Question on body's mechanisms on shutting down to exogenous testosterone

[ramacher]

So we all know when you use anabolic steroids, your body sees as extra being injected in the body and tells its HPTA axis to shut down its own production because it is not necessarily. But my question is since the body only produces testosterone, how/why does it see for ex. anavar as exogenous testosterone and stop producing its own? Anavar is not testosterone so why would the body see it/identify it as testosterone when Anavar is on its own its own compound?

[Lemonada8]

hey hey, an intelligent question! rare to find one of these among all the other stuff...

Just a real quick explanation:
there are 3 types of exogenous steroids used for muscle building. Test, 19nor, 17a.
Test with whatever ester
19nor -tren, deca, EQ *i think?
17a - winny, mast, var

the reason 17a arent extremely suppressive is because it depends on the indiidual person. 17a is a DHT derivative, so its stimilar in structure as DHT. DHT as many androgenic functions, but since its converted from test to DHT, DHT only typically doest shut down the HPTA. It slows the conversion from your natural test to DHT. If you have a high conversion rate, then you body will think you have enough, and slow making the test to convert to DHT. its all in the T, DHT/E ratio. So depending on ur ratios in ur on body, depend on how suppressive some orals are, aka 17a aka var.

The body notices extra estrogen which inhibits the test production, hence SERM treatment post cycle.

[jimmyinkedup]

hey hey, an intelligent question! rare to find one of these among all the other stuff...

Just a real quick explanation:
there are 3 types of exogenous steroids used for muscle building. Test, 19nor, 17a.
Test based:ie:test,dball,eq
19nor -ie:tren, deca,
DHT - ie:winny, mast, var

the reason 17a arent extremely suppressive is because it depends on the indiidual person. 17a is a DHT derivative, so its stimilar in structure as DHT. DHT as many androgenic functions, but since its converted from test to DHT, DHT only typically doest shut down the HPTA. It slows the conversion from your natural test to DHT. If you have a high conversion rate, then you body will think you have enough, and slow making the test to convert to DHT. its all in the T, DHT/E ratio. So depending on ur ratios in ur on body, depend on how suppressive some orals are, aka 17a aka var.

The body notices extra estrogen which inhibits the test production, hence SERM treatment post cycle.

Fixed brotha!
17aa refers to methylation which allows orals to survive first pass in an amount that will exert some effect. Its not a class of steroid.
Also - all steroids exert some androgenic effect - test is an androgen. The body will not differentiate - so any steroid that binds on any levels to the androgen receoptor will be viewed by the bpody as an active androgen thus reducing or eliminating the need for test production. Also as eluded too other factor come into polay to some extent like negative feedback etc...but thats the primary reason. So the steroids that tend to be viewed as less suppressive - you may notiuce have a low androgenic rating. Howver it is important to remeber that all steriods seem to , at least on some level, supress or shut down. People used to think anavar wouldnt shut you down or supress you - but recebntly wheter it be to higher effective dosages or something else , it has been shown and is acceopted that it does in fact cause gretaer supression or even shut down thatn was ever expected.

[Lemonada8]

gah i get those mixed up, usually cuz the DHT's are orals also.. yea the first pass on liver. Its the P450 enzymes i think, the main one that has all the drug interactions.
Thanks for the added info on the anabolic/androgenic ratio, i have to go refresh myself on it with certain compounds.
Although, theres only the ER receptor that suppresses production so its all about estro for suppression

[jimmyinkedup]

gah i get those mixed up, usually cuz the DHT's are orals also.. yea the first pass on liver. Its the P450 enzymes i think, the main one that has all the drug interactions.
Thanks for the added info on the anabolic/androgenic ratio, i have to go refresh myself on it with certain compounds.
Although, theres only the ER receptor that suppresses production so its all about estro for suppression

The bolded is inaccurate. Im on my phone at the moment but i have a couple studies that show androgen independant negative feedback clearly serpoate from that caused by aromitization. Later when im home ill see if i can find them and post the links.
A point that supports this - look at sarms - originally contended no supression whatsoever - they def dont artomitize...yet supression is being observed.

[Lemonada8]

Hmm... I would love to see them

Do sarms cross the BBB? ive never really looked at them because noone could answer my q's a while back...
I know there is AR in the testes, but I havent seen anything at the pituitary
thats why HCG is so useful