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Hey Smart Guys...Why is Anavar suppressive?

Are we still looking for the best bridge here or what? This has been going on for as long as I can remember. I have never tried var, but d-bol in the am is a viable option. Sure, there is definitely suppression but that's the decision you make with a bridge or with taking any AAS whatsoever really. That's the trade off. Nothing is free.
 
Nathan said:
Are we still looking for the best bridge here or what? This has been going on for as long as I can remember. I have never tried var, but d-bol in the am is a viable option. Sure, there is definitely suppression but that's the decision you make with a bridge or with taking any AAS whatsoever really. That's the trade off. Nothing is free.

cooking oil will not shut you down
 
Nathan said:
Are we still looking for the best bridge here or what?

Actually, no we're not. Please stick to the topic on this thread. If you want to start your own, "is var good for bridging thread" then feel free.

Anyways, back to the point....anyone know the actual mechanisms, processes, physiology, etc that goes on with administration of oxandrolone?
It must not have much of a signal, if once administration is ceased a quick return to full HPTA ensues without any type of pc therapy.
 
b1ewsw32 said:
There's 3 negative feedback loops that effect the HPTA- androgens,estrogens and progestogens.

I've read that oxandrolone has an affinity for the androgen receptor.
Also your study demonstrates that ox induced an increase in AR expression.

Binding to the AR by ox has been shown to be stronger then testosterone and nandrolone.

Therefore negative feedback via the androgen system will be the culprit in HPTA supression.

B32

Good explanation. It's through binding to the AR that thr HPTA gets supressed. HOWVER. This is very individualized. At 15-20mg/day, my test levels hover at around 600, while somebody else hover at around 100. This is wht it is crucial to get blood work done.

Also, I run 25-50mg Proviron about 4 weeks before my bridge(to saturate) the bloodstream of mesterolone, and increase the levels of endo LH as high as they can possibly go. This will also elevate your endo test by a small degree...100 or so points.
 
Well,
Let's just say a guy who really knows his shit...had this to say. Anyone here agree or disagree w/him and a reason why?

"Nope. It is the constant binding to the sytemic neuronet itself through these receptors that the LH levels decrease. Not the Hypothalamus, Pitutary or testes. Therefore not an HPTA issue."
 
Last edited:
atutt2 said:
Actually, no we're not. Please stick to the topic on this thread. If you want to start your own, "is var good for bridging thread" then feel free.

Anyways, back to the point....anyone know the actual mechanisms, processes, physiology, etc that goes on with administration of oxandrolone?
It must not have much of a signal, if once administration is ceased a quick return to full HPTA ensues without any type of pc therapy.

I was simply asking. Don't be rude princess.
 
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