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Hydrocortisone & Thyroid Hormone Use in ME/CFS + Misdiagnosing Rarer Hypothyroidisms as ME/CFS

Hip

Senior Member
Messages
17,798
Please note, this post and the following 93 posts have been split from this thread.

(http://forums.phoenixrising.me/inde...lgium-doctor-after-failed-by-nhs.32918/page-3)



A few years ago tried triiodothyronine (T3), at doses of around 5 to 20 mcg daily.

Looking back at my medication notes diary from 2012, I see that after around two weeks of taking T3 in daily doses ranging from 10 to 20 mcg, I suddenly began a two month period of frenetic energy and motivation, where I found myself working much, much harder than normal on various projects and activities.

I forgot about this uncharacteristic energetic period I had, but looking back at my notes, it seems that T3 might have been the cause of it. I think I will definitely try some T3 again, to see if I can replicate these results, and get a high energy period.

The reason I took T3 in he first place is because T3 is a potent inducer of mitochondrial biogenesis (the creation of new mitochondria in cells). Two potent inducers of mitochondrial biogenesis are T3 and nitric oxide (NO); however, NO cannot really be used to promote mitochondrial biogenesis, because NO levels are very tightly controlled by the body, so it is not easy to raise NO. But T3 levels are easy to raise, just by taking T3. Some people use T3 as a means to burn off fat, and I don't think there are any dangers in taking it, at least for short periods of a few months. If there are mitochondrial problems in ME/CFS, then you might expect mitochondrial biogenesis from T3 to be a useful treatment strategy.

I am not hypothyroid, since I was tested for this.
 
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Ema

Senior Member
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4,729
Location
Midwest USA
What are the risks involved in taking these hormones? As I understand it there are two possible situations. One is that corticosteroid and/or thyroid hormones are taken in a small supplemental dose that will suppress normal production and therefore have no significant continuing effect. The other is that the doses are big enough to produce a physiological effect which, unless there is pituitary, adrenal or thyroid disease, will produce a hormone excess syndrome.

I think you are missing the third situation which is, of course, the goal of any treatment with hormones. That is, the *optimal* hormone level will be replaced with exogenous hormones to provide the benefits of the hormones as nature intended while minimizing risks and side effects.

Appropriate, optimal hormone levels are mandatory for proper functioning of every system of the body. No system, including the immune system, can function efficiently (or sometimes even at all) without cortisol and thyroid hormones.

You are right that too small doses have either no effect or will make a person feel worse.

Hormone excess syndrome is not seen in physiological replacement, only in pharmacological dosing.

Note that in the first situation the person will feel 'improved' on starting cortisol, thyroid or oestorgen. All of these in different ways produce a 'lift' of a sort. That lift will disappear as soon as the gland is suppressed - maybe within a few days. But if the person stops the treatment they will feel lousy for a while.

All that means is the dose is too low and needs to be raised to optimal. It does not mean that the dose is too high. This is a common misconception typically made by those who have never actually taken hormones.

So 'improvement' on taking these hormones and 'worsening' on stopping them will happen to anybody who is down - and will have absolutely nothing to do with the hormones being useful for any disease they might have. Long term treatment will achieve nothing at all. The temporary effects will occur in people without ME. The situation is probably a bit like smoking or drinking coffee or alcohol or taking valium. Selling something that you get hooked on for reasons that have nothing to do with an illness may be OK for adults and it may cause no harm at this level but for most of these things we have laws protecting children against foolish usage. Note again that by definition at this level even if the person has ME and hormones turn out to be good for ME they will get no benefit, since gland suppression ensures that their hormone levels over time are essentially unchanged.

Comparing appropriate hormone treatment to drinking or smoking is so far off base it isn't even funny. Although, strangely enough, when you treat people with endocrine diseases with appropriate hormones, often times their urges to drink or smoke stop or are greatly lessened. Turns out nicotine and alcohol are pretty great hormonal stimulators. But of course, why do that when one can insist on a 12 step program with a recovery rate less than 5-10%? And, BONUS, then you get to blame the patient for being weak when it fails!

How does gland suppression ensure that their hormone levels over time are essentially unchanged? If the hormone level is unchanged, the dose is not high enough.

If the dosages are high enough to have a genuine effect on long term hormone levels there are serious complications to consider. For corticosteroids we have diabetes, juvenile cataract, bone loss, weight gain, skin atrophy, scarring acne, hair loss, coronary artery disease, etc etc even with doses that raise levels marginally. For thyroid hormones we have bone loss and at higher levels atrial fibrillation with cerebral embolism and stroke. Oestrogens have all sorts of effects too.

