder. Child Abuse Negl. 2008;32(1):139–53 Available from: http://www.sciencedirect.com/science/article/pii/S0145213407002633.
Swartz JR, Graham-Bermann SA, Mogg K, Bradley BP, Monk CS. Attention bias to emotional faces in young children exposed to intimate partner violence. J Child Adolesc Trauma 2011 1;4(2):109–22. doi: https://doi.org/10.1080/19361521.2011.573525.
Moritz S, Laudan A. Attention bias for paranoia-relevant visual stimuli in schizophrenia. Cogn Neuropsychiatry. 2007;12(5):381–90.
Green MJ, Phillips ML. Social threat perception and the evolution of paranoia. Neurosci Biobehav Rev. 2004;28(3):333–42.
Underwood R, Kumari V, Peters E. Cognitive and neural models of threat appraisal in psychosis: a theoretical integration. Psychiatry Res. 2016;239:131–8. https://doi.org/10.1016/j.psychres.2016.03.016.
Weissman DG, Bitran D, Miller AB, Schaefer JD, Sheridan MA, KA ML. Difficulties with emotion regulation as a transdiagnostic mechanism linking child maltreatment with the emergence of psychopathology. Dev Psychopathol. 2019;31(3):1–17 Available from: https://www.cambridge.org/core/product/identifier/S0954579419000348/type/journal_article. [cited 2019 Dec 13].
Combs DR, Penn DL, Michael CO, Basso MR, Wiedeman R, Siebenmorgan M, et al. Perceptions of hostility by persons with and without persecutory delusions. Cogn Neuropsychiatry. 2009;14(1):30–52.
Pinkham AE, Brensinger C, Kohler C, Gur RE, Gur RC. Actively paranoid patients with schizophrenia over attribute anger to neutral faces. Schizophr Res. 2011;125(2–3):174–8. https://doi.org/10.1016/j.schres.2010.11.006.
Gulley LD, Oppenheimer CW, Hankin BL. Associations among negative parenting, attention bias to anger, and social anxiety among youth. Dev Psychol. 2014;50(2):577–85 Available from: https://europepmc.org/articles/pmc4086836?pdf=render.
McLaughlin KA. Future directions in childhood adversity and youth psychopathology. J Clin Child Adolesc Psychol. 2016;45(3):361–82.
Glaser JP, van Os J, Portegijs PJM, Myin-Germeys I. Childhood trauma and emotional reactivity to daily life stress in adult frequent attenders of general practitioners. J Psychosom Res. 2006;61(2):229–36.
Heleniak C, Jenness JL, Vander Stoep A, McCauley E, KA ML. Childhood maltreatment exposure and disruptions in emotion regulation: a transdiagnostic pathway to adolescent internalizing and externalizing psychopathology. Cognit Ther Res. 2016;40(3):394–415 Available from: http://link.springer.com/10.1007/s10608-015-9735-z. [cited 2019 Dec 13].
McLaughlin KA, Kubzansky LD, Dunn EC, Waldinger R, Vaillant G, Koenen KC. Childhood social environment, emotional reactivity to stress, and mood and anxiety disorders across the life course. Depress Anxiety. 2010;27(12):1087–94. https://doi.org/10.1002/da.20762 [cited 2019 Dec 13].
Hein TC, Monk CS, TC. H, CS. M, Hein TC, Monk CS. Research Review: Neural response to threat in children, adolescents, and adults after child maltreatment – a quantitative meta-analysis. J Child Psychol Psychiatry. 2017 58(3):222–230. Available from: NS.
EJ MC, SASA DB, Viding E. The impact of childhood maltreatment: a review of neurobiological and genetic factors. Front Psychiatry. 2011;2:1–14.
McLaughlin KA, Peverill M, Gold AL, Alves S, Sheridan MA, et al. Child maltreatment and neural systems underlying emotion regulation. J Am Acad Child Adolesc Psychiatry. 2015;54(9):753–62 Available from: http://linkinghub.elsevier.com/retrieve/pii/S0890856715003937.
