In Brief: The Adrenal Glands and ME

April 1, 2014

The second in a new series of ‘In Brief’ articles, where Andrew Gladman provides a helpful insight into the science behind fairly common topics, exploring how they relate to ME/CFS. This time he discusses the adrenal glands and why they can be such a talking point …

Diagram showing the location of the adrenal glands, above the kidneys.

Diagram showing the location of the adrenal glands, above the kidneys

While the frequent topics of conversation relating to ME/CFS appear to now be infectious agents, autoimmunity and often a dysfunctional nervous system, many patients and researchers still turn their attention to problems within the endocrine system, namely the adrenal gland.

As the gland within the body centred around stress responses, it is initially quite a logical place to look for problems. There can be no denying that patients suffering with diseases of the adrenal glands certainly do share many symptoms and complaints of those afflicted with ME/CFS.

There is then good reason to query where the adrenal glands may relate to ME/CFS. While the initial reason for querying this may seem simple, the answers raise interesting questions for the potential pathophysiology and reasons for the symptomology of ME/CFS.

What are the Adrenal Glands?

The adrenal gland is one of the body’s most vital endocrine glands. The adrenals are glands which secrete their hormone directly into the bloodstream, often as a result of the glands being innervated with blood vessels. Sitting above each kidney, these glands’ primary function is releasing the hormones and chemicals which in turn stimulate a stress response, often known as a fight or flight reaction.

However the adrenal glands do carry out numerous other functions.

The stress response is initiated through the production and release of corticosteriods, such as cortistol, and a larger group of chemicals known as catecholamines of which adrenaline (epinephrine) and noradrenaline fall under.

Diagram showing the division between the adrenal medulla and cortex along with the chemicals produced by each.

Diagram showing the division between the adrenal medulla and cortex, along with the chemicals produced by each

The adrenal gland is composed of numerous layers although it is often discussed simply as being split into two main regions, the medulla and the cortex.

The medulla is the centre of the gland and the cortex is the outermost layers. The medulla is responsible for the production of adrenaline and noradrenaline. It achieves this through complex innervation with neurons of the sympathetic nervous system which stimulate the adrenal medulla in times of acute stress, increasing the rate of synthesis and release of these chemicals.

The cortex, on the other hand, is tasked with the production of corticosteroids, including cortisol and aldosterone, along with androgen hormones (the male sex hormones). The cortex is further sub-divided into three separate layers differentiated by which of the discussed chemicals is being produced by the specialised cells in that region, although the specifics of this sub-division are very rarely discussed.

The HPA axis.

The HPA axis

Given the importance of the adrenal gland in producing these vital chemicals, there has evolved a complex set of interactions between other endocrine glands, the adrenal gland and the brain to help regulate one another through a process known as negative feedback.

This set of interactions occurs between the hypothalamus (a region at the centre of the brain), the pituitary gland (a small gland located at the base of the brain) and the adrenal gland. This set of interactions between these three areas is known commonly as the  hypothalamic-pituitary-adrenal axis, often abbreviated to HPA axis.

It is this HPA axis that is frequently discussed in relation to ME/CFS.

Given the wide range of chemical messengers produced by the adrenal gland through the complex interactions it shares within the HPA axis, it is clear that the gland has far-reaching consequences within the homeostasis of the body.

These include playing roles in helping to control and regulate body temperature, digestion, immune system responses, mood sexuality and energy usage, along with the adrenal’s primary function of controlling the physiological reaction to stress, trauma and injury.

It is clear to see why any dysfunction in either the adrenal gland alone or in the HPA axis as a whole could potentially cause a plethora of problems and symptoms. Dysfunction in the HPA axis is well known to be involved in a wide variety of psychological illnesses and is now being understood to play quite a large role in many physiological conditions too — understandably, given the stress that disease itself causes.

Why are the Adrenal Glands important in ME?

For many years now studies have indicated finding abnormalities in HPA axis function within the ME/CFS cohort. These abnormalities are often described in the literature to include mild hypocortisolism, heightened negative feedback, and blunted HPA axis responsiveness.

Fundamentally, this means that in those patients observed, cortisol levels are persistently lower than is to be expected. This appears to be traced back to the hypothalamus and pituitary gland becoming somewhat unable to appropriately detect or respond to the low cortisol levels.

