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    Is Low Dose DHT Suppressive?

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    • NomanarchN
      Nomanarch
      last edited by

      I keep seeing anecdotal claims that physiological (non-replacement) DHT doses aren't suppressive and in fact permanently upregulates 5-AR. However I haven't found any studies supporting either claim (it could be a skill issue on my end, but I am critical of advocacy for exogenous hormone use that suppresses HPTA). So, is low dose DHT suppressive, and if not, is there any evidence for that claim? Does exogenous DHT supplementation permanently upregulate 5-AR (and might that make suppression worth it)?

      C sunsunsunS 2 Replies Last reply Reply Quote 0
      • C
        CrumblingCookie @Nomanarch
        last edited by CrumblingCookie

        Here you are:

        On the Role of Dihydrotestosterone in Regulating Luteinizing Hormone Secretion in Man

        Impact level of dihydrotestosterone on the hypothalamic-pituitary-leydig cell axis in men

        and as a bonus (+ Mauritio's linked studies about estrogen/aromatization but not DHT being the actually catabolic effector of high testosteron):
        Prolactin secretion in the human male is increased by endogenous oestrogens and decreased by exogenous/endogenous androgens

        Wrt ARs: Estrogens actually severely downregulate them. DHT both inhibits aromatization, seems to have some antagonizing effect on ERs IIRC, and it speeds up estrogen breakdown by EST estrogen sulfotransferase.
        And as you will read in the links above, DHT (in stark contrast to synthetic AIs) penetrates across the blood--testis barrier to exert the aforementioned effects also there.

        jamezb46J 1 Reply Last reply Reply Quote 0
        • sunsunsunS
          sunsunsun @Nomanarch
          last edited by

          @Nomanarch how could it be permanent up regulation lol

          1 Reply Last reply Reply Quote 0
          • jamezb46J
            jamezb46 @CrumblingCookie
            last edited by jamezb46

            @CrumblingCookie

            Pretty sure the aromatase inhibitor ATD (Androstatriendione) both inhibits aromatase and increases DHT by slowing the metabolic deactivation of DHT into the -diol metabolites

            So, theoretically ATD + something like Proviron would be anabolic

            https://en.wikipedia.org/wiki/1,4,6-Androstatriene-3,17-dione

            https://pubmed.ncbi.nlm.nih.gov/3773531/

            In time there is life but no knowledge; outside time there is knowledge but no life

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            • C
              CrumblingCookie @jamezb46
              last edited by CrumblingCookie

              @jamezb46 Does the inhibition of the -diol conversion make ATD notably better than ordinary exe?

              I've yet tried neither proviron nor DHT. But I'd like to use the latter first, as a benchmark, and not so much for a heavily criticized lack of anabolism of DHT but for its anticipated restorative effects, at some time when there's less essential conditions on my plate. Along with ARA-290 and other stuff then.

              jamezb46J 1 Reply Last reply Reply Quote 0
              • jamezb46J
                jamezb46 @CrumblingCookie
                last edited by jamezb46

                @CrumblingCookie

                I would be guessing as to whether one was better than the other. I assume what you mean by better is more anabolic to muscle?

                It would depend on the dose of course. But mechanistically it would seem that ATD would be better at a dose that achieved the same aromatase inhibition as a dose of Exemestane because of the inhibition of the metabolic deactivation of DHT.

                But that is an extremely rough guess. I don't know for sure. That is in part because the answer depends on the following two questions: how efficiently does the body convert either of the substances to the 3-ketone, 17b-hydroxyl metabolite and second, how anabolic is that metabolite.

                If you're not aware of the steroid chemistry: here is a brief crash course: the end-point androgens have a ketone group on position 3 and a hydroxyl group on position 17b. Both ATD and Exemestane have ketone groups on both position 3 and 17b. Therefore to be a full agonist of AR, they would need the ketone on 3 to be conserved and the one on 17 to be changed to a hydroxyl.

                Therefore, the metabolite with only the 17 functional group changed to hydroxyl will determine in part how anabolic the drug is when given orally. More specifically, we would need to know: (how anabolic is the 17b-hydroxyl metabolite) x (how efficiently that metabolite is created in a human body). Then we take the product and that would account for a big chunk of the anabolic potential of the compound.

                In time there is life but no knowledge; outside time there is knowledge but no life

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                • C
                  CrumblingCookie @jamezb46
                  last edited by CrumblingCookie

                  @jamezb46 said in Is Low Dose DHT Suppressive?:

                  I would be guessing as to whether one was better than the other. I assume what you mean by better is more anabolic to muscle?

                  Subjectively, mainly, as in a more wholesomely good and balanced feeling as opposed to the almost surgical single-sided effect of exe. So in between pure DHT and exe on a scale of AIs. ATD doesn't seem to be a thing anymore. Maybe discussing it is even of little use if there's both DHT and exe at hand. It sounded like you may had tried ATD when it still was available OTC.

                  jamezb46J 1 Reply Last reply Reply Quote 0
                  • jamezb46J
                    jamezb46 @CrumblingCookie
                    last edited by

                    @CrumblingCookie

                    Haven't tried it but it is available!

                    Just a head's up that I tend not to talk on this forum about mere possibilities or random pipe dreams that occur to me.

                    You can order from England: https://www.predatornutrition.com/us/testosterone-boosters/fusion-supplements/atd.html

                    In time there is life but no knowledge; outside time there is knowledge but no life

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