I've already addressed the myths of thyroxine supplementation causing osteoporosis. The scientific literature does not agree.

Hyperthyroidism produces fibrillation - but that means that the thyroid dose is too high, or the cortisol dose is too low, so in essence all this means is that the hormone treatment is again improperly managed. At optimal levels, these things do not happen.

Estrogens also are protective against heart disease and osteoporosis. The follow up to the WHI study showed this but to much less fanfare than the original study results because they were not nearly so fear-mongering as to provoke the attention of the media. This has resulted in women stopping BHRT for no good reason and suffering in vain.

As far as steroids, talk to any Addison's patient and read the literature - physiological doses of steroids do NOT cause the effects you list. If one is getting those side effects, the dose is pharmacological and too high. Here is the biggest side effect of too low cortisol: death by adrenal crisis. Most with ME/CFS do not have Addison's disease but low cortisol has been a consistent finding and should be treated rather than brushed off as most studies have tended to do.


Dr Hertighe appears to belong to a group of prescribers who feel that hormone deficiency can be diagnosed at normal test levels. My question would be how that diagnosis can be made. If it is on the basis that people feel a bit better when given a small dose of hormone, from what I have said above this would seem to be invalid - normal people or people feeling down for any reason may feel better for a brief period. If hormones are prescribed to a child with normal tests I think that does raise very serious legal and moral issues.

Tests are not the be all end all of medicine. I personally believe examining the patient and their symptoms is also of value, especially when there is so much that is not understood about hormones.

As far as I know, there is no "standard" level of optimal hormone levels, only antiquated ranges that encompass 95% of the population.

There is no mention of enzymes or binding proteins that might also be causing hormonal dysregulations as a factor in interpreting test results for the most part which is a huge oversight in my opinion.

Most endocrinologists don't even know how to administer the tests we do have properly and then make diagnoses based on these improperly performed tests all the time to the detriment of the patient.

Hertoghe may be over the top in terms of hormone treatment, but at least he is willing to treat the patient rather than a piece of paper. Subclinical deficiency is a real phenomenon due to the problems with the tests, not the problems with the patient.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
The Lancet says this on the issue;

We suggest that thyroxine alone does not have a significant effect on bone mineral density and hence on risk of osteoporotic fractures.

Yes but, for instance the more recent, http://www.medscape.com/viewarticle/408957 says

Conclusion: Our results suggest that women who begin long-term ( ˜ 10 years) thyroxine therapy in the premenopausal period can develop osteopenia by the beginning of menopause.

It may well depend in the dose and I strongly suspect you would need a fully suppressive dose to get an effect but I think the controversy continues. As you say, one wonders what the motives are for some of these studies. Anything below a suppressive dose would I think fall under my first scenario in which the patient's thyroid status is not actually changed. The result above might only occur with the generous or oversuppression preferred for treating thyroid cancer but I do not know the details.
 

Ema

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Yes but, for instance the more recent, http://www.medscape.com/viewarticle/408957 says

Conclusion: Our results suggest that women who begin long-term ( ˜ 10 years) thyroxine therapy in the premenopausal period can develop osteopenia by the beginning of menopause.

It may well depend in the dose and I strongly suspect you would need a fully suppressive dose to get an effect but I think the controversy continues. As you say, one wonders what the motives are for some of these studies. Anything below a suppressive dose would I think fall under my first scenario in which the patient's thyroid status is not actually changed. The result above might only occur with the generous or oversuppression preferred for treating thyroid cancer but I do not know the details.
Suppressive vs non-suppressive dosing is confusing for most patients. This is referring to the suppression of the TSH. The TSH is not a good measurement of thyroid hormone replacement. This has been shown time and time again yet the endocrinology associations cling to it for reasons unknown. So why would it be presumed to be a good measurement of thyroid function after thyroid removal? It wouldn't.

The thyroid status IS changed in appropriate therapy - it is raised to optimal. If there is no change, the doctor is doing it wrong!

That same Medscape article says this about suppressive and non-suppressive thyroxine replacement:

Suppressive doses of thyroid hormones have been reported to reduce or to have no effect on bone mineral density (BMD) in women. Meta-analysis of published reports has indicated that a 1% BMD loss occurs during the postmenopausal period in women who were administered suppressive doses of thyroxine.

