major breakthrough!! high dose hgh study GONE WRONGG

[AtrophicPyra]

No im a poorcell

erda probably the most affective for height probably better than pthrp and lr3 only

 

[iblamejordan1]

erda probably the most affective for height probably better than pthrp and lr3 only

Well, thank you bhay

 

[Stacyslayerᛉ]

Why’d they get an accelerated BA? Crosstalk with ER? Or directly misdialed? Cause in my case I’ve been on high dose GH, high androgens, but kept my E2 in range (0 lmao) and my bone age is delayed asf. (If yuo wanna see Look my latest thread)

 

[AtrophicPyra]

Why’d they get an accelerated BA? Crosstalk with ER? Or directly misdialed? Cause in my case I’ve been on high dose GH, high androgens, but kept my E2 in range (0 lmao) and my bone age is delayed asf. (If yuo wanna see Look my latest thread)

dam what the FUCK

just looked at it, im assuming ur on smth unaromatizable if i may ask??

and ur definitely taking letrozole, but dude high dose gh we can see in the study increased bone maturation independently out of sex hormones

 

[AtrophicPyra]

Why’d they get an accelerated BA? Crosstalk with ER? Or directly misdialed? Cause in my case I’ve been on high dose GH, high androgens, but kept my E2 in range (0 lmao) and my bone age is delayed asf. (If yuo wanna see Look my latest thread)

@Kojo

 

[Kojo]

yo im pretty sure these niggas got raped by hgh bec igf1 inhibits pthrp in the gp and that made the pz chrondrocytes differentiate into the hz faster than they could optimally proliferate in the pz

Feedback loops bro feedback loops

 

[Kojo]

@Kojo

He says his e2 is 0, so I don't know what you was trying to say

 

[Kojo]

Because they stopped at onset of puberty

Correct, it's almost as if no one even read this study

Pyra clearly didn't

 

[Kojo]

FAH in controls is -1.9

FAH in gh treatment is -2.1

There's only a 0.2 point different on the HSDS and they ran 100+ iu lmao

Not to mention, pubertal onset also advanced in the gh group which could explain the maturation

It wasn't all throughout puberty which is pretty shitty, I have theories as to why this happens anyways. GH definitely doesn't directly fuse plates tho

 

[Niebvll]

Why’d they get an accelerated BA? Crosstalk with ER? Or directly misdialed? Cause in my case I’ve been on high dose GH, high androgens, but kept my E2 in range (0 lmao) and my bone age is delayed asf. (If yuo wanna see Look my latest thread)

low iq take
if you hadnt blasted gh it would be even more delayed or you started gh too late for significant sc depletion
it is obvious that the e2 suppression is the reason for delay and it just covers for the acceleration gh gives
individual cases (You) which is also purely anecdotal doesnt influence the rule (acceleration in bone age maturation)

 

[jeremyy]

DAMN.

 

[AtrophicPyra]

FAH in controls is -1.9

FAH in gh treatment is -2.1

There's only a 0.2 point different on the HSDS and they ran 100+ iu lmao

Not to mention, pubertal onset also advanced in the gh group which could explain the maturation

It wasn't all throughout puberty which is pretty shitty, I have theories as to why this happens anyways. GH definitely doesn't directly fuse plates tho

gh OBVIOUSLY doesnt fuse plates

 

[AtrophicPyra]

Feedback loops bro feedback loops

????

 

[AtrophicPyra]

Correct, it's almost as if no one even read this study

Pyra clearly didn't

i read it all, just weird to have shitty fah on that high of gh dose, we see the same for kids on a short period of gh still reap benefits in fah?

 

[Stacyslayerᛉ]

low iq take
if you hadnt blasted gh it would be even more delayed or you started gh too late for significant sc depletion
it is obvious that the e2 suppression is the reason for delay and it just covers for the acceleration gh gives
individual cases (You) which is also purely anecdotal doesnt influence the rule (acceleration in bone age maturation)

I asked a question bro why so mad

Nah but still why does it accelerate BA, directly or through ER crosstalk?

