Adrenal Fatigue & Glucocorticoid Use

[Michael Scally MD]

Just to note: This study states that the HPA axis response was recovered in a (relatively) short amount of time for nearly every patient.

"Thus, it is not clear that the reduction in response to ACTH following low-dose prednisolone treatment revealed in the present study is of physiologic significance. Another question is whether the reduced response to ACTH is recovered quickly. In 14 patients who had been taking high doses of prednisone (up to 100 mg/m2/day) for up to 29 days, there was a clear suppression of adrenal function, but in the large majority of these patients, the HPA axis response was restored in fewer than 7 days (26). A further study of 75 patients who received at least 25 mg of prednisone daily for up to 30 days found that one-half had a reduced response to CRF on the day after stopping treatment. All but 2 of these patients recovered ACTH function within 2 weeks."

I am not sure if you are missing the point or merely pointing out what I said already. I do not believe that HPAA suppression is an issue. I only posted the study as an illumination of the HPAA. Recall, I said it was a short detour. It is the effects of GC administration. This has always been my contention, always! I will get into this soon, but it is clear that one area is osteoporosis.

I have searched unsuccessfully everywhere in PubMed for support of "adrenal fatigue" I did find the attached article: Head KA, Kelly GS. Nutrients and botanicals for treatment of stress: adrenal fatigue, neurotransmitter imbalance, anxiety, and restless sleep. Altern Med Rev 2009;14(2):114-40.

Research shows a dramatic increase in use of the medical system during times of stress, such as job insecurity. Stress is a factor in many illnesses - from headaches to heart disease, and immune deficiencies to digestive problems. A substantial contributor to stress-induced decline in health appears to be an increased production of stress hormones and subsequent decreased immune function. Non-pharmaceutical approaches have much to offer such patients. This article focuses on the use of nutrients and botanicals to support the adrenals, balance neurotransmitters, treat acute anxiety, and support restful sleep.

 

[CubbieBlue]

I am not sure if you are missing the point or merely pointing out what I said already. I do not believe that HPAA suppression is an issue. I only posted the study as an illumination of the HPAA. Recall, I said it was a short detour. It is the effects of GC administration. This has always been my contention, always! I will get into this soon, but it is clear that one area is osteoporosis.

I wasn't aware of what you meant by "this is a short detour". Sometimes you speak a little cryptically. Point noted however.

 

[CubbieBlue]

Just to note: This study states that the HPA axis response was recovered in a (relatively) short amount of time for nearly every patient.

"Thus, it is not clear that the reduction in response to ACTH following low-dose prednisolone treatment revealed in the present study is of physiologic significance. Another question is whether the reduced response to ACTH is recovered quickly. In 14 patients who had been taking high doses of prednisone (up to 100 mg/m2/day) for up to 29 days, there was a clear suppression of adrenal function, but in the large majority of these patients, the HPA axis response was restored in fewer than 7 days (26). A further study of 75 patients who received at least 25 mg of prednisone daily for up to 30 days found that one-half had a reduced response to CRF on the day after stopping treatment. All but 2 of these patients recovered ACTH function within 2 weeks."

I forgot a word in this post and cannot edit it anymore.

 

[HeadDoc]

so if I have this correct, the use of GC in anything that is not adrenal insufficiency may create a hyperadrenal condition. I searched Becker (2001 ed.) and could not find "adrenal fatigue". Did find some interesting material on hyperadrenal states and major depressive episode. I really should go back over the chapters (most are short) and work of a table to differentiate the two. Do you have such in your library? If not, that's ok. I almost avoided this post because I know that you (MS) are so committed to digging out the research. Believe me I've got my own shovel.

Becker also notes that serum assays are the only lab for hyperadrenal states. Becker did say that urine analysis is acceptible for hypo-adrenal states.

 

[Crazy Crew]

As I understand it, Adrenal Fatigue is a recent laymans term for adrenal insufficiency.

