Cortisol levels in ME/CFS

I did a salivary cortisol test (four samples throughout the day) quite a long time ago and my cortisol was well over the range in 3 out of the 4 samples, and 90% of the way through the range for the sample that wasn't over the range.

Much more recently I had my first ever blood cortisol test done at around 8.30am - 9am and that was over the range too.

I have read that very high stress can cause high cortisol and if the high cortisol lasts long enough then it becomes the patient's new "normal". If that is true then I wonder what causes cortisol to become low.
 
Post-COVID-19 condition in prospective inpatient and outpatient cohorts (2025, Scientific Reports)
PCC patients were manually distributed into three symptom clusters corresponding to their most dominant self-reported symptoms according to Global Burden of Disease Long COVID Collaborators guidelines (supplementary information).

Shortly, persistent fatigue with myalgia or mood swings (cluster 1) included bodily pain (myalgia), weakened muscular strength, numbness and tingling, fatigue, and mood disturbances.

Cognitive problems (cluster 2) included attention deficit and cognitive difficulties, and

ongoing respiratory problems (cluster 3) included exertional and resting dyspnea, persistent cough, and thoracic pain.
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During the 24-month follow-up, cluster 2 patients had lower cortisol levels than those belonging to clusters 1 and 3 (Supplementary Fig. 10 C). Twelve months post-infection, the difference was statistically significant (179 vs. 290 nmol/l, p = 0.031, and 179 vs. 351 nmol/l, p = 0.054). However, while the trend was similar throughout the follow-up, the differences did not reach statistical significance at any other time point, likely due to the small subgroup sizes.
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Between all long COVID (PCC) and healthy, it seems cortisol was only lower at the acute phase. Figure 4C:
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The overall cortisol levels were significantly lower in the acute phase – especially among inpatients with a severe disease. This can result from treatment with corticosteroids, suppressing endogenous cortisol production. However, we did not collect the samples uniformly at the same time of the day, resulting in increased variation in cortisol levels.
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Post-COVID-19 condition in prospective inpatient and outpatient cohorts (2025, Nature Scientific Reports)

In the whole group, spirometry results, orthostatic hypotension, or levels of soluble suppression of tumorigenicity 2, interleukin 6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), or cortisol had no association with PCC. However, using symptom clusters, patients with cognitive problems had lower cortisol levels, while patients with ongoing respiratory or myalgic symptoms had higher levels of IL-6 and hs-CRP.
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I read one thread talking about cortisol in me/cfs. Not sure I grasped what it was saying. I am understanding that cortisol levels are not just from types of insufficiencies or whatnot but from your routine as well?

I finally went and saw a private endocrinologist for my Hashimoto's which was a great appointment where someone finally cared about details even before I said anything.

One of the things he flagged was the nhs failed to ever test my cortisol to see if that plays any part in my symptoms.

While I have heard of cortisol it's not something I have ever looked into previously as a potential other issues. I will be having the cortisol at the end of April allowing for my new hashimoto's treatment to have an effect (if I tolerate it at all).

I don't often here cortisol mentioned with hypothyroidism so I am wondering if it fits in with cfs but found what I read so far less certain.

Also, not even sure how to understand results for myself (after I actually get the test). We are starting with the blood test at 9am to see if investigation is needed.
 
Cortisol Patterns Are Associated with T Cell Activation in HIV, 2013, Patterson et al
Abstract

Objective
The level of T cell activation in untreated HIV disease is strongly and independently associated with risk of immunologic and clinical progression. The factors that influence the level of activation, however, are not fully defined. Since endogenous glucocorticoids are important in regulating inflammation, we sought to determine whether less optimal diurnal cortisol patterns are associated with greater T cell activation.

Methods
We studied 128 HIV-infected adults who were not on treatment and had a CD4+ T cell count above 250 cells/µl. We assessed T cell activation by CD38 expression using flow cytometry, and diurnal cortisol was assessed with salivary measurements.

Results
Lower waking cortisol levels correlated with greater T cell immune activation, measured by CD38 mean fluorescent intensity, on CD4+ T cells (r = −0.26, p = 0.006). Participants with lower waking cortisol also showed a trend toward greater activation on CD8+ T cells (r = −0.17, p = 0.08). A greater diurnal decline in cortisol, usually considered a healthy pattern, correlated with less CD4+ (r = 0.24, p = 0.018) and CD8+ (r = 0.24, p = 0.017) activation.

Conclusions
These data suggest that the hypothalamic-pituitary-adrenal (HPA) axis contributes to the regulation of T cell activation in HIV. This may represent an important pathway through which psychological states and the HPA axis influence progression of HIV.
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This was interesting. They found the same pattern of lower waking cortisol levels that are reported in ME/CFS and found that it was associated with the level of T-cell activation.

I guess it is possible that lower waking cortisol levels are part of the sickness reponse. So, if your t-cells are activated, you are sick and it's probably not a good idea to be waking up, raring to get into your day. Instead, it's better to go 'ugh' and keep lying in bed. So there is some mechanism where activated t-cells (or some other response to the cause of the activated t-cells) dampens down the morning cortisol spike.

However, it's also possible that people with uncontrolled HIV feel pretty rubbish and aren't working and are spending more time in bed. And so perhaps it is their lifestyle (if I can call it that - the lifestyle of someone who is sick) that results in the lower waking cortisol. They routinely aren't leaping out of bed early in the morning, and so their cortisol production adjusts.

I don't think the authors have it right when they suggest psychological states influence progression of HIV. Rather, I suspect the causal mechanism goes in the other direction - the response to the virus makes you feel sick and possibly depressed, so you don't rush around in the morning, you sleep later - so you don't need that morning cortisol burst. And you probably don't load up on coffee first thing in the morning, which can also contribute to a morning cortisol spike.
 