Many studies have not just identified this as a fairly consistent finding in ME/CFS but have furthermore observed a correlation between this dysfunction and symptom severity. It is of note however that some studies dispute this finding.

This dysfunction in the HPA axis has been used somewhat deviously by some groups to verify the effectiveness of talking-based therapies such as cognitive behavioral therapy (CBT).

This is in part due to the effectiveness these therapies can appear to have in conditions such as anxiety disorders in which HPA axis dysfunction has also been proven to play a somewhat central role. However such a line of thought, while helpful in many diseases where HPA axis appears to be a disease mediator, is unlikely to be helpful in a disease where the HPA axis does not yet appear to be central.

While there are a large number of studies confirming their independent findings of HPA axis dysfunction, few make the leap to develop a hypothesis for this being the central disease mechanism. This is likely a result of the multitude of other research indicating a deeper physiological defect in ME/CFS of which HPA axis may simply be an unfortunate by-product.

One interesting study that bears thought as to HPA axis dysfunction developing as a secondary condition is a somewhat unrelated study by Dunn et al. This study focuses upon how cytokines can in turn activate the HPA axis, initiating a stress response. Cytokines are a rapidly emerging line of study in ME/CFS and we recently produced an article exploring why they are gaining increased exposure in the ME/CFS research field.

It’s an interesting notion that cytokines can directly influence the functioning of the HPA axis. When we consider the emerging results of researchers such as Prof. Lipkin outlining significant cytokine abnormalities in ME/CFS, perhaps we have a logical line of reasoning as to why the HPA axis appears somewhat blunted.

If the observed cytokine abnormalities prove repeatable and appear chronic, then it stands to reason that the HPA axis is under significant strain for a prolonged period of time. This could account for lower cortisol levels as time progresses, alongside a blunting of the HPA axis response when challenged with a stressor.

This hypothesis would also be supported by the HPA axis dysfunction seen in other chronic conditions with significant cytokine disturbance, such as lupus.

Overall, while problems with the adrenal glands and HPA axis function don’t yet appear to be a sole causative agent for ME/CFS, they do provide an interesting explanation for certain symptoms of ME/CFS from which patients suffer. As time progresses, and through the thorough research done every day, we learn more and more about the complex interconnections between different organs and systems such as the HPA axis.

The connections between these systems, while seemingly unrelated to many diseases, appear to play quite a substantial role in the symptomolgy of ME/CFS, perhaps tying together with increasing evidence of autonomic dysfunction within ME/CFS.

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32 comments

{ 32 comments… read them below or add one }

Ema April 1, 2014 at 1:14 pm

The common line here is inflammation…cortisol is an extremely powerful anti-inflammatory agent – the main one that we have at our disposal. And it is exquisitely tied to the immune system by the modulation of thousands of genes that regulate the immune response.

It seems quite clear now based on more recent studies that glucocorticoids both enhance and suppress immune function and are crucial for modulating inflammation. When the system is under constant stress of illness, it loses responsiveness to cortisol (resistance) and inflammation can run amok. And this does seem to happen mostly under the control of cytokines.

The immune system eventually stops working and we suffer symptoms of low cortisol that then can cascade to the rest of the endocrine system and eventually cause all kinds of metabolic distress (thyroid and diabetes, for example). And the body becomes even more vulnerable to infectious assaults.

The mistake many have made for years is assuming that the HPA axis dysfunction in ME/CFS *should* look exactly like the adrenal insufficiency of Addison's disease (an autoimmune disorder) or even like secondary AI which is a brain dysfunction. And it hardly ever does, though it is worth noting that infectious agents (such as CMV) can also cause adrenal insufficiency.

We need a new paradigm to explain the low cortisol state caused by the immune dysfunction found in ME/CFS.

voner April 1, 2014 at 3:20 pm

Andrew,

Thx for the article. Clear and concise. Not an easy task!

Any ideas on POTS and the adrenals/kidneys? I would love to see that as an article. Mineralcorticoids vrs glucocorticoids, etc.

It looks like the feedback loops signaling could break and thus cause the cortisol insufficiencies?

Simon April 2, 2014 at 12:12 am

Thanks, Andrew – a very clear and helpful article.

