“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
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
