Psychological distress as a risk factor for death from cerebrovascular disease

Mark Hamer; Mika Kivimaki; Emmanuel Stamatakis; G. David Batty

doi:10.1503/cmaj.111719

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Psychological distress and primary prevention of adverse outcomes
Ami Schattner

Posted on: 30 October 2012
This Could be due to an Increased Cortisol to DHEA Ratio
James M. Howard

Posted on: 21 June 2012

Posted on: (30 October 2012)
Page navigation anchor for Psychological distress and primary prevention of adverse outcomes
Psychological distress and primary prevention of adverse outcomes
Ami Schattner, Head, Department of Medicine
No less than the persuasive demonstration of a significant association between psychological distress (PSD) and cerebrovascular mortality (CMAJ, 18 September), I found the data indicating that 1:7 people (14.7%) of a large cohort of middle-aged British population had score ?4 consistent with significant PSD quite disturbing. In addition to an increased risk of cardiac and cerebrovascular mortality, PSD is associated with...
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No less than the persuasive demonstration of a significant association between psychological distress (PSD) and cerebrovascular mortality (CMAJ, 18 September), I found the data indicating that 1:7 people (14.7%) of a large cohort of middle-aged British population had score ?4 consistent with significant PSD quite disturbing. In addition to an increased risk of cardiac and cerebrovascular mortality, PSD is associated with an increase in all-cause mortality (including death from cancer and dementia) in a dose- response pattern (1). An adverse effect of PSD across a spectrum of infectious and inflammatory diseases is also supported by the literature (2, 3), not to mention its daily toll on patients' quality of life. Although the association does not prove causality, the potential mechanisms discussed by Hamer et al. suggest that it may be possible. Now that adverse associations of PSD have been confidently established, together with data confirming its high prevalence in the population (almost three times that of colorectal cancer), a pre-emptive strike might be contemplated. Although the treatment of emotional problems had not been convincingly shown to diminish associated mortality risk (4), primary care physicians should be encouraged to employ short practical screening tools such as the one used in this study which take less than 5 minute to complete, for the early detection of PSD. Considering ubiquitous physicians' time constraints, this can even be done in clinics by other health personnel or the patients who respond via touch-screen computers. Identified cases can complete more specific evaluation. They can then be advised, perhaps treated and followed, with the potential not only to alleviate their distress, but possibly also of attenuating their increased mortality risk.
1. Russ TC, Stamatakis E, Hamer M, et al. Association between psychological distress and mortality: individual participant pooled analysis of 10 prospective cohort studies. BMJ 2012; 345:e4933.
2. Straub RH, Dhabbar FS, Bijlsma JW, Cutolo M. How psychological stress via hormones and nerve fibers may exacerbate rheumatoid arthritis. Arthritis Rheum 2005; 52:16-26.
3. Chida Y, Mao X. Does psychological stress predict symptomatic herpes simplex virus recurrence? A meta-analytic investigation on prospective studies. Brain Behav Immun 2009; 23:917-25.
4. Frasure-Smith N, Lesperance F. Depression - a cardiac risk factor in search of treatment. JAMA 2003; 289:3171-3.
Conflict of Interest:
None declared
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Competing Interests: None declared.
Posted on: (21 June 2012)
Page navigation anchor for This Could be due to an Increased Cortisol to DHEA Ratio
This Could be due to an Increased Cortisol to DHEA Ratio
James M. Howard, Biologist
It is my hypothesis that conditions which are caused by, associated with, low dehydroepiandrosterone (DHEA) exhibit increased thrombosis. I think low DHEA increases susceptibility to thrombosis. ("Thrombosis may be Caused by Low DHEA," http://www.anthropogeny.com/Thrombosis%20May%20Be%20Caused%20by%20Low%20DHEA.htm )
In 1985, I developed my explanation of the "flight or fight" mechanism; it resulted from my w...
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It is my hypothesis that conditions which are caused by, associated with, low dehydroepiandrosterone (DHEA) exhibit increased thrombosis. I think low DHEA increases susceptibility to thrombosis. ("Thrombosis may be Caused by Low DHEA," http://www.anthropogeny.com/Thrombosis%20May%20Be%20Caused%20by%20Low%20DHEA.htm )
In 1985, I developed my explanation of the "flight or fight" mechanism; it resulted from my work on my explanation of human evolution. Basically, I suggested that the decision to fight, or run from, an adversary rested in the ratio of two hormones, dehydroepiandrosterone (DHEA) and cortisol, the two major hormones produced by the adrenal glands. At its most basic, my reasoning was that DHEA evolved to push biological mechanisms forward, that is cellular mechanisms. Since complex behavioral patterns (neurological mechanisms) result from evolution of cellular mechanisms, DHEA pushes behavior. In terms of amount, DHEA is the major adrenal hormone; cortisol is the other. Cortisol is produced during stress; cortisol produces stress. I reasoned that cortisol evolved to counteract DHEA, that is, to stop the actions of DHEA. If one's ratio of DHEA to cortisol is higher than DHEA, a behavior goes forward; one fights. If the ratio favors cortisol, one flees out of fear. According to my explanation, then, lack of cortisol would indicate a predisposition to fight.
Since psychological distress increases cortisol, I suggest the findings of Hamer, et al., may be explained by an increased cortisol to DHEA ratio.
Conflict of Interest:
None declared
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Competing Interests: None declared.