Ema April 2, 2014 at 11:00 am
Ema

We need a new paradigm to explain the low cortisol state caused by the immune dysfunction found in ME/CFS.

Or possibly we just need to extrapolate the paradigm already explored in AIDS all the way back in 1992…these patients had hypercortisolism despite an Addison's type presentation due to peripheral glucocorticoid resistance.

This also helps to possibly explain why some people have trouble with taking exogenous steroids…they already have enough but are just unable to use them properly so adding more is not helpful.

In conclusion, AIDS patients with hypercortisolism and clinical features of peripheral resistance to glucocorticoids are characterized by abnormal glucocorticoid receptors on lymphocytes. Resistance to glucocorticoids implies a complex change in immune-endocrine function, which may be important in the course of immunodeficiency syndrome.

http://www.ncbi.nlm.nih.gov/pubmed/1740494

Ema April 3, 2014 at 4:38 pm

So it turns out that our often low IgG levels may be due to low cortisol, as much or even more than defects in B cell production.

In 1981, Grayson and her associates (34) re-
ported that addition of hydrocortisone in low
concentration to peripheral blood lymphocytes
in culture resulted in dramatic induction of im-
munoglobulin production, including IgG, IgA and
IgM.

This effect occurred only with glucocorti-
coids, and not with estrogens or androgens, and
they suggested that glucocorticoids might play a
role in the normal function of the immune system.

Orson and associates (35,36), in a continuation of
the in vitro work of this group, reported that glu-
cocorticoids induce the synthesis and secretion of
all classes of immunoglobulins and that a steroid-
dependent cytokine appeared to participate in this
response.

In 1982, Nouri-Aria et al (37) reported
that physiologic concentrations of glucocorticoids
may inhibit natural killer (NK) cell activity in vitro
and that continuation of low dosages may main-
tain remissions in patients with autoimmune hep-
atitis. In 1985, Cupps et al (38) reported that the
effect of corticosteroids upon B cells varied not
only with the amount of steroid but also with the
phase of the B cell cycle, enhancement of secretion
of immune globulins occurring in the later stages
of the cycle. In the same year, Levo, Harbeck
and Kirkpatrick (39) confirmed that cortisol in
low concentrations enhanced synthesis of immune
globulins, whereas high concentrations inhibited
such synthesis.

Hence it appears that the initial observations of Dougherty et al (27) were valid and that failure to reproduce their results may have been due to differences in dosage of steroid administered, in the stage of the B cell at which the steroid was added, or in other aspects of protocols.

Med Hypotheses. 1991 Mar;34(3):198-208.
Cortisol and immunity.
Jefferies WM.
Abstract
The relationship between adrenocortical function and immunity is a complex one. In addition to the well-known detrimental effects of large, pharmacologic dosages of glucocorticoids upon the immune process, there is impressive evidence that physiologic amounts of cortisol, the chief glucocorticoid normally produced by the human adrenal cortex, is necessary for the development and maintenance of normal immunity. This evidence is reviewed, and the importance of differentiating between physiologic and pharmacologic dosages and effects is discussed. The popular use of synthetic derivatives of cortisol, which differ greatly from the natural hormone in strength, and the dynamic nature of the normal adrenocortical response, which varies with the degree of stress being experienced, have contributed to the confusion. Further studies of the nature of the beneficial effect of cortisol, and possibly of other normal adrenocortical hormones, upon immunity in humans are needed, especially in view of recent evidence of a feedback relationship between the immune system and the hypothalamic-pituitary-adrenal axis, and with the increasing awareness not only that the immune process provides protection against infection, but also that its impairment seems to be involved in the development of autoimmune disorders, malignancies and the acquired immunodeficiency syndrome (AIDS).

PMID:

2062254

[PubMed - indexed for MEDLINE]

heapsreal April 3, 2014 at 7:34 pm

I wonder if the newer cfs people, the less than 3 years people have high cortisol and those long term cfs patients have low cortisol? Is there any studies showing this at all?
Any ongoing stress can cause pregenolone steal i guess and then upset the apple cart of hormones??

Ema April 4, 2014 at 10:20 am

@heapsreal, this study shows a novel model for how cortisol may be affected over long term periods of stress similar to ME/CFS.