 

[Kojo]

low iq take
if you hadnt blasted gh it would be even more delayed or you started gh too late for significant sc depletion
it is obvious that the e2 suppression is the reason for delay and it just covers for the acceleration gh gives
individual cases (You) which is also purely anecdotal doesnt influence the rule (acceleration in bone age maturation)

Low iq take about gh and sc depletion

Good take about e2

 

[Kojo]

I asked a question bro why so mad

Nah but still why does it accelerate BA, directly or through ER crosstalk?

IGF-1 engages in cross talk with e2 and can amplify it's presence.

I mean running 180iu obviously isn't ideal as stem cell depletion is also a form of maturation WHEN E2 IS NOT CONTROLLED for the retards that might try to say I'm being contradictory

Additive Note: The onset of puberty was also earlier in the studies which also explains the maturation of bone

The maturation didn't amount to anything anyways, the height difference in the kids wasn't even an inch

People see maturation and think height was measurably stunted

 

[Kojo]

i read it all, just weird to have shitty fah on that high of gh dose, we see the same for kids on a short period of gh still reap benefits in fah?

The fah difference literally is 0.2sd's that's not even an inch difference

Learn how to understand studies and read every single word, don't only read the buzzwords/numbers

For reference, 0.2sd difference isn't even an inch in height difference.

It also says pubertal onset was earlier in the gh group, guess what early puberty is associated with? Shorter Stature.

Guess why you get shorter stature from early onset of puberty?

 

[AtrophicPyra]

The fah difference literally is 0.2sd's that's not even an inch difference

Learn how to understand studies and read every single word, don't only read the buzzwords/numbers

For reference, 0.2sd difference isn't even an inch in height difference.

It also says pubertal onset was earlier in the gh group, guess what early puberty is associated with? Shorter Stature.

Guess why you get shorter stature from early onset of puberty?

dude thats what im saying, the kids on gh on the study had a SHIT fah

 

[AtrophicPyra]

IGF-1 engages in cross talk with e2 and can amplify it's presence.

I mean running 180iu obviously isn't ideal as stem cell depletion is also a form of maturation WHEN E2 IS NOT CONTROLLED for the retards that might try to say I'm being contradictory

Additive Note: The onset of puberty was also earlier in the studies which also explains the maturation of bone

The maturation didn't amount to anything anyways, the height difference in the kids wasn't even an inch

People see maturation and think height was measurably stunted

also i have been thinking really hard abt the debate we had and realized from stacyslayer and you that…

letrozole trenbolone is probably all you need for a height stack as i saw with some studies i was looking at.. estrogen really is what fuses your gp from depleting rz obv.. and if androgens promote height velocity.. the only reason why it would be parallell to promoting bone maturation is because of estrogen..

so if u had a high androgen no e2 environment im pretty sure u could grow to like 7 foot

despite androgens forcing rz chrondrocytes to proliferate and enter the pz and promote pz chrondrocytes more into hz chrondrocytes as their dominant aspect maybe teriparatide could offset this by forcing pz chrondrocytes to proliferate a bit longer and further gaurentee positive fah from tren and letrozole obv gh would help too

you can also add in erdafitinib which also force pz and hz chrondrocytes to keep dividing and enlarging in their zones which could also help

but at the same time the rz can’t indefinitely assymetrically divide, and i have no idea how long they can divide for esp if tren is just raping the rz chrondrocytes into the pz and forcing them to hypertrophy.. meaning tren could just make u shorter fah wise since no more rz chrondrocytes left to divide and ur gp could never fuse due to no estrogen unless im wrong but im pretty sure im not since nothing can infinitely divide

 

[Niebvll]

Low iq take about gh and sc depletion

literally proven lol?
Its not an issue if you go through with the therapy but reducing the stem cell population in early childhood and then just leaving it like that is over

 

[percckk]

for like 3 days i used to pin in my fucking forearm dude, i was 14 what do u expect
but the rest did it properly lol.

you make mistakes n u learn

bro, i feel like im in that stage too and i really need some help, not pinning in forearm level tho. im just confused. i need about 10-12IU's of GH, so what quantity of vial do i buy? like lets say i buy a vial with 120IU's (ik its measured in mg), will that technically last me 10 days?

