rax1337
Iron
- Joined
- Feb 27, 2020
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Hello, I am an aspiring biochemist new to this forum. In my first post ill be exploring why taking DHT transdermally is not a good idea during puberty if you wish to maintain good HPTA function. As most of you probably know DHT is a testosterone metabolite synthesized when testosterone interacts with the 5 alpha reductase enzyme. It has a binding affinity in 5AR dense areas 5x that of testosterone for the androgen receptor, which plainly stated means it is quite androgenic. Androgens (and Estrogens) are the negative feedback used by the HPTA to lower GnRH which subsequently lowers FSH and LH lowering testosterone, meaning a strong androgen probably wouldnt be the best idea for HPTA upregulation, which plainly means it probably is quite suppressive. Luckily, for us someone already did the study for us using DHT gel. In this study you can see just how suppressed T is when 64mg of dht is used per day (after 14 days use is discontinued which is why they start to recover)
. If you wish to use DHT to simply increase your androgen index and care about your natural testosterone, this should be enough to make you reconsider using it. But if you are using DHT as a Androgen replacement and don’t care about natural testosterone production, im here to tell you this is not a good idea for a multitude of reasons. Firstly DHT is not very anabolic like testosterone, this means you will lose muscle. Another reason is the fact that it doesn’t interact with aromatase, meaning if you are doing this long term prepare to suffer low estradiol side effects which are crippling to quality of life. What do I suggest as an alternative to keep androgens high without severely hampering the HPTA you might ask? Well Proviron is quite decent at this (There are other ways to do this namely using an AI or HCG but they are both suboptimal solutions. HCG will cause Leydig desensitization after some time, and I personally cannot tolerate Aromasin even at a low dose because of low e2 side effects). Being an androgen it will always be suppressive of the HPTA but it is very readily bound (98%) by proteins (albumin and SHBG) meaning very little of it is free to bind to receptors sites which at a clinical dose is not enough to cause noticeable suppression. You might say, damn that means this shit is weak as fuck… but it being bound is actually a good thing because in simple terms it allows testosterone and dht (and e2) to not be bound since it is taking up all the binding protein. The amount of Proviron that is not bound is then free to bind to AR sites. The Proviron will then antagonize e2, leaving you with high free testosterone, high free dht and lowered e2 because of antagonism. In my next post ill be teaching you guys a method devised by me to extract pure Mesterolone which is the active ingredient in Proviron from Proviron pills which arent hard to source. The reason im going to do this is because the oral bioavailability is only 3%, so im going to extract the Mesterolone, suspend it in oil, and inject. Thank you for reading my post, I wrote this on very little sleep so I apologize if I made any grammatical mistakes. Thank you to @Dyorotic2 for inspiring me to get off my ass and write this. I'd love to have a friendly debate in the comments if you believe i made any mistakes.