Previous models of the HPA axis have not demonstrated bistability in steady state cortisol or ACTH. We believe this is because none of the previous models have explicitly accounted for nonlinear kinetics, such as the homodimerization of GR after cortisol activation [18,19]. This is essential for the negative feedback control of the HPA axis.

This homodimerization engenders the existence of two stable steady states and one unstable steady state in GR expression in the pituitary.

While increased cortisol following a short period of stress produces a small perturbation in GR concentration, long and repeated periods of stress resulting in elevated cortisol levels produce a large perturbation in GR concentration that force the HPA axis into an alternate steady state.

We were also able to demonstrate that these simulation results are qualitatively similar to cortisol levels measured in a human subject (Figure (Figure2).2). A large number of studies have investigated alterations of the HPA axis in CFS, including both studies of basal HPA axis activity as well as studies of HPA axis responsiveness to challenge (for review see [24]). A hypocortisol steady state, such as was demonstrated in this modelling and simulation study, is in keeping with many of these studies.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1804264/

Aerose91 May 6, 2014 at 7:57 pm
heapsreal

I wonder if the newer cfs people, the less than 3 years people have high cortisol and those long term cfs patients have low cortisol? Is there any studies showing this at all?
Any ongoing stress can cause pregenolone steal i guess and then upset the apple cart of hormones??

I have had ME for just over a year but before this had very severe adrenal fatigue which I think was a welcome mat for ME. Something very interesting happened though- the instant I got ME my adrenal fatigue nearly vanished. I mean I was as bad as they come, and instantly it almost completely went away. I have continued to do saliva cortisol tests throughout this past year as I have for the duration of my adrenal fatigue and my cortisol is still slightly low but not nearly as low as it was before ME. I have no explanation for this.

stridor May 27, 2014 at 6:10 pm

My adrenal function has gotten worse and I have no talent for stress-dosing. Crashed them again on the weekend. I am on 25 mg daily. I have to get better at this – but I'm nervous about osteoporosis.
At least in rats, mercury can permanently damage adrenals. These animals have normal a.m./p.m. cortisol levels but as soon as they are stressed the levels drop.
I have a bunch of cortisol receptor SNPs which would make me resistant to cortisol. And I have some corticotropin releasing hormone receptor SNPS.

Ema May 27, 2014 at 6:55 pm
stridor

My adrenal function has gotten worse and I have no talent for stress-dosing. Crashed them again on the weekend. I am on 25 mg daily. I have to get better at this – but I'm nervous about osteoporosis.
At least in rats, mercury can permanently damage adrenals. These animals have normal a.m./p.m. cortisol levels but as soon as they are stressed the levels drop.
I have a bunch of cortisol receptor SNPs which would make me resistant to cortisol. And I have some corticotropin releasing hormone receptor SNPS.

I just read a journal article by a conservative endocrinologist who wrote that she has never seen a case of HC induced osteo under 30 mg/day. So stress dosing for activity every now and again (or even raising your dose slightly if you find your daily dose insufficient for your activity level) is not going to be a major player in the development of osteoporosis. For that, your Vit D, K2 and A status will prove to be much bigger factors.

You'll learn to stress dose, it just takes time for everyone because there are no good hard and fast rules and we've all been brainwashed by the side effects of pharmacological doses opposed to physiological dosing. They just don't apply for the most part to us at all.

Aerose91 May 27, 2014 at 7:00 pm
stridor

My adrenal function has gotten worse and I have no talent for stress-dosing. Crashed them again on the weekend. I am on 25 mg daily. I have to get better at this – but I'm nervous about osteoporosis.
At least in rats, mercury can permanently damage adrenals. These animals have normal a.m./p.m. cortisol levels but as soon as they are stressed the levels drop.
I have a bunch of cortisol receptor SNPs which would make me resistant to cortisol. And I have some corticotropin releasing hormone receptor SNPS.

I think the SNP's may be your underlying problem as adrenal fatigue is really just a signaling problem from the brain- the adrenal glands themselves are fine. Your brain has lost the ability to respond accordingly to the environment which is why small stressors cause huge deficits. There's also a theory out there that leptin plays a huge role in signaling to the hypothalamus and controlling these minute changes.that we can't get right. Try googling "leptin reset" and see what you think.