Viding E, Sebastian CL, Dadds MR, Lockwood PL, Cecil CAM, De Brito SA, et al. Amygdala response to preattentive masked fear in children with conduct problems: the role of callous-unemotional traits. Am J Psychiatry. 2012;169(10):1109–16.
McLaughlin KA, Weissman DG, Bitran D. Childhood adversity and neural development: a systematic review. Annu Rev Dev Psychol. 2019;1(1):277–312.
Machlin L, Miller AB, Snyder J, McLaughlin KA, Sheridan MA. Differential associations of deprivation and threat with cognitive control and fear conditioning in early childhood. Front Behav Neurosci. 2019;13:1–14.
McLaughlin KA, Sheridan MA, Gold AL, Duys A, Lambert HK, Peverill M, et al. Maltreatment exposure, brain structure, and fear conditioning in children and adolescents. Neuropsychopharmacology. 2016;41(8):1956–64 Available from: http://www.nature.com/articles/npp2015365.
Weissman DG, Nook EC, Dews AA, Miller AB, Lambert HK, Sasse SF, Et al. Low emotional awareness as a transdiagnostic mechanism underlying psychopathology in adolescence. Clinical Psychological Science, in press.
Kim J, Cicchetti D. Longitudinal pathways linking child maltreatment, emotion regulation, peer relations, and psychopathology. J Child Psychol Psychiatry. 2010;51(6):706–16 Available from: https://europepmc.org/articles/pmc3397665?pdf=render.
Maughan A, Cicchetti D. Impact of child maltreatment and interadult violence on children’s emotion regulation abilities and socioemotional adjustment. Child Dev. 2002;73(5):1525–42.
Shields A, Cicchetti D. Emotion regulation among school-age children: the development and validation of a new criterion Q-sort scale. Dev Psychol. 1997;33(6):906–16.
Jenness JL, Peverill M, Miller AB, Heleniak C, Robertson M, Sambrook KA, et al. Alterations in neural circuits underlying emotion regulation following child maltreatment emerge across adolescence: a transdiagnostic mechanism underlying trauma-related psychopathology. Psychological Medicine, in press.
Milojevich HM, Norwalk KE, Sheridan MA. Deprivation and threat, emotion dysregulation, and psychopathology: concurrent and longitudinal associations. Dev Psychopathol. 2019;31(3):847–57 Available from: https://www.cambridge.org/core/product/identifier/S0954579419000294/type/journal_article.
Lambert HK, King KM, Monahan KC, KA ML. Differential associations of threat and deprivation with emotion regulation and cognitive control in adolescence. Dev Psychopathol. 2017;29(3):929–40 Available from: http://www.ncbi.nlm.nih.gov/pubmed/27424571.
Marusak HA, Martin KR, Etkin A, Thomason ME. Childhood trauma exposure disrupts the automatic regulation of emotional processing. Neuropsychopharmacology. 2015;40(5):1250–8 Available from: http://www.ncbi.nlm.nih.gov/pubmed/25413183.
Herringa RJR, Birn RMR, Ruttle PPL, Burghy CA, Stodola DE, Davidson RJ, et al. Childhood maltreatment is associated with altered fear circuitry and increased internalizing symptoms by late adolescence. Proc Natl Acad Sci. 2013;110(47):19119–24 Available from: http://www.ncbi.nlm.nih.gov/pubmed/24191026.
Thomason ME, Marusak HA, Tocco MA, Vila AM, McGarragle O, Rosenberg DR. Altered amygdala connectivity in urban youth exposed to trauma. Soc Cogn Affect Neurosci. 2015;10(11):1460–8 Available from: https://academic.oup.com/scan/article/10/11/1460/1640988. [cited 2019 Dec 16].
Kim-Spoon J, Cicchetti D, Rogosch FA, Kim-Spoon J, Cicchetti D, Rogosch FA. A longitudinal study of emotion regulation, emotion lability-negativity, and internalizing symptomatology in maltreated and nonmaltreated children. Child Dev. 2013;84(2):512–27. https://doi.org/10.1111/j.1467-8624.2012.01857.x [cited 2019 Dec 13].