AOL Search

 

[Crazy Crew]

wikipedea link

[ame="http://en.wikipedia.org/wiki/Adrenal_insufficiency"]Adrenal insufficiency - Wikipedia, the free encyclopedia@@AMEPARAM@@/wiki/File:Illu_adrenal_gland.jpg" class="image"><img alt="" src="http://upload.wikimedia.org/wikipedia/commons/thumb/1/14/Illu_adrenal_gland.jpg/230px-Illu_adrenal_gland.jpg"@@AMEPARAM@@commons/thumb/1/14/Illu_adrenal_gland.jpg/230px-Illu_adrenal_gland.jpg[/ame]

 

[CubbieBlue]

As I understand it, Adrenal Fatigue is a recent laymans term for adrenal insufficiency.

AOL Search

Right - adrenal fatigue is a term used to describe a hypoadrenal state, but not full fledged adrenal failure, or addisons disease. The question is whether or not this psuedo addisons condition exists, and whether or not the adrenals can be healed from it.

 

[Michael Scally MD]

For all out there using GC, are you aware of the adverse effects with the does used for AF? Thus far, no one has come forward with evidence for GC use in this fictitious disorder. I said I would get to the adverse effects, so here is a small introduction. There is more to come and it ain't good.

The consensus is for GC (HC) doses up to 40 mg, but typically 20-30mg daily. And this is for a long time in many. I will ask again, has your prescribing doctor bothered to obtain a bone mineral density (DXA) baseline? If you have not obtained a DXA scan, your doctor does not give a damn about you except for making money! Think About It.


Peacey SR, Guo CY, Robinson AM, et al. Glucocorticoid replacement therapy: are patients over treated and does it matter? Clin Endocrinol (Oxf) 1997;46(3):255-61.

BACKGROUND AND OBJECTIVES: Adequate assessment of patients on glucocorticoid replacement therapy is of great importance to avoid the consequences of under or over treatment, but no simple test is available for this. The aims of this study were (1) to assess adequacy of glucocorticoid replacement in hypoadrenal patients, (2) to correlate serum cortisol levels (cortisol day curve) with 24-hour urine free cortisol excretion and (3) to assess the impact of glucocorticoid dose optimization on markers of bone formation and bone resorption.

DESIGN: Cross-sectional study of current replacement therapy and a prospective study of the effect of dose alteration on bone turnover markers.

PATIENTS: Thirty-two consecutive patients on replacement glucocorticoid therapy (12 Addison's disease, 20 hypopituitarism) from a University teaching hospital out-patient department.

MEASUREMENTS: Serum and urinary cortisol, osteocalcin, N-telopeptide of type I collagen (NTX) and bone mineral density.

RESULTS: 28/32 (88%) patients required a change of therapy; 24/32 (75%) a total reduction in dose, 18/32 (56%) a change in replacement therapy regimen or drug and 14/32 (44%) both changes. The mean daily dose of hydrocortisone was reduced from 29.5 +/- 1.2 to 20.8 +/- 1.0 mg. A significant correlation was found between peak cortisol and 24-hour urine free cortisol/ creatinine (Spearman correlation r = 0.60, P < 0.0001; n = 51). Following hydrocortisone dose reduction, median osteocalcin increased from 16.7 micrograms/l (range 8.2-65.7) to 19.9 micrograms/l (8.2-56.3); P < 0.01, with no change in the NTX/creatinine ratio.

CONCLUSIONS: A high proportion of patients on conventional corticosteroid replacement therapy are over treated or on inappropriate replacement regimens. To reduce the long term risk of osteoporosis, corticosteroid replacement therapy should be individually assessed and over replacement avoided.


Lovas K, Gjesdal CG, Christensen M, et al. Glucocorticoid replacement therapy and pharmacogenetics in Addison's disease: effects on bone. Eur J Endocrinol 2009;160(6):993-1002.

Context: Patients with primary adrenal insufficiency (Addison's disease) receive more glucococorticoids than the normal endogenous production, raising concern about adverse effects on bone.

Objective: To determine i) the effects of glucocorticoid replacement therapy on bone, and ii) the impact of glucocorticoid pharmacogenetics.

Design, setting and participants: A cross-sectional study of two large Addison's cohorts from Norway (n=187) and from UK and New Zealand (n=105).