In contrast, substitution therapy with thyroid hormone shows no harmful effect on BMD.[1]

There's nothing in this article that warrants continuing fear-mongering about appropriate thyroid replacement leading to osteoporosis. Get a bone scan, by all means, if on long term treatment for hypothyroidism. That's probably a good idea for everyone. But there are many factors involved in osteoporosis and optimal thyroid hormone may very well be found to be protective against such states. There's a reason we have hormones, after all.







 

Jonathan Edwards

"Gibberish"
Messages
5,256
I think you are missing the third situation which is, of course, the goal of any treatment with hormones. That is, the *optimal* hormone level will be replaced with exogenous hormones to provide the benefits of the hormones as nature intended while minimizing risks and side effects.

As far as I know, there is no "standard" level of optimal hormone levels, only antiquated ranges that encompass 95% of the population.

I do not want to argue about this in detail because I am afraid the 'optimal' issue makes no logical sense to me. As you say, there is no standard. We have no idea how to define it except that the person likes the feel of it. They may not like the feel of the consequences 20 years later.

If TSH is pushed down then the dose must be 'more than the hypothalamus wants'. If it is not pushed down then you are having no effect on tissue delivery of hormone efficacy. I cannot see where 'optimal' comes in to this otherwise. All servo systems do have a finite sensitivity and response lag so there might be a teeny weeny window of level to nudge up but I don't see how you find it in reality or why it should be helpful. If there is pituitary disease then things are obviously different but that will be rare I presume.
 

Cheesus

Senior Member
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1,292
Location
UK
It may be relevant to comment that treatment with thyroxine tends to reduce bone mass - in lay terms it can induce premature osteoporosis. I would expect one of the most important long term consequences of childhood ME to be a risk of long term osteoporosis, because bone mass in adult life is critically dependent on peak bone mass at about 25, which is dependent on exercise. I would therefore be very concerned about giving thyroxine to children with ME unless someone has done a long term analysis and shown it to be safe. Premature osteoporosis can significantly shorten life expectancy.

People may be interested to view U-tubes of Dr Hertoghe at the anti-aging conference in Las Vegas in 2012.

Just out of curiosity, what happens if you suddenly and massively reduce activity at the age of 22? Would that potentially significantly impair bone mass at 25, or is bone mass fairly well established by that age?

Just to add, I am not trying to get personal medical information on the sly, but your comment gave me a little shock as I am currently 24 and have been lying in bed for 2 years.
 

Hip

Senior Member
Messages
17,798
Hello Hip,

I answered that question earlier, but to save you scrolling back the information was passed on by the patient advocate who is supporting the mum. At this juncture, of course, the amount of detail that can be posted is limited until the court case.

Thanks Countrygirl, I must have missed your earlier comment. I just wondered which hormones are being considered as "poison" and which are considered as benign, from the legal perspective of the court case. If we know which hormones are the issue, then we can search for supporting evidence for the safety and use of those hormones in ME/CFS.

From what you have written in your first post of this tread, it seems that the "poisonous" hormones are "natural thyroid extract" (which contains the hormones T4 and T3), oestrogen and hydrocortisone.

In the case of oestrogen, if the dose given was less than or equal to the dose found in a contraceptive pill, then I would think we can discount that as being toxic, just on that basis (depending on the age of the daughter).

Hydrocortisone has been used as an experimental treatment of ME/CFS, and often patients feel better in the short term, as Prof Jonathan Edwards mentioned above, likely due to the immune suppression of hydrocortisone which would mean any immune driven symptoms are reduced; but after some months patients may feel worse, probably as a result of their infections getting the up hand.

This study of hydrocortisone for ME/CFS found that low-dose hydrocortisone "was associated with some improvement in symptoms of CFS, the degree of adrenal suppression precludes its practical use for CFS". And this study concluded that "patients with chronic fatigue syndrome, low-dose hydrocortisone reduces fatigue levels in the short term. Treatment for a longer time and follow-up studies are needed to find out whether this effect could be clinically useful."

There is an article here about hypocortisolism is ME/CFS. Perhaps in patients who have some hypocortisolism, hydrocortisone replacement might be more appropriate.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
Just out of curiosity, what happens if you suddenly and massively reduce activity at the age of 22? Would that potentially significantly impair bone mass at 25, or is bone mass fairly well established by that age?

