Importance of the Wnt/B-catenin signaling pathway and the CXXC5 gene for growth plate senesence, chondrocyte profileration, and overall bone growth

MyDreamIsToBe183CM

MyDreamIsToBe183CM

i'll be 183 cm under soon
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Disclaimer: This is purely experimental and hypothetical only, so don't come crying to me when you retardedly start blasting these substances with no research and get testicular cancer

There are hundreds to even thousands of different pathways that contribute to height directly or indirectly, but most of them aren't worth looking into as optimizing them would barely give any height growth. We should be looking into what are the most important signaling pathways that contribute the most to height or longitudinal bone growth.

After the growth hormone signaling pathway, it seems the Wnt/B-catenin signaling pathway is the second most important pathway in regulating chondrocyte profileration within the growth plate, which can significantly impact bone growth and height

Basically what the Wnt/B-catenin signaling pathway does is coordinate and control chondrocyte profileration and differentation

Studies have demonstrated that Wnt signaling pathway plays an important role in cartilage development and homeostasis by regulating the growth, differentiation, and proliferation of chondrocytes

Specifically, the canonical Wnt/β-catenin signaling pathway plays a significant role in regulating chondrocyte phenotype, maturation, and function during the cartilage development process, which is crucial for cartilage defining cartilage boundaries and endochondral ossification

Genetic defects impacting the Wnt/B-catening signaling pathway can lead to some serious skeletal disorders and impaired bone growth

CXXC5 impact on the Wnt/B-Catenin signaling pathway

CXXC finger protein 5 (CXXC5) is a negative regulator of the Wnt/B-Catenin signaling pathway. As you progress further in puberty, CXXC5 expresison also progressively increases, and studies have shown that CXXC5 contributes to growth plate senesence at puberty, so we want to inhibit the CXXC5 gene. Inhibiting this gene can also lead to activation of the Wnt/B-Catenin pathway

"Collectively, our findings reveal an important role for CXXC5 as a suppressor of longitudinal bone growth involving growth plate activity."

"In summary, CXXC5, a protein induced with pubertal progression in the growth plate chondrocytes, is characterized as a key factor mediating termination of longitudinal bone growth by promoting growth plate senescence."

It has also been shown that estrogen, the main hormone contributing to growth plate closure induces CXXc5 expression, while also decreasing chondrocyte profileration.
In this study, we found that CXXC5 expression progressively increased in the resting, proliferative, and hypertrophic chondrocytes undergoing growth plate senescence. We also found that estrogen, a sex hormone that is elevated during the pubertal period, induced CXXC5 expression followed by decrement of β-catenin in chondrocytes.

Inhibiting this gene enhanced chondrocyte profileration and differentation
Furthermore, Cxxc5−/− mice displayed enhanced chondrocyte proliferation and differentiation in the late pubertal growth plate as well as longer tibiae at adulthood

Cxxc5-/- means the CXXC5 gene has been inhibited btw

Now although there are many other negative regulators of the Wnt/B-catenin signaling pathway, it seems the CXXC5 gene has the most detrimental effect. So, we will focus on this for now.
In summary, CXXC5, a protein induced with pubertal progression in the growth plate chondrocytes, is characterized as a key factor mediating termination of longitudinal bone growth by promoting growth plate senescence

Inhibition of the GSK-3B gene, which destablizies B-catenine, also resulted in tibial elongation through activaiton of Wnt/B-catenin signaling
In addition, treatment with an inhibitor of glycogen synthase kinase 3β (GSK3β), a serine/threonine kinase that destabilizes β-catenin resulted in tibial elongation in the ex vivo culture system

My theory on how to optimize the Wnt/B-catenin signaling pathway:
This is where the substance, KY-19382 comes into play. If you are a true heightmaxxer then you have probably heard of this drug atleast once during your research. It was originally used by some redditors as a potential cure to hair loss, but our goal is longitudinal bone growth so I will not talk about all the other potential positive effects of KY besides potential increased height

KY-19382 activates WNT/B-catening signaling via inhibition of CXXC5 and GSK-3B activity.