Main outcome measures: Bone mineral density (BMD) was measured; the Z-scores represent comparison with a reference population. Blood samples from 187 Norwegian patients were analysed for bone markers and common polymorphisms in genes that have been associated with glucocorticoid sensitivity.

Results: Femoral neck BMD Z-scores were significantly reduced in the patients (Norway: mean -0.28 (95% confidence intervals (CI) -0.42, -0.16); UK and New Zealand: -0.21 (95% CI -0.36, -0.06)). Lumbar spine Z-scores were reduced (Norway: -0.17 (-0.36, +0.01); UK and New Zealand: -0.57 (-0.78, -0.37)), and significantly lower in males compared with females (P=0.02). The common P-glycoprotein (ABCB1) polymorphism C3435T was significantly associated with total BMD (CC and CT>TT P=0.015), with a similar trend at the hip and spine.

Conclusions: BMD at the femoral neck and lumbar spine is reduced in Addison's disease, indicating undesirable effects of the replacement therapy. The findings lend support to the recommendations that 15-25 mg hydrocortisone daily is more appropriate than the higher conventional doses. [Note: Addisonian patients have No cortisol.] A common polymorphism in the efflux transporter P-glycoprotein is associated with reduced bone mass and might confer susceptibility to glucocorticoid induced osteoporosis.


Sadat-Ali M, Alelq AH, Alshafei BA, Al-Turki HA, Abujubara MA. Osteoporosis prophylaxis in patients receiving chronic glucocorticoid therapy. Ann Saudi Med 2009;29(3):215-8.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754428/?tool=pubmed

BACKGROUND AND OBJECTIVES: Glucocorticoid-induced osteoporosis (GIOP) is the most common form of secondary osteoporosis, yet few patients receive proper measures to prevent its development. We retrospectively searched prescription records to determine if patients receiving oral prednisolone were receiving prophylaxis or treatment for osteopenia and osteoporosis.

METHODS: Patients who were prescribed > or =7.5 milligrams of prednisolone for 6 months or longer during a 6- month period were identified through the prescription monitoring system. Demographic and clinical data were extracted from the patient records, and dual energy x-ray absorptiometry (DEXA) scans were retrieved, when available. Use of oral calcium, vitamin D and anti-resorptives was recorded.

RESULTS: One hundred males and 65 females were receiving oral prednisolone for a mean (SD) duration of 40.4 (29.9) months in males and 41.2 (36.4) months in females. Twenty-one females (12.7%) and 5 (3%) males had bone mineral density measured by DEXA. Of those, 10 (47.6%) females and 3 (50%) males were osteoporotic and 11(52.4%) females and 2 (40%) males were osteopenic. Calcium and vitamin D were prescribed to the majority of patients (60% to 80%), but none were prescribed antiresorptive/anabolic therapy.

CONCLUSIONS: Patients in this study were neither investigated properly nor treated according to the minimum recommendations for the management of GIOP. Physician awareness about the prevention and treatment of GIOP should be a priority for the local health care system.


Walsh LJ, Wong CA, Pringle M, Tattersfield AE. Use of oral corticosteroids in the community and the prevention of secondary osteoporosis: a cross sectional study. BMJ 1996;313(7053):344-6.
http://www.bmj.com/cgi/content/full/313/7053/344

Abstract Objective: To determine the prevalence of continuous use of oral steroids in the general population, the conditions for which they are prescribed, and the extent to which patients taking oral steroids are taking treatment to prevent osteoporosis.

Design: A cross sectional study with a four year retrospective review of drug treatment. Setting: Eight large general practices in central and southern Nottinghamshire.

Subjects: A population of 65 786 patients (52% women) registered with a general practitioner during 1995.

Results: 303 patients (65% (197) women) aged 12-94 years were currently taking "continuous" (for at least three months) oral corticosteroid treatment. This figure represents 0.5% of the total population and 1.4% (245/17 114) of patients aged 55 years or more (1.7% (166/9601) of women). The usual steroid was prednisolone (97% (294/303)), the mean dose was 8.0 mg/day, and the median duration of oral steroid treatment determined in 149 patients was three years. The most common conditions for which continuous oral steroids were prescribed were rheumatoid arthritis (23% (70)), polymyalgia rheumatica (22% (66)), and asthma or chronic obstructive airways disease (19% (59)). Only 41 (14%) of the 303 patients taking oral steroids had received treatment for the prevention of osteoporosis over the past four years. Although 37 of the 41 patients were women, only 10% (18/181) of the women over 45 years taking continuous oral corticosteroids were currently taking hormone replacement therapy.

