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The link between stress and disease has been of paramount interest to researchers and clinicians for decades. Hans Selye was among the first to recognize the effect of stress on disease relevant processes [1], and in tandem, Paul MacLean noted the associations among emotion, the brain, and health [2]. To date, some of the strongest associations have been established between stress and cardiovascular disease (e.g., Dimsdale [3]). For example, psychological stress can provoke acute cardiac events [4] and induce transient myocardial ischemia [5], and a number of epidemiological studies have linked anger, hostility, and chronic perceived stress to cardiovascular disease mortality (e.g., Haynes, Feinleib, and Kannel [6]; Rosengren et al. [7]). Critical to cardiovascular disease is the health of vascular endothelial cells, which play an essential role in maintaining vascular tone and the integrity of blood vessels. Endothelial injury causes endothelial cells to lose integrity, progress to senescence and detach into the circulation [8, 9]. Endothelial cell-derived microparticles (EMPs) are phospholipid rich, submicron particles derived and released from the membranes of activated or apoptotic endothelial cells [8, 10], and they can serve as markers of endothelial cell injury in humans. EMPs modulate inflammation via leukocyte activation and transendothelial migration and have procoagulant activity [11]. Thus, EMPs may have a direct role in atherosclerosis-related cardiovascular disease onset. EMPsmay also contribute to other vascular disorders, including stroke [12] and preeclampsia [13]. Although many studies have investigated stress effects on health-related physiology (e.g., cortisol [14], immune [15], and autonomic [16] responses), few studies have testedwhether psychological treatments can influence cellular processes directly relevant for disease. EMPs are a particularly important target in that regard; stress-induced EMP activity represents one plausible mechanism underlying the association between psychological stress and cardiovascular disease. In support of this hypothesis, experimentally provoked anger has previously been shown to elevate circulating EMPs [17], suggesting that psychological stress can cause endothelial cell injury. If psychological stressors can impact cellular processes relevant for cardiovascular disease risk, then psychological processes may be able to prevent them, and demonstrating such effects could lead to enhanced understanding and clinical deployment of psychological interventions. However, no prior research has investigated whether endothelial cell injury can be mitigated by a psychological inoculation. Among such procedures, values affirmation has emerged as a practice that is both effective at reducing stress—including cortisol reactivity [18], catecholamine secretion [19], and performance improvement [20–23]—and deployable on a large scale in diverse populations [20, 21, 23]. Here, we present a proof of principle study that tested whether social evaluative threat (SET) and values affirmation would have opposing effects on markers of endothelial cell injury. We recruited healthy participants who were randomized to one of three conditions: SETAlone, SET preceded by a buffering values affirmation task (SET+Values Affirmation), or a non-stressful Control task. Blood was sampled Julie Spicer Ph.D. and Daichi Shimbo M.D. contributed equally to this work.

Prevention of Stress-Provoked Endothelial Injury by Values Affirmation: a Proof of Principle Study