Objective: The stress reactivity hypothesis (SRH) posits that stressful early environments contribute to exaggerated stress responses, which increase risk for later cardiovascular (CV) disease. However, recent studies have revealed conflicting associations. The current study examined whether the biological sensitivity to context theory (BSCT) or SRH is a more accurate description of associations between early stress and CV reactivity and recovery, and determine which framework best explains sleep outcomes. This is the first article to conceptually link these theories and empirically examine competing hypotheses. Method: Participants were 213 adults who participated in the Pittsburgh Cold Study 3. Early environment stress was assessed by four self-report measures consistent with operationalizations of the BSCT. Average heart rate and mean arterial pressure reactivity to the trier social stress test were assessed on two occasions, and sleep parameters were assessed using wrist-worn actigraphy over 7 days. Results: Results generally did not support the SRH; little evidence that high-stress early environments were reliably associated with exaggerated CV reactivity or slower CV recovery, and little evidence that these CV stress responses were consistently associated with poor sleep. However, there was some support for the BSCT; both high-stress and low-stress early environments were associated with exaggerated CV reactivity, the combination of high-stress and high CV reactivity was associated with poor sleep, and the combination of low-stress and high CV reactivity was associated with better sleep. Conclusions: Associations proposed by the BSCT persist into adulthood and may help explain associations with poor health outcomes.
Public Significance StatementThis is the first article to conceptually link the stress reactivity hypothesis (SRH) and biological sensitivity to context theory (BSCT), and empirically examine their competing hypotheses. Findings provided some of the first evidence of the associations proposed by the BSCT in an adult sample and suggest this model may help explain associations between early environment stress, cardiovascular stress responses, and disease risk which contradict the SRH.