The acute effect of a laboratory shame induction protocol on endothelial function in young, healthy adults

Abstract

The objective of this study was to examine the impact of a shame induction protocol on endothelial function. Fifteen participants (n = 7 men, n = 8 women) completed both a written shame induction protocol and a control protocol on two different experimental days. Pre-and post-protocol we assessed: (1) endothelial function and arterial shear rate via a standard brachial artery reactive hyperaemia flow-mediated dilatation (FMD) test across two post-intervention time points (15 and 35 min post); (2) perceived shame via the experiential shame scale (ESS); and (3) cortisol and soluble tumor necrosis factor alpha receptor (sTNFαRII) through oral fluid analysis. Shame increased after the shame induction protocol (pre, 2.9 ± 0.6 vs. post, 3.7 ± 0.5, P < 0.001) but not the control protocol (pre, 3.0 ± 0.5 vs. post, 2.8 ± 0.5, P = 0.15; protocol by time interaction, P < 0.001). When all three time points were included in the analysis, %FMD did not change over time. Considering only the lowest post time point, %FMD decreased significantly in response to the shame protocol (pre, 4.8 ± 1.9 vs. post, 3.2 ± 1.6, P < 0.001) but not the control protocol (pre, 4.2 ± 1.8 vs. post, 3.8 ± 1.5, P = 0.45; protocol by time interaction, P = 0.035). Covariation of the shear rate stimulus for FMD did not alter the FMD results. When including both the control and shame protocols, but not the shame protocol alone, increased shame was significantly associated with decreased FMD (r = −0.37, P < 0.046). There were no significant time by protocol interaction effects for cortisol or sTNFαRII. In conclusion, temporary increases in shame might cause transient endothelial dysfunction which, if chronically repeated, could manifest as reduced vasoprotection against atherosclerosis.

Psychosocial vascular interactions: It's a ‘shame’ we don't kNOw more

“…Stress-induced excitation of the sympathetic nervous system can trigger the release of adrenaline and noradrenaline. Higher noradrenaline levels are associated with increased vasoconstriction, which is the likely culprit for the higher mean arterial pressure (81.9 ± 5.4 mmHg at baseline and 85.1 ± 5.5 mmHg at 15 min post) observed in the shame group compared with the control group in the study by McGarity-Shipley et al (2022) is driven by the release of angiotensin II, which also increases the release of adhesion molecules from the endothelium. The interaction of elevated blood pressure and adhesion molecules results in the development of vascular disease over time (Hinterdobler et al, 2021).…”

“…protocol might have triggered an increase in β-endorphins, resulting in disruption of vasoactive components (i.e., endothelin-1 and NO) and, ultimately, reduced the FMD observed byMcGarity-Shipley et al (2022). Analysis of circulating β-endorphin and nitric oxide levels, while also investigating the impact of naloxone inhibition of β-endorphins, in individuals experiencing both shame and mirthful laughter, would be a new and beneficial approach to reveal the mechanism involved in the psychosocial vascular dysfunction phenomenon.McGarity-Shipley et al (2022) have provided insight into the effects of emotions on our peripheral vasculature and have laid out the groundwork for a multitude of investigations.…”

“…Increased sympathetic nervous activity elevates circulating catecholamines, which alter the sensitivity of α‐ and β‐adrenergic receptors that can counter NO pathways involved in endothelium‐mediated relaxation (Hinterdobler et al., 2021 ). Increased pro‐inflammatory factors, such as cortisol, C‐reactive protein and interleukins, associated with higher stress hormone levels increase the risk of vascular dysfunction and disease (Hinterdobler et al., 2021 ; McGarity‐Shipley et al., 2022 ). Chronic psychosocial stress increases the risk of developing vascular dysfunction through prolonged exposure to circulating pro‐inflammatory factors and an increase in coping mechanisms (smoking, sedentary behaviour etc.)…”

The effect of shame on endothelial function: discussing potential mechanisms and future directions

“…We agree that further exploration of mechanisms including catecholamines and endorphins is important, as well as confirming findings, exploring the impacts of different forms of stress and stress protocols, and understanding the time course of psychophysiological effects. Relevant to our study (McGarity-Shipley et al, 2022), investigating shame physiology specifically is important since shame is used in many different contexts (e.g., public health campaigns, healthcare practice, parenting and coaching). It is therefore very important that we understand how the use of shame, and its sources such as stigmatization, affect human physiology and health on small and large scales.…”

“…'Stress' is typically defined in a very general way as a systemic reaction to a challenge. However, as discussed in our original article (McGarity-Shipley et al, 2022), previous researchers have put forth the integrated specificity model suggesting that different kinds of stress influence human physiology differently. Shame, a socially specific form of stress that comes from a decreased sense of social value (e.g., after being humiliated during a public speaking event), may have different impacts on human physiology than the stress that comes from responding to a physical threat (e.g., running out of a burning building).…”