By Kenzie MacDonald,


According to Dr. Hans Selye, the ‘Father’ of stress research, stress is a nonspecific reaction of the body to any demand upon it1. Stress can be a positive or beneficial response that facilitates adaptation and stimulates development2. Positive stress is often perceived to be within our coping abilities, short-lived, stimulates motivation and focus, and improves performance3. For example, planning for a trip, receiving a promotion, or taking an examination elicits a positive stress response. However, when the capacity to adapt to a given stressor or combination of stressors is exceeded, stress can be overwhelming and negative2.

The stress-response involves activation of various physiological systems, such as the hypothalamo-pituitary-adrenal (HPA) axis, the autonomic nervous system, and the cardiovascular, metabolic, and immune systems4. Continuous build-up of stressors and repetitive activation of the stress-response, also known as allostatic load, can result in the development of anxiety, depression, or other psychological conditions2. As the ‘predisposition-stress’ model describes, depending on an individual’s genetic, biological, and psychological context, experiences of stress can contribute to the pathogenesis of chronic psychological states such as depression2. Despite the fact that these chronic psychological states can be extremely emotionally, psychologically, and physically debilitating, they also exhibit a striking association with the development of cardiovascular disease (CVD)4.

The INTERHEART study, which investigated risk factors for acute myocardial infarction (AMI) in over 25,000 patients, found that psychological factors (i.e. anxiety, depression, etc.) are stronger risk factors for AMI than traditional risk factors such as diabetes, smoking, hypertension, or obesity5. This study investigated a group of psychosocial parameters, including depression, locus of control, perceived stress, and life events5. It has been suggested that depression is correlated to a 1.5-fold increase in an individual’s risk of CVD and that patients with existing CVD and depression have a 2- to 3-fold increased risk of suffering from a nonfatal or fatal cardiac event6. It was based on the findings of these and other studies that the 2010 Global Burden of Disease Study officially recognized depression as a risk factor for CVD6. Depression has also been correlated to an increased risk of recurrent total stroke, fatal stroke, and ischemic stroke7.

The association between CVD and psychological conditions has been acknowledged since the late 1930’s8. In 1937, Malzberg investigated the mortality rates in patients with ‘involutional melancholia’ or depression with onset in middle-age and determined that their age-adjusted mortality rate was 6 times greater that of controls8. For some time this relationship has been understood to reflect the association between psychological conditions and poor health behavior, maladaptive coping style, social isolation, and chronic stress.9 These factors may be considered confounding variables, as they often present concurrently with many psychological conditions and contribute to an increase in classic coronary risk factors.9 Although many psychological conditions are associated with non-adherence to cardiac prevention and treatment, there are numerous other manners in which these conditions theoretically contribute to the development of CVD [7-8]. Some of the biological factors that are thought to mediate the relationship between depression and CVD incidence and severity are: excess activation of the hypothalamo-pituitary-adrenal axis and sympathetic nervous system, greater catecholamine release, abnormal platelet activation, lower heart rate variability, toxicity from antidepressants, and inflammatory processes [7,10]. Mechanistically it is understood that increased activation of the sympathetic nervous system and release of catecholamines may result in damage to the vascular endothelium and excess release of fatty acids.10

The World Health Organization has forecasted that depression will be the second leading causes of disability worldwide by 202011. Further, the Anxiety and Depression Association of America estimates that approximately 6.7% of adults experience depression in a given year12. Given the prevalence of psychological conditions such as depression and the striking association between these conditions and the development of CVD, greater emphasis on psychological health is vital to the primary prevention and treatment of CVD. One of the most effective strategies to manage stress, anxiety, or depression is exercise.13 Exercise improves self-esteem, mood, energy, and cognitive function, alleviates social withdrawal, and provides stress relief.13 As an extremely effective intervention in mental health care, the importance of exercise to cardiovascular health is undeniable.

Also, of the utmost importance, speak to a professional, family members or anyone you feel comfortable with. The struggles of mental illness are not easy to cope with, especially on your own. Visit the Canadian Mental Health Association Website for more information.


  1. Goldstein, D. S., & Kopin, I. J. (2007). Evolution of concepts of stress. The International Journal on the Biology of Stress, 10(2), 109-120. doi:10.1080/10253890701288935.
  2. Orzechowska, A., Zajączkowska, M., Talarowska, M., & Gałecki, P. (2013). Depression and ways of coping with stress: A preliminary study. Medical Science Monitor: International Medical Journal of Experimental and Clinical Research, 19, 1050-1056.
  3. Mills, H., Reiss, N., & Dombeck, M. (2008). Types of stressors (eustress vs. distress). Retrieved from
  4. Brotman, D. J., Golden, S. H., & Wittstein, I. S. (2007). The cardiovascular toll of stress. Lancet, 370(9592), 1089-1100. doi:10.1016/S0140-6736(07)61305-1.
  5. Yusuf, S., Hawken, S., Ôunpuu, S., Dans, T., Avezum, A., Lanas, F., . . . Lisheng, Liu. (2004). Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study. Lancet, 364(9438), 937-952. doi:10.1016/S0140-6736(04)17018-9.
  6. Baune, B. T., Stuart, M., Gilmour, A., Wersching, H., Arolt, V., & Berger, K. (2012). Moderators of the relationship between depression and cardiovascular disorders: A systematic review.General Hospital Psychiatry, 34(5), 478. doi:10.1016/j.genhosppsych.2012.05.013.
  7. Elderon, L., & Whooley, M. A. (2013). Depression and cardiovascular disease. Progress in Cardiovascular Diseases, 55(6), 511-523. doi:10.1016/j.pcad.2013.03.010.
  8. McConnell, S., Jacka, F. N., Williams, L. J., Dodd, S., & Berk, M. (2005). The relationship between depression and cardiovascular disease. International Journal of Psychiatry in Clinical Practice, 9(3), 157-167. doi:10.1080/13651500510029138.
  9. Barth, J., Schumacher, M., & Herrmann-Lingen, C. (2004). Depression as a risk factor for mortality in patients with coronary heart disease: A meta-analysis. Psychosomatic Medicine, 66(6), 802-813. doi:10.1097/01.psy.0000146332.53619.b2.
  10. Thurston, R. C., Rewak, M., & Kubzansky, L. D. (2013). An anxious heart: Anxiety and the onset of cardiovascular diseases. Progress in Cardiovascular Diseases, 55(6), 524-537. doi:10.1016/j.pcad.2013.03.007.
  11. Murray, C. J. L., Lopez, A. D., World Bank, World Health Organization, & Harvard School of Public Health. (1996). The global burden of disease: A comprehensive assessment of mortality and disability from diseases, injuries, and risk factors in 1990 and projected to 2020. Cambridge, Mass.: Harvard School of Public Health on behalf of the World Health Organization and the World Bank.
  12. Anxiety and Depression Association of America. (2016). Facts and statistics. Retrieved from
  13. Sharma, A., Madaan, V., & Petty, F. D. (2006). Exercise for mental health. Primary Care Companion to the Journal of Clinical Psychiatry, 8(2), 106.