 

[Kojo]

dude thats what im saying, the kids on gh on the study had a SHIT fah

But the fah is barely different that's the point? Are you not trying to say it stunts

And I think 180iu's of GH would stunt with no e2 control

 

[AtrophicPyra]

But the fah is barely different that's the point? Are you not trying to say it stunts

And I think 180iu's of GH would stunt with no e2 control

no i meant the treatment was useless..

if u had zero e2 whilst taking tren and letro and took even 1000iu gh a week u would grow infinitely to 7’2

 

[Kojo]

also i have been thinking really hard abt the debate we had and realized from stacyslayer and you that…

letrozole trenbolone is probably all you need for a height stack as i saw with some studies i was looking at.. estrogen really is what fuses your gp from depleting rz obv.. and if androgens promote height velocity.. the only reason why it would be parallell to promoting bone maturation is because of estrogen..

so if u had a high androgen no e2 environment im pretty sure u could grow to like 7 foot

despite androgens forcing rz chrondrocytes to proliferate and enter the pz and promote pz chrondrocytes more into hz chrondrocytes as their dominant aspect maybe teriparatide could offset this by forcing pz chrondrocytes to proliferate a bit longer and further gaurentee positive fah from tren and letrozole obv gh would help too

you can also add in erdafitinib which also force pz and hz chrondrocytes to keep dividing and enlarging in their zones which could also help

but at the same time the rz can’t indefinitely assymetrically divide, and i have no idea how long they can divide for esp if tren is just raping the rz chrondrocytes into the pz and forcing them to hypertrophy.. meaning tren could just make u shorter fah wise since no more rz chrondrocytes left to divide and ur gp could never fuse due to no estrogen unless im wrong but im pretty sure im not since nothing can infinitely divide

Well you have to always remember when you talk about resting zone recruitment, they divide in different ways.

One division isn't losing a chondrocyte which is something I really want you to understand, You've got everything else figured out here

When a resting zone cell is recruited for example from an androgen or anything boosting velocity like you say, it doesn't mean much for fusion or "fusion by depletion" I suppose, because the resting zone chondrocyte will divide into 2 chondrocytes.

One will stay in the resting zone (aka nothing changed in the resting zone count) but you STILL get growth. This is why if anything androgens are a net-positive on your growth/FAH

Just for clarification if there was a lack of any beforehand, indefinitely doesn't mean infinite it just means it is not determinable but it also isn't a short time. I mean without e2, we already see them divide indefinitely in people without e2. 30 years old will growing plates that aren't fused.

I know you understand the concept of asymmetrical differentiation but I don't think you're factoring it in enough. For example when you say "tren is just raping the rz into the pz" it wouldn't be raping if you're not losing any chondrocytes..

I guess the only thing that would change is the hayflick limit obviously is slowly decreasing which is the amount of divisions you can get from one rz chondrocyte aka the indefinite depletion we was talking about

 

[Kojo]

no i meant the treatment was useless..

if u had zero e2 whilst taking tren and letro and took even 1000iu gh a week u would grow infinitely to 7’2

I agree

The reason a lot of peopel think heightmaxxing is cope is because literally not a single human being has done it right on this forum yet.

Now at least we have people who will do it right since the right information about heightmaxxing is actually coming out, @Paul.jnxy and @flowiza are my examples of people with open plates doing it right, I think their FAH's will be very promising for the entire heightmaxxing thing

So i'm just waiting on that

 

[AtrophicPyra]

Well you have to always remember when you talk about resting zone recruitment, they divide in different ways.