Ema May 27, 2014 at 7:29 pm
stridor

My adrenal function has gotten worse and I have no talent for stress-dosing. Crashed them again on the weekend. I am on 25 mg daily. I have to get better at this – but I'm nervous about osteoporosis.
At least in rats, mercury can permanently damage adrenals. These animals have normal a.m./p.m. cortisol levels but as soon as they are stressed the levels drop.
I have a bunch of cortisol receptor SNPs which would make me resistant to cortisol. And I have some corticotropin releasing hormone receptor SNPS.

What are the SNPs that you are referring to with regards to cortisol resistance?

stridor May 28, 2014 at 3:58 pm

@Ema @Aerose91
Thanks so much for the replies. I have to get this sorted out, as you seem to understand adrenal crashes are not any fun at all. I will look up leptin reset. I am delighted with the information on osteoporosis. I haven't been lucky in health and I get a bit too careful :)
I discovered my adrenal panel through Nutrahacker.
NR3C1 is the cortisol receptor = 7 ++
CRHR1 is the corticotropin releasing hormone receptor 1 ++ and 5 +-
My problem is that I think that I am only going to the garden for a minute and 2-3 hours later I notice that I feel a bit tired and by then it is too late. Nothing I can do will save me from the slide. Cortef will kick in hours later. brad

Ema May 28, 2014 at 4:09 pm

@stridor, try chewing the HC or taking it sublingually. It should kick in within about 15-20 minutes. But better to take a slightly higher dose overall than let yourself get in the hole constantly. That is really hard on your QOL.

Ema May 28, 2014 at 4:24 pm
stridor

I discovered my adrenal panel through Nutrahacker.
NR3C1 is the cortisol receptor = 7 ++
CRHR1 is the corticotropin releasing hormone receptor 1 ++ and 5 +-
[/USER]

What are the SNPs (rsid) that they are looking at on those genes?

Aerose91 May 28, 2014 at 4:40 pm

@stridor

Check this article out,
http://jackkruse.com/brain-gut-16-adrenal-fatigue-rx/

Dr. Jack Kruse is an extremely intelligent guy with very evolutionary ideas. Dr Romeo Mariano is another doctor who shares this theory of PVN signaling as the cause of adrenal fatigue.

I have been to hell and back with AF. It is what brought me to ME. I was so bad at one point no doctor would treat me without getting verified by an endocrinologist to not have Addisons. The ideas in this article are the best I've seen

Ema May 28, 2014 at 4:45 pm

I took Cycloset after reading Dr Jack Kruse for a while (or trying to read due to his ramblings and unwillingness to answer a straight question with a straight answer). It provoked a terrible crash that I'm still trying to recover from almost 9 months later.

Turns out Cycloset can drop norepinephrine levels up to 50%…which was extremely detrimental to my health.

I agree that he has some interesting ideas but be careful!

Aerose91 May 28, 2014 at 4:51 pm

I like his adrenal fatigue protocol because it's situational and he doesn't promote drugs and supplements. He uses particular diets and circadian rhythms which have helped me.

I feel you with crashing from random supplements, it has happened to me more times than I can count so I'm as careful as can be these days!

He is definitely an eccentric guy

stridor May 29, 2014 at 3:06 pm

@Ema I do take it sublingual but find that once I crash it takes a substantial amount of time (hours) to regain the ground I lost. It seems that either I will have to stress dose before working or I get to write off my day. Anyone else have this?
Cortisol receptor site.
NR3C1 rs2918419 ++
rs860458 ++
rs852997 ++
rs6188 ++
rs6198 ++
rs1866388 ++
rs258750 ++

Corticotropin Releasing Hormone receptor
CRHR1 rs173365 ++
rs7209426 +-
rs110402 +-
rs242924 +-
CRHR2 rs2267710 +-
rs2284217 +-

@Aerose91 I am going to look at the site. I don't have adrenal fatigue. I have "Chronic Adrenal Insufficiency" that seems to be slipping towards a close to Addison's presentation. I do have a bit of production left. I could go for a walk right now without any problem. A bit of work in the gardens for 2-3 hours is a problem.
My adrenals just keep getting worse. It may have been adrenal fatigue 7 years ago. My Dr said that I was 10 years too late moving against mercury and that my adrenals are not treatable.
I did 35-40 ACE and vitamin IV's at considerable expense. They did nothing but at least I can take comfort in knowing that I tried.
There are no options, I have to get better with stress-dosing. brad

Aerose91 May 29, 2014 at 3:26 pm

@stridor

I was so bad I could only get out of bed to crawl to the bathroom. I would shower once a month. I was so dizzy I couldn't look down because the floor would fall out from under my feet and I would start throwing up. I've personally never met someone who had AF as bad as me that wasn't clinical Addisons. I personally hate the name adrenal fatigue because it sounds so minor.
I needed 20 mg hydrocortisone to get out of the hole but I made it. I feel that if I didn't get M.E. I would be healed by now.

