“Therefore, in this study, we hypothesize that understanding cortisol patterns in both these syndromes may be a crucial factor in characterizing FMS and CFS.” The authors
HPA axis stress response.
More than any other substance, cortisol demonstrates how integral a role the stress response plays in the functioning of our body. Our main stress hormone, cortisol is best known for the role it plays in jacking up our fight or flight system, but this versatile substance also affects our metabolism, tamps down inflammation, regulates blood pressure, affects glucose levels, and even impacts our sleep/wake cycle.
Too much cortisol can result in anxiety, depression, headaches, memory and concentration problems, digestion issues, heart disease, and trouble sleeping. Too little cortisol can result in fatigue, muscle weakness, digestive issues (diarrhea, nausea, vomiting) and low blood pressure and weight loss.
Cortisol is clearly something we would want our body to get right.
The Studies
Most ME/CFS studies have found low morning salivary cortisol levels but these researchers, hailing out of the University of Houston, as well as two top research institutions – UCSF and Vanderbilt – think that may not be the end of the story.
The idea that one-and-done measurements can tell us much have been taking a beating lately. Because cortisol is secreted according to a circadian rhythm, the authors asserted that that rhythm – which is unique to each individual – must be taken into account. They believe that asking whether we have too much or too little cortisol is much too simple a question for this dynamic hormone.
They threw the kitchen sink at these two diseases, assessing cortisol secretion patterns, timings, amplitudes, and the number of the underlying pulses, as well as infusion and clearance rates – and they did that every ten minutes for 24 hours.
Characterization of Cortisol Dysregulation in Fibromyalgia and Chronic Fatigue Syndromes: A State-Space Approach. Pednekar DD, Amin MR, Fekri Azgomi H, Aschbacher K, Crofford LJ, Faghih RT.IEEE Trans Biomed Eng. 2020 Mar 5. doi: 10.1109/TBME.2020.2978801. Online ahead of print.PMID: 32149617
A System Theoretic Investigation of Cortisol Dysregulation in Fibromyalgia Patients With Chronic Fatigue. Divesh Deepak Pednekar, Md Rafiul Amin, Hamid Fekri Azgomi, Kirstin Aschbacher, Leslie J Crofford, Rose T Faghih. Conf Proc IEEE Eng Med Biol SocJul;2019:6896-6901. doi: 10.1109/EMBC.2019.8857427.
Linking Disease Symptoms and Subtypes With Personalized Systems-Based Phenotypes: A Proof of Concept Study“Kirstin Aschbachera,b,* , Emma K. Adamc , Leslie J. Croffordd, Margaret E. Kemenya, Mark A. Demitracke, and Amos Ben-Zvif. Brain Behav Immun. 2012 October ; 26(7): 1047–1056. doi:10.1016/j.bbi.2012.06.002.
While the daytime cortisol levels were similar to healthy controls, things went a bit haywire during the night. With their crappy sleep, night isn’t the best time for people with ME/CFS and FM – but this study suggests it may be a good time to assess biological factors.
The researchers’ recent study produced a split between FM and ME/CFS: cortisol appear to be dysregulated in both diseases, but in different ways.
Fibromyalgia
FM patients had a blunted cortisol feedback loop. (Positive feedback loop- Wikimedia)
Cortisol was not being cleared, or taken up, by FM patients’ cells as quickly as it usually is. That extra supply of cortisol resulted in cortisol being pulsed through the system fewer times and at lower levels than usual compared to the healthy controls. That was an indication of “blunted feedback signaling”; i.e. cortisol production was not shut down when it should be and tended to go on longer than normal in FM patients.
When hormones like cortisol become overly available like that, the glucocorticoid receptor that usually responds to it may start ignoring it. The authors believed this could explain the blunted inhibitory feedback other studies have found. It could also be bad news for tamping down inflammation and pain control.