Aldao A, Nolen-Hoeksema S, Schweizer S. Emotion-regulation strategies across psychopathology: a meta-analytic review. Clin Psychol Rev. 2010;30:217–37.
Burns EE, Jackson JL, Harding HG. Child maltreatment, emotion regulation, and posttraumatic stress: the impact of emotional abuse. J Aggress Maltreatment Trauma. 2010;19(8):801–19. https://doi.org/10.1080/10926771.2010.522947.
O’Mahen HA, Karl A, Moberly N, Fedock G. The association between childhood maltreatment and emotion regulation: two different mechanisms contributing to depression? J Affect Disord. 2015;174:287–95 Available from: https://www.sciencedirect.com/science/article/pii/S0165032714007381.
Kimhy D, Gill KE, Brucato G, Vakhrusheva J, Arndt L, Gross JJ, et al. The impact of emotion awareness and regulation on social functioning in individuals at clinical high risk for psychosis. Psychol Med. 2016;46(14):2907–18.
McLaughlin KA, Aldao A, Wisco BE, Hilt LM. Rumination as a transdiagnostic factor underlying transitions between internalizing symptoms and aggressive behavior in early adolescents. J Abnorm Psychol. 2014;123:13–23.
Messman-Moore TL, Bhuptani PH. A review of the long-term impact of child maltreatment on posttraumatic stress disorder and its comorbidities: an emotion dysregulation perspective. Clin Psychol Sci Pract. 2017;24(2):154–69.
Belsky J, Steinberg L, Draper P. Childhood experience, interpersonal development, and reproductive strategy: an evolutionary theory of socialization. Child Dev. 1991;62(4):647–70 Available from: http://doi.wiley.com/10.1111/j.1467-8624.1991.tb01558.x. [cited 2016 Oct 17].
Ellis BJ, Figueredo AJ, Brumbach BH, Schlomer GL. Fundamental dimensions of environmental risk: the impact of harsh versus unpredictable environments on the evolution and development of life history strategies. Human Nature. 2009;20:204–68.
Ellis BJ, Garber J. Psychosocial antecedents of variation in girls’ pubertal timing: maternal depression, stepfather presence, and marital and family stress. Child Dev. 2000;71(2):485–501 Available from: http://www.ncbi.nlm.nih.gov/pubmed/10834479. [cited 2012 Nov 1].
Boynton-Jarrett R, Harville EW. A prospective study of childhood social hardships and age at menarche. Ann Epidemiol. 2012;22(10):731–7 Available from: NS.
Deardorff J, Abrams B, Ekwaru JP, Rehkopf DH. Socioeconomic status and age at menarche: an examination of multiple indicators in an ethnically diverse cohort. Ann Epidemiol. 2014;24(10):727–33 Available from: NS.
Mendle J, Leve LD, Van Ryzin M, Natsuaki MN, Ge X. Associations between early life stress, child maltreatment, and pubertal development among girls in foster care. J Res Adolesc. 2011;21(4):871–80 Available from: http://onlinelibrary.wiley.com/doi/10.1111/j.1532-7795.2011.00746.x/full. [cited 2013 May 7].
Negriff S, Saxbe DE, Trickett PK. Childhood maltreatment, pubertal development, HPA axis functioning, and psychosocial outcomes: an integrative biopsychosocial model. Dev Psychobiol. 2015;57(8):984–93 Available from: NS.
Price LH, Kao H-T, Burgers DE, Carpenter LL, Tyrka AR. Telomeres and early-life stress: an overview. Biol Psychiatry. 2013;73(1):15–23 Available from: http://www.ncbi.nlm.nih.gov/pubmed/22831981. [cited 2013 Aug 7].
Coimbra BM, Carvalho CM, Moretti PN, Mello MF, Belangero SI. Stress-related telomere length in children: a systematic review. J Psychiatr Res. 2017;92(PG-47-54):47–54 Available from: https://www-clinicalkey-com.laneproxy.stanford.edu/service/content/pdf/watermarked/1-s2.0-S0022395616304022.pdf?locale=en_US. [cited 2017 Jul 21].
