Cortisol levels in Chronic Fatigue Syndrome and atypical depression measured using hair and saliva specimens, 2020, Cleare/Chalder/others

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Senior Member (Voting Rights)
Source: Journal of Affective Disorders
Preprint
Date: January 29, 2020
URL:
https://www.sciencedirect.com/science/article/abs/pii/S0165032719314466


Cortisol levels in Chronic Fatigue Syndrome and atypical
depression measured using hair and saliva specimens
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Andres Herane-Vives(a,b,*), Andrew Papadopoulos(a), Valeria
de Angel(a), Kia-Chong Chua(a), Lilian Soto L(c), Trudie
Chalder(a), Allan H Young(a), Anthony J Cleare(a)
a Centre for Affective Disorders, Department of Psychological
Medicine, Institute of Psychiatry, Psychology & Neuroscience,
King's College London, London, UK
b Institute of Cognitive Neuroscience. University College of
London (UCL), London, UK
c Facultad de Medicina, Universidad de Chile.
* Corresponding aithor.Centre for Affective Disorders,
Department of Psychological Medicine, Institute of Psychiatry,
Psychology and Neuroscience, King's College London, 103,
Denmark Hill, London, United Kingdom, SE5 8AF, Email
andres.herane@kcl.ac.uk

Received 31 May 2019
Revised 9 December 2019
Accepted 25 January 2020
Available online 29 January 2020.


Abstract

Background
Several diagnostic criteria for major depressive disorder (MDE) overlap
with those of Chronic Fatigue Syndrome (CFS). Furthermore, atypical MDE
(A-MDE), a subtype of MDE characterised by profound fatigue and which
has frequently been linked with CFS, exhibits similar low cortisol
levels to CFS. However, this result has been only found in specimens
designed for measuring acute cortisol levels. In this study, we measure
cortisol levels in subjects with CFS and in subjects with atypical MDE
(A-MDE), without psychiatric comorbidity, using both hair and saliva
specimens, to gain a measure of both short and long-term cortisol levels
in these two conditions.

Methods

Hair cortisol concentration, representing the cortisol concentration of
the previous three months, and salivary cortisol, measured at six
time-points across one day and including the cortisol awakening response
(CAR), post-awakening delta cortisol and the total daily output, were
assessed in an age and gender matched group of 34 controls, 15 subjects
with A-MDE and 17 with CFS.

Results
CFS (92.2 nmol/l.h, s.d=33.2 nmol/l.h) and A-MDE (mean=89.1 nmol/l.h,
s.d=22.6 nmol/l.h) subjects both showed lower cortisol total daily
output in saliva (AUCg) in comparison to healthy controls (mean=125.5
nmol/l.h, s.d=40.6 nmol/l.h). However, hair cortisol concentration was
not lower than that of controls in either patient group. CFS and A-MDE
did not differ from one another on any cortisol measures. CFS subjects
reported fewer daily hassles and less severe psychic anxiety symptoms in
comparison to A-MDE subjects (all p<0.05). However, they did not differ
in the severity of somatic anxiety symptoms. There was also no
difference in the presence of overlapping symptoms such as fatigability
and memory problems between A-MDE and CFS subjects.

Conclusion
Low levels of cortisol found using short-term measures of daily output
may be transient, since cortisol levels were normal when a long-term
measure (hair) was studied. This might be explained by a potential
cortisol rhythm alteration. Although these disorders have their
distinctive depressive and somatic features, they may from part of a
wider group of Somatic Symptom Disorders (SSD), given the findings of
the same pattern of cortisol secretion in both disorders and increased
frequency of overlapping clinical features.

--------
(c) 2020 Elsevier B.V.
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Cortisol is a feed-forward metabolic hormone, so if there are corresponding alterations in sleep-wake cycle, daily activity (and intensity of activity) compared to healthy controls, then the altered cortisol cycle may in fact be working normally and the cortisol cycle correctly predicting daily metabolic demand.

I wonder whether there was a similar level of (un)employment among the "A-MDE" group. I don't yet have access to the article so I can't check as to whether they recorded this.
 
Snow Leopard said:
Cortisol is a feed-forward metabolic hormone, so if there are corresponding alterations in sleep-wake cycle, daily activity (and intensity of activity) compared to healthy controls, then the altered cortisol cycle may in fact be working normally and the cortisol cycle correctly predicting daily metabolic demand.
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Could this also explain the similarity in readings from the A-MDE and CFS groups, albeit for different reasons? Both groups having restricted predicted physical activity, but for psychological reasons in the first case and physical reasons in the second. I don't understand much of this but it seems like this measure would have no way to distinguish.
 
As far as I can see the results show that their measures do not measure what they thought they measured. Hair levels were supposed to be the average over the short term levels, indicated by saliva. They weren't, so it looks as if their assumptions about interpretation were wrong.

There is nothing to suggest that the low cortisol salivary levels caused symptoms. So I cannot see that the results tell us anything either surprising or informative.
 
Presumably, getting it printed in the Journal of Affective Disorders aligns with the King's College view that CFS is a mood disorder....

"blogs.plos.org
Affective disorders are a set of psychiatric disorders, also called mood disorders. The main types of affective disorders are depression, bipolar disorder, and anxiety disorder. Symptoms vary by individual and can range from mild to severe. ... Affective disorders can be disruptive to your life."

I guess they would say that this is merely because they are comparing CFS to Major depression (MDE) or what they describe as Atypical Major depression (A-MDE).

Methinks they are trying to align CFS with A-MDE...
 
Jonathan Edwards said:
There is nothing to suggest that the low cortisol salivary levels caused symptoms.
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I can't pretend to understand this, but going by @Snow Leopard's post. Is it more that low cortisol salivary levels are anticipatory of the day's activity? And if the activity is similar for two different people, even though the reasons may be completely different, then their levels might be similar? So not causing symptoms, but caused by the consequences of symptoms?
 