One division isn't losing a chondrocyte which is something I really want you to understand, You've got everything else figured out here

When a resting zone cell is recruited for example from an androgen or anything boosting velocity like you say, it doesn't mean much for fusion or "fusion by depletion" I suppose, because the resting zone chondrocyte will divide into 2 chondrocytes.

One will stay in the resting zone (aka nothing changed in the resting zone count) but you STILL get growth. This is why if anything androgens are a net-positive on your growth/FAH

Just for clarification if there was a lack of any beforehand, indefinitely doesn't mean infinite it just means it is not determinable but it also isn't a short time. I mean without e2, we already see them divide indefinitely in people without e2. 30 years old will growing plates that aren't fused.

I know you understand the concept of asymmetrical differentiation but I don't think you're factoring it in enough. For example when you say "tren is just raping the rz into the pz" it wouldn't be raping if you're not losing any chondrocytes..

I guess the only thing that would change is the hayflick limit obviously is slowly decreasing which is the amount of divisions you can get from one rz chondrocyte aka the indefinite depletion we was talking about

yess the hayflick limit was what i was referring to..

i found a study and made a whole thread, where i found that DHT did not increase dna synthesis in the rz and showed differentiation markers in the rz.. u should check it out, it might be evidence that smth as potent as dht like trenbolone what it would do to a chrondrocytes in rz

 

[Kojo]

also why does no one consider the concept of competitive binding on here? @Paul.jnxy I just remembered your letrozole + exemestane theory, It really wouldn't make sense because both the ai's have to compete for the enzyme so using both is redundant.

Letrozole binds to the aromatase enzyme with a much higher affinity

 

[Kojo]

yess the hayflick limit was what i was referring to..

i found a study and made a whole thread, where i found that DHT did not increase dna synthesis in the rz and showed differentiation markers in the rz.. u should check it out, it might be evidence that smth as potent as dht like trenbolone what it would do to a chrondrocytes in rz

Well DHT on chondrocytes isn't talked about enough because people only think of test, other androgens and igf-1/gh. It has interesting effects there, when i debated someone on androgens supposedly fusing plates through ROS oxidation (Retarded) I came across literature about DHT on chondrocytes. I'll send it to you

I suspect it stimulates PKC-Zeta which helps the growth plates health and shields it from estrogen oxidation

 

[AtrophicPyra]

also why does no one consider the concept of competitive binding on here? @Paul.jnxy I just remembered your letrozole + exemestane theory, It really wouldn't make sense because both the ai's have to compete for the enzyme so using both is redundant.

Letrozole binds to the aromatase enzyme with a much higher affinity

i would think using aromasin with letrozole, with aromasin being there to negate and estrogen rebound from a missed dose or near dose for the letrozole..

idk much abt that theory u r talking abt

 

[AtrophicPyra]

Well DHT on chondrocytes isn't talked about enough because people only think of test, other androgens and igf-1/gh. It has interesting effects there, when i debated someone on androgens supposedly fusing plates through ROS oxidation (Retarded) I came across literature about DHT on chondrocytes. I'll send it to you

I suspect it stimulates PKC-Zeta which helps the growth plates health and shields it from estrogen oxidation

ye there is very little 5ar in cartillage and bone so u cant rlly see dht affecting anybodys bone or cartillage so this is only applicable to vitro..

but atleast we know its role in the zones..
pkc-zeta stimulation in rz right?

also ROS and inflammation markers like tnf can be negated through pentoxyfilyine

 

[Kojo]

i would think using aromasin with letrozole, with aromasin being there to negate and estrogen rebound from a missed dose or near dose for the letrozole..

idk much abt that theory u r talking abt

Yeah the theory is that aromasin does this, but how? Only one ligand can bind to aromatase at once

Aromasin would essentially just be there doing nothing

 

[Kojo]

ye there is very little 5ar in cartillage and bone so u cant rlly see dht affecting anybodys bone or cartillage so this is only applicable to vitro..