Gassen NC, Chrousos GP, Binder EB, Zannas AS. Life stress, glucocorticoid signaling, and the aging epigenome: implications for aging-related diseases. Neurosci Biobehav Rev. 2017;74(PG-356-365):356–65.
Wolf EJ, Maniates H, Nugent N, Maihofer AX, Armstrong D, Ratanatharathorn A, et al. Traumatic stress and accelerated DNA methylation age: a meta-analysis. Psychoneuroendocrinology. 2018;92:123–34 Available from: https://doi.org/10.1016/j.psyneuen.2017.12.007. [cited 2018 mar 5].
Sumner JA, Colich NL, Uddin M, Armstrong D, McLaughlin KA. Early experiences of threat, but not deprivation, are associated with accelerated biological aging in children and adolescents. Biol Psychiatry. 2019;85(3):268–78 Available from: https://linkinghub.elsevier.com/retrieve/pii/S0006322318318511.
Negriff S, Blankson AN, Trickett PK. Pubertal timing and tempo: associations with childhood maltreatment. J Res Adolesc. 2015;25(2):201–13 Available from: NS.
Colich NL, Platt JM, Keyes KM, Sumner JA, Allen NB, KA ML. Earlier age at menarche as a transdiagnostic mechanism linking childhood trauma with multiple forms of psychopathology in adolescent girls. Psychol Med. in press.
Drury SS, Mabile E, Brett ZH, Esteves K, Jones E, Shirtcliff EA, et al. The association of telomere length with family violence and disruption. Pediatrics. 2014;134(1):e128–37 Available from: NS.
Shalev I, Moffitt TE, Sugden K, Williams B, Houts RM, Danese A, et al. Exposure to violence during childhood is associated with telomere erosion from 5 to 10 years of age: a longitudinal study. Mol Psychiatry. 2013;18(5):576–81 Available from: NS.
Jovanovic T, Vance LA, Cross D, Knight AK, Kilaru V, Michopoulos V, et al. Exposure to violence accelerates epigenetic aging in children. Sci Rep. 2017;7(1):8962. https://doi.org/10.1038/s41598-017-09235-9.
Colich NL, Rosen ML, Williams ES, McLaughlin KA. Biological aging in childhood and adolescence following experiences of threat and deprivation: a systematic review and meta-analysis. bioRxiv. 2019:1–85.
Harden KP, Mendle J. Gene-environment interplay in the association between pubertal timing and delinquency in adolescent girls. J Abnorm Psychol. 2012;121(1):73–87.
Copeland WE, Adair CE, Smetanin P, Stiff D, Briante C, Colman I, et al. Diagnostic transitions from childhood to adolescence to early adulthood. J Child Psychol Psychiatry. 2013; Available from: http://www.ncbi.nlm.nih.gov/pubmed/23451804. [cited 2013 Mar 6].
Hamilton JL, Hamlat EJ, Stange JP, Abramson LY, Alloy LB. Pubertal timing and vulnerabilities to depression in early adolescence: differential pathways to depressive symptoms by sex. J Adolesc. 2014;37(2):165–74 Available from: http://www.ncbi.nlm.nih.gov/pubmed/24439622. [cited 2014 Nov 17].
Mendle J, Leve LD, Van Ryzin M, Natsuaki MN. Linking childhood maltreatment with girls’ internalizing symptoms: early puberty as a tipping point. J Res Adolesc. 2014;24(4):689–702 Available from: NS.
Hamlat EJ, Snyder HR, Young JF, Hankin BL. Pubertal timing as a transdiagnostic risk for psychopathology in youth. Clin Psychol Sci. 2019;7(3):411–29.
Platt JM, Colich NL, McLaughlin KA, Gary D, Keyes KM. Transdiagnostic psychiatric disorder risk associated with early age of menarche: a latent modeling approach. Compr Psychiatry. 2017;79:70–9 Available from: http://linkinghub.elsevier.com/retrieve/pii/S0010440X17300706.
