Salivary cortisol output before and after cognitive behavioural therapy for chronic fatigue syndrome, 2008, Roberts

dreampop · Jul 21, 2020

Abstract
Background:There is evidence that patients with chronic fatigue syndrome (CFS) have mild hypocortisolism. One theory about the aetiology of this hypocortisolism is that it occurs late in the course of CFS via factors such as inactivity, sleep disturbance, chronic stress and deconditioning. We aimed to determine whether therapy aimed at reversing these factors–cognitive behavioural therapy for CFS–could increase cortisol output in CFS.

Methods:We measured diurnal salivary cortisol output between 0800 and 2000h before and after 15 sessions (or 6 months) of CBTin 41 patients with CDC-defined CFS attending a specialist, tertiary outpatient clinic.

Results:There was a significant clinical response to CBT, and a significant rise in salivary cortisol output after CBT.

Limitations:We were unable to control for the passage of time using a non-treated CFS group.

Conclusions:Hypocortisolism in CFS is potentially reversible by CBT. Given previous suggestions that lowered cortisol may be amaintaining factor in CFS, CBT offers a potential way to address this.
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https://www.kcl.ac.uk/ioppn/depts/pm/research/cfs/publications/assets/2009/Robertssalivary.pdf

dreampop · Jul 21, 2020

This is a small, self-controlled study with a long, variable treatment (CBT ofc) duration up to 6 months. 47% were "responders" to CBT. (sidenote: in this case, I believe as the outcomes are subjective by the therapist rather than the patient). The authors include Wessley and Chalder.

The response to CBT was not consistent with the change in cortisol levels, undermining the hypothesis involving the pathophysiology of the HPA axis. Both non-responders and responders showed an increase in total daily cortisol output. In fact, non-responders showed greater increases in cortisol (+12.8 vs +8)

There was no differential effect of whether patients were judged to have responded to CBT or not apparent in salivary cortisol measures (Table 3). We also calculated the change in the endocrine variables after CBT (i.e. pre-treatment values subtracted from post-treatment values)and performed an independentt-test on these values between responders and non-responders. There were no significant differences detectable (data not shown).We also looked to see if there were any correlations between clinical and cortisol measures after CBT. There were no correlations with total or mean cortisol output.
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CBT responders were nearly 6 points higher in total output, almost as much as the increase from CBT, suggesting a slightly better off treatment group to begin with.

However, after CBT, a flatter cortisol day curve (i.e. areduced diurnal change) was associated with worse functioning on the SF-36 social function subscale (r=−0.40,P=0.015) and higher BDI depression scores(r=0.41,P=0.013).
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4. Discussion
As outlined, hypocortisolism is one of the most oftenreported biological changes in CFS (Cleare, 2003). We have shown for the first time that cortisol levels can be increased by CBT, with a 16% increase in total cortisol output from 0800–2000h apparent after 6 months of therapy. Our findings are robust due to the careful selection of medication-free subjects, and because patients acted as their own controls before and after CBT, thus excluding other inter-individual factors that might complicate comparisons of HPA axis assessments. Other advantages of the present study include the careful assessment of psychiatric and other comorbidities, and theuse of salivary cortisol, a non-stressful method ofassessing biologically active hormone.
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Ok, so +16% total output refers to *responders and non-responders* to CBT.

CBT responders experienced an +11.2% costisol outpot and non-responders experienced a +19.6% change !

Not only is this conclusion very deceitful, the following is a pure contradiction when combined with Wessley's own results. If cortisol increased more in patients that didn't respond to therapy either the therapy or the cortisol finding is being misinterpreted.

We are not directly able to deduce the mechanism bywhich CBT increases cortisol levels from this study.However, there is accumulating evidence that HPA axischanges are not a primary feature of CFS, but instead couldbe a secondary effect of illness. Thus, chronic fatigue sixmonths after Epstein–Barr virus (Candy et al., 2003)orsurgery (Rubin et al., 2005) is not associated with HPA axischanges. However, patients who have had CFS for severalyears, do show HPA axis changes (Cleare, 2003). Since sleep pattern, habitual physical activity levels, physical deconditioning and perceived stress can all exert marked effects on the HPA axis (Cleare, 2003), we hypothesise that these factors, together with potential effects of comorbid psychiatric illness and medication, are largely responsible for the varying degrees of hypocortisolism in longstanding CFS (Cleare, 2004). Since CBT for CFS concentrates on addressing many of these factors, it is plausible that it is via the reversal of these cognitive–behavioural factors that both clinical and endocrine change is produced
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Except that the larger change coincided with the unresponsiveness to CBT. So, how can that be. And how can the HPA axis, lifestile and deconditioning *not* be correlated with responsiveness to CBT if BPS model holds.

A final limitation was that we did not use an untreated group of CFS sufferers: since there is clear evidence of theefficacy of CBT we did not feel it would be ethical to delaythis for 6 months to act as a control for this experiment.
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...

Thus, we cannot exclude the increase in cortisol output being due to factors independent of CBT such as illness progression or repeated testing.
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Final conclusion:

Although previous research suggests that some CFS patients may benefit from low dose hydrocortisone replacement, we suggest that our results, together with the superior evidence base for CBT in CFS, point to CBT being the treatment of choice for the observed mild hypocortiso-lism in CFS at this time
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Sarah94 · Jul 21, 2020

Doesn't cortisol reflect stress? So CBT made them more stressed

dreampop · Jul 21, 2020

Anyone on twitter (I am not) might want to show this paper to Dr. Keith Geraghty as it seems very relevant to the question he asked. Ironically, it's a BPS paper that seems to undermine the position he was querying.

Snow Leopard · Jul 21, 2020

Sarah94 said: ↑

Doesn't cortisol reflect stress? So CBT made them more stressed
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Cortisol is a feed-forward metabolic hormone, it's purpose is to provide sufficient blood glucose upon wakening and smooth the blood glucose level over the day given anticipated activity demands (insulin is a feed-back metabolic hormone...).

Despite all the pop-psychology on the contrary, it's more correct to say that cortisol levels reflect sleep-wake and activity patterns than "stress".

obeat · Jul 21, 2020

dreampop said: ↑

Anyone on twitter (I am not) might want to show this paper to Dr. Keith Geraghty as it seems very relevant to the question he asked. Ironically, it's a BPS paper that seems to undermine the position he was querying.
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Done

Midnattsol · Jul 21, 2020

obeat said: ↑

Done
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Could you also share the protocol for the CEBA project with the "sustained arousal model"?

It is the "Forskningsprotokoll" found when one clicks on "Relevant sentral informasjon" at this link:

https://www.ahus.no/fag-og-forsknin...esyke-hos-ungdom#relevant-sentral-informasjon

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Salivary cortisol output before and after cognitive behavioural therapy for chronic fatigue syndrome, 2008, Roberts

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