Just to add, I am not trying to get personal medical information on the sly, but your comment gave me a little shock as I am currently 24 and have been lying in bed for 2 years.

I cannot give you expert advice on that but my guess is that by 22 you are at least pretty close to peak bone mass. Inactivity is associated with bone loss at any age but it is slow so I guess you will not have lost much ground. My rheumatological colleagues tend to think about bone protection for almost anyone with immobility these days but I suspect that using something like a bisphosphonate would not be common in your situation.
 
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12
It may be relevant to comment that treatment with thyroxine tends to reduce bone mass - in lay terms it can induce premature osteoporosis. .

Here are some studies on the Thyroid/Osteoporosis Connection - or non-connection!

A study released in June, 2000, at the World Congress on Osteoporosis in Chicago, Illinois, found that taking thyroxine (i.e., Synthroid) does not increase the risk of osteoporosis. The research, presented by Dr. Martin Stenstrom of the University of Gothenburg in Sweden, studied more than 750 women who were taking prescribed thyroid medication for thyroid disease. Over an 18 month period, bone mineral density was measured, and compared to a control group who were not taking thyroid hormone. No differences were noted in bone mineral density between those taking the thyroid hormone, and the control group. An October, 1998 study reported on in the Journal of Gynecological Endocrinology found that levothyroxine suppressive therapy, if carefully carried out and monitored, has no significant effect on bone mass. ( Gynecol Endocrinol 1998 Oct;12(5):333-7, "Bone mineral density in premenopausal women receiving levothyroxine suppressive therapy.").

The highly regarded Journal of Clinical Endocrinology and Metabolism found that even "suppressive," levothyroxine therapy -- prescribing medicine that lowers TSH levels to hyperthyroid levels below normal range -- if carefully carried out and monitored, has no significant effect on bone metabolism or bone mass. ( J Clin Endocrinol Metab 1994 Apr;78(4):818-23, "Carefully monitored levothyroxine suppressive therapy is not associated with bone loss in premenopausal women.")

A major thyroid-related journal, Thyroid, found that long-term levothyroxine therapy using suppressive doses has no significant adverse effects on bone. (Thyroid, 1995 Feb;5(1):13-7, "Suppressive doses of thyroxine do not accelerate age-related bone loss in late postmenopausal women.")

Finally, in 1998, the Journal of Hormonal and Metabolic Research found that there was no difference in bone mineral density between thyroid patients and controls, and that the main factor in bone density and bone turnover is menopausal status. The researchers found that slightly suppressive levothyroxine doses constitute neither an actual risk factor for bone loss nor, consequently, for osteoporotic fractures. (Horm Metab Res 1995 Nov;27(11):503-7, "A slightly suppressive dose of L-thyroxine does not affect bone turnover and bone mineral density in pre- and postmenopausal women with nontoxic goitre.")

On the other hand, there is some research that suggests that the osteoporosis risk may be a legitimate concern.

A May 2000 study in the European Journal of Endocrinology found that long-term treatment with levothyroxine to normal range TSH levels was associated with a slightly increased risk for osteoporotic fracture. (Eur J Endocrinol 2000 May;142(5):445-450, "The effect of long-term, non-suppressive levothyroxine treatment on quantitative ultrasonometry of bone in women.").

And the Journal of Clinical Endocrinology and Metabolism has said that, although controversies exist on the possible adverse effect of T4 on bone mass, most studies reported bone loss in estrogen-deprived postmenopausal women taking suppressive doses of levothyroxine. Levothyroxine- suppressive therapy was associated with bone loss in postmenopausal women, however, it could be prevented by either calcium supplementation or intranasal calcitonin. ( J Clin Endocrinol Metab 1996 Mar;81(3):1232-6, "Prevention of bone loss induced by thyroxine suppressive therapy in postmenopausal women: the effect of calcium and calcitonin.")
 

Ema

Senior Member
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I do not want to argue about this in detail because I am afraid the 'optimal' issue makes no logical sense to me. As you say, there is no standard. We have no idea how to define it except that the person likes the feel of it. They may not like the feel of the consequences 20 years later.

If TSH is pushed down then the dose must be 'more than the hypothalamus wants'. If it is not pushed down then you are having no effect on tissue delivery of hormone efficacy. I cannot see where 'optimal' comes in to this otherwise. All servo systems do have a finite sensitivity and response lag so there might be a teeny weeny window of level to nudge up but I don't see how you find it in reality or why it should be helpful. If there is pituitary disease then things are obviously different but that will be rare I presume.