Ema May 29, 2014 at 3:51 pm

@stridor, Stress dosing is hard. It has taken me years to get anywhere near reasonable at it. Steroid fear, for the most part; it's hard to get over.

I would suggest that if it is still taking you hours to get over a low cortisol episode that a) your daily dose is still insufficient or b) your stress dose is insufficient either in quantity or type of steroid.

I personally find that stress dosing with Medrol often works better than HC for other than out and out emergency situations (like a broken bone or car wreck) because it gives you a longer lasting baseline from which to re-build your reserves. You might ask your doctor to give you a trial to see if that helps.

It usually takes me at least 10-20 mg of HC (or 4 mg of Medrol) to get out of a low cortisol hole within 20-30 minutes. If I dribble in 5 mg over the course of the day, I never really get out of the hole. A bigger dose is required for me and then I'm pretty normal in a short amount of time. This took me a LONG time to learn.

The important thing to remember is that you will never hurt yourself short term by taking more steroid than you need. So you can feel free to experiment and find the dose that is right for you that gets you out of the hole without having to write off the rest of the day.

I also know many people that find themselves to be more stable on a combo of dex/Medrol and HC on a daily basis for exactly that reason as well. It's another thing to consider if you metabolize steroid quickly like I do as well.

stridor May 30, 2014 at 3:53 am

@Aerose91 When I read your post I got that sinking feeling in my stomach. Took me back to 2011 when I couldn't get any help as Dr's kept saying that I was depressed. Finally, I bought hydrocortisone ointment and put that into capsules to swallow. That is how I finally got some HC on board. Man those were dark days….I hear you loud and clear.

@Ema Yep, I have steroid fear. Looking at what you do, I am being way too conservative with the stress dosing. This is precisely the type of information that I was looking for. My Dr is an HC guy but I can work with that at least for now. I have been under-treating these crashes. I take take HC 5 times a day to help stabilize levels (weighted towards the morning). Thanks a million for giving me the confidence to experiment more. brad

heapsreal May 30, 2014 at 5:20 am

Pred and methyl Pred maybe better suited as they are more slowly broken down. Ema mentioned a possible combo, maybe 1mg methylpPred and 5mg of hc for a more quicker increase in cortisol on first awakening? The methyl Pred will taper off slower. Maybe just a once a morning appropriate dose of methyl pred and hc for stress dosing when required.

Some are fast and some are slow metabolizes of steroids? ?

stridor May 30, 2014 at 3:11 pm

I will mention to my Dr about the trouble I have been having. but honestly, I really can't wait to try some of the other ideas around stress-dosing. I was only using 5-6 mg. I have to read Safe Uses of Cortisol again now that I am not buried in illness.
My Dr has an open mind and if I need to change, he will think about it. but generally he is a HC guy.Maybe he would push me to 30 mg from 25…..brad

heapsreal May 30, 2014 at 6:42 pm
stridor

I will mention to my Dr about the trouble I have been having. but honestly, I really can't wait to try some of the other ideas around stress-dosing. I was only using 5-6 mg. I have to read Safe Uses of Cortisol again now that I am not buried in illness.
My Dr has an open mind and if I need to change, he will think about it. but generally he is a HC guy.Maybe he would push me to 30 mg from 25…..brad

Ask him about an equal strength dose of methyl pred and see if it makes a difference. Help tell if your a fast metabolizer of hc, so might not really need an increase in dose but just something that has a longer half life, then take it from there.

you might have mentioned this, but have u had other hormones checked like dhea and testosterone, these could also need to play a part.

