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Pregnenolone Is A Potent Aldosterone Antagonist (antimineralocorticoid)

Discussion in 'Scientific Studies' started by haidut, Jan 25, 2017.

  1. haidut

    haidut Member

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    Ray has written a number of articles on the hypertension, heart and kidney failure, eclampsia, and CVD in which he describes the central role of aldosterone in the pathogenesis of these conditions. Aldosterone antagonists (antimineralocorticoid) are mainstream therapy for heart failure and prevention of both first and subsequent heart attacks. I posted a thread some time ago showing that cyproheptadine can reliably lower aldosterone. This study shows that pregnenolone (just like progesterone) is a potent aldosterone antagonist in low nanomolar concentrations (IC50: 72nM/L).

    Occurrence of androgens in sewage treatment plants influents is associated with antagonist activities on other steroid receptors. - PubMed - NCBI
    http://www.sciencedirect.com/science/article/pii/S0043135412000334

    "...Highlights ► Steroid receptor profiling of STPs extracts using in vitro steroid receptor bioassays. ► Presence of agonist ER and AR, and antagonist GR, PR and MR activities in samples. ► Analysis of the STPs activities due to human steroids. ► AR, anti-GR and PR activities were not due to known human androgens. ► The steroid precursor pregnenolone is a potent anti-mineralocorticoid."

    "...Interestingly, using LC MS/MS (Liquid chromatography coupled to tandem mass spectrometry), we detected the presence of pregnenolone at high concentrations in the S2 and S4 samples. Using our bioluminescent reporter cells, pregnenolone was identified as a potent MR antagonist with a faint antagonist activity on PR and AR (Fig. 4B and Table 4 for the IC50) and a weak agonist activity on ERa (Fig. S3). Chemical analysis indicated that pregnenolone significantly contributed to the Bio-Spiro-Eqs (54.9 and 7.3% see Table 3). Altogether, these results identify pregnenolone as a novel EDCs acting as an important contributor to the detected antimineralocorticoid activity."
     
  2. Velve921

    Velve921 Member

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    What would you consider high aldosterone symptoms?
     
  3. OP
    haidut

    haidut Member

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    Did you Google "high aldosterone symptoms"?
     
  4. dfspcc20

    dfspcc20 Member

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    My mom was "diagnosed" by her idiot doctors with Secondary Hyperaldosteronism. They didn't even consider it could have been caused by the super low-sodium diet they recommended for her many years prior for her Ménière's disease, along with potassium supplements. I've been trying unsuccessfully ever since to get her to add more salt again, while watching her basically fall apart and develop many more issues.

    Maybe I'll be able to convince her to try pregnenolone, progesterone, and/or cyproheptadine for the Secondary Hyperaldosteronism, rather than what ever else they're giving her for it. I doubt it though, unless the doctor says it. Those would likely help with the Ménière's as well, according to previous Peat quotes.
     
  5. Velve921

    Velve921 Member

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    Got it! Thanks.
     
  6. Drareg

    Drareg Member

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    When you consider the actions of HSD11B2, do you think anything that inactivates/lowers cortisol will leave aldosterone unopposed in some cases? I understand they have a sensitive ratio where cortisol outcompetes aldosterone.

    Niacinamide,creatine and aspirin can cause slight water retention,puffiness in some cases,the creatine complaints are well known,it seems using these substances without checking the aldosterone could be causing it?
     
  7. OP
    haidut

    haidut Member

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    It is actually the elevated cortisol that can outcompete aldosterone for binding to the MR receptor and this is what causes the water retention, puffiness and hypertension in high cortisol states. Aldosterone is primarily driven by sodium levels in the blood so the control mechanism is (usually) not dependent on cortisol levels. What aldosterone can cause is fibrosis if it is elevated chronically. I think aldosterone is also driven by serotonin, which is not surprising since serotonin is de-activated in a sodium-dependent fashion (i.e. the SERT protein), so it's down to sodium again.
     
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