Ok, I’m learning alot here and I really appreciate you taking your time to answer my questions.
Ive been pinning daily since I started. Shit kind of sucks but its become routine and I don’t mind.
Ok, So I get that it will eventually unbind and take one of the aforementioned pathways even if you have adequate SHBG levels, nothing I can do about that. But wouldn’t having the higher SHBG mean less of it is converting at once? So even if it will eventually convert, it won’t be happening as quickly and in as high of a concentration, meaning lower dht and e2 levels at a more consistent rate? In my mind having more testosterone bound up would mean a lower level of conversion happening at once as apposed to big spikes equating out to overall lower levels of the converted hormones. I’m sorry if I’m not understanding an aspect of this, I haven’t really gone super deep into this shit until now, so again, I appreciate your time here and I enjoy getting some good info. I was on the phone with my current trt doc today and he told me he has no idea and it sounds like I’ve done more research on this than he has lol.
No problem we are all learning here. Honestly, I had no clue testosterone was neutralized in the liver via oxidation to be excreted. It makes sense since the liver usually does have a process to change substances form (like ammonia to BUN) to then allow for easier excretion but I didn't know the specifics of it.
Is this for TRT or Blasting?
If you are looking to use a higher SHBG as a buffer for any initial injection, it is doubtful it will be impactful? As only 1-3% of T is unbound naturally, SHBG has a high affinity for binding so it is already bound with androgens, more transiently, albumin would be better to initially bind as there is a lesser chance that it is fully bound due to its weak affinity.
It is kind of hard to explain.
Initially, it may help a little bit... But if you slam exogenous hormones you will have a small upshoot in your blood regardless, it will take time to bind to anything.
Eventually, either binding stops or occurs at the same rate as unbinding, making it useless unless you continuously increase SHBG which is not sustainable or really possible. The only real function of SHBG is to hold onto DHT,E2, or T until a receptor has a higher affinity for it than the SHBG. SHBG has an affinity to bind E2 and DHT due to the molarity but again it will then also unbind faster since androgen receptors also have a high affinity for them haha. I mean it may be a tad bit healthier since there is research saying that if an androgen receptor NEEDS a hormone to be bound, it may have a small advantage to be transported on a weakly bound albumin or strongly bound SHBG. Again though, in any excess of hormones TRT or Blast this would never be the case...
Then actually increasing SHBG is hard to impossible, low insulin or high thyroxine increases SHBG, high E2 or low T will too. A
nticonvulsant drugs can increase SHBG, while IGF1, non-aromatizing androgens, and Hgh decrease it.
If you are just looking for a steady release undecanoate T is best bet.