Small adrenal glands in chronic fatigue syndrome: a preliminary computer tomography study, 1999, Scott et al

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Small adrenal glands in chronic fatigue syndrome: a preliminary computer tomography study
Scott LV, Teh J, Reznek R, Martin A, Sohaib A, Dinan TG.

https://pubmed.ncbi.nlm.nih.gov/10451910/

Abstract
No inclusive or satisfactory biomedical explanation for chronic fatigue syndrome (CFS) has as yet been forwarded. Recent research suggests that a dysregulated hypothalamic-pituitary-adrenal axis (HPA) may be contributory, and in particular that there may be diminished forward drive and adrenal under-stimulation. In this preliminary study we wished to examine a cohort of CFS patients in whom evidence for such hypofunctioning was found.

Our aim was to establish whether these patients had altered adrenal gland size. Patients were recruited from a fatigue clinic. Those who fulfilled the Centre for Disease Control and Prevention (CDC) criteria underwent a 1 microgram adrenocorticotropin (ACTH) stimulation test, a test of adrenal gland functioning. Eight subjects (five females, three males) with a subnormal response to this test underwent a computer tomography (CT) adrenal gland assessment.

Measurements were compared with those from a group of 55 healthy subjects. The right and left adrenal gland bodies were reduced by over 50% in the CFS subjects indicative of significant adrenal atrophy in a group of CFS patients with abnormal endocrine parameters.

This is the first study to use imaging methods to measure adrenal gland size in CFS. It is a limitation of this study that a selected CFS sample was employed. A future larger study would optimally employ an unselected cohort of CFS patients. This study has implications not only for the elucidation of CFS pathophysiology, but also for possible therapeutic strategies.
 
So, they screened people in a fatigue clinic for adrenal gland functioning (using the ACTH test). They don't say how many people they screened, but they do say that they only found 8 people with faulty adrenal gland functioning.

Comparing the size of the adrenal glands of these 8 subjects with 55 heathy controls, they found that the selected CFS subjects had smaller adrenal glands.

Of course, this tells us nothing about people with CFS with normal ACTH test results. Possibly these 8 people don't even have CFS - perhaps they have some other medical issue. Given there is no good evidence for people with ME/CFS having, on average, abnormal ACTH or cortisol levels, I don't think this study contributes to knowledge about ME/CFS.

And yet, it has recently been cited as evidence for an HPA axis-based theory of ME/CFS etiology.
 
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I have occasional calls* with an endocrinologist who has been forced by NICE guidance to scan and review a small nodule on my adrenal gland every so often to see if it does anything exciting. Sample of one, but I’ll remember to ask whether the size or any other characteristics of the gland itself are unusual.

At one point I was rather hoping for a grand unifying theory that would tie together the NSTEMI and the ME symptoms with the endocrine investigations, but that was never likely.


*He switched from meetings quite happily. It’s only neurologists and rheumatologists and psychiatrists who hate us, other clinicians can be perfectly accommodating to ME.
 
This was originally posted here UK Parliament: ME/CFS Announcements: Statement by Health Secretary Sajid Javid, 12 May 2022
in response to a discussion about a 2022 media article that mentions this study

There was this (small) study:
https://pubmed.ncbi.nlm.nih.gov/10451910/
Small adrenal glands in chronic fatigue syndrome: a preliminary computer tomography study
L V Scott 1, J Teh, R Reznek, A Martin, A Sohaib, T G Dinan
Affiliations
Abstract


