The experience of negative emotions is associated with an increased risk of incident atherosclerosis-related cardiovascular disease (CVD) events, independent of traditional risk factors. The strongest data supporting this relation is with provoked anger. There is also some evidence that becoming acutely depressed or anxious are also triggers of incident CVD. The underlying putative mechanisms are poorly understood. Vascular endothelial cells (ECs) play an essential role in maintaining vascular tone and the integrity of blood vessels. Evidence suggests that dysfunction of the endothelium is an early pathogenic process underlying atherosclerosis development and CVD event onset.
The aims of this study are to primarily examine the acute effects of provoked anger and secondarily depressed mood and anxiety on EC health. Examination of these critical pathways will help determine whether endothelial dysfunction is a biological mechanism linking the experience of core negative emotions and incident CVD risk. In this application, a state-of-the-art, laboratory-based, randomized controlled experiment is proposed that will test whether provoked anger, depressed mood and anxiety will induce endothelial dysfunction in humans. We hypothesize that compared to an emotionally neutral condition;an anger recall task will impair endothelium-dependent vasodilatation, injure ECs, and reduce EC reparative capacity. We will also examine whether a depressed mood and anxiety induction task will similarly induce endothelial dysfunction, as well as whether levels of provoked self-reported anger, depressed mood, and anxiety are associated with the degree of endothelial dysfunction. Finally, given that endogenous nitric oxide (NO) inhibition plays a central role in exacerbating endothelial dysfunction, we will explore whether NO inhibition partially mediates the acute adverse effects of provoked anger, depressed mood, and anxiety on endothelial function. In the United States, atherosclerosis-related CVD events remain the leading cause of morbidity and mortality. Further, anger, depressed mood, and anxiety are negative emotions commonly experienced by adults in the general population on a day-to-day basis. Therefore, evaluation of these hypotheses is timely and highly significant, as it will help identify a putative biological pathway linking the experience of core negative emotions to CVD incidence, for a large number of individuals who are at increased risk for CVD events.

Public Health Relevance

Although the experience of negative emotions acutely increases cardiovascular disease (CVD) risk, the reasons for this relation are not known. This study will help determine why anger and secondarily depressed mood and anxiety increase the risk of cardiovascular disease, and may suggest ways to develop more effective strategies to reduce the CVD risk associated with negative emotions.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
3R01HL116470-02S1
Application #
8843603
Study Section
Biobehavioral Mechanisms of Emotion, Stress and Health Study Section (MESH)
Program Officer
Stoney, Catherine
Project Start
2013-02-01
Project End
2018-01-31
Budget Start
2014-06-01
Budget End
2015-01-31
Support Year
2
Fiscal Year
2014
Total Cost
$128,056
Indirect Cost
$48,021
Name
Columbia University
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
621889815
City
New York
State
NY
Country
United States
Zip Code
10032
Yoon, Sunmoo; Schwartz, Joseph E; Burg, Matthew M et al. (2018) Using Behavioral Analytics to Increase Exercise: A Randomized N-of-1 Study. Am J Prev Med 54:559-567
Ensari, Ipek; Burg, Matthew M; Diaz, Keith M et al. (2018) Putative mechanisms Underlying Myocardial infarction onset and Emotions (PUME): a randomised controlled study protocol. BMJ Open 8:e020525
Diaz, Keith M; Krupka, David J; Chang, Melinda J et al. (2018) Wrist-based cut-points for moderate- and vigorous-intensity physical activity for the Actical accelerometer in adults. J Sports Sci 36:206-212
Diaz, Keith M; Booth 3rd, John N; Seals, Samantha R et al. (2017) Physical Activity and Incident Hypertension in African Americans: The Jackson Heart Study. Hypertension 69:421-427
Diaz, Keith M; Goldsmith, Jeff; Greenlee, Heather et al. (2017) Prolonged, Uninterrupted Sedentary Behavior and Glycemic Biomarkers Among US Hispanic/Latino Adults: The HCHS/SOL (Hispanic Community Health Study/Study of Latinos). Circulation 136:1362-1373
Booth 3rd, John N; Abdalla, Marwah; Tanner, Rikki M et al. (2017) Cardiovascular Health and Incident Hypertension in Blacks: JHS (The Jackson Heart Study). Hypertension 70:285-292
Redmond, Nicole; Booth 3rd, John N; Tanner, Rikki M et al. (2016) Prevalence of Masked Hypertension and Its Association With Subclinical Cardiovascular Disease in African Americans: Results From the Jackson Heart Study. J Am Heart Assoc 5:e002284
Booth 3rd, John N; Muntner, Paul; Diaz, Keith M et al. (2016) Evaluation of Criteria to Detect Masked Hypertension. J Clin Hypertens (Greenwich) 18:1086-1094
Diaz, Keith M; Booth 3rd, John N; Seals, Samantha R et al. (2016) Sedentary behavior and subclinical atherosclerosis in African Americans: cross-sectional analysis of the Jackson heart study. Int J Behav Nutr Phys Act 13:31
Spicer, Julie; Shimbo, Daichi; Johnston, Natalie et al. (2016) Prevention of Stress-Provoked Endothelial Injury by Values Affirmation: a Proof of Principle Study. Ann Behav Med 50:471-9

Showing the most recent 10 out of 18 publications