aac21
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The key concept to understand here is the difference between 2 events. Epiphyseal plate CLOSURE, and proliferation/differentiation of chondrocytes inside the growth plate.
When chondrocytes are proliferated within the growth plate, the growth plate subsequently ages as a result. This is because there is a finite amount of chondrocytes that can proliferate which is what determines your FAH. (Final Adult Height)
When androgens such as Halotestin, or Anavar are present in the body, the pool of finite chondrocytes gets consumed, slowly. Over months or years. This results in an increase of growth velocity. GH also does this through the IGF-1 axis. And also results in a more aged growth plate. (Downstream effect) Erdafitinib should also be noted as being exceptional for improving chondrocyte proliferation through removal of the FGFR3 brake.
Estrogen, is widely known and regarded as the primary driver of epiphyseal plate closure, which is different from proliferation of chondrocytes I was talking about.
Now, here comes the big scary question that fearmongerers love to spread, using androgens such as anavar or halotestin (at low doses) would induce a premature epiphyseal plate closure.
NO! This is not true, those compounds simply act on the finite pool of chondrocytes, yes it will age the growth plate, but aging is downstream of chondrocyte proliferation, meaning the growth velocity will either be on par, or outpace plate fusion with the correct stack.
Letrozole is complete and absolute king in nuking your E2 into the floor. 2.5mg / day shows robust 98% suppression. (If this is healthy for your body is a seperate discussion.)
When combining letrozole 2.5mg / day with GH at the correct dose, alongside orals like Anavar or Halotestin, chondrocytes can proliferate at a substantial rate, (making you taller and aging the growth plate), whilst keeping the plate OPEN for long enough through letrozole where estrogen has NO chance to shut those plates down. This is not to say that epiphyseal plate closure is inevitable.
At the end of the day, what is important for us is the NET effect. More chondrocytes proliferated, over a larger period of time. (typically many years) Will result in an increase of FAH or predicted FAH which is the whole point of us heightmaxxers.
Minimalist stack:
TRT base (find your endogenous T and match it or add a little more, wont matter)
15 iu rHGH ed
2.5mg halo ed
2.5mg letrozole ed
4-8mg erda ed
Sure, you can do the safe route without androgens but you potentially leave some height on the table.
And remember, this concept entirely falls without an aromatase inhibitor, with reference range or higher levels of estrogen, premature closure is induced and therefore we can see a net loss on FAH, or simply no change which would defeat the purpose, which is typically seen in a majority of studies that use anavar and halotestin. Even those studies with reference or higher E2 actually see positive effects in FAH, or no change.
When chondrocytes are proliferated within the growth plate, the growth plate subsequently ages as a result. This is because there is a finite amount of chondrocytes that can proliferate which is what determines your FAH. (Final Adult Height)
When androgens such as Halotestin, or Anavar are present in the body, the pool of finite chondrocytes gets consumed, slowly. Over months or years. This results in an increase of growth velocity. GH also does this through the IGF-1 axis. And also results in a more aged growth plate. (Downstream effect) Erdafitinib should also be noted as being exceptional for improving chondrocyte proliferation through removal of the FGFR3 brake.
Estrogen, is widely known and regarded as the primary driver of epiphyseal plate closure, which is different from proliferation of chondrocytes I was talking about.
Now, here comes the big scary question that fearmongerers love to spread, using androgens such as anavar or halotestin (at low doses) would induce a premature epiphyseal plate closure.
NO! This is not true, those compounds simply act on the finite pool of chondrocytes, yes it will age the growth plate, but aging is downstream of chondrocyte proliferation, meaning the growth velocity will either be on par, or outpace plate fusion with the correct stack.
Letrozole is complete and absolute king in nuking your E2 into the floor. 2.5mg / day shows robust 98% suppression. (If this is healthy for your body is a seperate discussion.)
When combining letrozole 2.5mg / day with GH at the correct dose, alongside orals like Anavar or Halotestin, chondrocytes can proliferate at a substantial rate, (making you taller and aging the growth plate), whilst keeping the plate OPEN for long enough through letrozole where estrogen has NO chance to shut those plates down. This is not to say that epiphyseal plate closure is inevitable.
At the end of the day, what is important for us is the NET effect. More chondrocytes proliferated, over a larger period of time. (typically many years) Will result in an increase of FAH or predicted FAH which is the whole point of us heightmaxxers.
Minimalist stack:
TRT base (find your endogenous T and match it or add a little more, wont matter)
15 iu rHGH ed
2.5mg halo ed
2.5mg letrozole ed
4-8mg erda ed
Sure, you can do the safe route without androgens but you potentially leave some height on the table.
And remember, this concept entirely falls without an aromatase inhibitor, with reference range or higher levels of estrogen, premature closure is induced and therefore we can see a net loss on FAH, or simply no change which would defeat the purpose, which is typically seen in a majority of studies that use anavar and halotestin. Even those studies with reference or higher E2 actually see positive effects in FAH, or no change.
