That long-term stress is linked to cardiovascular disease is not breaking news. However, despite the well-known connection, exactly how the two are coupled has been difficult to pinpoint. Two studies published this week provide new insight.
Psychological stress carries with it a wealth of ills. In fact, excessive stress is known to contribute to a range of conditions, including hypertension (high blood pressure), ulcers, asthma, and irritable bowel syndrome.
It also has a well-documented impact on heart health. Some of this negative influence could be due to coping mechanisms – such as drinking alcohol or smoking tobacco – but there also appears to be a direct link between elevated stress levels and heart complaints.
Although this relationship is common knowledge to medical researchers and laypeople alike, the exact physiological processes behind it have remained difficult to unpick.
How can an emotion that is constructed in the brain influence the physical health of the heart?
“While the link between stress and heart disease has long been established, the mechanism mediating that risk has not been clearly understood.”
Dr. Ahmed Tawakol, lead author
Studies in animals have found that stress increases the manufacture of white blood cells in bone marrow. This, in turn, leads to an increase in inflammation. How this fits into the full picture is yet to be understood.
Researchers from Massachusetts General Hospital (MGH) and Icahn School of Medicine at Mount Sinai (ISMMS) in New York designed a double-pronged investigation to gain insight into this fascinating question.
The results, published this week in The Lancet, provide new information regarding the links between cardiac health and psychological stress.
Dr. Tawakol’s paper describes two studies that aimed to combat the same problem in a similar way. The first study, conducted at MGH, analyzed positron emission tomograph (PET) and computed tomography (CT) scans of nearly 300 individuals. The scans utilized a radiopharmaceutical called fluorodeoxyglucose (FDG), which can simultaneously measure activity in the brain and the level of inflammation in arteries.
All participants were healthy at the time of the scan and had information in their medical records of at least three additional clinical visits within the following 5 years.
The second study was carried out at the Translational and Molecular Imaging Institute at ISMMS. This smaller study involved 13 participants with a history of post-traumatic stress disorder (PTSD). The researchers assessed their current levels of perceived stress and carried out FDG-PET scans.
Dr. Tawakol and his team were able to show an association between the likelihood of a cardiac event and a specific part of the brain: the amygdala, a region known to be involved in emotional processing.
High levels of activity in the amygdala at the start of the study were associated with an increased risk of experiencing a cardiac event. Even after adjusting for other cardiovascular risk factors and atherosclerosis, the association was significant. The link became even stronger when the analysis only took into account more serious cardiac events.
They also showed that activity in the amygdala could predict the timing of the events. Higher levels of activity at baseline were associated with the occurrence of cardiac events sooner in time.
Greater activity levels in the amygdala were also associated with increased metabolism in regions of the body responsible for creating blood cells (bone marrow and spleen) and an increase in arterial inflammation.
The results from the smaller ISMMS study add weight to the MGH findings. Participants’ stress levels were, again, significantly associated with activity in the amygdala and arterial inflammation.
“This pioneering study provides more evidence of a heart-brain connection, by elucidating a link between resting metabolic activity in the amygdala, a marker of stress, and subsequent cardiovascular events independently of established cardiovascular risk factors. We also show that amygdalar activity is related to increased associated perceived stress and to an increased vascular inflammation and hematopoietic activity.”
Zahi A. Fayad, Ph.D., co-senior author
Further research will help to deepen our understanding of the so-called amygdala-bone marrow-arterial axis. In the future, medications that target this mechanism may be useful for controlling or minimizing cardiovascular disease. The findings also underscore the importance of addressing stress in order to reduce health risks.
As Dr. Tawakol says: “It would be reasonable to advise individuals with increased risk of cardiovascular disease to consider employing stress-reduction approaches if they feel subjected to a high degree of psychosocial stress.”