Conclusions: If our figures are typical then they suggest that over 250 000 people in the United Kingdom are taking continuous oral steroids and that most of these are taking no prophylaxis against osteoporosis. Key messages The prevalence of use of oral corticosteroids in a community based population of 65 786 was 0.5%, rising to 1.7% in women aged >/=55 years The main indications for oral steroids were rheumatoid arthritis, polymyalgia, and asthma or chronic obstructive pulmonary disease Only 14% of patients taking oral steroids had received any treatment to prevent or treat osteoporosis These data suggest that over a quarter of a million people in the United Kingdom are currently taking oral corticosteroids and hence at risk of adverse effects

 

[Michael Scally MD]

In one of the most comprehensive reviews of GIOP, their findings show a substantial risk of fracture, FRACTURE! Osteoporosis is the prodromal event. The studies "clearly indicate a substantial risk in individuals taking between 2.5 and 7.5 mg [prednisolone] daily." [Next: The mental disturbances with these "low" doses.]

Recall, Prednisolone 5 mg = 20 mg HC = 25 mg Cortisone.


Kanis JA, Stevenson M, McCloskey EV, Davis S, Lloyd-Jones M. Glucocorticoid-induced osteoporosis: a systematic review and cost-utility analysis. Health Technol Assess 2007;11(7):iii-iv, ix-xi, 1-231.

The prevalence of oral glucocorticoid use was similar between men and women and was 0.9% of the total adult population, but increased with age. The prevalence of current utilisation was 0.2% at the age of 20–29 years, rising to 2.5% between the ages of 70 and 79 years. Of the three dose categories studied, the intermediate dose (2.5–7.5 mg prednisolone or equivalent daily) was the most frequently used (0.4% of the adult population). The prevalence of a higher dose therapy (more than 7.5 mg daily) was 0.3% and that of lower dose treatment (<2.5 mg daily) was 0.1%. . . . In this study of eight large general practices with a catchment population of nearly 66,000 individuals, current continuous use of glucocorticoids was defined as individuals taking glucocorticoids for at least 3 months.


Although most patients received glucocorticoids for a short period, treatment for longer than 6 months was observed in 22% of patients and treatment for more than 5 years in 4.3%.


It has been difficult to demonstrate clear dose–response effects because of the heterogeneity of skeletal response to glucocorticoids and the small samples studied. The most extensive data available to date, undertaken within the general practice research framework, indicate dose responsivity in that the risks of a fracture are higher, the higher is the dose of glucocorticoids. With a standardised daily dose of prednisolone of <2.5 mg, hip fracture risk was 0.99 (95% CI 0.82–1.20), rising to 2.27 (95% CI 1.94–2.66) at doses of 7.5 mg or greater. Dose responses were also observed for vertebral fracture. These findings indicate that doses hitherto regarded as of little importance to osteoporosis carry a substantial risk. The guidelines for osteoporosis produced by the Royal College of Physicians gave a daily dose of 7.5 mg or more of prednisolone as the threshold at which one should be concerned about fracture risk, whereas more recent studies clearly indicate a substantial risk in individuals taking between 2.5 and 7.5 mg daily, a risk that was significantly higher than individuals taking a low dose (2.5 mg daily or less) for nonvertebral fracture, hip fracture or vertebral fracture.

 

[CubbieBlue]

Dr. John Crisler discussed pregnenelone and adrenal fatigue at length in this radio segment:

http://superhumanradio.com/super-human-radio-show/460-pregnenolone-the-progenitor-hormone.html

He notes that AF is a real disorder, that is treated purely on symptoms. He states that it is not necessarily a diminished cortisol response, but rather, incorrect response times.

It is fairly interesting.