If the glucocorticoid receptors on FM patients’ immune cells turn a blind eye to cortisol, they may keep the pro-inflammatory cytokines that produce pain. Inflammation could run amok, producing longer than normal periods of pain – and perhaps sensitizing the pain neurons. One study found evidence of a blunted anti-inflammatory response to exercise.
Fifteen years ago a study found “strong relationship” between cortisol levels and pain early in the day in FM. Other studies have clearly shown a relationship between balky cortisol production and increased pain sensitivity. Cortisol is definitely a player in FM: how big a player it is – we don’t know.
Chronic Fatigue Syndrome (ME/CFS)
ME/CFS patients, on the other hand, had more secretory events than usual, but produced lower levels of cortisol during the early morning hours compared to the healthy controls. That suggested that the increase in secretory events was a (failed) attempt to compensate for the low cortisol levels present. As cortisol should pump some energy into us as we wake up in the morning, the low cortisol could contribute to the early morning blues and perhaps even the pain people with ME/CFS often feel at that time.
Sensitive Responders!
This study also found that people with ME/CFS/FM exhibited an ultrasensitive cortisol response characterized by more rapid or more sustained release of cortisol during the night. The authors called this unusual response a “high sensitivity phenotype”. That wouldn’t seem to jive with better health, but it may have been there for a reason: the study also found that the ME/CFS/FM patients who produced more cortisol (per unit of ACTH) at night had reduced symptoms.
A high sensitivity phenotype is not, as one might think, associated with hypercortisolism. Instead, this kind of hyperactivity – which could result from chronic stress – appears to be associated with hypocortisolism, or low cortisol levels.
That authors speculated that that “high sensitivity phenotype” may be helping the ME/CFS/FM patients to counter-balance high levels of neuroinflammation.
Aberrant cortisol activity, no matter how helpful in one way, still comes at a cost, though, in others. In this case, a constant state of arousal at night and poorer sleep. Greater cortisol reactivity has been associated with increased pain and poor sleep. Determining what the chicken and the egg is may be difficult. One review concluded that poor sleep results in greater cortisol reactivity.
Circadian Pattern Lost
Cortisol is produced according to a circadian rhythm. It hits rock bottom during the early evening – a good time for a stress response hormone to shut down – and then climbs to a peak in the morning. The study found that a quicker cortisol rebound at night was associated with better sleep in the healthy controls. That pattern, though, was completely missing in the FM and ME/CFS patients. A quick cortisol rebound didn’t improve ME/CFS/FM patients’ sleep at all. It was another indication of something broken in this system.
The Other Overactive Stress Response
HPA axis and the stress response.
This isn’t the first study to suggest that an overactive stress response may be wreaking havoc with sleep in ME/CFS and FM. A Several Australian studies and the CDC found that sympathetic nervous system activation was associated with poor sleep in ME/CFS. In fact, SNS activation was the only factor an FM study could link to poor sleep. When the Aussies added an exercise session in the ME/CFS patients, SNS activation increased at night. The 2007 CDC study went the farthest tying together a batch of factors:
“… the presence of increased HR and reduced HRV in CFS during sleep coupled with higher norepinephrine levels and lower plasma aldosterone suggest a state of sympathetic ANS predominance and neuroendocrine alterations”.
If these studies are correct, then both of the major stress response axes – the HPA axis and the sympathetic nervous system – are overactivated during sleep in ME/CFS/FM. If the cortisol studies are correct about the link to neuroinflammation – and note that idea was introduced in 2012, well before the Watanabe ME/CFS paper was published – then tamping down neuroinflammation might also help the night-time HPA axis problems as well. Interestingly, Mackay and Tate recently proposed that HPA axis dysfunction was linked with neuroinflammation as well.
The authors didn’t offer any treatment options other possibly mineralocorticoids, but are going to add ACTH – the factor responsible for synthesizing cortisol – to their modeling efforts. Way back in 2008, though, a study suggested that intranasal insulin, of all things, was able to reduce hyperactivity of the HPA axis. How it would affect people with ME/CFS – who have increased secretory events, but reduced cortisol production in the early morning hours, or FM patients, with their reduced cortisol clearance – is unclear.