"Likes the feel of it" is quite a disparaging way to say "feels healthy" that brings back your earlier comments comparing hormone replacement to drug abuse. It's offensive.

The TSH is not a good measure of either thyroid hormone status (measure the free thyroid hormone levels instead for *some* idea of actual thyroid hormone status). Why use a roundabout measure like a pituitary hormone when one can measure the hormone directly? Again, it's antiquated thinking so I can understand why one would not want to argue about this in detail.

Most hypothyroid patients feel best with a TSH between 1 and 2. That's hardly "pushed down". In fact, it's quite "normal" - despite the "normal" range going all the way up to 5 in some countries.

However, many thyroid patients also feel fine with a TSH as low as 0.2-0.3. This *is* suppressed but has not been shown to have any ill effects (probably because the TSH doesn't have as much to do with thyroid hormone levels as was once thought).

Frank suppression, on the other hand, has been shown to have side effects which is why no one advocates dosing thyroid hormone that high. This is why using the TSH to measure thyroid hormone status is foolish and antiquated though it is amusing to think of what the hypothalamus "wants" even though TSH is actually a pituitary hormone.

Optimal is where a particular patient feels best and it is most usually within the bounds of the normal range which encompasses 95% of the population. I'm not sure why doctors would have any problem treating to those numbers considering that they fall into the "normal" range for the most part. But especially in the UK, doctors seem content to let patients continue to suffer from hypothyroid symptoms. Doctors that treat patients rather than lab results have found that patients typically feel best with a FT4 in the range of 1.2-1.5 ng/dl and a FT3 in the top third of the range. If a patient continues to have symptoms with numbers lower than this, they are not optimally treated. Seems pretty simple to me.
 

Ema

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Hydrocortisone has been used as an experimental treatment of ME/CFS, and often patients feel better in the short term, as Prof Jonathan Edwards mentioned above, likely due to the immune suppression of hydrocortisone which would mean any immune driven symptoms are reduced; but after some months patients may feel worse, probably as a result of their infections getting the up hand.

Physiological dosages of hydrocortisone do not cause immune suppression. In fact, hypocortisolism causes loss of immune function. Too little cortisol is just as bad as too much.
 

alex3619

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Hormone excess syndrome is not seen in physiological replacement, only in pharmacological dosing.

This is a point I agree with. Low dose treatments, designed to improve hormones within normal physiological ranges, are typically not an issue. Lots of these concerns arose with cortisol, which in physiological doses is lifesaving and highly beneficial with almost no downside. Yet a lot of focus in the literature has been on immunosuppressive doses. Such doses are very dangerous long term. The two dosage regimes are however confused. I suspect something similar may be happening with thyroid hormones, but have not researched this.

Lets talk testosterone as another example. Abusive steroid regimes designed for bodybuilding are dangerous. Yet used within physiological ranges, what is the harm? The key is monitoring and adjusting dosage, and that includes monitoring other physiological factors that might be affected.
 
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It's hard to know just how much of this is driven by the acrimony of divorce, with the father out of spite painting a very negative picture of the mother to the authorities.

But certainly I have tried all these three hormones myself to see if they might help my ME/CFS, so I am astounded that simply treating an ME/CFS patient with them can lead to a court case.

A few years ago tried triiodothyronine (T3), at doses of around 5 to 20 mcg daily.

Looking back at my medication notes diary from 2012, I see that after around two weeks of taking T3 in daily doses ranging from 10 to 20 mcg, I suddenly began a two month period of frenetic energy and motivation, where I found myself working much, much harder than normal on various projects and activities.

I forgot about this uncharacteristic energetic period I had, but looking back at my notes, it seems that T3 might have been the cause of it. I think I will definitely try some T3 again, to see if I can replicate these results, and get a high energy period.

The reason I took T3 in he first place is because T3 is a potent inducer of mitochondrial biogenesis (the creation of new mitochondria in cells). Two potent inducers of mitochondrial biogenesis are T3 and nitric oxide (NO); however, NO cannot really be used to promote mitochondrial biogenesis, because NO levels are very tightly controlled by the body, so it is not easy to raise NO. But T3 levels are easy to raise, just by taking T3. Some people use T3 as a means to burn off fat, and I don't think there are any dangers in taking it, at least for short periods of a few months. If there are mitochondrial problems in ME/CFS, then you might expect mitochondrial biogenesis from T3 to be a useful treatment strategy.