Through this action, studies show KY-19382 has shown drastic increase in chondrocyte profileration and differentation, which induced increased longitudinal bone growth while also delaying growth plate senesence

We further demonstrated that KY19382 markedly enhanced proliferation and differentiation of chondrocytes and induced longitudinal tibiae growth in adolescent mice by delaying growth plate senescence


KY-19382 effects on chondrocytes and growth plate height:

"The total growth plate height, monitored by COL2A1 immunostaining, was significantly increased by KY19382 treatment. This effect was confirmed by increased numbers of both proliferative and hypertrophic chondrocytes per column,"

"nuclear β-catenin was dramatically increased in the growth plate chondrocytes by KY19382 treatment"

"These functional and structural changes demonstrate the ability of KY19382 in delaying growth plate senescence."


"These results demonstrate that KY19382 promotes chondrocyte proliferation and differentiation via specific activation of the Wnt/β-catenin pathway."

TL;DR: Ideal optimization of the Wnt/B-catenin has some crazy potential for heightmaxxing, it is the second most important pathway after the growth hormone signaling pathway for height in my opinio.

KY-19382 also achieves increased chondrocyte profileration and delayed growth plate senesence through different methods and pathways then HGH and AI, so just imagine pairing up KY-19382 with HGH and AI:aheago::aheago::aheago::aheago: we could actually keep grow until fucking age 25 if we find a way to properly optimize this pathway. (sadly the only studies of ky-19382 affecting growth plates were done on rats)


Ky-19382 side effects aren't revealed yet, but according to redditors who used it for hair loss they reported 0 sides. It is also expensive as shit, dosage is around 0.1 mg/kg per bw every single day. But some people were able to get a way cheaper source. And you need to larp your way on being a researcher and shit... but i already found my way around it (not allowed to leak jfl so dont ask)

I already have a source for ky-19382 at a semi-reasonable price. Problem is im still trying to figure out how to mix the powder into an injectable solution.

Anyways my bad for the poor formatating and text, I made this whole thing in a rush out of boredom. But still, an interesting topic.

Tagging heightmaxxers/educated members:
@org3cel.RR @The Homelander @Cyrus @enchanted_elixir @Corpuscula

Anyways if i do end up hopping on ky-19382, ill create a log on it and if it actually worked or not
@
 
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@Newday*V3 @wastedspermcel @halloweed @HandsomeHustler @Osie

gtfihh heightmaxxers
 
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1741149503716


This is actual broscience. You are not mentally well to be writing all this and expecting someone to read your misinterpreted schizo mentally ill pseudoscience research from pubmed sources
 
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@TrueRamirez @Zagro @playxiing i would tag that supposdely high iq regulus but the way he speaks pmo and hes kinda slow ngl
 
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View attachment 3539813

This is actual broscience. You are not mentally well to be writing all this and expecting someone to read your misinterpreted schizo mentally ill pseudoscience research from pubmed sources
whats your point nigger
 
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View attachment 3539813

This is actual broscience. You are not mentally well to be writing all this and expecting someone to read your misinterpreted schizo mentally ill pseudoscience research from pubmed sources
can you send that discord server bro pls
 
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rep= for the foort will read after my sleep
 
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blast hgh and hop off retracted aslyum bullshit
im already on hgh, bro what is your point supposed to be? and what was that ss even supposed to prove

im discussing new ways to combat height growth

also send that discord server please
 
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im already on hgh, bro what is your point supposed to be? and what was that ss even supposed to prove

im discussing new ways to combat height growth

also send that discord server please

mentally illl by the way
 
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just imagine pairing up KY-19382 with HGH and AI:aheago::aheago::aheago::aheago: we could actually keep grow until fucking age 25 if we find a way to properly optimize this pathway
Why would you take this lab substance for that when you can have sub5 pg e2 relatively easily? That would actually keep your plates open for longer
 
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Why would you take this lab substance for that when you can have sub5 pg e2 relatively easily? That would actually keep your plates open for longer
It delays growth plate senesnece through different ways bro, estrogen isn’t the only thing that contributes to growth plate closure
 
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I may be retarded
 
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View attachment 3539813

This is actual broscience. You are not mentally well to be writing all this and expecting someone to read your misinterpreted schizo mentally ill pseudoscience research from pubmed sources
Why would you take this lab substance for that when you can have sub5 pg e2 relatively easily? That would actually keep your plates open for longer
You fucking niggers read my theory before questioning me
 
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It delays growth plate senesnece through different ways bro, estrogen isn’t the only thing that contributes to growth plate closure
Estrogen and glucocorticoids are the only hormones that can close growth plates on their own as far as I know, unless you're talking about extremely specific things like FGFs that will most likely barely make a difference in that process
 
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Estrogen and glucocorticoids are the only hormones that can close growth plates on their own as far as I know, unless you're talking about extremely specific things like FGFs that will most likely barely make a difference in that process
Your already wrong on that, did you forget about androgen ossification ?

