Stress: The Silent Killer. Chronic Stress and CVD

“Not everything that matters can be measured, and not everything that is measured matters.” – Elliot Eisner

Cardiovascular diseases (CVDs) are the number one cause of death globally. In 2008, more than 17 million people died from them. On a national level, based on the 2004-2005 National Health Survey, 3.7 million Australians are estimated to have existing cardiovascular problems; CVDs were the direct cause of 35% of total mortality in 2005, again the number one cause of death ^1,2. This is despite the billions of dollars spent on medications to reduce the risk and intensity of cardiovascular diseases ³. CVD is no longer considered a disorder of lipid (fat) accumulation, but rather a disease process characterized by low-grade inflammation of the vascular (artery) lining and an inappropriate wound healing of the blood vessels. The answer is to treat the cause of inflammation not cholesterol.

A study in 2004 known as the INTERHEART study found that 90% of all myocardial infarctions (heart attacks) could be attributed to nine potentially modifiable risk factors ^4,5. These factors include tobacco use, atherosclerosis, hypertension, diabetes, abdominal obesity, psychosocial factors, alcohol consumption, physical inactivity and poor diets ^4,6.

Despite convincing evidence linking psychosocial factors such as chronic and acute stress to the risks of cardiovascular disease ^7,8,9, there remains a lack of focus on stress reduction for the prevention and treatment of cardiovascular disease. Risk reduction for stress is low-cost, simple to administer, and “non-pharmaceutical” ¹⁰.

Stress is the failure of an individual to cope with an emotional or physical threat. It results in both psychological and physical effects on individuals by means of two main stress groups: acute stress and chronic stress. Chronic stress occurs from exposure to stressors such as family, society (traffic, population, etc.) and, almost all the time, the workplace. When the body is stressed, a large number of biological and chemical processes can occur that put the body at increased risk of CVD. Chemical mediators are released, which cause the prolonged activation of the sympathetic nervous system ⁷ and increase heart rate and blood pressure, which puts a lot of strain on the heart and cardiovascular system ¹¹. Over time, the strain on the system leads to deterioration of the heart muscle, arteries and vessels ¹¹. Chemical mediators can also result in sleep deprivation, elevated cortisol levels, elevated insulin and blood glucose levels and increases in ghrelin, the hormone that increases appetite ¹¹.

Chronic stress, which is what we are often confronted with in our daily busy lives, plays a huge role in these increases, as it can cause the prolonged activation of the sympathetic nervous system ⁷. This results in an increase in blood pressure and heart rate, which remain elevated, leading to an increased risk of cardiovascular disease. In extreme circumstances this is also linked with endothelial dysfunction (inability of arteries to dilate) and possible necrosis of artery walls ⁷.

Stress increases the release of hormones like cortisol, adrenaline and noradrenaline, which act to increase the heart rate and contractile volume, as well as constricting arteries in the gastrointestinal tract, whilst dilating those in the periphery. Aldosterone and vasopressin, two lesser hormones in the stress response, are also released and act to increase blood volume through increased water retention. One of the functions of cortisol is to increase the concentration of fatty acids carried by lipoproteins and sugars in the bloodstream, leading to more damage to the arterial wall, producing excessive levels of cholesterol that may then bond to the artery walls (and lead to high cholesterol readings by your doctor), a process called atherosclerosis ¹². Atherosclerosis is the process in which a blood vessel wall thickens due to a build-up of fatty substances. The combined effect of these hormones is a marked increase in blood pressure, which may over time result in damage to the vascular tissue in the form of small micro-tears in the vessel walls. These minute tears heal by bonding with molecules floating in the blood (that is, cholesterol acts as a Bandaid). This cholesterol then forms a hard fibrous plaque with calcium, which may build up over time, constricting blood flow in the artery. Stress also causes the blood to become stickier in preparation of potential injury, increasing the likelihood of an artery‑clogging blood clot ¹³. One study found that those who expressed feeling high levels of stress and despair had a 20% greater chance of developing atherosclerosis over a four-year period. This was the same magnitude of increased risk as seen in a pack-a-day smoker.  Studies on animals have shown similar results. A study on hypertensive rats and normal rats found that the hypertensive rats suffering from stress had a higher rate of these events ¹⁴.