 

[Michael Scally MD]

Dr. John Crisler discussed pregnenelone and adrenal fatigue at length in this radio segment:

http://superhumanradio.com/super-human-radio-show/460-pregnenolone-the-progenitor-hormone.html

He notes that AF is a real disorder, that is treated purely on symptoms. He states that it is not necessarily a diminished cortisol response, but rather, incorrect response times.

It is fairly interesting.

If what you are saying is true, this is being treated as a psychiatric disorder. Where does one find any support that this is a real disorder. They are not talking about adrenal insufficiency if the treatment is on symptoms alone. Also, it is clearly dangerous to treat with GC, which interferes with the hormonal status of the patient. Is the proposed treatment pregnenolone, not GC? I do not have the time to listen. Maybe someone will chime in on what is said in the web cast.

 

[CubbieBlue]

If what you are saying is true, this is being treated as a psychiatric disorder. Where does one find any support that this is a real disorder. They are not talking about adrenal insufficiency if the treatment is on symptoms alone. Also, it is clearly dangerous to treat with GC, which interferes with the hormonal status of the patient. Is the proposed treatment pregnenolone, not GC? I do not have the time to listen. Maybe someone will chime in on what is said in the web cast.

No. He talks about preg for something else. I didn't get that far, the AF segment is at the beginning.

 

[HeadDoc]

there are some small studies indicating a positive effect for dhea and/or pregnenolone for depression. I haven't seen any for these substances and adrenal insufficiency. I don't recall that Wilson (of adrenal fatigue fame) advocates supplementing w. either. Sorry---someone borrowed my copy of Wilson and I cannot verify the point regarding dhea and pregnenolone.

See the following for more information about Wilson and adrenal fatigue

http://www.adrenalfatigue.org/

 

[Michael Scally MD]

One of the well explained phenomenon with cortisol administration is adverse psychiatric effects. Unfortunately, the euphoria observed with cortisol administration is seen by most as a benefit. It is not. Because it feels as if it relieves stress or depression is NOT a reason to take these drugs!

Further, cortisol administration, even in small doses used by those for “adrenal fatigue” cause memory deficits. These deficits can cause problems in work and everyday activities.

And do not be fooled by HAN all of a suddenly saying that “adrenal fatigue” is not the proper term, but use adrenal insufficiency. HAN’s knowledge of the adrenals is worthless. HAN does not know SHIT, which might speak more to his knowledge on the bowels.


Warrington TP, Bostwick JM. Psychiatric Adverse Effects of Corticosteroids. Mayo Clinic Proceedings 2006;81(10):1361-7.

Psychiatric adverse effects during systemic corticosteroid therapy are common. Two large meta-analyses found that severe reactions occurred in nearly 6% of patients, and mild to moderate reactions occurred in about 28%. Although disturbances of mood, cognition, sleep, and behavior as well as frank delirium or even psychosis are possible, the most common adverse effects of short-term corticosteroid therapy are euphoria and hypomania. Conversely, long-term therapy tends to induce depressive symptoms. Dosage is directly related to the incidence of adverse effects but is not related to the timing, severity, or duration of these effects. Neither the presence nor the absence of previous reactions predicts adverse responses to subsequent courses of corticosteroids. Corticosteroid-induced symptoms frequently present early in a treatment cycle and typically resolve with dosage reduction or discontinuation of corticosteroids. In severe cases or situations in which the dose cannot be reduced, antipsychotics or mood stabilizers may be required. This review offers an approach to identifying and managing corticosteroid-induced psychiatric syndromes based on the type of symptoms and anticipated duration of corticosteroid treatment.


Brown ES, Chandler PA. Mood and Cognitive Changes During Systemic Corticosteroid Therapy. Prim Care Companion J Clin Psychiatry 2001;3(1):17-21.

BACKGROUND: Physicians in the United States write approximately 10 million new prescriptions for oral corticosteroids each year. Common side effects of corticosteroids include weight gain, osteoporosis, and diabetes mellitus. This article reviews the available literature on psychiatric and cognitive changes during corticosteroid therapy.