And there’s pathways as well
 
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It delays growth plate senesnece through different ways bro, estrogen isn’t the only thing that contributes to growth plate closure
1741150352527


id = 879915020853596260

DNR a single molecule.

As a human being with somewhat sympathy and emotions, I hope that you will grow to 6ft tall. Still, I think you are mentally ill. Pubmed is full of shit and is ran by the government for ill lurkers to see.
 
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Bro yall are so smart and shit go take a moment to pat yourself on the back wtf
 
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View attachment 3539858

id = 879915020853596260

DNR a single molecule.

As a human being with somewhat sympathy and emotions, I hope that you will grow to 6ft tall. Still, I think you are mentally ill. Pubmed is full of shit and is ran by the government for ill lurkers to see.
Bro why are you mad? And what is doxxing my discord ID supposed to even do?

Literally the first sentence is that it’s purely hypothetical, j never stated it would work for sure
 
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Bro why are you mad? And what is doxxing my discord ID supposed to even do?

Literally the first sentence is that it’s purely hypothetical, j never stated it would work for sure
to make you pee your pants & be scared by my autist abilties.
 
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to make you pee your pants & be scared by my autist abilties.
Nigga is actually hating for no reason, leaking discord id is crazy
 
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Disclaimer: This is purely experimental and hypothetical only, so don't come crying to me when you retardedly start blasting these substances with no research and get testicular cancer

There are hundreds to even thousands of different pathways that contribute to height directly or indirectly, but most of them aren't worth looking into as optimizing them would barely give any height growth. We should be looking into what are the most important signaling pathways that contribute the most to height or longitudinal bone growth.

After the growth hormone signaling pathway, it seems the Wnt/B-catenin signaling pathway is the second most important pathway in regulating chondrocyte profileration within the growth plate, which can significantly impact bone growth and height

Basically what the Wnt/B-catenin signaling pathway does is coordinate and control chondrocyte profileration and differentation

Studies have demonstrated that Wnt signaling pathway plays an important role in cartilage development and homeostasis by regulating the growth, differentiation, and proliferation of chondrocytes

Specifically, the canonical Wnt/β-catenin signaling pathway plays a significant role in regulating chondrocyte phenotype, maturation, and function during the cartilage development process, which is crucial for cartilage defining cartilage boundaries and endochondral ossification

Genetic defects impacting the Wnt/B-catening signaling pathway can lead to some serious skeletal disorders and impaired bone growth

CXXC5 impact on the Wnt/B-Catenin signaling pathway

CXXC finger protein 5 (CXXC5) is a negative regulator of the Wnt/B-Catenin signaling pathway. As you progress further in puberty, CXXC5 expresison also progressively increases, and studies have shown that CXXC5 contributes to growth plate senesence at puberty, so we want to inhibit the CXXC5 gene. Inhibiting this gene can also lead to activation of the Wnt/B-Catenin pathway

"Collectively, our findings reveal an important role for CXXC5 as a suppressor of longitudinal bone growth involving growth plate activity."

"In summary, CXXC5, a protein induced with pubertal progression in the growth plate chondrocytes, is characterized as a key factor mediating termination of longitudinal bone growth by promoting growth plate senescence."

It has also been shown that estrogen, the main hormone contributing to growth plate closure induces CXXc5 expression, while also decreasing chondrocyte profileration.
In this study, we found that CXXC5 expression progressively increased in the resting, proliferative, and hypertrophic chondrocytes undergoing growth plate senescence. We also found that estrogen, a sex hormone that is elevated during the pubertal period, induced CXXC5 expression followed by decrement of β-catenin in chondrocytes.

