was successfully added to your cart.

I did my MSc dissertation on cortisol resistance in chronic fatigue syndrome (mechanism diagram below) and it was one of the most worthwhile things I have done in my development as a clinician/coach. Our understanding of the HPA axis, which regulates cortisol production has substantially increased over the last few years. The 3 stage model of adaptation, that is still so popular in the complimentary medicine world, I believe is outdated. Another important lesson I learned was around the issues we have investigating cortisol status. Two key points to highlight straight away are:

  1. If you are testing cortisol you simply have to test thyroid and sex hormones alongside it.
  2. It seems urine testing, to help shed light on cortisol metabolism, may be more worthwhile that performing the popular saliva test

HPA activity is intertwined with the behaviour of the hypothalamic-pituitary-gonadal (HPG) axis and the immune system, among others, and this interplay should not be ignore

More important than these two points is the question, what would you do with the results anyway? As you will see, cortisol imbalances are often secondary to other imbalances – and thus, at least in most situations, would you do anything with the results, and thus do you want to invest money in testing cortisol levels? As always there is no universal right or wrong answer to these questions, but clients, and clinicians, need to understand the reasons as to why you would test in the first place.

There is a real skill (and a vast amount of knowledge – as I keep on discovering) required to interpret results from laboratory testing  and taking numbers at face value is not an effective way to practice.

Low Cortisol Production or Clearance in CFS?

Low cortisol production, called hypocortisolim, is one of the most common findings in patients with chronic fatigue syndrome. There has been a lot of discussion around the term ‘adrenal fatigue’ over the years, many now saying the condition doesn’t exist. One of the problems is simply how hard it is to pin point where the ‘imbalance’ is. For example if someone is found to have low cortisol levels via salivary testing, or any other method, are they producing low levels of the hormone or are they metabolising the hormone and excreting it at an enhanced rate?

More than 95% of cortisol is metabolised before excretion. Free cortisol can thus not only be considered a consequence of cortisol production, but, in addition, of cortisol clearance in the liver. In patients with chronic fatigue, for example, low salivary cortisol levels have been discussed to be associated with a faster clearance of cortisol (Jerjes et al., 2006)

 This is a pretty significant point to be aware of!

Low Cortisol As A Protective & Beneficial Response

In an interesting article published in the journal Psychoneuroendocrinology (Fries et al., 2005) discussed the potential protective mechanisms and beneficial effects of hypocortisolism. This quote sums up one of the key points from the article:

“prolonged or repeated exposure to immune stimuli might predispose an individual to reduced glucocorticoid [cortisol] signaling as a means of freeing bodily defences from inhibitory control in the face of an ongoing infectious threat. Thus, an enhanced release of inflammatory compounds may be adaptive under conditions in which recurrent infection is likely and immune readiness is an attendant requirement.”

This raises the question of whether we want to directly interfere with what may be a natural and protective response. It is also a good example of why we often want to take a comprehensive and detailed approach when exploring the underlying causes of a patients symptoms/state of health.

Another interesting highlight is that results of Hellhammer et al. (2004) (cited in  Fries et al., 2005) demonstrate a significantly higher allostatic load index in older compared to younger subjects with the exception of hypocortisolemic elderly who had a comparable allostatic load to young people even though they scored far higher on perceived stress scales.

Considering the fact that allostatic load has been associated with a higher risk for mortality, these data suggest that a hypocortisolemic response to stress may rather be protective than damaging (Fries et al., 2005)

Cortisol And The Nervous System

Interestingly another important concept that is discussed in the article is around the relationship between cortisol and the sympathetic nervous system (SNS). The SNS activates what is often termed the fight or flight response via the release of adrenaline from the adrenal gland.

“increased catecholamine concentrations [such as adrenaline] have been reported in patients with stress related disorders characterised by hypocortisolemic stress responses.”

Summary

As always we need to appreciate that Chronic Fatigue Syndrome is not a single disease entity and that the cause in one person can be very different to the cause in another. This is why research is so mixed and can be contradictory.

One of the most common findings is low cortisol production and based on an infection being a potential trigger for the condition this makes sense. Cortisol is an anti-inflammatory and immune modulating hormone. If someone is experiencing prolonged exposure to an immune stimulus (a viral or bacterial infection for example) then suppression of cortisol production may be the body’s way of trying to deal with this.

A great perspective on this comes from a paper published which states:

“These findings seem to suggest that the underlying disease mechanisms of CFS are more related to altered neuroendocrine control than to altered hormone levels per se”

Screen Shot 2016-07-08 at 10.50.46

My MSc Mechanism Diagram