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My understanding of treating adrenal fatigue

Discussion in 'Adrenal Dysfunction' started by heapsreal, Apr 17, 2012.

  1. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    My experience is that i have felt worse trying to increase cortisol as well, but have found slowly increasing dhea first is important, then it seems that i can tolerate treatments that increase cortisol better, but thats still a work in progress.

    cheers!!!
  2. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    There seems to be abit of an arguement over the name or where the problem actually lies, is it in the adrenals or is it in the hpa axis, at the moment who cares, treating these difiencies can help, is it a long term solution? Well nothing is in cfs, most treatments seem to be ongoing to maintain benefit, theres nothing wrong with that if it helps, diabetics keep taking insulin??

    One of the points i was trying to make in my initial thread was the importance of slowly increasing dhea levels before doing anything with cortisol levels. Nothing may need to be done with cortisol levels if dhea improves. This is what i wanted to share with people as i have found this an important point in treating adrenal fatigue and i have read many people say they have had bad reactions from trying to increase cortisol from adrenal extracts, pregnenolone etc. Im also not saying its going to work for everyone but its worth ba shot.

    Hopefully this has resuscitated my thread that has been shot to pieces,
  3. lansbergen

    lansbergen Senior Member

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    Too high virus load?
  4. adreno

    adreno 3% neanderthal

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    Alex, I think rituximab is not the only road to Rome. Treating the viral infections, that lead to the autoimmune reaction, and dampening the excessive immune response (inflammation) might be another way to go. It's the road I'm taking, as I still find rituximab too risky at the moment.

    Again, curcumin looks very promising in treating autoimmune, inflammatory, and fatigue conditions. It's a very powerful inhibitor of NF-kB. I think you'll find the following interesting:


    Downregulation of B lymphocyte stimulator expression by curcumin in B lymphocyte via suppressing nuclear translocation of NF-?B.

    Huang G, et al.

    Eur J Pharmacol. 2011 Jan 10;650(1):451-7. Epub 2010 Oct 13.

    Department of Biochemistry and Molecular Biology, College of Basic Medical Science, Third Military Medical University, Chongqing 400038, China.
    Abstract

    Overexpression of B lymphocyte stimulator (BLyS) is closely involved in the pathogenesis and progression of some autoimmune diseases. Curcumin, a pharmacologically safe agent, has been shown to possess potent anti-inflammatory properties. However, it is not clear whether curcumin affects the expression of BLyS. In this study, we report that curcumin inhibits the expression of BLyS and that a DNA-binding site for the transcriptional factor NF-?B in the BLyS promoter region is required for this regulation. Moreover, we find that curcumin reduces the DNA-binding activity of NF-?B to the BLyS promoter region and suppresses nuclear translocation of p65, suggesting that curcumin may suppress BLyS expression via negatively interfering with NF-?B signaling. These results suggest that curcumin may serve as a novel therapeutic agent in the treatment of autoimmune diseases by targeting BLyS.

    PMID 20950605
  5. adreno

    adreno 3% neanderthal

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    I don't know where you got this information, but it is simply not correct. Cortisol is a known immunosuppressant, that suppresses the immune system in a dose dependent manner. It is mainly there to modulate the immune system, and keep inflammation from getting out of hand. That is why it is used as a treatment for autoimmune conditions. Cortisol is contraindicated in infections, because it worsens them.


    [Immunosuppressive effects of glucocoriticoid].

    Tanaka Y.

    Nihon Rinsho. 2008 Jan;66(1):83-8.

    The First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health.

    Abstract

    Although glucocorticoid (GC) is widely used to treat a variety of autoimmune diseases, inflammatory diseases, allergic diseases and many, GC causes a number of significant side effects. Among them, bacterial, fungal and viral infections, based on immunosuppressive conditions induced by GC, are major complications of GC therapy. GC exerts its biological effects through binding to the GC receptor (GR), a ligand activated transcription factor(TF). Recent findings indicate that the crosstalk between GR and certain TF induced by cytokines or toll-like receptor (TLR) signaling, results in the modulation of genes targeted by these specific TF, including NF-kappaB, AP-1, STAT and IRF3. The modification of these TF by GR regulate the transcription of targeted genes involved in innate immunity, acquired immunity, allergy and inflammation, which results in the final outcome of the immune responses.