METHOD: A search of the MEDLINE and psycINFO databases was conducted to find clinically relevant articles on psychiatric and cognitive side effects with corticosteroids using search terms including corticosteroid, prednisone, mania, depression, psychosis, mood, memory, and cognition.

RESULTS: Symptoms of hypomania, mania, depression, and psychosis occur during corticosteroid therapy as do cognitive changes, particularly deficits in verbal or declarative memory. Psychiatric symptoms appear to be dose-dependent and generally occur during the first few weeks of therapy. Patients who must remain on corticosteroids may benefit from pharmacotherapeutic approaches, such as lithium and the new antipsychotic medications.

CONCLUSION: Mood and cognitive changes with corticosteroids appear to be common but generally mild and reversible side effects. More studies are needed to determine effective treatment for steroid-induced psychiatric disorders.


Tollenaar MS, Elzinga BM, Spinhoven P, Everaerd W. Immediate and prolonged effects of cortisol, but not propranolol, on memory retrieval in healthy young men. Neurobiology of Learning and Memory 2009;91(1):23-31.

Background While acute cortisol administration has been found to impair retrieval of emotional memories in healthy subjects, the duration of this memory impairment is still unknown. Propranolol, on the other hand, may impair the reconsolidation of emotional memories during reactivation, although human studies examining such effects are scarce. The present investigation was therefore undertaken to examine the immediate and prolonged effects of a single administered dose of cortisol or propranolol on memory retrieval in a double-blind placebo controlled design.

Methods Eighty-five healthy male participants were asked to retrieve previously learned emotional and neutral information after ingestion of 35 mg cortisol, 80 mg propranolol or placebo. After a washout period of 1 week, recall was again tested.

Results Memory retrieval of neutral and emotional information was impaired by a single dose of cortisol compared to placebo. The memory impairment due to cortisol remained, even after a washout period of 1 week. No immediate or prolonged effects of propranolol on memory retrieval were found, despite significant reductions in sympathetic arousal.

Conclusions These results lend support to the hypothesis that cortisol is able to attenuate (emotional) memory recall in men over longer time spans and may therefore augment the treatment of disorders like post-traumatic stress disorder and phobias, but do not clarify the mechanism(s) through which propranolol exerts its therapeutic effects.


de Quervain DJF, Aerni A, Roozendaal B. Preventive Effect of {beta}-Adrenoceptor Blockade on Glucocorticoid-Induced Memory Retrieval Deficits. Am J Psychiatry 2007;164(6):967-9.

OBJECTIVE: Elevated glucocorticoid levels impair retrieval of emotional information, and animal studies indicate that this effect depends on concurrent emotional arousal-induced increases in noradrenergic transmission within the brain. The authors investigated whether the {beta}-adrenoceptor antagonist propranolol blocks glucocorticoid-induced memory retrieval impairments in human subjects.

METHOD: In a double-blind, placebo-controlled study, 42 healthy volunteers were presented a set of words with variable emotionality and asked to learn them for recall. A day later, cortisone (25 mg), propranolol (40 mg), or both drugs were administered orally 1 hour before a free-recall test.

RESULTS: Cortisone selectively impaired the recall of emotionally arousing words by 42%. This impairment was blocked by the concurrent administration of propranolol. Propranolol alone did not affect recall of either emotional or neutral words.

CONCLUSIONS: A pharmacological blockade of {beta}-adrenoceptors prevents glucocorticoid-induced memory retrieval deficits in human subjects. This finding may have important implications for the treatment of memory deficits in hypercortisolemic states, such as stress and depression.


de Quervain DJF, Roozendaal B, Nitsch RM, McGaugh JL, Hock C. Acute cortisone administration impairs retrieval of long-term declarative memory in humans. Nat Neurosci 2000;3(4):313-4.

 

[MetalMX]

That is interesting. I can tell you from first hand experience that i had horrible memory. When i started HC i started remembering everything.

IMO studies aren't as useful as first hand experience. I think you are highly mistaken about HAN he really does know his shit

[)]

 

[boon]

Mr. Scally:

I listened to the section of the broadcast about adrenal fatigue and transcibed the following statements made by Dr. Crisler.