Ullsperger JM, Nikolas MA. A meta-analytic review of the association between pubertal timing and psychopathology in adolescence: are there sex differences in risk? Psychol Bull. 2017;143(9):903–38. https://doi.org/10.1037/bul0000106.
Ridout KK, Ridout SJ, Price LH, Sen S, Tyrka AR. Depression and telomere length: a meta-analysis. J Affect Disord. 2016;191(5):237–47 Available from: https://linkinghub.elsevier.com/retrieve/pii/S0165032715310788.
Malouff JM, Schutte NS. A meta-analysis of the relationship between anxiety and telomere length. Anxiety Stress Coping. 2017;30(3):264–72. https://doi.org/10.1080/10615806.2016.1261286.
Li X, Wang J, Zhou J, Huang P, Li J. The association between post-traumatic stress disorder and shorter telomere length: a systematic review and meta-analysis. J Affect Disord. 2017;218:322–6. https://doi.org/10.1016/j.jad.2017.03.048.
Kao H-T, Cawthon RM, DeLisi LE, Bertisch HC, Ji F, Gordon D, et al. Rapid telomere erosion in schizophrenia. Mol Psychiatry. 2008;13(2):118–9 Available from: http://www.nature.com/articles/4002105.
Polho GB, De-Paula VJ, Cardillo G, dos Santos B, Kerr DS. Leukocyte telomere length in patients with schizophrenia: a meta-analysis. Schizophr Res. 2015;165(2–3):195–200. https://doi.org/10.1016/j.schres.2015.04.025.
Jeste DV, Wolkowitz OM, Palmer BW. Divergent trajectories of physical, cognitive, and psychosocial aging in schizophrenia. Schizophr Bull. 2011;37(3):451–5.
Wade M, Fox NA, Zeanah CH, Nelson CA, Drury SS. Telomere length and psychopathology: specificity and direction of effects within the Bucharest Early Intervention Project. J am Acad Child Adolesc Psychiatry. 2019. https://doi.org/10.1016/j.jaac.2019.02.013.
Haskett ME, Kistner JA. Social interactions and peer perceptions of young physically abused children. Child Dev. 1991;62(5):979–90. https://doi.org/10.1111/j.1467-8624.1991.tb01584.x.
Rogosch FA, Cicchetti D, Aber JL. The role of child maltreatment in early deviations in cognitive and affective processing abilities and later peer relationship problems. Dev Psychopathol. 1995;7(4):591–609 Available from: http://www.cambridge.org/core/journals/development-and-psychopathology/article/role-of-child-maltreatment-in-early-deviations-in-cognitive-and-affective-processing-abilities-and-later-peer-relationship-problems/66316FC7BCA5177612A26479425A844E.
Cohen S. Social relationships and health. Am Psychol. 2004;59(8):676–84.
Cohen S, Wills TA. Stress, social support, and the buffering hypothesis: a theoretical analysis. Psychol Bull. 1985;98(2):310–57.
Herman-Stahl M, Petersen AC. The protective role of coping and social resources for depressive symptoms among young adolescents. J Youth Adolesc. 1996;25(6):733–53.
Trickey D, Siddaway AP, Meiser-Stedman R, Serpell L, Field AP. A meta-analysis of risk factors for post-traumatic stress disorder in children and adolescents. Clin Psychol Rev. 2012;32:122–38.
Alto M, Handley E, Rogosch F, Cicchetti D, Toth S. Maternal relationship quality and peer social acceptance as mediators between child maltreatment and adolescent depressive symptoms: gender differences. J Adolesc. 2018;63:19–28 Available from: http://www.sciencedirect.com/science/article/pii/S0140197117302026.
DDL C, Kleiman EM, Glenn CR, Millner AJ, Nock MK. The dynamics of social support among suicide attempters: a smartphone-based daily diary study. Behav Res Ther. 2019;120:103348 Available from: http://www.sciencedirect.com/science/article/pii/S0005796718301979.