A recent and sure to be controversial study also reported that hydrocortisone pills allowed people with fibromyalgia, ME/CFS, rheumatoid arthritis, neuropathy and/or many other disorders, to achieve a “minimum symptom state” via control of inflammation.
Conclusion
The most comprehensive cortisol study ever in ME/CFS and FM found cortisol abnormalities during the night in ME/CFS but not during the day. The two groups differed: the FM patients demonstrated reduced cortisol clearance which appear to result in reduced numbers and levels of secretory events. The ME/CFS group showed more secretory events but reduced cortisol production during the early morning hours.
The authors characterized the ME/CFS/FM group as a whole as having a “high sensitivity phenotype”; i.e they either produced cortisol more rapidly (ME/CFS) or produced it for longer periods (FM). Since individuals who produced more cortisol (per ACTH production) had reduced symptoms, they proposed that the HPA axis was attempting to tamp down neuroinflammation at night.
Since the receptors that respond to cortisol tend to ignore the hormone when it is too present, it’s possible that cortisol is not tamping down inflammation as it should – resulting in increased pain in FM patients. The low clearance rate also appeared to retard normal cortisol production, with the FM patients showing fewer and smaller secretory events.
Time will tell how important or not important these findings are but the study does provide more evidence of HPA axis abnormalities in these diseases. It bears noting that these researchers have twice gone to extraordinary lengths – doing blood draws every ten minutes for 24 hours – to assess cortisol/ACTH levels.
Leslie Crofford, one of the co-authors, has been studying cortisol on and off in these and other disorders for years. Back in 1996, she reported that “Patients with FM exhibit disturbances of the major stress-response systems, the HPA axis and the sympathetic nervous system”, and that “FM patients display a unique pattern of HPA axis perturbation“.
She stated that “Many clinical features of FM and related disorders, such as widespread pain and fatigue, could be related to the observed neuroendocrine perturbations”, and that “Further clarification of the role of neuroendocrine abnormalities in patients with FM, and the relationship of these disturbances with particular symptoms, may lead to improved therapeutic strategies.” It’s crazy that 25 years later we’re still waiting.
The authors didn’t provide treatment suggestions, but are now going to dig into patterns of the ACTH – the hormone that tells the adrenals to produce cortisol.
“Since the receptors that respond to cortisol tend to ignore the hormone ***when it is too present*** it’s possible that that cortisol is not tamping down inflammation as it should – resulting in increased pain in FM patients”
***emphasis added, “TOO PRESENT”: this is reminiscent of the substrate-inhibition of IDO1 in Phair’s metabolic trap theory.
I was reading a study on “Dark Microglia” when I saw you’d posted this article, Cort. The study contains many interesting statements, but one that jumps out at me in (potential) relations to cortisol is:
“[dark microglia are over expressed] in wild‐type mice following 2 weeks of chronic unpredictable stress”
In broad terms it does seem like biological feedback loops get strained, this cascades into neighboring systems and overloads their feedback loops. I’m not really saying anything new in that regard, but it’s nice that the research is honing in on the specifics more. E.g. An infectious trigger during a high-stress period dysregulates the microglia, which then dysregulates cortisol which in turn dysregulates sleep and the endocrine system. Perhaps IDO2 polymorphisms influence how “stuck” microglia get. The species of triggering pathogen likely also modulates the intensity, rapidity, and “flavor” of this pattern.
Whether one is a “lumper” or a “splitter”, the gut and the mitochondria can be tied in too, I imagine.
I hope that was at least somewhat coherent; I’ve given myself a headache.
Thanks for another great article, Cort!
-Sean
Fascinating Sean, and a nice possible pathway there – “An infectious trigger during a high-stress period dysregulates the microglia, which then dysregulates cortisol which in turn dysregulates sleep and the endocrine system.”
Thanks!