No inclusive or satisfactory biomedical explanation for chronic fatigue syndrome (CFS) has as yet been forwarded. Recent research suggests that a dysregulated hypothalamic-pituitary-adrenal axis (HPA) may be contributory, and in particular that there may be diminished forward drive and adrenal under-stimulation. In this preliminary study we wished to examine a cohort of CFS patients in whom evidence for such hypofunctioning was found. Our aim was to establish whether these patients had altered adrenal gland size. Patients were recruited from a fatigue clinic. Those who fulfilled the Centre for Disease Control and Prevention (CDC) criteria underwent a 1 microgram adrenocorticotropin (ACTH) stimulation test, a test of adrenal gland functioning. Eight subjects (five females, three males) with a subnormal response to this test underwent a computer tomography (CT) adrenal gland assessment. Measurements were compared with those from a group of 55 healthy subjects. The right and left adrenal gland bodies were reduced by over 50% in the CFS subjects indicative of significant adrenal atrophy in a group of CFS patients with abnormal endocrine parameters. This is the first study to use imaging methods to measure adrenal gland size in CFS. It is a limitation of this study that a selected CFS sample was employed. A future larger study would optimally employ an unselected cohort of CFS patients. This study has implications not only for the elucidation of CFS pathophysiology, but also for possible therapeutic strategies.
 
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That study appears to be from 20 years ago and, again as far as I know, has not been replicated - for such a drastic size reduction (50%) I find this surprising, if the result was both valid, and considered to mean anything.

If there was a condition where people had drastically reduced mobility, and close medical examination determined that a contributing factor may be that one of their legs was 50% smaller then I would expect comment to be made by others than the research team that came up with the idea.
 
This study is a perfect example of how rubbish research keeps turning up to influence public opinion. People don't read past the abstract study title. And then it gets taken as truth, and referenced in science journals (by the Chief Medical Officer of OMF in a paper discussing a hypothesis about ME/CFS causes) as well as popular media.
 
I haven't read the original paper, but this review (The Neuroendocrinology of Chronic Fatigue Syndrome, Cleare, 2003) points out that:

"However, because subjects were chosen specifically to have a blunted cortisol response to ACTH, the authors admit that this may not generalize to all CFS subjects; indeed, it is possible that normals selected for low cortisol responses would also show smaller adrenal glands."

Seems fairly damning to me, so if no one has followed up with a study to address this, there doesn't seem to be anything here.
 
I am playing around with making a table out of the studies in the cortisol thread (if I get anywhere on this through the brain fog I can post a prototype and we can decide if it's any good, and modify/extend it as needed).

Anyway I was trying to figure out how many patients they screened to get the 8 subjects and found the full paper is on sci-hub. So I'll just quote the selection process here for posterity.
The subjects were recruited from a specialist fatigue clinic which accepted referrals from primary care and other hospital settings. Of 52 consecutive referrals to the clinic, and 40 had a diagnosis of CFS (CDC; Fukuda et al., 1994). Thirty patients had a low-dose ACTH test. Eight patients (five female, three male) between the ages of 20 and 49 were recruited for this study, having given fully informed written consent.

In each case a viral influenza type illness anteceding the symptoms was documented. All underwent a structured psychiatric interview (SCID; Spitzer et al., 1987) based on DSM IIIR (American Psychiatric Association, 1987) to exclude the presence of current formal psychiatric illness. Two subjects had a past history of major depression.

Each of the eight subjects had a blunted response to the low dose ACTH (1 mg) infused at 14: 00 h; blunting was defined as a failure to achieve a peak cortisol of greater than 600 nmol/l at 30 min post-infusion (Hurel et al.,1996). The testing procedure was as previously described (Scott et al., 1998b).
Click to expand...
 
Was trying to figure out how to summarize the issues here in one sentence and honestly the author's own limitations put it well:
Would a comparison group of CFS patients who did not display the above endocrine abnormalities show similar alterations or, by selecting subjects with abnormally low cortisol responses, as in this study, is one simply selecting a group with the smallest adrenal glands?
Click to expand...

They also claim this:
Demitrack et al. (1991) demonstrated a blunted CRH/ACTH response in CFS subjects. This has since been replicated by our group (Scott et al., 1998a).
Click to expand...
So those would be something to dig up maybe if they aren't already in the cortisol thread.

I wonder if part of the problem here is just that back in the day the CFS category included a lot of people with regular endocrine problems that weren't been screened for properly and now the ghost of that is with us forever.
 
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