Stress has long been associated with increased risk of cardiovascular disease. New research suggests that a potential explanation for this correlation is due to increased activity of the amygdala, which may upregulate bone marrow activity and arterial inflammation. (Photo Credits: Flickr Creative Commons, bottled_void)
Whether it’s from upcoming exams, unpaid bills, or simply a long day at work, stress is an inevitable part of life. However, poor stress management can lead to severe health impairments, with several studies showing that chronic stress is particularly correlated with higher risk of heart disease, although scientists have been unable to provide a biological explanation for these observations until now. A new study, led by Dr. Ahmed Tawakol of Harvard Medical School, has recently identified a potential mechanism for how stress causes cardiovascular disease. The study, published in The Lancet, demonstrated that high levels of activity in the amygdala, a brain structure primarily associated with emotional processing and the stress response, is linked to increased blood cell production and inflammation of the arteries, and can be used to accurately predict the onset of cardiovascular disease years in advance (1).
The longitudinal portion of the study followed 293 healthy individuals over the age of 30 for four years. During this time, subjects underwent regular PET/CT scans to gather data on the resting metabolic rates of their amygdala, bone marrow, and spleen, as well as tests to assess severity of arterial inflammation. The bone marrow and spleen are both structures involved in generating blood cells and some cells of the immune system, in a process called haematopoiesis (2). In the following years, cardiologists, who were blinded to the participants’ initial data, evaluated their cardiovascular health based on health records and noted any significant and adverse cardiovascular events. To confirm that amygdalar activity and inflammation was correlated with perceived stress, the researchers also performed a separate, cross-sectional study tracking these markers in subjects with a known history of chronic stress (1).
Results of the longitudinal study showed that the 22 participants that eventually developed cardiovascular disease had shown significantly higher amygdalar activity 3-7 years prior, even when data was adjusted for several cardiovascular disease risk factors. Furthermore, the data showed that among these subjects, the higher the amygdalar activity levels, the earlier they developed cardiovascular disease, suggesting that amygdalar activity could provide a robust, time-associated prediction of cardiovascular disease development. Researchers also noted that there was increased bone-marrow activity and subsequent arterial inflammation following increased amygdalar activity (1).
The team concluded that the amygdala appears to be a key player in mediating stress-induced cardiovascular disease, through the upregulation of bone marrow activity and arterial inflammation, and that activity in the amygdala detected by PET scans may be a useful predictor of cardiovascular disease. However, the researchers caution that additional studies will be needed to confirm their results (1).
References:
1. Tawakol, A., Ishai, A., Takx, R. A., Figueroa, A. L., Ali, A., Kaiser, Y., … & Tang, C. Y. (2017). Relation between resting amygdalar activity and cardiovascular events: a longitudinal and cohort study. The Lancet. doi:10.1016/s0140-6736(16)31714-7
2. Ho, M. S., Medcalf, R. L., Livesey, S. A., & Traianedes, K. (2015). The dynamics of adult haematopoiesis in the bone and bone marrow environment. British journal of haematology, 170(4), 472-486.
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