Differential associations between childhood trauma subtypes and adolescent HPA-axis functioning
Introduction
Approximately 10% of children in the United States are maltreated (Finkelhor et al., 2009) and 66% report a major traumatic event before adulthood (Read et al., 2011). Exposure to trauma during childhood increases the risk for lifelong physical and mental health problems (Chapman et al., 2007, Dube et al., 2003). The hypothalamic–pituitary–adrenal-axis (HPA-axis) modulates multiple biological, affective, behavioral and cognitive responses to stress (Lupien et al., 2009), thus dysregulation of the HPA-axis may be one mechanism through which stress impacts health. Animals (Pryce et al., 2002) and humans (Gunnar and Quevedo, 2007) exposed to early life stress exhibit anomalies in HPA-axis functioning, although this research in youth has been equivocal. For example, trauma exposure has been linked to both diurnal HPA-axis hyper- and hypo-activity (Lupien et al., 2009, McEwen, 1998), as well as hyper- and hypo- reactivity to stress (MacMillan et al., 2009, Peckins et al., 2012, Saltzman et al., 2005, Trickett et al., 2014). The inconsistencies may be accounted for by different subtypes of childhood trauma contributing to different HPA-axis anomalies.
Traumatic events rarely occur in isolation (Finkelhor et al., 2007), yet the majority of published studies have either isolated one subtype of trauma exposure, such as parental loss (Kaplow et al., 2013) and marital violence (Saltzman et al., 2005), or collapsed subtypes of childhood trauma into a single category (e.g., adversity; Gustafsson et al., 2010). Both approaches limit our understanding of how different types of stress influence the HPA-axis. Neglect, physical abuse, and natural disaster may demand different physiological responses to promote learning and survival (Miller et al., 2007). Repeated exposure to any one of these categories could result in divergent processes (e.g., inhibiting emotional responses vs. responding quickly to a physical threat), reflecting different patterns of HPA-axis activation over time, and whose output may influence the long-term regulation of the system. Therefore, previous inconsistencies linking childhood trauma to the HPA-axis may reflect the heterogeneity of effects by different types of trauma.
The HPA-axis indices most commonly examined among youth include cortisol awakening response (CAR), diurnal regulation, and stress reactivity. These indices represent underlying neuroendocrine processes that may have different biopsychosocial meaning (Tsigos and Chrousos, 2002), but our understanding of how different types of trauma impact these indices is limited. CAR refers to a surge in cortisol following awakening and is used increasingly as a stress biomarker as it may reflect chronic, daily stress and affected physiological systems (Fries et al., 2009). In adults, greater CAR is most consistently associated with recent stress (Chida and Steptoe, 2009). Yet, surprisingly few studies have examined the relationship between childhood trauma and CAR. One study found that 1–2 adverse childhood events predicted greater CAR compared with none (Gustafsson et al., 2010), suggesting that any exposure may sensitize CAR. However, associations between number of adversities and CAR are not consistently observed (Michels et al., 2012), while singular experiences such as death of a caregiver have been linked to decreased CAR (Meinlschmidt and Heim, 2005). Thus, the previous inconsistencies may be explained by the type of childhood adversity examined which may be more critical to our understanding of the impact of stress on CAR than number of adversities.
More studies have examined the association between childhood trauma and diurnal regulation, but results have also been mixed. Cortisol follows a circadian pattern, with highest concentrations in the morning and lowest at night. Decline in cortisol throughout the day is a marker of the physiological capacity to maintain homeostasis (Tsigos and Chrousos, 2002), and deviation from this pattern is a predictor of risk for poor health (e.g., Sephton et al., 2000, Sjögren et al., 2006). Childhood maltreatment, inclusive of physical, sexual, and emotional abuse has been linked to high cortisol during the day (Cicchetti and Rogosch, 2001), specifically in the afternoon (Bevans et al., 2008, Hart et al., 1996). Similarly, children in foster care do not exhibit a decline in cortisol across the day (Linares et al., 2008), while some groups of maltreated youth do not exhibit anomalies in diurnal cortisol regulation at all (MacMillan et al., 2009, Ouellet-Morin et al., 2011). These conflicting findings may suggest that comparing maltreated and non-maltreated youth, or using a variable that collapses across multiple types of abuse and neglect does not inform our understanding of HPA-axis function or development. Thus, the simultaneous examination of trauma subtypes within the same sample may help us clarify how different types of maltreatment are associated with diurnal cortisol regulation.
