That’s the word on integrative medicine street. I had a sense this was coming, not just a tightening of our terminology but also a challenge of the very concept of ‘adrenal burnout’. Hear me out.
This important information was presented by Dr. Kamal Karl, an experienced integrative GP from NZ at the ACNEM thyroid adrenal module in Adelaide, and his point about the inappropriateness of this ‘diagnosis’ was twofold:
- In most instances the gland itself is not actually the source of the low cortisol problem. Even in patients who have endured chronic stress for years & exhibit low cortisol in blood, saliva or urine, administration of ACTH (which is what we do in the medical test called Syncathen when actual adrenal failure i.e. Addison’s disease is suspected) provokes – a jump in cortisol secretion indicative of a ‘normal healthy response’
- So, if the gland itself is able to produce and secrete sufficient cortisol given a dose of ACTH then this suggests strongly that the ‘adrenal issues’ are actually coming from ‘higher up’ i.e. the patient’s own ACTH level is too low to stimulate adequate cortisol. Therefore their low cortisol really is a consequence of a hypothalamus or pituitary ‘sleeping on the job’ or a case of damaged or altered glucocorticoid receptors, which produces this excessively vigilant or over-sensitive negative feedback loop to the pituitary. Both underpinning causes are increasingly discussed in the scientific literature.
So how does this change things? Well, Dr. Karl’s suggestion first is to use more technically correct terminology and describe these patients as having simply HPA dysfunction, and, when low cortisol has been confirmed, you could add that they exhibit hypocortisolism. But much more importantly than this, it should change our treatment approach in some patients.
Think about this example: a PTSD patient presents with a picture we might have previously described as one of ‘adrenal fatigue’ and has suboptimal levels of cortisol in test results, if the assumption remains that the adrenal glands are simply incapable of producing adequate corticosteroid then we might assume the remedy is to boost cortisol – with herbs, or glandulars or even low dose cortisone. But what if we had a test that measured corticosteroid receptor numbers and we could see that this patient had an abnormally small number of these – hence only small amounts of cortisol were triggering negative feedback inhibition (the ‘off switch’) at the pituitary – as has been demonstrated in several patient groups, especially those subjected to childhood trauma? How would this treatment effect them? Would it make things better? Probably not and there is a risk it could make this ‘down-regulation’ of receptors worse –> further disturbed HPA and low endogenous cortisol.
I really see the merit in this important re-framing and challenging. It is something I have been thinking about for a while and I think, in order to choose the right treatment approach being able to identify the true underpinning cause is critical. I am left, however, with one piece of the puzzle not fitting and I wish I had thought of this when Dr. Karl was in front of me to bring it up for discussion. That is the issue of DHEAs depletion.
We all appreciate that DHEAs levels decline with aging, but if my patients are remotely representative of the rest out there then we are facing an epidemic of premature DHEAs decline – patients in their 30s and 40s with DHEAs values < 2 umol/L. While there is substantial evidence that DHEAs levels are inversely related to almost all major diseases (cancer, CVD, diabetes, inflammatory diseases) I am seeing this in patients who have none of these overt diagnoses and remain ‘relatively well’. The low DHEAs therefore to me, speaks of this depleted adrenal reserve more so than the low cortisol values which as we know are dynamic, diurnal and could be due to HPA dysfunction rather than actual tissue integrity issues. I still measure cortisol and find it can be insightful however I do find myself placing equal if not more weight on patients’ blood DHEAs levels (take note saliva is not accurate for DHEAs only DHEA and most labs are not testing for this!) While DHEAs levels are impacted by the HPA axis, this is much less potent and absolute than we see with cortisol and the other aspects of regulation and influences upon DHEAs are still being fully mapped. So let’s keep watching this space and in the meantime – let’s bury the ‘adrenal fatigue’ diagnosis and sharpen our understanding of true HPA dysfunction.
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