How Does Stress Increase Your Risk for Stroke and Heart Attack?
A new study in Biological Psychiatry provides a link
A new study in Biological Psychiatry provides a link
Philadelphia, PA, May 5, 2014
Scientists have shown that anger, anxiety, and depression not only affect the functioning of the heart, but also increase the risk for heart disease.
Stroke and heart attacks are the end products of progressive damage to blood vessels supplying the heart and brain, a process called atherosclerosis. Atherosclerosis progresses when there are high levels of chemicals in the body called pro-inflammatory cytokines.
It is thought that persisting stress increases the risk for atherosclerosis and cardiovascular disease by evoking negative emotions that, in turn, raise the levels of pro-inflammatory chemicals in the body.
Researchers have now investigated the underlying neural circuitry of this process, and report their findings in the current issue of Biological Psychiatry.
“Drawing upon the observation that many of the same brain areas involved in emotion are also involved in sensing and regulating levels of inflammation in the body, we hypothesized that brain activity linked to negative emotions – specifically efforts to regulate negative emotions – would relate to physical signs of risk for heart disease,” explained Dr. Peter Gianaros, Associate Professor at the University of Pittsburgh and first author on the study.
To conduct the study, Gianaros and his colleagues recruited 157 healthy adult volunteers who were asked to regulate their emotional reactions to unpleasant pictures while their brain activity was measured with functional imaging. The researchers also scanned their arteries for signs of atherosclerosis to assess heart disease risk and measured levels of inflammation in the bloodstream, a major physiological risk factor for atherosclerosis and premature death by heart disease.
They found that individuals who show greater brain activation when regulating their negative emotions also exhibit elevated blood levels of interleukin-6, one of the body’s pro-inflammatory cytokines, and increased thickness of the carotid artery wall, a marker of atherosclerosis.
The inflammation levels accounted for the link between signs of atherosclerosis and brain activity patterns seen during emotion regulation. Importantly, the findings were significant even after controlling for a number of different factors, like age, gender, smoking, and other conventional heart disease risk factors.
“These new findings agree with the popular belief that emotions are connected to heart health,” said Gianaros. “We think that the mechanistic basis for this connection may lie in the functioning of brain regions important for regulating both emotion and inflammation.”
These findings may have implications for brain-based prevention and intervention efforts to improve heart health and protect against heart disease.”
“It is remarkable to see the links develop between negative emotional states, brain circuits, inflammation, and markers of poor physical health,” said Dr. John Krystal, Editor of Biological Psychiatry. “As we identify the key mechanisms linking brain and body, we may be able to also break the cycle through which stress and depression impair physical health.”
The article is “An Inflammatory Pathway Links Atherosclerotic Cardiovascular Disease Risk to Neural Activity Evoked by the Cognitive Regulation of Emotion” by Peter J. Gianaros, Anna L. Marsland, Dora C.-H. Kuan, Brittney L. Schirda, J. Richard Jennings, Lei K. Sheu, Ahmad R. Hariri, James J. Gross, and Stephen B. Manuck (doi: 10.1016/j.biopsych.2013.10.012). The article appears in Biological Psychiatry, Volume 75, Issue 9 (May 1, 2014), published by Elsevier.
Notes for editorsFull text of the article is available to credentialed journalists upon request; contact Rhiannon Bugno at +1 214 648 0880 or Biol.Psych@utsouthwestern.edu. Journalists wishing to interview the authors may contact Peter Gianaros at +1 412 624 9578 or firstname.lastname@example.org.
The authors’ affiliations, and disclosures of financial and conflicts of interests are available in the article.
John H. Krystal, M.D., is Chairman of the Department of Psychiatry at the Yale University School of Medicine, Chief of Psychiatry at Yale-New Haven Hospital, and a research psychiatrist at the VA Connecticut Healthcare System. His disclosures of financial and conflicts of interests are available here.
About Biological PsychiatryBiological Psychiatry is the official journal of the Society of Biological Psychiatry, whose purpose is to promote excellence in scientific research and education in fields that investigate the nature, causes, mechanisms and treatments of disorders of thought, emotion, or behavior. In accord with this mission, this peer-reviewed, rapid-publication, international journal publishes both basic and clinical contributions from all disciplines and research areas relevant to the pathophysiology and treatment of major psychiatric disorders.
The journal publishes novel results of original research which represent an important new lead or significant impact on the field, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Reviews and commentaries that focus on topics of current research and interest are also encouraged.
Biological Psychiatry is one of the most selective and highly cited journals in the field of psychiatric neuroscience. It is ranked 4th out of 135 Psychiatry titles and 13th out of 251 Neurosciences titles in the Journal Citations Reports® published by Thomson Reuters. The 2012 Impact Factor score for Biological Psychiatry is 9.247.
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