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  • Why is HCG Important for Men on Testosterone Replacement Therapy?



    Nelson Vergel from www.ExcelMale.com explains the benefits of human chorionic gonadotropin (hCG) use in men with low testosterone beyond fertility and testicular atrophy reversal. For more details go to:https://www.excelmale.com/showthread.... and watch https://www.youtube.com/watch?v=0uXoB...

    This article was originally published in forum thread: Why is HCG Important for Men on Testosterone Replacement Therapy?
    Comments 4 Comments
    1. Weasel's Avatar
      Weasel -
      Nelson,

      Couple Questions,

      1. Can the same results be achieved by supplementing PREG/DHEA vs HCG?

      2. Have you saw any studies or evidence that HCG will increase DHT more than just testosterone will?
    1. MikeXL's Avatar
      MikeXL -
      What always bothered my about the concept of back filling the pathways is that it Presumes that the pathways need to be back filled. I realize that once on TRT, less of the higher-up-the-chain hormones are produced. However, that could merely be because less are needed given the patient is now on TRT. Pregnenolone, progesterone and DHEA are still needed when you commence TRT. And we see a decrease, but we don't see a complete shutdown like we do with LH and FSH. Perhaps the body merely down regulates them just enough to give the patient only what is needed, which would be less now that none is needed for producing T.


      And that leads me to the next thing. If LH really was needed for something other than testosterone, why would the body produce zero just because of TRT ?
    1. Nelson Vergel's Avatar
      Nelson Vergel -
      Excellent observation. Evolution has made it possible to get every hormone axis to self-regulate depending on the amount of hormones in it. It was never intended to get hormones supplied from the outside world. The downregulation of the HPTA shuts down LH and FSH with obvious physiological disadvantages like low or no fertility. Replacing T via physiologic TRT normalizes only one hormone while leaving LH, FSH, pregnenolone and progesterone low or nil. DHT and E2 remain OK since they are downstream of T. If the body was just slowing down production of all those suppressed hormones to adjust them due to less need for them, why would the axis keep an important hormone like FSH shut down. That hormone ensures the survival of our species via sperm production. If this self-regulation was just part of homeostasis, then all organ functions would eventually be normalized (including testicular sperm production). We can speculate all day since we have hardly any data on the subject.

      There are references showing that LH itself may also have other roles since LH receptors are everywhere including the brain. Unfortunately, we do not have any scientific information of what happens to those receptor with long term LH shutdown. The same thing can be said about the shut down of pregnenolone and progesterone. Those two hormones have some limited references about their role in men's health:

      https://www.excelmale.com/showthread...cursor-Hormone and

      https://www.excelmale.com/showthread...1-Progesterone

      This is an emerging field and we hope to see more studies that actually provide solid data on issues surrounding long term shut down of the HPTA and upstream steroid hormones caused by TRT.
    1. Nelson Vergel's Avatar
      Nelson Vergel -
      Effects of Hormones on Sleep

      Horm Res 1998;49:125–130


      Neuroactive Steroids

      As early as 1942, Selye [55] reported hypnotic and anesthetic effects of certain steroid hormones. Previous preclinical research had indicated that apart from classic genomic mechanisms of action, certain steroids are capable of acting through membrane sites such as the GABAA-receptor complex [56]. These hormones are called ‘neuroactive steroids’ and can accumulate in the CNS independent from peripheral sources. A series of studies demonstrated that several neuroactive steroids exert specific effects on the sleep EEG which may be explained by a modulation of the GABAA receptor.

      A single oral dose of pregnenolone in young normal men increased the amount of SWS and depressed EEG sigma power. Nocturnal secretion of cortisol and GH remained unchanged [57]. In the rat, subcutaneous injection of pregnenolone enhanced slow wave activity during nonREM sleep and tended to increase the amount of REM sleep [58]. The sleep-EEG changes after pregnenolone in humans and rats are the opposite to some of those induced by GABAA receptor agonists such as benzodiazepine hypnotics. Therefore, these findings suggest an inverse agonistic interaction of pregnenolone or its metabolites at the GABAA receptor. A single oral dose of dehydroepiandrosterone (DHEA) prompted an increase in REM sleep whereas all other sleep variables remained unchanged. EEG spectral analysis showed enhanced EEG activity in the sigma frequency range during REM sleep in the first REM sleep period after DHEA administration. In contrast, the EEG power spectrum of nonREM sleep was not affected nor was the nocturnal secretion of cortisol, GH or testosterone. These findings suggest that DHEA or its metabolites exert a mixed GABAA agonistic/antagonistic effect [59]. In contrast, sleep-EEG changes after progesterone in humans and in rats point to an agonistic modulation of the GABAA receptor. After oral progesterone administration to normal male controls the amount of nonREM sleep increased significantly. The EEG spectral power during nonREM sleep showed a significant decrease in the slow wave-frequency range, whereas spectral power in the higher frequency range tended to be elevated [60]. In rats, progesterone was given intraperitoneally at light onset: Progesterone dose dependently shortened nonREM-sleep latency, lengthened REM latency, decreased the amount of wakefulness and REM sleep and markedly increased pre-REM sleep, an intermediate state between nonREM and REM sleep. Furthermore, progesterone induced dose-related changes in EEG power densities. NonREM-sleep EEG activity was diminished in the lower frequencies and was enhanced in the higher frequencies. In addition, REM-sleep EEG activity was markedly enhanced in the higher frequencies [61]. The sleep-EEG changes after progesterone appear to be mediated via the conversion of progesterone into its major metabolite allopregnanolone [60, 61].