Murberg TA, Bru E. The role of coping styles as predictors of depressive symptoms among adolescents: a prospective study. Scand J Psychol. 2005;46(4):385–93. https://doi.org/10.1111/j.1467-9450.2005.00469.x.
Prinstein MJ, Boergers J, Spirito A, Little TD, Grapentine WL. Peer functioning, family dysfunction, and psychological symptoms in a risk factor model for adolescent inpatients’ suicidal ideation severity. J Clin Child Psychol. 2000;29(3):392–405. https://doi.org/10.1207/S15374424JCCP2903_10.
Rockhill CM, Vander Stoep A, McCauley E, Katon WJ. Social competence and social support as mediators between comorbid depressive and conduct problems and functional outcomes in middle school children. J Adolesc. 2009;32(3):535–53 Available from: http://www.sciencedirect.com/science/article/pii/S0140197108000821.
Bal S, De Bourdeaudhuij I, Crombez G, Van Oost P. Predictors of trauma symptomatology in sexually abused adolescents: a 6-month follow-up study. J Interpers Violence. 2005;20(11):1390–405. https://doi.org/10.1177/0886260505278720.
Brewin CR, Andrews B, Valentine JD. Meta-analysis of risk factors for posttraumatic stress disorder in trauma-exposed adults. J Consult Clin Psychol. 2000;68(5):748–66 Available from: https://psycnet.apa.org/record/2000-02835-001.
Pine DS, Cohen JA. Trauma in children and adolescents: risk and treatment of psychiatric sequelae. Biol Psychiatry. 2002;51(7):519–31 Available from: http://www.sciencedirect.com/science/article/pii/S000632230101352X.
Gee DG, Gabard-Durnam L, Telzer EH, Humphreys KL, Goff B, Shapiro M, et al. Maternal buffering of human amygdala-prefrontal circuitry during childhood but not during adolescence. Psychol Sci. 2014; Available from: http://www.ncbi.nlm.nih.gov/pubmed/25280904. [cited 2014 Oct 9].
van Rooij SJH, Cross D, Stevens JS, Vance LA, Kim YJ, Bradley B, et al. Maternal buffering of fear-potentiated startle in children and adolescents with trauma exposure. Soc Neurosci. 2017;12(1):22–31 Available from: https://www.tandfonline.com/doi/full/10.1080/17470919.2016.1164244[cited 2019 Dec 16].
Farchione TJ, Fairholme CP, Ellard KK, Boisseau CL, Thompson-Hollands J, Carl JR, et al. Unified protocol for transdiagnostic treatment of emotional disorders: a randomized controlled trial. Behav Ther. 2012;43(3):666–78.
Weisz J, Bearman SK, Santucci LC, Jensen-Doss A. Initial test of a principle-guided approach to transdiagnostic psychotherapy with children and adolescents. J Clin Child Adolesc Psychol. 2017;46(1):44–58.
McLaughlin KA, DeCross SN, Jovanovic T, Tottenham N. Mechanisms linking childhood adversity with psychopathology: Learning as an intervention target. Behav Res Ther. 2019;118:101–9 Available from: https://doi.org/10.1016/j.brat.2019.04.008. [cited 2019 Dec 13];.
Jacobs TL, Epel ES, Lin J, Blackburn EH, Wolkowitz OM, Bridwell DA, et al. Intensive meditation training, immune cell telomerase activity, and psychological mediators. Psychoneuroendocrinology. 2011;36(5):664–81.
This research was supported by the National Institute of Mental Health (R01-MH103291; R01-MH106482; R56-119194 to McLaughlin; F32-MH114317 to Colich).
Ethics approval and consent to participate
The authors have no competing interests to declare.
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Rights and permissions
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
About this article
Cite this article
McLaughlin, K.A., Colich, N.L., Rodman, A.M. et al. Mechanisms linking childhood trauma exposure and psychopathology: a transdiagnostic model of risk and resilience. BMC Med 18, 96 (2020). https://doi.org/10.1186/s12916-020-01561-6
- Childhood trauma
- Social information processing
- Emotion regulation
- Emotional processing
- Accelerated aging
- Biological aging