There is a large body of evidence demonstrating the relationship between increased stress and increased CVD. A study commenced before the terrorist attacks in the U.S. on September 11, 2001 examined the degree to which acute stress reactions as a result of the terrorist attacks could predict future cardiovascular outcomes through follow-up surveys over three years ¹⁵. In a sample of 2,592 adults, researchers found that the acute stress response was associated with a 53% increased incidence of cardiovascular ailments ¹⁵. Those individuals who had high levels of acute stress following the attacks also reported a two-fold increase in physician-diagnosed hypertension and a three-fold increase in other heart-related problems over the three-year period.

In a study of 11,119 patients found that those patients who had experienced a myocardial infarction reported a higher prevalence of all four stress factors: stress at home, stress at work, financial stress and major life events in the prior year ¹⁶. The study also found that the four stress factors worsened coronary atherosclerosis and endothelial dysfunction and increased inflammation ¹⁶.

The Whitehall II study found a 2.15-fold (215%) increased risk for cardiovascular disease in men who experienced a disparity between effort and reward at work ¹⁷. The study also concluded that high-risk individuals included those who were overcommitted at work, had poor promotion prospects, blocked or stalled careers as well as competitive and hostile work environments. Similarly, in a study of nearly two thousand male workers over a six-year period, researchers found that those who experienced chronic work-related stress were four times more likely to experience cardiovascular ailments ¹⁶. A study at the Beth Israel Deaconess Medical Centre in Boston found evidence that managers who fire someone run twice the usual risk of heart attack in the week following the dismissal; the greatest danger occurred to those who had conducted the firing while working under a high-pressure deadline. Another study found that chronic work stress and divorce increased the risk of cardiovascular mortality ¹⁷.

In a study of 791 patients, researchers reported that high-pressure deadlines increased the risk of heart attacks by 2.3 times within the seven days after the stress of the deadlines. Specific time pressures dramatically increase the risk of heart attack and early death. In a study of 60 women ages 30 to 45, researchers found that those under stress who secreted the highest levels of cortisol were also the ones who turned to high-fat foods in attempts to cope with their stress.

The results are similar for younger populations. In a study of 158 healthy adolescents who undertook self-report measures of chronic stress over 3.3 years, adolescents exposed to chronic, negative stressors that worsened over time demonstrated heightened cardiovascular risk ¹⁸. In a study investigating the responses of university students to stressful situations, researchers found that students exposed to stressful laboratory tasks displayed high levels of cardiovascular responses, which extended into a continued increase in blood pressure during instances of perceived stress in everyday life situations ¹⁹.

Being angry more than doubles the risk of cardiac arrest. In a study of 1,500 people who had suffered heart attacks who were surveyed and asked what their feelings were a few hours prior to the heart attack, it was found that the heightened risk appears to last for about two hours after the episode of anger. 

Psychosocial stress also results in changes in physiological behaviours ^5,7,11, which can put a person at increased risk of CVD. These behaviours include increased smoking and drinking, unhealthy eating and reductions in physical activity ^20,21,22. In addition, chronic stress can lead to constrained appetites or overeating, leading to problems of anorexia or obesity ²³. In extreme cases, anorexia or extreme weight loss can have an effect on heart rhythms and even lead to heart failure ²⁰¹⁰, while overeating may lead to obesity that has significant health risks associated with coronary heart disease, hypertension and type 2 diabetes ²⁵.

Stress is our great silent killer. Despite the growing body of evidence of this, we continue to focus on pharmaceutical treatments to reduce CVD and we continue to fail. The mechanisms behind stress being such a large contributing factor are now understood and numerous major studies have shown that the effects of chronic stress increase the risk from two to nine times. By contrast, medication to reduce cholesterol reduces the risk by 1% or 0.001 times (that is more than 2,000 times less important than stress). The next stage then is to invest in stress management practices. It’s that simple. Or is it?

1.     NHMRC 2009

2.     Bonthuis et al. 2010

3.     Ademi et al. 2009

4.     Yusef et al. 2004

5.     Dimsdale 2008

6.     Begg et al. 2008).

7.     Rozanski et al. 1999

8.     Black and Gabutt 2002

9.     Siegrist 1995

10.  Cade et al. 2010).

11.  McEwen 2008

12.  Brotman et al. 2007

13.  Newton et al. 1990

14.  Hallbäck and Folkow 2008

15.  Holam et al. 2008

16.  Rosengren et al. 2004

17.  Dimsdale 2007

18.  Low et al. 2009

19.  Loft et al. 2007

20.  Sturmer et al. 2006

21.  Logan and Barksdale 2008

22.  Hamer, Bates and Mishra 2011

23.  Rutledge and Linden 1997

24.  Bell 2010

25.  Rapoport, Clark and Wardle 2000

Acknowledgements. Brigitta Curley, Amy Williams