but atleast we know its role in the zones..
pkc-zeta stimulation in rz right?

also ROS and inflammation markers like tnf can be negated through pentoxyfilyine

Correct about 5ar and the fact dht doesn't effect people yeah, it was actually in vivo btw -- https://www.sciencedirect.com/science/article/abs/pii/S1388198121001566#abstracts

pkc-zeta stimulation overall

ROS was just a stupid myth from a tiktok user anyways

 

[AtrophicPyra]

Yeah the theory is that aromasin does this, but how? Only one ligand can bind to aromatase at once

Aromasin would essentially just be there doing nothing

because lets say u miss a dose of letrozole..

since the aromasin has a relatively long half life, it can still have an e2 lowering affect even a day later, kind of suspending the ERB resensitization from raping the plates a little bit, its 100% better than nothing

and letrozoles half life is rlly short, if u didnt take it for one day ur er sensitivity already high, shits going to go bad

 

[Kojo]

because lets say u miss a dose of letrozole..

since the aromasin has a relatively long half life, it can still have an e2 lowering affect even a day later, kind of suspending the ERB resensitization from raping the plates a little bit, its 100% better than nothing

and letrozoles half life is rlly short, if u didnt take it for one day ur er sensitivity already high, shits going to go bad

I think you're thinking about anastrozole, anastrozole has a really short half life. It's like 12-24 hours or something. letro is like 2-4 days

I understand the missing the dose thing but I don't see why he'd miss one. I'm pretty sure his thought process was that they essentially "stack" on top of each other so whilst letro is nuking, aromasin is simultaneously deleting the enzyme but that doesn't make sense

 

[Niebvll]

if u had zero e2 whilst taking tren and letro and took even 1000iu gh a week u would grow infinitely to 7’2

You wouldnt

 

[AtrophicPyra]

Correct about 5ar and the fact dht doesn't effect people yeah, it was actually in vivo btw -- https://www.sciencedirect.com/science/article/abs/pii/S1388198121001566#abstracts

pkc-zeta stimulation overall

ROS was just a stupid myth from a tiktok user anyways

pkc-zeta stimulation means that androgens DO cause rz chrondrocytes to differentiate though and probably could cause fusion

but its probably nothing near estrogens rate of fusion

ros could be a reason tho bec androgens esp more potent ones if taken for like years will put u in a high inflammatory environment and that could rape ur growth potential

but nobody is taking a gram of tren without atleast glutathione and plus pentoxyfiline negates these inflammation markers

 

[AtrophicPyra]

I think you're thinking about anastrozole, anastrozole has a really short half life. It's like 12-24 hours or something. letro is like 2-4 days

I understand the missing the dose thing but I don't see why he'd miss one. I'm pretty sure his thought process was that they essentially "stack" on top of each other so whilst letro is nuking, aromasin is simultaneously deleting the enzyme but that doesn't make sense

well there r so much receptors i dont think one overlapping another would ever be a problem

 

[AtrophicPyra]

You wouldnt

ya ik, kind of over exxageration, u could probably grow till ur like mid 40’s on 100mg tren for a few decades with zero e2

nowhere bear estrogens rate of fusion ofc

 

[Kojo]

pkc-zeta stimulation means that androgens DO cause rz chrondrocytes to differentiate though and probably could cause fusion

but its probably nothing near estrogens rate of fusion

ros could be a reason tho bec androgens esp more potent ones if taken for like years will put u in a high inflammatory environment and that could rape ur growth potential

but nobody is taking a gram of tren without atleast glutathione and plus pentoxyfiline negates these inflammation markers

There's no ROS pathway from androgens that could oxidate the growth plate chondrocytes though

It's not possible for any signalling of the ar to cause ROS and the mechanism they used was calcium influxes causing pkc-alpha activation down p47phox phosphorylation activating nox cascades, ergo ROS. Which ar signalling can't induce, as ar induces PC-PLC not PI-PLC

and nah pkc zeta doesn't cause chondro differentiation, it just protects chondrocytes from cell toxicities and inhibits apoptosis from these toxicities.