    PMID 18193547
  6. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    if cortisol is too low then infections can greatly increase inflammation, we need the right amount, its not a matter of cortisol being good or bad.

    cheers!!!
  7. adreno

    adreno 3% neanderthal

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    And how do you know that the downregulation of the HPA axis seen in ME/CFS is not adaptive? I find it very possible that this could be a way of avoiding infections from getting any worse.

    My point is, I'm not convinced that raising cortisol levels will be beneficial to us in the long run. I find it a wiser strategy to focus on dampening the excessive inflammation.

    It does look like DHEA has anti-inflammatory effects, and could be helpful in treating autoimmune conditions. So I'm not saying that DHEA isn't useful. DHEA does not increase cortisol levels, from the evidence I have seen, though.
  8. iacyi

    iacyi

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    A few years back after getting off SSRIs I tried to jump straight back into life and ran into all the"adrenal fatigue" symptoms (Uncontrolable shaking, bursting out in sweat and the room spinning if I became slightly stressed, also took me hours to become conscious enough to get out of bed). Hydrocortisone knocked out all those problems and greatly improved my sleep, for a while at least. I stopped taking it from a combination of frightened doctors, lack of money and possibly the return of some symptoms...

    Any pregnenolone gives me negative feedback within hours; I can't do anything but lie down and I feel like I'm standing on Jupiter. It takes about a day to get back to where I was. If I take really high doses my brain starts to feel weird and I feel kinda spaced out.

    I used to do fine on 25mg DHEA twice a day, but then I started taking sulforaphane to try and help my Gilbert's... I started getting mega feedback again. IIRC I cut down to 25mg which helped, but got feedback again after a couple days, then cut down to nothing and started getting feedback from the sulforaphane itself. Now I can't take either DHEA or sulforaphane without feedback.

    I seem to get the same effect from bee propolis, and I'm not sure, but I think curcumin too. I bought all these supplements to help with my Gilbert's and to reduce my oestrogen, which they do temporarily.

    I have taken <7mg of sublingual DHEA just now as an experiment. Maybe I can build up slow and then add the pregnenolone like you say.

    My other experiment ideas were to use some of my leftover hCG to boost pregnenolone, or to try aggressive carb feeding as described on blogs like 180DegreeHealth or some Ray Peat-inspired ones. Unfortunately I did a test round of DMSA and my gut flora has gone absolutely beserk, so the carb idea looks incompatible now...
  9. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    It might be adaptive but maybe it drives cortisol too low, which is why there is alot of inflammation and oxidative stress in cfs/me. DHEA helps protect us from the negative effects of cortisol. but i think we need to work on low dhea first, may never need to worry about cortisol once this is corrected. I agree with you that high cortisol levels should be avoided. Maybe im also getting a good response from dhea as antivirals have lowered my cmv/ebv load and antibiotics have finally sorted my chronic sinus issues out.

    cheers!!!
  10. Ema

    Ema Senior Member

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    It probably is adaptive...for the infection that wishes to continue to proliferate without sufficient cortisol to help halt it! If cortisol is so bad for infection, why does the body produce double or triple the normal levels when one has an infection? Eventually the body cannot keep up with the demand with chronic infection and cortisol levels become too low to help the immune system. As heapsreal stated, it is a matter of dose. The amount needs to be just right...not too low or too high.

    DHEA needs to be taken along with cortisol if it also tests low as it is also an important adrenal hormone.
    heapsreal likes this.
  11. Ema

    Ema Senior Member

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    Your response and cite prove my point...it is a dose dependent manner. I'm not talking about large immunosuppressive doses.

    The effects you list simply do not occur at physiological dosing and are a great way to keep people needlessly afraid of steroid treatment which may be greatly beneficial for their healing.
  12. adreno

    adreno 3% neanderthal

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    The article I quoted does not support your claim that cortisol fight viral infections.

    So your argument is that physiological doses of cortisol are immunosupportive, whereas pharmacological doses are immunosuppressive? Do you have any evidence of that? Is there a cut-off point?

    Here is a recent study showing glucocorticoids can reactivate latent EBV. Note that this occurs at physiological doses. This is also why you are prone to getting cold sores during times of stress.


    Glucocorticoids activate Epstein Barr virus lytic replication through the upregulation of immediate early BZLF1 gene expression.

    Yang EV, et al.

    Brain Behav Immun. 2010 Oct;24(7):1089-96. Epub 2010 May 11.

