Childhood trauma exposure and autonomic nervous system changes among children in a South African birth cohort

The developmental origins of disease hypothesis posits that early life stress, such as childhood trauma and adversities, can permanently affect health in later life (Gluckman et al., 2005). Consistent with this hypothesis, childhood trauma exposure has been robustly associated with both mental and physical health problems throughout the lifespan (Hogg et al., 2022; Suglia et al., 2015). It has been theorised that neurobiological changes in the body’s stress response systems, including in the autonomic nervous system (ANS), drive these long-term adverse effects of childhood trauma (Agorastos et al., 2018; Beilharz et al., 2020). A key area of growing concern is the robust association between childhood trauma and an increased risk of cardiovascular diseases (CVDs; Jacquet-Smailovic et al., 2022; Suglia et al., 2015), which are among the leading causes of death worldwide (WHO, 2019). However, robust evidence investigating early markers of cardiovascular function is limited. Given that research has consistently found that elevated heart rate (HR) measured in the aftermath of a traumatic event is associated with subsequently reporting more post-traumatic stress symptoms (Morris et al., 2016), and that both childhood trauma and elevated resting HR are associated with increased risk of CVDs (Aune et al., 2017), it is theorised that childhood trauma is associated with a persistently elevated HR. However, research has yielded mixed findings across both adult and youth samples, with trauma linked to both elevated (Beilharz et al., 2020; Pretty et al., 2013) and reduced resting HR (Bailey et al., 2025; Krenichyn et al., 2001) in some studies, and no effects in others (MacMillan et al., 2009; Sigrist et al., 2021). It has been theorised that trauma exposure, particularly cumulative or prolonged traumas, during critical developmental periods could result in chronic hyperactivation or hypoactivation of the stress response system, dependent on trauma timing (e.g., early childhood vs. adolescence; Agorastos et al., 2018) or the type and extent of trauma exposure (Herzog et al., 2018), which could offer some explanation for this mixed pattern of findings. However, there are several key limitations of the existing evidence which may have also contributed to these findings. Firstly, most research has been conducted with relatively small sample sizes and has been conducted primarily in high-income countries. Youth in low- and middle-income countries (LMICs) are especially underrepresented despite the majority of the world’s children living in LMICs (UNICEF, 2005), and these youth being disproportionately more likely to be exposed to traumas than youth in high-income countries (WHO, 2002). More than 75% of children in South Africa were estimated to have been exposed to at least one traumatic event before age 6 years (Tsunga et al., 2023); estimates from high-income country cohorts demonstrate substantially lower rates of trauma exposure even when participants are older (Lewis et al., 2019). Secondly, most studies have used cross-sectional designs. For studies with adults, childhood trauma exposure is therefore reported retrospectively which may introduce significant recall bias. Additionally, cross-sectional studies recruit participants following trauma exposure; therefore the ability to draw causal conclusions regarding trauma-HR associations is limited. Furthermore, because participants have been recruited following trauma exposure, most individuals have been exposed to single-incident traumas, such as road traffic accidents and other accidental injuries. Research has shown that interpersonal childhood traumas, especially those occurring within the family, such as physical, sexual, and domestic violence, are the strongest predictors of psychopathology (Green et al., 2010; McLaughlin et al., 2010). The underrepresentation of these more severe or chronic/repeated traumas in the existing literature may therefore offer some explanation for the mixed findings across studies. Finally, a limitation of all the aforementioned studies is that HR was measured at a single timepoint. HR is not static and decreases naturally with age (Sarganas et al., 2017). Research should therefore utilise repeated measurements of HR to investigate whether childhood trauma exposure is associated with changes in HR development (e.g., slowing of the normal pattern of decline with advancing age). Heart rate variability (HRV), the variation in time intervals between heartbeats, has also been of particular interest in the traumatic stress literature, as it is viewed as a more sensitive measure of ANS function (Appelhans & Luecken, 2006), through indices that capture sympathetic and parasympathetic activity (Nagpal et al., 2013). Lower HRV is thought to reflect impaired functioning/regulation of the ANS, which negatively affects the body’s ability to cope with stressors (Sigrist et al., 2021), and research has shown lower HRV to be associated with an increased risk of cardiovascular events (Hillebrand et al., 2013). Research with adults has shown associations between childhood trauma and reduced resting HRV (Bussone et al., 2023; Jin et al., 2018), though research with youth samples has not observed such effects (MacArthur, 2011; Michels et al., 2013), suggesting that the impact of childhood trauma on HRV may not be evident until later life. Finally, childhood trauma exposures have been associated with blunted ANS reactivity to stressors (Busso et al., 2017; Voellmin et al., 2015). However, again, this evidence is limited by small sample sizes, the use of cross-sectional designs, and an underrepresentation of LMIC samples. To address these limitations of the existing literature, the present study will use data from the Drakenstein Child Health Study (Donald et al., 2018; Stein et al., 2015; Zar et al., 2015), an ongoing prospective birth cohort located in Cape Town, South Africa, to conduct a longitudinal investigation of the impact of childhood trauma on ANS functioning in children living in a LMIC. Research Questions & Aims: 1. Does childhood trauma exposure predict the average levels and rate of change of resting HR during childhood? We aim to estimate change in resting HR between ages 4 and 8 years using growth curve modelling, and to examine trauma exposure up to age 4.5 years as a time-invariant predictor of the resultant growth factors. 2. Is childhood trauma exposure associated with resting HRV during childhood? We aim to use linear regression analyses to examine cross-sectional and longitudinal associations between childhood trauma exposure (assessed at ages 4.5 and 8 years) and indices of resting HRV at age 8. 3. Is childhood trauma exposure associated with altered autonomic reactivity to stress? We aim to use linear regression analyses to examine cross-sectional and longitudinal associations between childhood trauma exposure (assessed at ages 4.5 and 8 years) and HR and HRV reactivity in response to stress at age 8 years (captured via residualized change scores).