I was going to ask about how the study dealt with ME/CFS/FM.
As i have both but had ME.years before.
I was in a terrible high stress childhood.
It lasted 19 years.
Even in childhood when i woke up i never felt refreshed.
I never have in my life.
Even if i sleep for very long periods.
I always new these diseases were somehow resulting in my stress and brutal childhood.
Although it was mono that triggered the ME in 1997.
One day they will get to the bottom of all this but it will be too late for me .
Im 60.
Age 32 got mono during hi-stress period – later diagnosed w/CFS and subsequent subclinical hypothyroidism followed by partial thyroidectomy for recurring goiter. Comprehensive blood & saliva testing since 1992 w/several yrs of repeating thyroid & adrenal panels 3x in SAME DAY. Data supports pharmaceutical statement under CONTRAINDICATIONS [in full pamphlet] that thyroid Rx will cause [hepatic] over-clearance of cortisol. 1.8M cortisol tests in 10 mos @ just 1 lab, most taking thyroid Rx. Is there a connection?
Bit late to the party, but had to put a comment to say this (Sean/Cort) is the best hypothesis I’ve read. A chain reaction of problems, such as you have written, explains the plethora, variation and severity of symptoms in ME. Each feedback loop may not be affected to the same degree person to person. The cortisol levels also correspond nicely to when I feel best/worst… I don’t think this is coincidental.
If this is the case, why the body can’t self correct itself is the interesting question (amongst many others!)
Hi Cort,
I opened the 3th link you put there: Linking Disease Symptoms and Subtypes With Personalized Systems-Based Phenotypes: A Proof of Concept Study“Kirstin Aschbachera,b,* , Emma K. Adamc , Leslie J. Croffordd, Margaret E. Kemenya, Mark A. Demitracke, and Amos Ben-Zvif. Brain Behav Immun. 2012 October ; 26(7): 1047–1056. doi:10.1016/j.bbi.2012.06.002.
but or my head is to bad, or they simply did not mention how many patients they studyd with cfs or fm or cfs and fm. I am so tired of many studus on a handfull of papients that has no statistic value. And the larger studys are so few and are not dupplicated or more by other researchers.
I look allways if I can on how many study participants, if there are controls, the . p value.
Do you maybe know how many patient of each group where involved and the .p value?
Thanks!!!
As you can imagine 24 hour studies that measure factors every 10 minutes are not cheap. Get this – the 2012 study took data from a 2004 study (!) that included forty individuals with FM, CFS, or both disorders and 40 healthy controls. The 2020 study included 72 subjects (36 age-matched healthy control subjects and 36 patients) The p values vary – (p = 0:0013) (p = 0:0052).0.0455 and 0.0249, (p = 0:0198).(p = 0:0464) (p = 0:0277
thank you Cort for the information!!!
I must have been verry ill that I could not find it.
Ofcourse studys are not cheap but over more then 3 decades almost allways the small numbers… and for fm, me/cfs, … everything is not cheap while for other deseases there is trowing with millions and millions.
It is no blame on the researchers or anyone, just all our goverments. 1000’s of studys, most of them so small just because it is for me/cfs or fm , …
Look for excample at covid-19 and how the world can throw with money if they want.
Wow, human physiology is sooo complex.
Can anyone clarify what is meant by ‘poor sleep’!
My daughter ‘sleeps’ for 10 hours each night ….and NEVER feels rested. Never remembers any dreams. And goes into the deepest sleep (she believes) around the 5am mark…through to 9am when her alarms goes. The alarm is just to keep some kind of routine. Sometimes she is not aware she has turned it off and she goes into deep oblivion for another hour!
BTW she did (long ago) cortisol spit testing over 24 hours. All 4 readings came back high yet her symptoms overlap from those of high and low cortisol.
There is still a lot to unpick here. I hope they work quickly…some machine learning might speed up some of these processes!
No kidding…I read and reread and reread this study and the others. So complex…I hope I got it right.