Keep in mind the following:

I didn't include any questions/comments by the host (for whatever that's worth).

The host and Dr. Crisler were talking about medical subjects in conversational language and didn't include any preparatory info about the things they were going to say; they just said what they said with no prior elaboration.

I tried to post the gist of Dr. Crisler's comments and left out what I considered fluff so perhaps I missed a few details you may or may not have found important.

But overall I stand by the accuracy of what I'm including here. Remember these are all statements made by Dr. Crisler (not the radio host).


AF first recognized in 1898...regularly treated in 1920-1940s now difficult to get doctors to admit it exists.

Some people have been brought from bedridden state to full vigorous lifestyle with 10-20 MG of HC a day. These people are not making this up.

Been proven with lab analysis these people are not responding appropriately to stress hormones due to the stimulus. (Not sure what he was saying but this is how it sounded to me after several listenings so this is how I worded it.)

Conventional medical opinion is that HC dangerously supresses the system. It's been shown that people can take up to 40 mg orally a day without supressing the system.

Too many millions of people who've had their lives turned around with nonsuppressive physiologic - not pharmacologic - doses of a very mild and safe level or dose of HC.

Crisler recalls that he's likely never had to go above 30 mg a day to get results with patients. This is well below suppressive dosing.

As far as diagnosing AF, all lab work can be normal but this is unreliable given that "normal" lab ranges cover a statistical evaluation of the population which includes sick people so these sick people are included in the "normal" range for lab values.

Diagnosing AF is a completely clinical judgement.

Some questions that can be asked to diagnose AF:

Does salt/salty food taste very good to you? if patient says "yes I love it, would eat a lot of it if I could" this suggests AF.

Trouble getting up in AM?

Have more energy at night than in the morning and very fatigued in the AM after waking up?

Does cup of strong coffee put you to sleep (due to change in blood sugar level)?

Main point about AF which all doctors should know is that the primary purpose of glucocorticoids (including HC) is to maintain blood sugar levels. That's why of the stress hormones, cortisol is the only one you can't live without.

To illustrate this, patients are often released from longterm care of some kind while on prednisone for example (much much stronger than HC and these patients are completely suppressed) and transferred to another facility without anyone noting these patients are on prednisone and they would die in a few hours if no one caught it.

At this point the radio show host changed topics and began a discussion of pregnenolone as the "progenitor hormone" in which pregnenolone can "travel downstream" and convert into various other hormones based on certain enzymatic processes.

I didn't transcribe any comments made about this topic except that the host asked if taking pregnenolone can balance out all other hormones through a "cascading downward" process or would any enzymatic deficiencies cause you to have more of certain hormones and less of others depending on your age. Dr. Crisler said both things are true and that you can balance hormones by making higher levels of some of the "intermediate steps" than others as things progress down the stream.

Dr. Crisler used the analogy of filling buckets stacked on top of each other. As the top buckets fill up they over flow and fill the buckets under them and so on.

This lead Dr. Crisler to say that:

A Dr. Mark Gordon treats AF exclusively with transdermal pregnenolone waiting for it to travel downstream.

Dr. Crisler has had patients completely transform themselves on the first day of treatment with only 10 MG of HC.

Dr. Crisler usually starts with 10 MG of HC...sometimes 5 MG...taken first thing in the morning.

Dr. Crisler stated that if a patient has great trouble getting out of bed (which indicates the presence of AF) to take 5 MG of HC upon waking (putting the pill and a glass of water by the bed the night before) and the patient will get up easily.

Also if you have an afternoon crash at whatever time take 5 MG. If this fixes the crash then you're in good shape. If not take another 5 MG.

The afternoon crash is a significant indicator of AF.

The next day about the same time take the dose that helped you on the day before. Some people - not many - crash 3 or 4 times a day.

They went to commercial break and after returning Dr. Crisler said the following about AF:

AF isn't necessarily about not producing enough stress hormone but rather the ill-timed release of stress hormone in response to stressful life events, which is why you can have normal lab results but still feel lousy.

Example: You're cut off while driving in traffic. You ignore it and have no reaction. But 15-20 min later at home reading the paper you have a stress reaction (feeling like an anxiety attack).

