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.
Just coming back to add the link: Perspective: Drawing on Findings From Critical Illness to Explain ME/CFS, 2022, Stanculescu, Bergquist
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 PMID: 10451910 DOI: 10.1016/s0306-4530(99)00028-1 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.
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.