Resilient people are proven to work smarter because they can negotiate the inevitable changes that are the one certainty of life.  People who know what teamwork really means can turn good teams into great ones.

Derek Roger is a leading UK-registered business psychologist who shares his insight with you here in his regular blog, "Psychobabble," which will provoke thought and stimulate interest in the fields of Resilience, Wellbeing and Stress Management.

It's not black and white!

In the Challenge of Change Resilience training programme we emphasise that there is no 'good stress', and that all that stress offers is a life that may be shorter and will definitely be more miserable.  Once you define stress properly, as ruminating about emotional upset, the miserable part is self-evident to everyone.  We illustrate the 'short' part during the training by referring to the impact on your health of sustained high levels of adrenaline and cortisol, which are secreted when the system involving the hypothalamus and the pituitary and adrenal glands (the h-p-a axis) is activated.  The dramatic increase in adrenaline and cortisol in response to demand is called 'fight or flight', and these are not 'stress hormones' at all – they're doing exactly what they're designed to do, facilitate action, but they're adaptive only in the short term. 

In the longer term, adrenaline has the effect of unnecessarily prolonging cardiovascular strain, and continued elevations in cortisol secretion can compromise immunity by suppressing the production of white blood cells.  However, a recent paper in Nature Medicine appears to contradict these effects for cortisol, in showing that white blood cell production is increased during stress.  How are these findings to be reconciled?  They are in fact both correct.  This requires a lot more detail than is needed for the purposes of the training programme, but we need to put the findings into the perspective of the Challenge of Change.

First, the main findings were obtained by studying mice placed under laboratory stress.  Using mice doesn't negate the findings, but the effects may not necessarily generalise across species.  Second, the paper attributes the effects of enhanced white blood cell activity to chronic as opposed to acute stress, and to make sense of this we need a proper understanding of stress.   The CoC training programme is aimed at replacing misleading psychobabble with simple English, and 'stress' is reserved only for ruminating about emotional upset.  We distinguish between that and pressure, which is just a demand to perform.  It starts when you wake up: the demand is to get out of bed.  You get to work and something goes pear-shaped; this is just greater pressure, not stress.  It will involve an increase in adrenaline and cortisol – fight or flight – but that's appropriate: we need to act, and provided there is recovery afterwards it isn't a problem.  Pressure corresponds to 'acute stress'; rumination sustains activation inappropriately and corresponds to chronic stress.

Finally, we need to be wary of generalisations like 'white blood cells'.  There are in fact different kinds, and they have different functions.  The two types of white blood cell that increased under stress were monocytes and neutrophils, which are stimulated in chronic stress by noradrenaline.  Broadly speaking, adrenaline is associated with provocation to action and noradrenaline is associated with recovery, and the monocytes and neotrophils cluster around sites of inflammation to enhance healing.  In the cardiovascular system, inflammation is commonly at points where there is increased cardiovascular strain, for example, at bends and forks in arteries, particularly in the coronary artery system.  Cholesterol accumulates at the site of the inflammation, resulting in the formation of plaques, and the monocytes and neutrophils that also accumulate there serve to augment and exacerbate plaque formation.  Plaques lead to a narrowing of the arterial bore – atherosclerosis, which significantly restricts blood-flow to the heart, and the plaques can also break off and form life-threatening clots.

These effects have now been shown to be associated with the increase in monocytes and neutrophils, but elevated cortisol levels that are sustained can compromise the production of other white blood cells, especially lymphocytes called T-cells.  These regulate the immune response: helper T-cells facilitate it, while suppressor T-cells return the immune system to resting levels after infection, and sustained levels of cortisol compromises the helper-suppressor ratio.  Taken together, what the findings indicate is a double-whammy from ruminating.  Sustained levels of adrenaline increase cardiovascular strain and inflammation, leading to the formation of arterial plaques which are enhanced by some white blood cells that increase in the circulatory system as a result of sustained levels of noradrenaline.  At the same time, the action of other white blood cells is compromised by sustained levels of cortisol.  This is why stress, properly defined as rumination, will not only make you miserable but could indeed shorten your life.

 

 


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