This column originally appeared in Psychology Today on July 17, 2024.
Have you ever wondered how well science supports the adage “Stress kills”? Of course, a convincing answer would not fit into a Psychology Today article, because stress neuroscience has shown us that for all of us there are many possible pathways from stress to death.
But one of the more intriguing pathways from stress to early death is through the formation of blood clots. And who is better qualified to tell us about the state of the science of stress and blood clots than Roland von Känel, MD, [link to his ResearchGate website: https://www.researchgate.net/profile/Roland-Von-Kaenel ] an internist and psychiatrist, a prolific researcher, and the Director of the Department of Consultation-Liaison Psychiatry and Psychosomatic Medicine at the University of Zurich, Switzerland?
In 2007 at the annual meeting of the American Psychosomatic Society (APS)1 in Budapest, when Prof von Känel won the APS Weiner Research Scientist Award, he told us how “stress thickens the blood” summarizing the highlights of his research into this topic since 2000. Earlier this year Prof von Känel published a thorough review (13 pages, 271 references) on “Stress-induced Hypercoagulability” [link to: https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1787660 ], and here are a few pearls from that paper.
The first pearl von Känel helps us appreciate is the sheer number of measurable factors that contribute to the miracle of maintaining our blood at the optimal thickness for its many functions, including nourishing our cells, waste removal, and wound healing. Every chef appreciates the delicate task of finding the right mix of thickness for any soup or souffle. Our bodies master this task for our blood day in and day out, thin enough to flow freely, thick enough to clot when needed. Table 1 of the paper lists 36 measures in six categories that contribute either to the formation of clots or the lysing of clots. This delicate balance between clot formation and clot dissolution is constantly at work, and, as stress increases, this balance shifts toward clot formation at the site of injury.
How does our stress response system adjust this balance? One mechanism is through stress hormones, such as epinephrine and cortisol, that raise the release of proteins facilitating coagulation. Or stress hormones may decrease the release of proteins that guide the lysing of clots. Stress hormones also increase the release and the stickiness of platelets, which form the fiber of the clot. Inflammation accelerates this process.
Von Känel’s review emphasizes that, in general, healthy people maintain the optimal blood thickness and readiness to clot, in response to and in spite of the stresses of daily life. But people at risk for heart disease are more likely to have serious trouble with excessive clotting. He cites 31 observational studies that show that stress raises the risk for the development of atherosclerotic heart disease, and another 11 studies show that stress adds to the poor prognosis for clotting risks in people who already have heart disease.
Heart attacks, strokes, muscle cramping with exercise (“claudication”), pulmonary emboli, and deep vein thrombosis are the big clotting events that come more often with either acute or chronic stress in people with heart disease. Behaviors that contribute to the risk for these events include physical inactivity, sleep disorders, overeating and obesity, smoking, alcohol—all of which drive excessive sympathetic activity in the autonomic nervous system and higher levels of stress hormones. Chronic stress thickens the blood, and then acute stress is more likely to crystallize a clot.
If this sounds like a slam-dunk argument for aggressive stress management regimens in people with risks for heart disease, Prof von Känel cautions that one crucial piece of the puzzle is still missing. This too is a pearl. The field lacks the necessary number of clinical trials in which stress interventions reduce measures of hypercoagulability and then also reduce the frequency of clotting problems, such as heart attacks and strokes. That is, we don’t yet know what kinds of stress interventions, at what intensity and for how long, are required to confidently protect the most vulnerable people from stress-induced clotting events.
Prof von Känel’s review of progress in the 25-year journey to explore the role of stress in the blood clotting process, much of which he has led, gives us another mile marker for the growth of stress neuroscience. The elusive holy grail for many fields in stress neuroscience is now the task of finding stress interventions that deliver powerful effects on the course of common stress-related illnesses, such as heart disease, diabetes, and obesity. This task will require large, long, and expensive clinical trials to give us the final piece we need to put a dent in the current wave of stress-related disorders.
1 The American Psychosomatic Society has changed its name this year to the Society for Biopsychosocial Science and Medicine.