Inhibiting this gene enhanced chondrocyte profileration and differentation
Furthermore, Cxxc5−/− mice displayed enhanced chondrocyte proliferation and differentiation in the late pubertal growth plate as well as longer tibiae at adulthood

Cxxc5-/- means the CXXC5 gene has been inhibited btw

Now although there are many other negative regulators of the Wnt/B-catenin signaling pathway, it seems the CXXC5 gene has the most detrimental effect. So, we will focus on this for now.
In summary, CXXC5, a protein induced with pubertal progression in the growth plate chondrocytes, is characterized as a key factor mediating termination of longitudinal bone growth by promoting growth plate senescence

Inhibition of the GSK-3B gene, which destablizies B-catenine, also resulted in tibial elongation through activaiton of Wnt/B-catenin signaling
In addition, treatment with an inhibitor of glycogen synthase kinase 3β (GSK3β), a serine/threonine kinase that destabilizes β-catenin resulted in tibial elongation in the ex vivo culture system

My theory on how to optimize the Wnt/B-catenin signaling pathway:
This is where the substance, KY-19382 comes into play. If you are a true heightmaxxer then you have probably heard of this drug atleast once during your research. It was originally used by some redditors as a potential cure to hair loss, but our goal is longitudinal bone growth so I will not talk about all the other potential positive effects of KY besides potential increased height

KY-19382 activates WNT/B-catening signaling via inhibition of CXXC5 and GSK-3B activity.

Through this action, studies show KY-19382 has shown drastic increase in chondrocyte profileration and differentation, which induced increased longitudinal bone growth while also delaying growth plate senesence

We further demonstrated that KY19382 markedly enhanced proliferation and differentiation of chondrocytes and induced longitudinal tibiae growth in adolescent mice by delaying growth plate senescence


KY-19382 effects on chondrocytes and growth plate height:

"The total growth plate height, monitored by COL2A1 immunostaining, was significantly increased by KY19382 treatment. This effect was confirmed by increased numbers of both proliferative and hypertrophic chondrocytes per column,"

"nuclear β-catenin was dramatically increased in the growth plate chondrocytes by KY19382 treatment"

"These functional and structural changes demonstrate the ability of KY19382 in delaying growth plate senescence."


"These results demonstrate that KY19382 promotes chondrocyte proliferation and differentiation via specific activation of the Wnt/β-catenin pathway."

TL;DR: Ideal optimization of the Wnt/B-catenin has some crazy potential for heightmaxxing, it is the second most important pathway after the growth hormone signaling pathway for height in my opinio.

KY-19382 also achieves increased chondrocyte profileration and delayed growth plate senesence through different methods and pathways then HGH and AI, so just imagine pairing up KY-19382 with HGH and AI:aheago::aheago::aheago::aheago: we could actually keep grow until fucking age 25 if we find a way to properly optimize this pathway. (sadly the only studies of ky-19382 affecting growth plates were done on rats)


Ky-19382 side effects aren't revealed yet, but according to redditors who used it for hair loss they reported 0 sides. It is also expensive as shit, dosage is around 0.1 mg/kg per bw every single day. But some people were able to get a way cheaper source. And you need to larp your way on being a researcher and shit... but i already found my way around it (not allowed to leak jfl so dont ask)

I already have a source for ky-19382 at a semi-reasonable price. Problem is im still trying to figure out how to mix the powder into an injectable solution.

Anyways my bad for the poor formatating and text, I made this whole thing in a rush out of boredom. But still, an interesting topic.

Tagging heightmaxxers/educated members:
@org3cel.RR @The Homelander @Cyrus @enchanted_elixir @Corpuscula

Anyways if i do end up hopping on ky-19382, ill create a log on it and if it actually worked or not
@
Anyways bumpmaxx bruh
 
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Your already wrong on that, did you forget about androgen ossification ?

And there’s pathways as well
Androgens won't close growth plates on their own, you're probably talking about specific substances such as anavar.

Pure DHT for example has a minimal effect on growth plate closure, it's like saying HGH can close growth plates, it's technically true, but it doesn't make a noticeable difference like estrogen and cortisol could. Androgens would be great for growth either way, as they are one of the primary signalers of long bone growth.
 