Hutan said:
I don't think the authors have it right when they suggest psychological states influence progression of HIV. Rather, I suspect the causal mechanism goes in the other direction - the response to the virus makes you feel sick and possibly depressed, so you don't rush around in the morning, you sleep later - so you don't need that morning cortisol burst. And you probably don't load up on coffee first thing in the morning, which can also contribute to a morning cortisol spike.
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I agree that's such a weird framing. And I think it ignores the most obvious connection: that T cell activation modulates the HPA axis directly, independent of "psychological stressors." I continually see this weird insistent belief that HPA axis activity must somehow only be influenced by psychosocial stress and that changes in its activity must somehow be indicative of psychosocial stress. But it's a system that responds to a million and one things, psychosocial stress or lifestyle being only one
 
Immunological and Clinical Markers of Post-acute Sequelae of COVID-19: Insights from Mild and Severe Cases 6 Months Post-infection (2025)

cortisol was quantified in 160 of the available 175 samples (with enough volume), and significantly higher levels were observed in severe patients, as compared with mild patients (90.9 [73.9–124.4] vs. 74.9 [60.9–101.4] pg/mL, p = 0.0045). However, no significant difference in cortisol levels was found between patients with and without PASC, neither in the mild (93.6 [63.4–109.2] vs. 71.2 [55.3–93.4] pg/mL, p = 0.070) nor in the severe cohort (90.4 [67.6–125.3] vs. 100.3 [80.4–118.3] pg/mL, p = 0.38).
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Can Low Cortisol Predict Long COVID? A Controversial Issue (2025)

98.84% of our LC participants had normal (62.79%) or elevated (36.05%) cortisol.
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Thus, our cohort results suggest that low cortisol may not define LC […] Our plasma cortisol levels were collected between 5:00 a.m. and 10:00 a.m., well within typical cortisol peak windows. Normal and elevated cortisol did not significantly correlate with specific LC characteristics or symptoms.
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The general absence of hypercortisolism and hypocortisolism in these EMP and MMP circadian rhythm alignment sub-groups suggests that cortisol secretion is not severely dysregulated in LC-induced sleep disorders and may be less sensitive to circadian misalignments. No correlations were found between cortisol levels and time of awakening.
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Low Vasopressin In Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (2025, Endocrine Practice)

The demographic data of the 124 study participants is shown in Table 2. Sex distribution, age ranges and body mass indices were typical of patients with ME/CFS. The average/median disease duration was 7.3/7.5 years.
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As standard clinical routine, all 141 recruitable patients delivered morning samples […] The standard diagnostic procedure included brain MRI and measurements of plasma glucose, sodium, and potassium, as well as serum TSH and cortisol.
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Blood chemistry including sodium, potassium, glucose, thyroid stimulating hormone (TSH) and cortisol levels were within normal range.
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Hormonal alterations in adolescent chronic fatigue syndrome (2010, Acta Paediatrica)

Their definition of CFS is 3 months of disabling fatigue:
Adolescent CFS patients were consecutively recruited from the Paediatric outpatient clinic, Oslo University Hospital, Norway, which serves as a national referral centre for children and adolescents with unexplained chronic fatigue. [...] in this study, three consecutive months of disabling fatigue was sufficient for inclusion and no accompanying symptoms were required.
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serum cortisol was slightly and non-significantly lower (p = 0.07) [334 (301–375) mmol/L for CFS vs. 400 (370–447) for controls]
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SNT Gatchaman said:
We can almost close the thread I would have thought! Cortisol is clearly irrelevant.
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Would that disappoint those 1st responders who only want the stress-response option with a multiple choice MUS question to pass their easy-read neuro-rehab exam for re-enablement of crippled sufferers with medically unexplained, endearing but enduring and persistent symptoms of dysregulating, factitious, false illness-belief, which "we all believe and teach" making it the only realistic and pragmatic opportunity (by proxy)?

Especially for wannabee 1st-and-only responders who prefer a psycho-social history from before ME/CFS onset to warrant a traumatised shut-down stress-response - of the most primitive sort - that is playing dead, which didn't work often enough to prevent predators eating the person. Or do these highly trained and subsidised responders have a work-around - for if their other working-theory falls through too

e.g the exaggerated significance of minor pathology, or the misinterpretation of normal sensations - all more or less modifiable illness-beliefs (unless its an intractable illness-belief) therefore I say none of it is NICE-compliant. Its all been clinically explained to put the whole misunderstanding straight, so no more medically unexplained MUS, but the stress-response must explain physiological manifestation of factitious false illness-belief.

So maybe rollout PUS next - the pathology of unknown significance - just not sure where the reflex FND malfunctions fit into the stress. Or would our stress-response vanish from the working-theory in clinical practice? Can the clinicians stop saying: "gut-brain axis - you know - we all know any anxiety always upsets any gut on the planet, so stop worrying, and the 2-way feedback isn't at all relevant .... no ... Oh no:

"our visceral organs do not cause any encephalopathy, ever, that is not what gut-brain axis means". Oh. Ok, but I do agree that sustained stress-chemicals poison the brain, if any. And I finally worked out that axis-blurb is an example of what @bobbler calls "the hand-waving". Also - no its not la-la land it is the "realistic and pragmatic" opportunity on offer, and for our next trick we shall explain the pragmatic psychosomatic approach to GI vasculitis (without cortisol).

What I want to know is - which is the neurotransmitter that keeps the brain awake, if not cortisol? And how might cortisol interact with our RAAS thing that is said to be remarkably anomalous? Anyway I must read up the vasopressin thing. My liable kidney is quite upset (on and off and only if... ... ...). But 1st I must read page 1 of this thread.
 
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