Unrefreshing sleep is a key symptom in ME/CFS. Since she’s getting enough sleep she’s probably not getting the right kind of sleep. Too much sleep, though, is as bad physiologically as poor sleep. It’s good you’re keeping her to a routine.
I think these researchers would love, love, love to do more on the HPA axis and ME/CFS/FM. After quite a hiatus they’ve published three studies in the past couple of years. Next they’re going to work on their ACTH findings.
I have CFS and my cortisol runs high, especially in the am. I, too, have symptoms of high and low cortisol at various times.
I think you are not alone. In fact, the variability we see in the studies may reflect people’s cortisol levels bouncing around.
I have consistently borderline high AM serum cortisol. Twice it was slightly over the range. In fact for a while I was chasing a cyclical cushing’s diagnosis. I’ve had 6 serum cortisol tests, 3 x 24hr urines, and 1 dex suppression test. Urine and dex tests came back normal.
Im just like your daughter in my sleep patterns .I was diagnosed with ME/CFS in 1997.
Got fibro five years latter.
Have now got 7 autoimmune diseases as well.I go to bed at 2am.
Sleep on and off .Then awake for hours until about 6am i fall i to a really deep sleep not waking until 10am.
I feel like ive done 45 rounds with mike tyson.
Then i read or go on my phone .
Then the next thing i wake up and its always past 12 pm.
I cant function much.
But do a bit of cooking gardening or housework.
Then after dunner im straight back on the couch till 2am again.
I was called lazy all my life yet ive never been lazy.
Good luck to your daughter i no exactly how she feels.
I’m not sure how accurate the saliva tests are. Here in Australia they are not used for diagnosis of the condition. I did one with a private lab which takes 4 x samples 6-8 hours apart. 1 of the samples was borderline high and the other high above range. The recommendation was to take DHEA. I kind of had my doubts about the legitimacy of the test and interpretation. I have consistently borderline high AM serum cortisol, but from the several 24 hr urinary tests they are all in range and on the dex suppression(which I believe is the most accurate) my cortisol excretion did suppress as normal.
I’m curious as to the comparison between these cortisol levels in these ME/CFS and Fibromyalgia studies to Cushing’s disease? My CFS illness was showing similar fluctuating cortisol levels as those found with Cushing’s. No tumors were seen on scans of the pituitary gland. A recent death in the family has activated something causing BP spikes, increased inflammation and migraines.
I imagine that they are much worse in Cushing’s diseases. While HPA axis findings are generally “positive” i.e. they find something wrong there are studies which don’t. I think the medical profession doesn’t really know what to do with cortisol and ME/CFS/FM. Is the HPA axis a causal factor or is it reacting to something? And how much of role does it play?
My guess is that this is a multisystem problem. Cushing’s disease is so much easier!
Found the info of increased research into ACTH very interesting. I was diagnosed with CFS in 1986 by a doctor who had spent 16 years actively researching why I was sick. He used to give me ACTH injections when I was not doing well. He said he published the first medical journal article on ACTH and went to his bookcase to get the article for me to read. It’s very frustrating now when I am in a bad flare to know that 40 years ago there was a medicine that helped me with no side effects that is not available to me now.
I have Cfs. My cortisol tends to run high, especially in the am. I know that cortisol is deeply involved in cfs. High cortisol drives the air hunger that so many of us with Cfs experience. I had autonomic testing done and it was determined that I am mildly sympathetic nervous system dominant. Do you think it’s possible the drug Cortene might be a treatment for the issues this study brings up?
I’m interested in cortene too and hoping it can be a solution for some. I have consistently high AM cortisol.
Cort, why is that one study controversial?
Ah, the failures of conservative endocrinologists. About 5 years ago I had a morning cortisol test where I was somewhat above the reference range. I recently got tested again, saliva, just before bedtime, two nights in a row, and the tests came back 30 one night and 60 the next with ‘normal’ being under 100. There were no other test times.