Similar inconsistencies emerge among investigations of acute HPA-axis responses to stress. For example, greater cortisol reactivity to laboratory stress has been shown in school-aged youth exposed to any traumatic events (Ivanov et al., 2011), marital violence (Saltzman et al., 2005), and victims or witnesses of violence in the past year (Peckins et al., 2012). This is not surprising given the abundance of animal research suggesting sensitization of the axis in response to aversive events (Pryce et al., 2002) and that the presence of physical threat is a robust activator of the HPA-axis (Miller et al., 2007). Compared with emotional abuse and accidental trauma, physical abuse may be more likely to sensitize the axis to stressors. However, youth exposed to maltreatment, such as chronic abuse and neglect, demonstrate blunted reactivity to laboratory stress (MacMillan et al., 2009, Trickett et al., 2014). Therefore frequent exposure to adversity during childhood may accumulate to dampen the axis, although which types of stress drive this phenomenon are currently unknown. Here, we aimed to identify the contribution of physical abuse, emotional abuse, and non-intentional trauma to multiple indices of neuroendocrine functioning (CAR, diurnal regulation, acute reactivity) hypothesizing that each trauma subtype would be associated with distinct anomalies in neuroendocrine functioning such that physical abuse exposure may sensitize the HPA-axis to acute stress, while emotional abuse and neglect may be associated with impaired diurnal regulation of glucocorticoids.
Section snippets
Participants
Participants were 121 youth (51% male), ages 9–16 (Mage = 12.8; SDage = 2.3) from a study aimed to characterize the mechanisms that underlie adolescent anxiety and depression. Participants were recruited from communities in and around Southeast Michigan via flyers, referrals from clinicians and primary care providers, and advertisements on websites targeting parents of adolescents who have concerns about their child's mental health. Participants in this study were 70% Caucasian, 10% biracial, 6%
Childhood trauma exposure and adolescent HPA-axis functioning
Per parent report, 85% of youth in our sample were exposed to at least one traumatic event where 71% reported at least one non-intentional trauma, 48% reported at least one incident of physical abuse, 31% reported at least one emotional abuse experience, and 6% of our sample reported at least one sexual abuse experience. Among the participants exposed to non-intentional trauma, the most frequently endorsed non-intentional traumatic events were: serious personal injury or illness (25%), family
Discussion
In this study, we characterized the association between different types of childhood trauma exposure and HPA-axis functioning. More non-intentional trauma exposure was associated with greater CAR, however not when controlling for exposure to physical and emotional abuse. Youth with reported exposure to more non-intentional trauma throughout their childhood demonstrated a steeper decline in cortisol from morning to evening, and higher cortisol at bedtime compared to youth with less exposure to
Role of the funding source
The sponsors of this research had no involvement in study design, data collection, analysis or interpretation of data, composition of this manuscript, or the decision to submit the article for publication.
Conflict of interest statement
The authors have no conflict of interest to declare.
Acknowledgements
This research was funded by the Blue Cross Blue Shield of Michigan Foundation, Barabara A. Oleshansky Memorial Award, American Psychological Foundation Elizabeth Munsterberg-Koppitz Award, and The University of Michigan Rackham Graduate School. We also thank the faculty and fellows of the International Max Planck Research School “The Life Course: Evolutionary and Ontogenetic Dynamics” for valuable feedback on this work.
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