KSman your thoughts on this reply (below) to my question please? Confusing, because I thought everyone that was using HGH while on TRT was also continuing with Testosterone at same dosages as prior to addition of the HGH. 100mg/wk is a pretty small dose already no? How much lower would I be going?
*The combo of HGH and test from what I can gather provides a synergistic affect
OVERVIEW:
In your case you would boost growth hormone to let you reduce your T and quit the arimidex, or reduce it to almost zero, as well as improve your sleep (if your sleep is not maximum refreshing), but you will need to naturally produce more cortisol, or supplement appropriately (eg: pregnenolone) to create more cortisol if you can’t produce more cortisol naturally.
DETAILS:
T and GH trigger many of the same repairs (not 100% overlap).
Our genetic optimum for T is set at somewhere which assumes plenty of GH. When we only boost T to trigger the repairs which are ordinarily triggered by both T and GH, then we have to boost our T far above our genetic-setpoint-for-optimum-T.
This causes our body’s defenses to kick in, and our body defends itself from T-which-is-far-above-our-genetic-setpoint-for-optimum-T by one or more of 5 different mechanisms, ie:
…1) Lower SHBG to allow T to remain as “free T” which can be quickly metabolized by the liver into urinary metabolites
…2) Raise SHBG to bind excess T to SHBG, thus taking T-bound-to-SHBG permanently out-of-action until the liver metabolizes T-bound-to-SHBG by stripping the SHBG and converting the free T into urinary metabolites
…3) Dump excess T into E2 and DHT
…4) Suppress LH to starve the testicles of raw materials (pregnenolone), as well as inhibit the production of Leydig cells which produce testosterone in the testicles.
…5) Suppress ACTH to starve the testicles of raw materials (pregnenolone), but this also reduces cortisol production.
In your case your body has definitely invoked “3)” and “4)”.
We can’t escape “4)” but by boosting GH considerably we can escape “3)” because boosting GH allows us to reduce our T accordingly, and the reduction in T puts our T at much closer to our genetic-setpoint-for-optimum-T, which means we slow down the rate at which T converts into E2 and DHT, to much closer to their optimum levels. Thus we can reduce our arimidex to zero or almost zero.
Usually boosting GH this way this means our ability to manage our T-to-E2 ratio is almost 100% reliable. Ie: we get erections on demand, and maintain them for longer. On the other hand, our libido is not as strong because not only do we reduce the amount of T dumping into E2, but we reduce the amount of T dumping into DHT. And DHT is the main hormone responsible for libido.
Usually boosting GH this way, at night time, improves our neurotransmitter balance greatly too, to the point where we get a fantastic night’s sleep and wake up very refreshed indeed.
Usually boosting GH this way, at night time, requires us to produce (or supplement appropriately) more cortisol at night time, because GH at night requires plenty of cortisol at night time, because GH and cortisol work synergistically to produce the benefits which are incorrectly attributed to GH alone. Without a cortisol boost (natural or supplement) then boosting GH will achieve no benefits.
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Warning:
A) Slow excreters have pooly functioning livers. They must monitor hormone levels very carefully, to ensure their dosages are low enough to prevent accumulation of hormones to the point where levels become excessive, or even toxic, after several days or weeks of supplementation.
B) Fast excreters have excessive liver enzyme activity. These people require relatively high and frequent doses of hormones, and the cost of hormone supplementation, for these people, is relatively high.