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Androgens won't close growth plates on their own, you're probably talking about specific substances such as anavar.

Pure DHT for example has a minimal effect on growth plate closure, it's like saying HGH can close growth plates, it's technically true, but it doesn't make a noticeable difference like estrogen and cortisol could. Androgens would be great for growth either way, as they are one of the primary signalers of long bone growth.
How much androgens contribute to growth plate closure isn’t revealed, but yes estrogen is rhetorical main hormone but that doesn’t mean there’s not other factors that lead to growth plate senesence

In studies it’s shown specific androgens such as anavar or tren for example significantly sped up bone age, resulting in higher bone age then chronical age

However, it wasn’t stated whether if it was from the excess estrogen conversion from testosterone or the drug itself
 
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The hair loss by PGD2 was restored by Cxxc5 knock-out or treatment of protein transduction domain-Dishevelled binding motif (PTD-DBM), a peptide activating the Wnt/β-catenin pathway via interference with the Dishevelled (Dvl) binding function of CXXC5
Also the knockout version of Cxx5 is able to reverse balding. Some people are just born better than others.
shookt-shocked.gif4
 
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Also the knockout version of Cxx5 is able to reverse balding. Some people are just born better than others.
shookt-shocked.gif4
Nigga cxxc5 knockout means cxxc5 was inhibited not a knockout version
 
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Also the knockout version of Cxx5 is able to reverse balding. Some people are just born better than others.
shookt-shocked.gif4
And PTD BDM is literally the same thing as ky
 
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How much androgens contribute to growth plate closure isn’t revealed, but yes estrogen is rhetorical main hormone but that doesn’t mean there’s not other factors that lead to growth plate senesence

In studies it’s shown specific androgens such as anavar or tren for example significantly sped up bone age, resulting in higher bone age then chronical age

However, it wasn’t stated whether if it was from the excess estrogen conversion from testosterone or the drug itself
There's no evidence to androgens alone closing growth plates, if that was the case men deficient in DHT would have a lower bone age progression. At the very least, that shows it's effects are barely noticeable, if any.

Anavar on the other hand is a modified androgen, it's not just DHT, it accelerates height growth before fusing growth plates, although I don't think there is any specific cause that would make it close them on it's own, could just be a coincidence due to higher e2 levels from fluctuation. Tren can't close growth plates on it's own though, if anything it would slow them down due to less e2.

If you're worried about growing longer you can just have zero e2 levels with AIs and modified testosterone if needed. Aren't you on HGH already anyway?
 
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There's no evidence to androgens alone closing growth plates, if that was the case men deficient in DHT would have a lower bone age progression. At the very least, that shows it's effects are barely noticeable, if any.

Anavar on the other hand is a modified androgen, it's not just DHT, it accelerates height growth before fusing growth plates, although I don't think there is any specific cause that would make it close them on it's own, could just be a coincidence due to higher e2 levels from fluctuation. Tren can't close growth plates on it's own though, if anything it would slow them down due to less e2.

If you're worried about growing longer you can just have zero e2 levels with AIs and modified testosterone if needed. Aren't you on HGH already anyway?
I already raped my E2 levels with 2.5 mg of letrozole.

Also zero E2 levels is impossible you know that, even 2.5 mg of letrozole daily usage only brought some niggas estrogen levels to 20 pg/ml
:lul::lul::lul::lul::lul::lul::lul:
 
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There's no evidence to androgens alone closing growth plates, if that was the case men deficient in DHT would have a lower bone age progression. At the very least, that shows it's effects are barely noticeable, if any.

Anavar on the other hand is a modified androgen, it's not just DHT, it accelerates height growth before fusing growth plates, although I don't think there is any specific cause that would make it close them on it's own, could just be a coincidence due to higher e2 levels from fluctuation. Tren can't close growth plates on it's own though, if anything it would slow them down due to less e2.

If you're worried about growing longer you can just have zero e2 levels with AIs and modified testosterone if needed. Aren't you on HGH already anyway?
Well, I still need to do more research on androgens.

