A cornerstone for research into the link between stress and health has been the reactivity hypothesis; cardiovascular reactivity to psychological stressors, if prolonged or exaggerated, can promote the development of cardiovascular disease. However, it has recently been argued that low or blunted reactivity is also associated with negative health outcomes. As such, in this special issue we present further evidence implicating that cardiovascular and stress hormone responses to acute stress at the other end of the response spectrum can also be considered a pathway to ill health. In this introductory article, we explore and review the origins of and potential mechanisms underlying blunted responses to acute stress. In so doing, we aim to highlight: what is currently known regarding this new conceptualization of the reactivity hypothesis; the potential explanations for blunted reactivity; the pathways underlying associations with health outcomes; and where this field is headed in terms of developing our understanding of the link between reactivity and health.

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Anxiety confers increased risk for inflammatory diseases, and elevated inflammatory activity in anxious individuals may contribute to this increased risk. One complication, however, is that anxiety could be associated with inflammatory activity either through a specific anxiety pathway or through a more general negative emotionality pathway. To investigate, we measured levels of the stress hormone cortisol, the pro-inflammatory cytokine interleukin-6 (IL-6), and the systemic inflammatory marker C-reactive protein (CRP), as well as depression and neuroticism, in clinically anxious and non-anxious adults. Compared with non-anxious participants, clinically anxious participants exhibited significantly lower levels of morning cortisol and significantly higher levels of IL-6, independent of age, sex, and depressive symptoms. These group differences were robust when controlling for neuroticism. Conversely, the groups had equivalent levels of CRP in all analyses. Results are indicative of anxiety-specific effects on inflammatory activity, and highlight a pathway by which anxiety may increase risk for inflammatory diseases.

This study examined concordance in heart rate (HR) and respiratory sinus arrhythmia (RSA) in a sample of 104 child-maltreating (CM) and nonCM mother–preschooler dyads (208 individuals). In a laboratory setting, mother and child cardiac physiology was simultaneously monitored via ECG in a 5-min resting period. Mothers ranged in age from 20 to 49 years; children ranged in age from 3 to 5 years. Significant within-dyad (WD) and between-dyad (BD) associations were observed for mother HR and both child HR and RSA, and the associations were moderated by CM status. Only CM dyads exhibited BD associations: Higher average maternal HR was associated with higher child HR and lower child RSA. By contrast, when the time interval was divided into 30 s epochs, nonCM dyads exhibited positive WD (dynamic) associations in mother and child HR, and both CM and nonCM dyads showed negative WD associations in mother HR and child RSA. Further, mothers’ mean HR levels moderated the extent of epoch-by-epoch WD concordance observed in mother and child, such that elevated average maternal HR was associated with lower levels of WD (dynamic) concordance. No BD or WD concordance in maternal and child RSA was observed. The findings suggest that measures of intraindividual variation provide useful, alternate perspectives in the study of dyadic processes in at-risk families.

Background: Type-D personality is treated as a categorical variable and caseness has