I am not hypothyroid, since I was tested for this.
You say you are not hypothyroid but you also state that T3 might have been the cause of an uncharacteristic energetic period. Do you not think the doctors may have been wrong and you more than likely have a low functioning thyroid. There is much worldwide debate on diagnosis and treatment surrounding thyroid issues.
 

Hip

Senior Member
Messages
17,798
Physiological dosages of hydrocortisone do not cause immune suppression. In fact, hypocortisolism causes loss of immune function. Too little cortisol is just as bad as too much.

If you give hydrocortisone to an ME/CFS patient whose cortisol is normal, then you have supraphysiological levels. So it depends on whether you are giving hydrocortisone to correct hypocortisolism, or as a corticosteroid treatment for ME/CFS.

Interestingly enough, Dr John Chia has observed that patients who were given glucocorticoids like hydrocortisone or prednisone by a doctor during the acute phase of an infection — because doctor thought the symptoms were suggestive of asthma — have a high risk of developing ME/CFS later. This combination of glucocorticoids during acute infection is a recipe for precipitating ME/CFS, Chia has found.

To quote Dr Chia:
"Glucocorticoids: if the patient developed a viral infection, and with symptoms suggestive of asthma, they are often given steroids, because it's the mainstay of therapy. That can shift the immune response to Th2, not to mention you'll drop the T-lymphocytes down to practically zero."

"If the patient already had chickenpox before and they then develop flu-like illness with chickenpox-like rashes that's enterovirus until proven otherwise. But the rash could look like measles, German measles, it could look like hives. So very often people travel, eat some shellfish, and develop this hives, all over. Went to the emergency room, the emergency room doctor will say, "Oh Well, you ate lobster, you must be allergic to shellfish. " So what's the next thing they get? They get some prednisone, steroids, and that disease never ended. They develop chronic fatigue syndrome after that. We hear this hundreds of times."

Source: Enteroviruses in ME/CFS Presentation, Invest in ME International ME/CFS Conference, London 2010


So one etiology for ME/CFS that Dr Chia says he has observed hundreds of times is the incorrect prescription of glucocorticoids when a patient has initially come down with a viral infection. One might guess that the immunosuppression caused by these glucocorticoids during the acute infection stage prevents the immune system from dealing with the virus, so that perhaps the virus is able to insinuate itself more into the body, leading to ME/CFS.

Of course, giving glucocorticoids like hydrocortisone once the patient already has ME/CFS is not associated with any known risk. It is only during the acute phase of infection that glucocorticoids appear to be able to precipitate ME/CFS.

Chia says he now tells every doctor to only prescribe glucocorticoids to a patient if their life depends on it, due to the significant risk he has uncovered connecting glucocorticoids during acute infections to the later development of ME/CFS.

I wish more research would be undertaken on this connection that Chia seems to have found.

I also think that this data from Dr Chia is extremely important in terms of understanding ME/CFS viral etiologies in general. It suggests that the enterovirus itself is not the main etiological determinant; rather, it is the state of your immune health when you caught the infection that may play a major role in whether that infection leads to ME/CFS or not.
 
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Ema

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It's very hard to add to your own cortisol due to the feedback mechanism. So even a person taking 10-15 mg of hydrocortisone would not likely end up with higher levels of cortisol than they had prior to taking it. In fact, they often end up with lower levels due to suppressing more than they replace. They certainly would not end up with higher than physiological levels or immune suppression. This is true for everyone whether they have low or normal levels of cortisol to start.

At higher than 20-25 mg, typically full reversible adrenal suppression is seen but many say that doses under 40mg a day are not immunosuppressive. In fact, for acute infections, those with adrenal insufficiency are instructed to double or even triple their normal daily dose in order to fight an infection. So (in the short term) even those doses up to 100 mg or so would not be considered immunosuppressive though they certainly would lead to side effects if carried on long term.

It's a real problem - how do you make sure a patient has enough cortisol for proper immune function without crossing the line? The natural system gets all mucked up in the face of chronic infections.

I completely agree with the risks of giving pharmacological doses of steroids.
 

Hip

Senior Member
Messages
17,798
You say you are not hypothyroid but you also state that T3 might have been the cause of an uncharacteristic energetic period. Do you not think the doctors may have been wrong and you more than likely have a low functioning thyroid. There is much worldwide debate on diagnosis and treatment surrounding thyroid issues.