So what are your thoughts on tren for height growth? It unregulates the wnt/b caten in pathway as well

Not sure if it’s worth the sides tho
 
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Disclaimer: This is purely experimental and hypothetical only, so don't come crying to me when you retardedly start blasting these substances with no research and get testicular cancer

There are hundreds to even thousands of different pathways that contribute to height directly or indirectly, but most of them aren't worth looking into as optimizing them would barely give any height growth. We should be looking into what are the most important signaling pathways that contribute the most to height or longitudinal bone growth.

After the growth hormone signaling pathway, it seems the Wnt/B-catenin signaling pathway is the second most important pathway in regulating chondrocyte profileration within the growth plate, which can significantly impact bone growth and height

Basically what the Wnt/B-catenin signaling pathway does is coordinate and control chondrocyte profileration and differentation

Studies have demonstrated that Wnt signaling pathway plays an important role in cartilage development and homeostasis by regulating the growth, differentiation, and proliferation of chondrocytes

Specifically, the canonical Wnt/β-catenin signaling pathway plays a significant role in regulating chondrocyte phenotype, maturation, and function during the cartilage development process, which is crucial for cartilage defining cartilage boundaries and endochondral ossification

Genetic defects impacting the Wnt/B-catening signaling pathway can lead to some serious skeletal disorders and impaired bone growth

CXXC5 impact on the Wnt/B-Catenin signaling pathway

CXXC finger protein 5 (CXXC5) is a negative regulator of the Wnt/B-Catenin signaling pathway. As you progress further in puberty, CXXC5 expresison also progressively increases, and studies have shown that CXXC5 contributes to growth plate senesence at puberty, so we want to inhibit the CXXC5 gene. Inhibiting this gene can also lead to activation of the Wnt/B-Catenin pathway

"Collectively, our findings reveal an important role for CXXC5 as a suppressor of longitudinal bone growth involving growth plate activity."

"In summary, CXXC5, a protein induced with pubertal progression in the growth plate chondrocytes, is characterized as a key factor mediating termination of longitudinal bone growth by promoting growth plate senescence."

It has also been shown that estrogen, the main hormone contributing to growth plate closure induces CXXc5 expression, while also decreasing chondrocyte profileration.
In this study, we found that CXXC5 expression progressively increased in the resting, proliferative, and hypertrophic chondrocytes undergoing growth plate senescence. We also found that estrogen, a sex hormone that is elevated during the pubertal period, induced CXXC5 expression followed by decrement of β-catenin in chondrocytes.

Inhibiting this gene enhanced chondrocyte profileration and differentation
Furthermore, Cxxc5−/− mice displayed enhanced chondrocyte proliferation and differentiation in the late pubertal growth plate as well as longer tibiae at adulthood

Cxxc5-/- means the CXXC5 gene has been inhibited btw

Now although there are many other negative regulators of the Wnt/B-catenin signaling pathway, it seems the CXXC5 gene has the most detrimental effect. So, we will focus on this for now.
In summary, CXXC5, a protein induced with pubertal progression in the growth plate chondrocytes, is characterized as a key factor mediating termination of longitudinal bone growth by promoting growth plate senescence

Inhibition of the GSK-3B gene, which destablizies B-catenine, also resulted in tibial elongation through activaiton of Wnt/B-catenin signaling
In addition, treatment with an inhibitor of glycogen synthase kinase 3β (GSK3β), a serine/threonine kinase that destabilizes β-catenin resulted in tibial elongation in the ex vivo culture system

My theory on how to optimize the Wnt/B-catenin signaling pathway:
This is where the substance, KY-19382 comes into play. If you are a true heightmaxxer then you have probably heard of this drug atleast once during your research. It was originally used by some redditors as a potential cure to hair loss, but our goal is longitudinal bone growth so I will not talk about all the other potential positive effects of KY besides potential increased height

KY-19382 activates WNT/B-catening signaling via inhibition of CXXC5 and GSK-3B activity.

Through this action, studies show KY-19382 has shown drastic increase in chondrocyte profileration and differentation, which induced increased longitudinal bone growth while also delaying growth plate senesence

We further demonstrated that KY19382 markedly enhanced proliferation and differentiation of chondrocytes and induced longitudinal tibiae growth in adolescent mice by delaying growth plate senescence


KY-19382 effects on chondrocytes and growth plate height:

"The total growth plate height, monitored by COL2A1 immunostaining, was significantly increased by KY19382 treatment. This effect was confirmed by increased numbers of both proliferative and hypertrophic chondrocytes per column,"

"nuclear β-catenin was dramatically increased in the growth plate chondrocytes by KY19382 treatment"

"These functional and structural changes demonstrate the ability of KY19382 in delaying growth plate senescence."