I suppose this only means I don’t have Cushings, and really doesn’t shed much light on what my cortisol levels are doing throughout the day. Is this really a common practice? My endocrinologist only said, ‘normal’ with no other comment so I don’t know if my values are high or low normal.
I’m quite sure I have hyper-POTS and probably there is some relationship to cortisol as well as my Hashimotos.
I find it very frustrating when doctors are ‘just taking a snapshot’ rather than trying to document ‘a process’ to try to find out what may not be functioning optimally.
This might explain my still crappy sleep – thanks!!
Do you know if the scientists are looking at Seriphos for reregulating dysregulated cortisol production?
My daughter’s salivary cortisol test results fit right in with the ME pattern. Normal except for very low first thing in the morning. First thing that I found to help her–small but noticeable reduction in symptoms–was liquorice, which has a mineralocorticoid affect.
The drug Florinef has the same affect as licorice. I took it for 20 years and it helped quite a bit, until it stopped working. I also took Thermotab buffered salt tablets with a lot of water with the Florinef.
The only time I’ve showed any improvement was the years on low dose steroids, I was still able to work part-time, sleep and occasionally do something fun.
Hi G, I know this is an old thread but wanted to reply snyway. I had a similar experience, as I was given hydrocortisone to ease my symptoms for over 2 years after my first real ‘crash’ – and it worked pretty well, I had to manage it carefully but I felt semi-normal much of the time. I had no health insurance and was paying out of pocket to see a DPC functionalist, who of course said it was adrenal fatigue.
Then I got on Kaiser Permanente through my job, and they wont give it to me. Their Endo did do an ACTH Stim test and said it was normal, so no HC needed; she thought the benefit i was getting from it was outweighed by the risks of long term steroid use, and that it was likely covering up the real issue – which was NOT the adrenals. Since then, I have been in a steady decline. I am still hanging on to my job but its getting really hard to do – and have given up almost everything else in my life in order to just keep working. I usually have a brief period of feeling almost normal again when fall/winter arrive (anything over 70 degrees is almost debilitating, so when fall arrives its like a tremendous weight/pressure is lifted for a time), but not this year. I have considered going back to the functionalist just to get the HC again, but the kaiser docs are very against it and I am concerned maybe they are right. But it did seem to help so much!
SImon Wessely and Michael SHarpe would probably agree with this stress related cause. This is what they have been trying to say for a long time now.
I don’t think so Martin. My understanding of what Wessley, Sharpe and the others think, is that ME/CFS is caused by mistaken beliefs that a person may have about their symptoms and activity levels.
So they therefore need Cognitive Behavioural Therapy (CBT) to challenge their incorrect beliefs about being ill.
They also need Graded Exercise Therapy (GET) to increase their activity levels, until they reach normal levels because Wessley et al don’t, I think, believe there’s any valid reason for ME/CFS patients to be unable to achieve this goal.
From my own personal experience I believe my HPA axis and sympathetic nervous system went into overdrive, causing a multitude of issues, which had a domino effect throughout my body.
As far as I’m aware, Wessley et al would believe that my illness was based on my perception of being unwell and that there was no basis in reality to back up my belief.
As far as I can see, they are not talking about the disruption of powerful systems within the brain/body, they are focused instead on incorrect beliefs within the mind.
This one was a little over my head. My takeaway is that the relationship between cortisol and our symptoms is probably more complex than what we’re told by both conventional endocrinologists (e.g. your hormone levels are normal) and alternative health practitioners (e.g. the functionalist who confidently diagnoses “adrenal fatigue,” solving the mystery of ME, during your initial 15 minute consult).
Tracey Anne Yes you are right. They must also secretly know the haemohemorlogicql reason for PEM and probably the disease itself. Read Ramsay’s Disease on Amazon.
Yes, that book looks very interesting. Do you get ME Essential from the ME association in the UK?
I see from Dr Charles Shepherd, that the publication of the new NICE guidelines on ME/CFS has been put back from October to December 2020.