Some borderline hypothyroidism is a possibility I guess. And I am certainly going to investigate this further. I have just ordered some more liothyronine (T3), to try to repeat my results. I only noticed the connection between T3 and my frenetic energy period while reviewing my records, due to this thread.

However, this frenetic period I had lasted for 5 weeks after I stopped taking the T3 (I only took T3 daily for around two weeks, and then I stopped).

T3 is a fast acting thyroid hormone, and has a relatively short half life of around 1.5 days. So if I were hypothyroid, you would expect that on cessation of taking T3, within a few days my energy would have dropped down again. But my high energy went on for 5 more weeks after stoping T3.
 
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Hip

Senior Member
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17,798
At higher than 20-25 mg, typically full reversible adrenal suppression is seen but many say that doses under 40mg a day are not immunosuppressive. In fact, for acute infections, those with adrenal insufficiency are instructed to double or even triple their normal daily dose in order to fight an infection. So (in the short term) even those doses up to 100 mg or so would not be considered immunosuppressive though they certainly would lead to side effects if carried on long term.

It's a real problem - how do you make sure a patient has enough cortisol for proper immune function without crossing the line? The natural system gets all mucked up in the face of chronic infections.

Those studies I cited earlier used daily hydrocortisone doses in the 5 mg to 30 mg range in ME/CFS patients, so these are below the doses typically used in medicine, which are around 100 to 500 mg.

It's very hard to add to your own cortisol due to the feedback mechanism. So even a person taking 10-15 mg of hydrocortisone would not likely end up with higher levels of cortisol than they had prior to taking it. In fact, they often end up with lower levels due to suppressing more than they replace. They certainly would not end up with higher than physiological levels or immune suppression. This is true for everyone whether they have low or normal levels of cortisol to start.

So how can you tell whether the 10-15 mg of hydrocortisone you are taking is actually increasing your cortisol levels, or decreasing them due to a feedback mechanism? Would you need to take a salivary cortisol test to check this?
 

Ema

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Those studies I cited earlier used daily hydrocortisone doses in the 5 mg to 30 mg range in ME/CFS patients, so these are below the doses typically used in medicine, which are around 100 to 500 mg.



So how can you tell whether the 10-15 mg of hydrocortisone you are taking is actually increasing your cortisol levels, or decreasing them due to a feedback mechanism? Would you need to take a salivary cortisol test to check this?
You can tell once you've been taking HC for a while. I know it sounds bizarre but there are certain symptoms that always come on when my cortisol drops a bit low. But it does make it hard for someone just starting out. It took me about two years to get confident with what was what and I still struggle with stress dosing. It's the hardest part of trying to "drive" the adrenals in manual.

It would be amazing if they would finally come out with that saliva cortisol app for the phone. I think it would revolutionize treatment to be able to cheaply and easily test whenever you wanted.
 

bertiedog

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It's very hard to add to your own cortisol due to the feedback mechanism. So even a person taking 10-15 mg of hydrocortisone would not likely end up with higher levels of cortisol than they had prior to taking it. In fact, they often end up with lower levels due to suppressing more than they replace. They certainly would not end up with higher than physiological levels or immune suppression. This is true for everyone whether they have low or normal levels of cortisol to start.

At higher than 20-25 mg, typically full reversible adrenal suppression is seen but many say that doses under 40mg a day are not immunosuppressive. In fact, for acute infections, those with adrenal insufficiency are instructed to double or even triple their normal daily dose in order to fight an infection. So (in the short term) even those doses up to 100 mg or so would not be considered immunosuppressive though they certainly would lead to side effects if carried on long term.

It's a real problem - how do you make sure a patient has enough cortisol for proper immune function without crossing the line? The natural system gets all mucked up in the face of chronic infections.

I completely agree with the risks of giving pharmacological doses of steroids.
I wish there was a way of measuring one's cortisol level in the same way one can measure one' blood sugar. It would help so much to know what is going on when dealing with low cortisol symptoms. Perhaps one day there will be such a test, I for one would find it so helpful.

Pam
 

Jonathan Edwards

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@Jonathan Edwards

Thank you for the information. I am seeing a rheumatologist soon for an EDS assessment. Would he be the right person to speak to for personal advice? Despite my referral I am not entirely sure what a rheumatologist is!

A rheumatologist deals with bones and joints. Bone mass is something they tend to think of in relation to almost any illness but it would be worth raising specifically.