At this point the discussion went back to pregnenolone and I stopped listening.


Hope this helps.

Edit: I've never had any contact with Dr. Crisler and I'm not trying to subject him to ridicule or put him on the chopping block. I'm very interested in the issue of whether or not AF is a real condition and thought highlighting the comments he made in the radio broadcast would be usesful in furthering the discussion.

 

[nickatnite]

I'm taking roughly 12.5mg per day in divided doses. That seems to be helping a bit.


here are my saliva results:

7am-9am: 0.22mcg/dL
11am-1pm: 0.04mcg/dL
3pm-5pm: 0.05mcg/dL
10pm-12am:<0.03mcg/dL

I got a long way to go though. Apparently I have some serious adrenal issues. I have no libido, have been gaining weight around my midsection like I'm getting paid for it. HANS has been helping me a lot. Him and Dr. O seem to really know their shit.

 

[MetalMX]

I'm taking roughly 12.5mg per day in divided doses. That seems to be helping a bit.


here are my saliva results:

7am-9am: 0.22mcg/dL
11am-1pm: 0.04mcg/dL
3pm-5pm: 0.05mcg/dL
10pm-12am:<0.03mcg/dL

I got a long way to go though. Apparently I have some serious adrenal issues. I have no libido, have been gaining weight around my midsection like I'm getting paid for it. HANS has been helping me a lot. Him and Dr. O seem to really know their shit.

"Gaining weight around my midsection like i'm getting paid for it" HAHAHA

Man i love that quote. Same symptoms we're happening to me. 15mg of HC completely turned my life around right now. Although i have the more dreaded problem of adjust thyroid meds (for my hashimotos) and Hydrocortisone (for my adrenal fatigue) but my thyroid meds could not work if my AF isn't being treated plain and simple.

I experienced:

Severe morning tiredness gets better at night (at night i felt as if i just woke up)
salt cravings
no libido
shortness of breath or "sighing"
gaining weight around my midsection
loss of appetite or heavily reduced
no smell or taste
sugar cravings
constant awakening from sleep with hunger (due to low blood sugar)
awful memory

Some Symptoms are still their but nowhere near as bad as before. Its a process takes time to heal. I didn't think i could ever be able to work or do much now i have initiative and drive in my life.

This is just my experience with it. I was hypothyroid for a LONG LONG (since early childhood) time before i got on meds and diagnosis so this is the likely cause of my AF.

 

[techlogik]

There seems to be a discussion going far off track of what most people consider "adrenal fatigue" and "adrenal insufficiency" .

I have never heard/read anybody advocating the use of powerful GCs in high doses, like prednisone, to treat adrenal fatigue.

I am confused why articles from PubMed keep being quoted that have nothing to do with the point of fatigue and insufficiency as it relates to the typical health discussions on the forums.

The most that is recommended for adrenal fatigue using HC is approximately 20mg/day in divided doses, like 10,5,2.5,2.5 mg respectively every 3hrs upon rising, or something like that.

Nobody have ever suggested that adrenal fatigue be treated with 75mg/prednisone and such like has been quoted off PubMed articles and how this plays into psychological issues taking such. If so, please find that info and post it.

 

[Michael Scally MD]

There seems to be a discussion going far off track of what most people consider "adrenal fatigue" and "adrenal insufficiency" .

I have never heard/read anybody advocating the use of powerful GCs in high doses, like prednisone, to treat adrenal fatigue.

I am confused why articles from PubMed keep being quoted that have nothing to do with the point of fatigue and insufficiency as it relates to the typical health discussions on the forums.

The most that is recommended for adrenal fatigue using HC is approximately 20mg/day in divided doses, like 10,5,2.5,2.5 mg respectively every 3hrs upon rising, or something like that.

Nobody have ever suggested that adrenal fatigue be treated with 75mg/prednisone and such like has been quoted off PubMed articles and how this plays into psychological issues taking such. If so, please find that info and post it.

It is clear that you did not take the time to read the thread or the abstracts. If you did, you would see the adverse effects occur with doses of 20-30 mg cortisone. Why don't you learn how to read before spouting off?