"These results demonstrate that KY19382 promotes chondrocyte proliferation and differentiation via specific activation of the Wnt/β-catenin pathway."

TL;DR: Ideal optimization of the Wnt/B-catenin has some crazy potential for heightmaxxing, it is the second most important pathway after the growth hormone signaling pathway for height in my opinio.

KY-19382 also achieves increased chondrocyte profileration and delayed growth plate senesence through different methods and pathways then HGH and AI, so just imagine pairing up KY-19382 with HGH and AI:aheago::aheago::aheago::aheago: we could actually keep grow until fucking age 25 if we find a way to properly optimize this pathway. (sadly the only studies of ky-19382 affecting growth plates were done on rats)


Ky-19382 side effects aren't revealed yet, but according to redditors who used it for hair loss they reported 0 sides. It is also expensive as shit, dosage is around 0.1 mg/kg per bw every single day. But some people were able to get a way cheaper source. And you need to larp your way on being a researcher and shit... but i already found my way around it (not allowed to leak jfl so dont ask)

I already have a source for ky-19382 at a semi-reasonable price. Problem is im still trying to figure out how to mix the powder into an injectable solution.

Anyways my bad for the poor formatating and text, I made this whole thing in a rush out of boredom. But still, an interesting topic.

Tagging heightmaxxers/educated members:
@org3cel.RR @The Homelander @Cyrus @enchanted_elixir @Corpuscula

Anyways if i do end up hopping on ky-19382, ill create a log on it and if it actually worked or not
@
ok so wtf am i supposed to do. Buy it? i just searched it up on google and nothing pops up
 
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ok so wtf am i supposed to do. Buy it? i just searched it up on google and nothing pops up
This is in theory

And you can’t just buy it like you can with steroids, most companies only sell to actual researchers
 
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I already raped my E2 levels with 2.5 mg of letrozole.

Also zero E2 levels is impossible you know that, even 2.5 mg of letrozole daily usage only brought some niggas estrogen levels to 20 pg/ml
:lul::lul::lul::lul::lul::lul::lul:
It may not always stay at 0pg but you can have levels close to that with an AI and a non-aromatising test derivate. For example tren as you mentioned doesn't aromatase into estrogen at all so theoretically you'd not have estrogen while on it, or extremely minimal levels.

2.5mg of letro may not be enough for everyone, I was taking 7.5mg once.
 
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It may not always stay at 0pg but you can have levels close to that with an AI and a non-aromatising test derivate. For example tren as you mentioned doesn't aromatase into estrogen at all so theoretically you'd not have estrogen while on it, or extremely minimal levels.

2.5mg of letro may not be enough for everyone, I was taking 7.5mg once.
7.5 mg will absolutely rape your BMD, but atleast it makes you taller aye?
 
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Well, I still need to do more research on androgens.

So what are your thoughts on tren for height growth? It unregulates the wnt/b caten in pathway as well

Not sure if it’s worth the sides tho
It can be great but effects vary for everyone, one guy here reported he supposedly had another growth spurt right after taking tren with HGH. It makes sense since it could stimulate long bone growth as other androgens would.
 
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It may not always stay at 0pg but you can have levels close to that with an AI and a non-aromatising test derivate. For example tren as you mentioned doesn't aromatase into estrogen at all so theoretically you'd not have estrogen while on it, or extremely minimal levels.

2.5mg of letro may not be enough for everyone, I was taking 7.5mg once.
Also I don’t know if completely nuking your estrogen levels to 0 is ideal, I might be wrong but a bit of estrogen is still required to grow taller and overall development
 
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7.5 mg will absolutely rape your BMD, but atleast it makes you taller aye?
Personally I didn't feel any sides while on it, I think AIs side effects are overblown here or at least have a huge margin on how different they affect everyone. Gotta do what you gotta do for them bones though.
 
