aac21
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I made this thread since i saw a lack of awareness for this compound and its properties
I will explain simply why winstrol is the best dht deriv and a compound that should be used in every height stack
Its more complex than this, but estrogen signaling is actually required for chondrocyte proliferation. particularly ERA.
At the core, every chondrocyte in the growth plate is actually estrogen-dependent for the most part.
Now don't get me wrong, there is a small reference range of estrogen that can promote proliferation, but going above this threshold quickly shifts into a rapid maturation and fusing signal which obviously we don't want.
Now where it gets interesting, winstrol a typical dht deriv has genuinely odd and fascinating effects on ERA. the reasoning is because winstrol is a NAAAS now you may ask how does it affect estrogen then? Good question bhaijan, the reasoning lies in the chemical structure of winstrol
Pyrazole ring fused to the A-ring
Unless ur a science nerd all you need to know is it creates a chemical shape that can occupy " estradiol A-ring binding pocket" we dont really give a fuck
Anyways, ERA is not end all be all, there's more.
ERα cross-talks with IGF-1R and converges on ERK1/2. Stanozolol raised p-ERα, p-IGF-1R and p-ERK1/2 together.
This is very important for local growth plate function
Third important factor, winstrol is anti-catabolic and anti-inflammatory
In IL-1β-stimulated equine articular chondrocytes, stanozolol reduced MMP-13, MMP-1, IL-6 and COX-2, and reduced ADAMTS4 in normal chondrocytes
Again, helps with local growth plate function
Now, a properly dosed aromatase inhibitor alongside winstrol will put your estrogen signaling in the right spot. Obviously combined with high dose gh, erda ky etc will severely improve your FAH.
thanks for reading
I will explain simply why winstrol is the best dht deriv and a compound that should be used in every height stack
Its more complex than this, but estrogen signaling is actually required for chondrocyte proliferation. particularly ERA.
At the core, every chondrocyte in the growth plate is actually estrogen-dependent for the most part.
Now don't get me wrong, there is a small reference range of estrogen that can promote proliferation, but going above this threshold quickly shifts into a rapid maturation and fusing signal which obviously we don't want.
Now where it gets interesting, winstrol a typical dht deriv has genuinely odd and fascinating effects on ERA. the reasoning is because winstrol is a NAAAS now you may ask how does it affect estrogen then? Good question bhaijan, the reasoning lies in the chemical structure of winstrol
Pyrazole ring fused to the A-ring
Unless ur a science nerd all you need to know is it creates a chemical shape that can occupy " estradiol A-ring binding pocket" we dont really give a fuck
Anyways, ERA is not end all be all, there's more.
ERα cross-talks with IGF-1R and converges on ERK1/2. Stanozolol raised p-ERα, p-IGF-1R and p-ERK1/2 together.
This is very important for local growth plate function
Third important factor, winstrol is anti-catabolic and anti-inflammatory
In IL-1β-stimulated equine articular chondrocytes, stanozolol reduced MMP-13, MMP-1, IL-6 and COX-2, and reduced ADAMTS4 in normal chondrocytes
Again, helps with local growth plate function
Now, a properly dosed aromatase inhibitor alongside winstrol will put your estrogen signaling in the right spot. Obviously combined with high dose gh, erda ky etc will severely improve your FAH.
thanks for reading