    Institute for Behavioral Medicine Research, The Ohio State University Medical Center, 460 Medical Center Drive, Columbus, OH 43210, USA.

    Abstract

    Psychological stress-associated immune dysregulation has been shown to disrupt the steady-state expression and reactivate latent herpes viruses. One such virus is the Epstein Barr virus (EBV), which is associated with several human malignancies. EBV infects >90% of people living in North America and persists for life in latently infected cells. Although several studies have shown that glucocorticoids (GCs) can directly induce reactivation of the latent virus, the mechanism of stress hormone involvement in the control of EBV gene expression is not well understood. In this study, we tested the hypothesis that GCs can induce the latent EBV genome to lytically replicate through the induction of the EBV immediate early gene BZLF1 which encodes the lytic transactivator protein ZEBRA. We show a dose-dependent upregulation of BZLF1 mRNA expression by hydrocortisone (HC) and dexamethasone (Dex) in Daudi cells, an EBV genome positive Burkitt's lymphoma cell line, and Dex-induction of the early gene products BLLF3 (encoding for the EBV dUTPase) and BALF5 (encoding for the EBV DNA polymerase). We show that Daudi cells express glucocorticoid receptors (GR) that mediate Dex-dependent upregulation of BZLF1 mRNA levels. This effect was inhibited by both the glucocorticoid receptor antagonist RU486 and by cycloheximide. The results suggest that GCs, in addition to inducing stress-related immune dysregulation, can mediate latent EBV reactivation through the induction of the BZLF1 gene.

    PMID 20466055
  13. adreno

    adreno 3% neanderthal

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    Here is an article showing that cortisol is detrimentally involved in HIV. Again, this is at physiological doses.


    A possible role for the cortisol/anticortisols imbalance in the progression of human immunodeficiency virus.

    Clerici M, et al. Show all Journal

    Psychoneuroendocrinology. 1997;22 Suppl 1:S27-31.

    Cattedra di Immunologia, Universit degli Studi di Milano, Padiglione L.I.T.A., Ospedale L. Sacco, Italy. mago@imiucca.csi.unimi.it

    Abstract

    The progression of HIV infection is accompanied by complex alterations in the production of adrenal steroids. Cortisol levels are increased in HIV infection whereas those of dehydroepiandrosterone (DHEA), a physiologic antagonist of the immunoregulatory activities of cortisol, decrease. The progression of HIV infection to AIDS is also characterised by a shift from a type 1 to type 2 cytokine production. Thus, defective production of interferon gamma (IFN gamma), interleukin (IL)-2, and IL-12 as well as increased production of IL-4, IL-5, IL-6, and IL-10 are observed in HIV-seropositive individuals and are proposed to be in vitro immunologic marker of progression. Cortisol and pharmacological doses of glucocorticoids (GC) suppress IL-2 and IFN gamma production and favour the production of IL-4. Furthermore, GC and IL-4 stimulate the differentiation of B lymphocytes into IgE producing plasma cells, the concentration of which augments in HIV infection. Finally, GC induce programmed cell death (PCD) in a variety of different cells, including mature T lymphocytes, and type 2 cytokines were recently proposed to augment the susceptibility of T lymphocytes to PCD. It was suggested that the progressive shift from type 1 to type 2 cytokine production characteristic of HIV infection could be at least partially provoked by the increase in the production of cortisol and the reduction of DHEA. This hypothesis is discussed within the scenario of an endrocrinologic imbalance being responsible for HIV progression at least partially via increased susceptibility of HIV + CD4 lymphocyte to PCD.

    PMID 9264144
  14. adreno

    adreno 3% neanderthal

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    This study shows that the glucocorticoid antagonist mifepristone is effective at inhibiting HIV replication:


    Antiviral effects of mifepristone on human immunodeficiency virus type-1 (HIV-1): targeting Vpr and its cellular partner, the glucocorticoid receptor (GR).

    Schafer EA, et al.

    Antiviral Res. 2006 Dec;72(3):224-32. Epub 2006 Jul 7.

    Department of Infectious Diseases & Microbiology, University of Pittsburgh, Graduate School of Public Health, 130 Desoto Street, Pittsburgh, PA 15261, USA.

