Mounting evidence has demonstrated long-term negative physical and psychological health effects of stressors experienced in early childhood (Repetti, Taylor, & Seeman, 2002). But as health psychology researchers, what we’re interested in is why. How is it possible that something that happened in childhood could affect your health 50 or 60 years later? What are the mechanisms by which this would be possible?
Deregulation of the body’s stress response systems is thought to be one of the culprits. We have two main systems that respond to a stressor (imagine you’re about to be eaten by a lion). These systems are the hypothalamic-pituitary-adrenal axis (HPA axis for short), and the autonomic nervous system (ANS)

Both cross-sectional and experimental studies support the hypothesis that early life stress leads to a deregulated HPA stress response. Indeed, experimental studies have shown that those with early life adverse experiences show significantly different HPA responses to acute stress. For example, women who were abused as children exhibited increased pituitary-adrenal and autonomic responses to the Trier Social Stress Task (TSST; Heim et al., 2000). Luecken et al. (2009) found that participants from families characterized as negative versus positive in relationship quality exhibited significantly lower cortisol responses to acute stress. Other studies of early life stress and HPA deregulation have reported similar findings (eg. Bremner et al., 2003; Heim et al., 1998; Rao et al., 2008).

Although exposure to chronic family adversity during childhood has been linked to HPA deregulation, the evidence is weaker for deregulation of the autonomic nervous system. The majority of work on ANS responses to acute stressors has focused on cardiovascular reactivity such as changes in heart rate. For example, males from risky families had significantly higher HR at baseline, immediately following TSST, and at recovery (Taylor, Lerner, Sage, Lehman, & Seeman, 2004). Heim et al. (2000) found that women with a history of childhood abuse exhibited increased heart rate response to the TSST. Heart rate is an inadequate measure of ANS because of the numerous factors that influence it (i.e. movement, depth of breath) and it is unclear whether it is a measure of the sympathetic or parasympathetic nervous system. Only a handful of studies have used sophisticated measures of the ANS, and in these studies we see preliminary evidence of significant differences based on history of early life stress. In a longitudinal study of adolescent girls, Miskovic et al. (2009) found that maltreated girls had lower resting cardiac vagal tone (indicating weaker parasympathetic nervous system basal level) than matched controls that were not maltreated as children. Oosterman et al. (2010) demonstrated that children with a background of neglect showed more sympathetic reactivity (measured via pre-ejection period) during the Strange Situation paradigm. Further investigation is needed to understand whether there is a true difference in ANS stress response and whether the difference is primarily driven by the sympathetic or parasympathetic nervous system. Why is it important which system is deregulates, the SNS or PNS? Because nerves in those two systems link to different organs, and thus if we want to understand how deregulation of the ANS leads to disease, we need to know  which organs are potentially affected by stress.