stridor May 31, 2014 at 5:46 am

I take testosterone as my levels were low. The Dr wanted me to try DHEA and Pregnenolone (sp?) at the same time. I did not respond well to them. I am high estrogen and really didn't care much about having success with DHEA anyway from that perspective. But it is supposed to help with age spots and I have lots but my real interest was whether it was generally good for skin as I have many skin ailments.
The pregnenolone gave me a good initial response but then went on to increase fatigue and brain-fog. I took this to mean that it was trying to push energy production somehow. I do not respond well to the traditional approaches to CFS like ribose or creatine. brad

heapsreal May 31, 2014 at 9:08 am
stridor

I take testosterone as my levels were low. The Dr wanted me to try DHEA and Pregnenolone (sp?) at the same time. I did not respond well to them. I am high estrogen and really didn't care much about having success with DHEA anyway from that perspective. But it is supposed to help with age spots and I have lots but my real interest was whether it was generally good for skin as I have many skin ailments.
The pregnenolone gave me a good initial response but then went on to increase fatigue and brain-fog. I took this to mean that it was trying to push energy production somehow. I do not respond well to the traditional approaches to CFS like ribose or creatine. brad

with pregnenolone i think its tablet versions if dosed too high can cause a spacey type of feel as they can affect benzo receptor sites. Supposedly transdermal preg creams work better and best to start with low doses like 5-10mg and slowly increase from there. Dhea pills i think is best to start low also say 10mg pills and slowly increase to say 25mg, if more is needed then add some at night, i use 25mg twice a day and that has me in the upper third of the normal range. For me pregnenolone helped increase cortisol, didnt do alot for other hormones but i think its an individual thing.

U might also try looking into ways to help increase dopamine as this is normally low in us and can help with energy and pain etc??

bertiedog May 31, 2014 at 12:56 pm
heapsreal

Pred and methyl Pred maybe better suited as they are more slowly broken down. Ema mentioned a possible combo, maybe 1mg methylpPred and 5mg of hc for a more quicker increase in cortisol on first awakening? The methyl Pred will taper off slower. Maybe just a once a morning appropriate dose of methyl pred and hc for stress dosing when required.

Some are fast and some are slow metabolizes of steroids? ?

This is so true. I metabolized h/c too quickly, a dose of even 10 mg in the morning would run out well before midday and so would the next dose so my doctor said I would probably do better with Prednisolone and he was so right. That was in 2002 and I have been on it ever since. I take 2.5mg on waking around 5 am, go back to sleep and then when I wake around 6.30 am I take another 2.5 mg.Pred That will last me till about 3 pm and then I need another 1mg Pred and 2.5 mg h/c. However if I have done more physical stuff or have a virus then I will probably need another 2.5 mg h/c in the evening. It still takes me till about 9 am at the earliest to get any real energy through but this seems to be typical of the Addison sufferers too.

BTW I had a Dexa scan on my bone about 3 years ago and I had the bones of a young woman which is great seeing that I was 62 at the time! They said it was very unusual to see this but I have always taken lots of supplements and have carried on with some estrogen plus I take dessicated thyroid too so taking steroids if you need them doesn't mean you have to get osteoporosis. I think there is a lot more to it.

If you are too low on your dose of steroid then you will feel horrendous, I can always tell when I am running low. I agree it is really difficult to get the balance right as to what your body needs and not to overdose.

Pam

stridor June 1, 2014 at 5:03 am

@bertiedog @heapsreal
I am feeling a bit foolish right now. I have been so focused on Mercury-detox and Freddd's protocol that I have made no effort to really understand what I can do for my adrenals. I just took my 25 mg/day with an occasional extra 5 mg when I was in trouble.
At this point I am unsure whether my adrenals have gotten worse or if now that I am recovering from ME, my activity level is revealing limitations that were there all along.
Yesterday I took an extra 10 mg HC before going outside to pull dandelions. I took another 7.5mg during and after the activity. I did need to rest for a while but the day was not a write-off. That's over 40 mg of HC.
I will ask the Dr what he thinks about other products with longer half-lives.
I read somewhere that oral DHEA is more likely to increase estrogen production and that transdermal is superior. I don't feel particularly led to take it either way. My DHEA levels were in the normal range. The Dr was trying to sort out why my testosterone was low and DHEA was an experiment. I am willing to look at the pregnenolone again.