It’ll be interesting to see what happens when they are published…
No I don’t get that mag. I spoke to them about various things lately and they did not want to answer my question about why JB got better from ME when I said she had had thyroid cancer and had it out. TB said he could not understand it at all but they did not want to talk about it (and dismissed CCI as the reason) The Nice people as I saw it are still very BPS so I have my doubts! 😉 😉
tracey, People just say that about Wessely but he has at least researched CFS as this paper on immune function shows http://www.simonwessely.com/Downloads/Publications/CFS/149.pdf
I’ll have a look Martin
‘A systematic review and critical evaluation of the immunology of chronic fatigue syndrome’. Marc Lyall, Mark Peakman, Simon Wessely
They’re reviewing the literature, which was available at the time (2001). I wouldn’t be able to comment on how good their review was, but they say – “As regards the aetiology of CFS, our results do not rule out the possibility that the syndrome is caused, at least in part, by immunological dysfunction.”
Yes you are right Tracey. Actually I looked at Simon Wessely’s earlier papers on his website and he seems to scorn ME/CFS as though he knows or knew it is/was a psychological illness the way he talks in these papers.
http://www.simonwessely.com/Downloads/Publications/CFS/2.pdf
This one in 1989 he was suggesting CFS is an affective disorder.
Wessely talks the talk but does not come up with anything viable. He likes discounting things and scorning this illness for some reason I don’t understand. Same for his Gulf War Illness research I think. Yet Wessely has changed the way ME/CFS is seen and treated by GPs in the UK and it is not getting any better. In fact I think it has only got worse over the last 15 years or so that he has been on the scene.
I’ll have a look at that one tomorrow, Tues. Am trying to have a bit of discipline and avoid the law of diminishing returns…
What kind of Blood work should we ask our physician to do to get some clue about our cortisol levels and possible just a clue about what going on with us more if anything.
Wow talk about interesting reading my head and mind are whirring.
So these conditions both of them ME/CFS and fibromyalgia are really linked.Does one get Me/CfS first and Fibromyalgia becomes an add on.I have been told by a doctor that they are the same condition but reading this research I think there are differences in both of these conditions.
I do feel however they are definitely linked to the Pituritory Gland.
Would love something concrete to come out if these studies and a plan to help us with these conditions.
They seem to do the research and then trail away when it comes to treatment.
I am 72 now no hope of any help in my life time but hope they progress to a positive outcome for the future.
I’m hypopituitary now (sheehan’s syndrome). I was dxed with FMS in 2011, then adrenal insufficiency in 2014.. been taking steroids daily since… I feel better right after dosing, but have to dose 5x/day since hydrocortisone doesn’t stay in the system as long as prednisone or other more damaging steroids. When I have to stress dose (infection, surgery, etc), and take 3x normal steroid dosing for 3 days, I feel wonderful… almost normal… my FMS pain is minimal, etc… I am an ultra rapid metabolizer and seem to need more meds than the average person for the same effect.
For those getting cortisol levels tested, it’s important to do the first one at around 8am, that is when your level should be the highest… (top of the normal range). For those drs who say it’s fine, within range, but heck it’s at the bottom, they are not educated in the normal circadian rhythm of cortisol. Also a good idea is to test ACTH at the same time as morning cortisol, this will differentiate if you have primary adrenal issues with low cortisol or secondary (pituitary related). Very interesting article, thanks.
I’ve had ME/CFS for about 6 years. When I was trying to figure out what I had years ago, I met with an autoimmune doc. He told me that he has had some success with cortizone and other immune suppressing drugs with ME/CFS patients. He offered to try it on me. At the time, I turned him down.
Recently, to treat an unrelated issue, I was on low-dose oral cortizone for one week. It was the most energy and best sleep I’ve had for months. Its making me wonder if an over-active inflammatory response is the primary culprit. Now after feeling so much better on cortizone, I may be willing got back to this doc to give it a try, at least to experiment to see what happens.