High cardiovascular reactions to psychological stress are associated with the development of hypertension, systemic atherosclerosis, and cardiovascular disease. However, it has become apparent that low biological stress reactivity also may have serious consequences for health, although less is known about the mechanisms of this. The objectives of this narrative review and opinion article are to summarize and consider where we are now in terms of the usefulness of the reactivity hypothesis and reactivity research, given that both ends of the reactivity spectrum seem to be associated with poor health, and to address some of the key criticisms and future challenges for the research area.
This review is authored by the members of a panel discussion held at the American Psychosomatic Society meeting in 2019, which included questions such as the following: How do we measure high and low reactivity? Can high reactivity ever indicate better health? Does low or blunted reactivity simply reflect less effort on task challenges? Where does low reactivity originate from, and what is a low reactor?
Cardiovascular (and cortisol) stress reactivity are used as a model to demonstrate an increased understanding of the different individual pathways from stress responses to health/disease and show the challenges of how to understand and best use the reconstruction of the long-standing reactivity hypothesis given recent data.
This discussion elucidates the gaps in knowledge and key research issues that still remain to be addressed in this field, and that systematic reviews and meta-analyses continue to be required.