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Personally I didn't feel any sides while on it, I think AIs side effects are overblown here or at least have a huge margin on how different they affect everyone. Gotta do what you gotta do for them bones though.
Yeah I agree as well. @TrueRamirez was freakinf out because I recommended 2.5 mg of letrozole every day.

But it does mentally cuck you though, horrible neurological imbalance sides. Gets better after a bit tho.

Honestly as long as you have a proper diet and getting all the proper nutrients for bone health, AI shouldn’t even be that detrimental on your bones
 
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Also I don’t know if completely nuking your estrogen levels to 0 is ideal, I might be wrong but a bit of estrogen is still required to grow taller and overall development
A bit may be good but it's not like anyone does a tren-only cycle, even if some steroid only converts like 20% of itself into e2 you'd most likely have more than 0pg in your system.
 
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A bit may be good but it's not like anyone does a tren-only cycle, even if some steroid only converts like 20% of itself into e2 you'd most likely have more than 0pg in your system.
What e2 levels do you think are ideal?

I think you need atleast 5 pg honestly, estrogen isn’t always the enemy
 
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Yeah I agree as well. @TrueRamirez was freakinf out because I recommended 2.5 mg of letrozole every day.

But it does mentally cuck you though, horrible neurological imbalance sides. Gets better after a bit tho.

Honestly as long as you have a proper diet and getting all the proper nutrients for bone health, AI shouldn’t even be that detrimental on your bones
If bone density is a concern you could just take something else with it, some steroids are great for increasing bone density so they would counteract AI's supposed effect, or you could just take vitamin K2. Either way it's not like you're gonna get glass bones due to inhibiting estrogen, and if you somehow do you'd probably be notified with other side effects first.
 
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If bone density is a concern you could just take something else with it, some steroids are great for increasing bone density so they would counteract AI's supposed effect, or you could just take vitamin K2. Either way it's not like you're gonna get glass bones due to inhibiting estrogen, and if you somehow do you'd probably be notified with other side effects first.
Usually HGH is used with AI anyways, which is amazing for increasing bone density
 
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Bookedmarked will read later
 
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What e2 levels do you think are ideal?

I think you need atleast 5 pg honestly, estrogen isn’t always the enemy
Estrogen levels fluctuate throughout the day, if you read a specific level on a blood test it doesn't mean you're gonna stay with that 24/7.

But how much you should crush it may vary from person to person. I've not felt low estrogen affect me negatively at all so in my case I'd probably be fine with having constant near or complete zero levels. If one doesn't feel the side effects or is willing enough to tolerate them, I don't think there's much harm on having it at 0pg. From what I remember (read this long ago so may not be fully accurate), estrogen's effect on growth is that higher natural e2 could also result to periods of higher natural IGF-1, so if you're obtaining HGH from external sources having low e2 shouldn't affect your growth negatively. Estrogen is bad for men in general.
 
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Estrogen levels fluctuate throughout the day, if you read a specific level on a blood test it doesn't mean you're gonna stay with that 24/7.

But how much you should crush it may vary from person to person. I've not felt low estrogen affect me negatively at all so in my case I'd probably be fine with having constant near or complete zero levels. If one doesn't feel the side effects or is willing enough to tolerate them, I don't think there's much harm on having it at 0pg. From what I remember (read this long ago so may not be fully accurate), estrogen's effect on growth is that higher natural e2 could also result to periods of higher natural IGF-1, so if you're obtaining HGH from external sources having low e2 shouldn't affect your growth negatively. Estrogen is bad for men in general.
I guess your right, I only used 2.5 mg of letrozole EOD, but maybe I should switch to to ED.

My main concern is that estrogen contributes to brain development though? Or so I heard, and I really don’t wanna fuck with my brain development at all
 
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I guess your right, I only used 2.5 mg of letrozole EOD, but maybe I should switch to to ED.

My main concern is that estrogen contributes to brain development though? Or so I heard, and I really don’t wanna fuck with my brain development at all
It can be extremely important for brain development in females as it aids in the process of "feminizing" the structure. I've not seen any study showing aromatase deficient men have inferior cognitive development compared to non-deficients. If you start to see signs of getting "slow" or something while on AI you will obviously notice it though, bodybuilders stay on multiple drugs and AI for years and don't see permanent changes.

The most important things for the brain is animal fat and omega-3 either way.
 
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