Barry said:
So not causing symptoms, but caused by the consequences of symptoms?
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That seems very reasonable to me. If the person's strategy for managing their illness includes not doing things that require sudden changes in activity or diurnal schedule (i.e. not getting up for a 6 o clock flight or pollarding a tree or swatting for an exam or hiking in freezing conditions) then you would expect cortisol levels to be on the low side on average.
 
strategist said:
How exactly do these findings support the classification of CFS as psychiatric disorder?
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To me it seems that the definition of psychiatry is not made by its subject but by its way to treat problems - which is highly dubious.

Subject-wise psychiatry is somewhere between psychology and neurology. But where are the two borders?

I think psychiatry could be defined through nerve-dysfunction not leading to any degeneration. In this sense ME even may be a psychiatric disorder.

Jonathan Edwards said:
If the person's strategy for managing their illness includes not doing things that require sudden changes in activity or ...
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E.g. - some heart problems in ME also have been associated with lying around.

I am not so sure if this is the right interpretation.
 
Snow Leopard said:
Cortisol is a feed-forward metabolic hormone, so if there are corresponding alterations in sleep-wake cycle, daily activity (and intensity of activity) compared to healthy controls, then the altered cortisol cycle may in fact be working normally and the cortisol cycle correctly predicting daily metabolic demand.

I wonder whether there was a similar level of (un)employment among the "A-MDE" group. I don't yet have access to the article so I can't check as to whether they recorded this.
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This. It seems very likely to me that cortisol levels in ME are reduced because of activity levels.

I think we've also discussed sleep times, elsewhere, and it's been postulated that later wakening times might account for blunted levels in the morning.

If they want to prove their thesis, they're being very selective. I wonder if they'd find similar results in other fatiguing, life-limiting long-term conditions, such as MS and Parkinson's.
 
adambeyoncelowe said:
If they want to prove their thesis, they're being very selective. I wonder if they'd find similar results in other fatiguing, life-limiting long-term conditions, such as MS and Parkinson's.
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This is a particular bug bear of mine. They never (or at least I've not seen) compare with an established organic disease. I suppose they cant can they, because they might start getting results where we looked more like those with organic disease than those with depression.
 
People here seem to be worried about depression being misdiagnosed as ME/CFS when I think the other way around might be much more likely (maybe not with these authors but in general). Depression seems to be even more heterogeneous and less well defined than ME/CFS. It's not reliable point of reference to use.

For all we know a lot of these depressed patients could have CFS or that's being particularly badly managed which causes distress. An easy way to mismanage CFS would be to tell a a patient they have depression and must make an effort to do more, exercise and not give up so easily. The outcome of that is likely to be a lot of repeated relapses and despair.
 
Arnie Pye said:
I thought that measuring anything using hair had been dismissed as quackery. There is far too much interference from shampoo, other hair products, and pollution.
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No, the quackery is when you measure a single hair sample from a single individual and propose all sorts of health consequences.

Hair sampling can be valid for groups of participants within scientific studies, but those other things you mentioned can obviously increase the variation and thus reduce the signal to noise ratio of results.
 
That's pretty confused since those researchers consider depression and anxiety to be the disease itself, so I have no idea how it makes sense for them to separate what they consider to be the same thing. There is basically no telling who the participants in this trial are.

I also have no idea what is the scientific measurement of "daily hassles".

Just got curious and, cortisol:
It functions to increase blood sugar through gluconeogenesis, to suppress the immune system, and to aid in the metabolism of fat, protein, and carbohydrates.
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That's quite the list of functions. Nice cherry-picking, but it tells us absolutely nothing.
 
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strategist said:
People here seem to be worried about depression being misdiagnosed as ME/CFS when I think the other way around might be much more likely (maybe not with these authors but in general). Depression seems to be even more heterogeneous and less well defined than ME/CFS. It's not reliable point of reference to use.

For all we know a lot of these depressed patients could have CFS or that's being particularly badly managed which causes distress. An easy way to mismanage CFS would be to tell a a patient they have depression and must make an effort to do more, exercise and not give up so easily. The outcome of that is likely to be a lot of repeated relapses and despair.
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That is my main concern. I have no issues or fears about any association with the two, they are clearly completely different and only superficially similar to either the untrained eye or the ideological mind.

The problem is we have no idea what depression is, how to diagnose it, how to define it, how to quantify or qualify its severity, how it works, what it affects, what it is at all. So this isn't comparing apples to oranges, it's comparing a box labeled apples with a box label oranges without knowing anything about what's inside. It also increasingly appears to have nothing whatsoever to do with psychology other than as a consequence, almost definitely not a cause.

It sure tells us things about those labels but we know those labels have massive inner complexity that we simply don't understand. And pretty ironic considering that until recently medicine completely dismissed depression and now basically everything is depression all the time and everywhere. We still don't understand any of it but it sure is everywhere and explains everything. Somehow. Don't ask for details, it's a philosophical split, or something like that.
 
strategist said:
People here seem to be worried about depression being misdiagnosed as ME/CFS when I think the other way around might be much more likely (maybe not with these authors but in general). Depression seems to be even more heterogeneous and less well defined than ME/CFS. It's not reliable point of reference to use.

For all we know a lot of these depressed patients could have CFS or that's being particularly badly managed which causes distress. An easy way to mismanage CFS would be to tell a a patient they have depression and must make an effort to do more, exercise and not give up so easily. The outcome of that is likely to be a lot of repeated relapses and despair.
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I’ve talked on other threads about the high chances of a depression diagnosis masking gradual onset ME. This ties in with my experience although it’s not clear cut as I was experiencing grief before I started having the regular viral illness episodes.
 
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