    Abstract

    The HIV-1 viral protein R, Vpr, increases virus replication in T cells and is necessary for the optimal infection of primary monocytes/macrophages and other non-dividing cells. Vpr interacts with the cellular glucocorticoid receptor (GR) and transactivates the HIV-1 LTR through glucocorticoid response element (GRE), an event that can be blocked by the GR antagonist, mifepristone. Results demonstrated that Vpr-induced transactivation of the HIV-1 LTR was inhibited by mifepristone in a dose-dependent manner by >60% at a 10 microM concentration. Infectivity assays using X4 and R5 viruses demonstrated antiviral effects on a dose-dependent regimen of mifepristone. The effects of mifepristone were also tested in latently infected cells that could be activated with extracellular Vpr protein and results indicated specific inhibition of virus reactivation in the presence of this antagonist.

    PMID 16889838
  15. lansbergen

    lansbergen Senior Member

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    i avoid cortico's as the plaque. I noticed consequences opposite of what is supposed to happen.
  16. Ema

    Ema Senior Member

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    Again, proving the point that *pharmacological* doses are immunosuppressive.
  17. Ema

    Ema Senior Member

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    "Treatment of Daudi cells with physiological concentrations of HC (1 nM) did not result in a significant increase in BZLF1 expression above that of untreated controls at any time point. However, cells treated with stress levels (100 nM) and pharmacological levels (10 ?M) of HC induced BZLF1 gene expression, reaching a maximum increase of 3.07 1.28 fold above control levels (p = 0.001) after treatment with 10 ?M HC for 72 hrs."

    This is a quote from the article cited above...again it is not referring to physiological levels.

    If physiological levels of cortisol were the problem, then all people with healthy HPA axis function should be running around with raging chronic infections when the opposite is true.
  18. bertiedog

    bertiedog Senior Member

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    From personal experience I know that it is true that one's immune system can improve when taking physiological doses of cortisol because I have been on Prednisolone 5mg plus a bit extra hydrocortisone since 2002 and gradually my immune system has got stronger and even though I might get a virus I am finding that my body fights it in a day or so without it developing. Before being on cortisol I used to have horrendous tummy bugs and vomitting and frequent viruses and infrections. I haven't had a tummy bug since being on cortisol and my gut is great these days. The throat infections I used to get are also a lot better but I think this might also be because I have improved my Vitamin D level.

    I also have a life and do things like running a local support group for Fibromyalgia sufferers which involves putting together a newsletter every other month and running monthly meetings. I also do volunteer work at a Visitor Centre near my home. Most days I walk my dog and I don't have many cognitive problems either which as I am 64 years old isn't bad.

    For me taking cortisol in the form of Prednisolone always felt completely natural, actually for me more natural than hydrocortisone which tended to run out too quickly in my body. I don't have any problems with Osteoporosis either and for me it has helped me so much especially my nervous system. I used to have horrendous adrenaline problems but these are miles better now, in general I am very calm and can cope with most things without too many problems.

    I am still left with an inability to walk for more than 25 minutes at a time but I do recover usually by the next day even if I overdo things. Cortisol gave me my life back and when I read of so many sufferers' symptoms I recognise them as being related to poor adrenal function but people are scared of cortisol. The way I see it is if the adrenals aren't producing what is necessary for life then why not take some in pill form.

    Dr William Jefferies book "The safe use of Cortisol" is a great read and really put my mind at rest. I should say that also I have Hashimotos thyroid disease and I think the fact that I need around the equivalent of 25mg cortisol each day is partly because the adrenals have to be strong in order to take T3.

    Finally it does seem that the adrenals can improve too even on steroids because I needed Fludrocortisone for very bad POTS for 3 years but recently I have been able to discontinue it and just stick with a very low dose of betablocker to keep the POTS under control.

    Pam
  19. garcia

    garcia Aristocrat Extraordinaire

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    I agree with this and all adreno's posts. The bottom line for something like corticosteroids is whether they work for the patient. They didn't for me. I find even the smallest doses to be immunosuppressive. However I acknowledge that there is a minority of patients for whom they do help.
  20. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    Agree, it depends on the persons hormonal profile before using corticosteriods. The HIV study mentioned a drop in dhea as well as increase in cortisol, so dhea may treat the negative effects of cortisol. Other studies showing dhea lowering IL6 which is a major inflammatory cytokine in cfs/me. I think this is showing what i have been saying that u need a good level of dhea before looking into increasing cortisol levels, dhea on its own maybe enough.
    Sallysblooms likes this.

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