I just did trial of tyrosine again and had an initial (+) response. I took it with tryptophan this time (as opposed to 5-HTP).
I was getting headaches and my hard to control blood pressure got worse so I took a break. Too bad, as my thinking improved otherwise.
BP is running in the 130-160 / 80-90 range right now with 3 meds on board. Looks like I will need one more increase. Was running 180/100 two months ago so definitely the meds help. If I push the adrenals it drops to 90/60 and I have a hard time standing as all the strength leaves me. I will dust off "Safe Uses of Cortisol". I have to get better at this. Thanks, brad

heapsreal June 1, 2014 at 8:09 am

@stridor if your dhea levels are within normal range then i probably dont see a need for it and probably would increase your estrogen level, if your dhea was low though it probably wouldnt effect estrogen too negatively??

It can take alot of experimenting to find what helps you personally, we all seem to be slightly different.

good luck,
keep us posted,
cheers!!!

bertiedog June 1, 2014 at 10:01 am
stridor

@bertiedog @heapsreal
I am feeling a bit foolish right now. I have been so focused on Mercury-detox and Freddd's protocol that I have made no effort to really understand what I can do for my adrenals. I just took my 25 mg/day with an occasional extra 5 mg when I was in trouble.
At this point I am unsure whether my adrenals have gotten worse or if now that I am recovering from ME, my activity level is revealing limitations that were there all along.
Yesterday I took an extra 10 mg HC before going outside to pull dandelions. I took another 7.5mg during and after the activity. I did need to rest for a while but the day was not a write-off. That's over 40 mg of HC.
I will ask the Dr what he thinks about other products with longer half-lives.
I read somewhere that oral DHEA is more likely to increase estrogen production and that transdermal is superior. I don't feel particularly led to take it either way. My DHEA levels were in the normal range. The Dr was trying to sort out why my testosterone was low and DHEA was an experiment. I am willing to look at the pregnenolone again.

I just did trial of tyrosine again and had an initial (+) response. I took it with tryptophan this time (as opposed to 5-HTP).
I was getting headaches and my hard to control blood pressure got worse so I took a break. Too bad, as my thinking improved otherwise.
BP is running in the 130-160 / 80-90 range right now with 3 meds on board. Looks like I will need one more increase. Was running 180/100 two months ago so definitely the meds help. If I push the adrenals it drops to 90/60 and I have a hard time standing as all the strength leaves me. I will dust off "Safe Uses of Cortisol". I have to get better at this. Thanks, brad

@stridor I don't take any extra DHEA as I don't seem to need it. When I did the last saliva test it was right in the middle of the range. I have heard that DHEA can deplete the benefits of cortisol as it sort of opposes it so if you aren't too low in it anyway then I wouldn't bother.

One other thing that I have found out so many times that makes me worse is taking herbal medicines although I like the idea of them. What seems to happen with me is that the herbs block the steroid so I don't do at all well. I think it is to do with the detoxification pathways being the same in the liver for both steroids and most herbs. Something else to onsider!

If your testosterone was low I would have thought you would do far better to just take a small amount of that rather than take pregnenolone because with that you don't know what it is going to convert into. Unless your liver is perfect you might well not get what you are hoping for. If you have adrenal and pituitary issues its better to get established on a basic regime that works before you start adding in other stuff then if you find you are worse you can always go back to the basic regime only.

Good luck with it all I know how difficult it can be to find out exactly what you need and how much of it!

Pam

stridor June 1, 2014 at 10:47 am

@heapsreal @bertiedog
HOLD THE PHONE! After typing this mornings entry I went to set up the days meds and it seems that I miscounted. I stress dosed 12.5 mg yesterday = 5 mg extra before the activity + 5 mg when I first started to note symptoms = 1.5 hours later and 2.5 mg when I finished. I had a mild crash and stopped activity around noon. My spark returned around 3 pm.
This morning I added 10 mg and have taken breaks every hour. I am working harder and am definitely on the right track. I am a bit tired but not in trouble yet. My BP is 112/72 down from 160/88 this morning after meds. I will take another 5 mg and then hit the gardening again. So by 1 p.m my intake will be 30 mg for a total of 40 mg today. Very seldom can I go back out after lunch. This is great.
Thanks guys, I'm just going to keep mucking about with this. brad

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