 

[Kojo]

well there r so much receptors i dont think one overlapping another would ever be a problem

well aromatase isn't a receptor it's an enzyme, and most receptors/enzymes have one active binding sight not multiple so overlap couldn't really occur

 

[AtrophicPyra]

There's no ROS pathway from androgens that could oxidate the growth plate chondrocytes though

It's not possible for any signalling of the ar to cause ROS and the mechanism they used was calcium influxes causing pkc-alpha activation down p47phox phosphorylation activating nox cascades, ergo ROS. Which ar signalling can't induce, as ar induces PC-PLC not PI-PLC

and nah pkc zeta doesn't cause chondro differentiation, it just protects chondrocytes from cell toxicities and inhibits apoptosis from these toxicities.

i have to look more into pkc zeta maybe m thinking abt smth else

 

[AtrophicPyra]

well aromatase isn't a receptor it's an enzyme, and most receptors/enzymes have one active binding sight not multiple so overlap couldn't really occur

i mean like one letrozole molecule enters an aromatase enzyme and one aromasin molecule enters an aromatase enzyme etc. etc., whatever letrozole doesnt bind to, aromasin does vice versa leading to an even lower e2 level

 

[Kojo]

i have to look more into pkc zeta maybe m thinking abt smth else

Possible, PKC-zeta is just an atypical protein kinase c isoform. I can send you the literature on protein kinase c.

it's by far one of my favourite parts about cell biology

https://www.sciencedirect.com/science/article/pii/S0021925822006366#fig1

 

[Kojo]

i mean like one letrozole molecule enters an aromatase enzyme and one aromasin molecule enters an aromatase enzyme etc. etc., whatever letrozole doesnt bind to, aromasin does vice versa leading to an even lower e2 level

Well letrozole already nukes 99.1%

Letrozole also has a higher binding affinity than Aromasin so that shits never getting through

 

[AtrophicPyra]

Possible, PKC-zeta is just an atypical protein kinase c isoform. I can send you the literature on protein kinase c.

it's by far one of my favourite parts about cell biology

https://www.sciencedirect.com/science/article/pii/S0021925822006366#fig1

will look into it

 

[AtrophicPyra]

Well letrozole already nukes 99.1%

Letrozole also has a higher binding affinity than Aromasin so that shits never getting through

well as letrozoles half life slowly dies out, it will be nuking 50% lets say at the half point..

aromasin with a greater half life would induce aromatase suicide and make up for that letrozoles half life dying and further inhibit e2 at points where letrozole is weakest

idk.. aromasin seems like shit to me now that u brought up letrozoles half life

 

[Kojo]

well as letrozoles half life slowly dies out, it will be nuking 50% lets say at the half point..

aromasin with a greater half life would induce aromatase suicide and make up for that letrozoles half life dying and further inhibit e2 at points where letrozole is weakest

I'll think more about this later I'm kinda hungry

idk.. aromasin seems like shit to me now that u brought up letrozoles half life

Eh, anastrozole is the worst. 85-92% suppression

Shit binds to era

Least tissue selective

I just don't know why anyone would use it

 

[Kojo]

literally proven lol?
Its not an issue if you go through with the therapy but reducing the stem cell population in early childhood and then just leaving it like that is over

very nuanced

 

[flowiza]

I agree

The reason a lot of peopel think heightmaxxing is cope is because literally not a single human being has done it right on this forum yet.

Now at least we have people who will do it right since the right information about heightmaxxing is actually coming out, @Paul.jnxy and @flowiza are my examples of people with open plates doing it right, I think their FAH's will be very promising for the entire heightmaxxing thing

So i'm just waiting on that

yo ty and yeah i grew 1cm in the last 2 weeks and im starvemaxxing aswell people r just tards and should pay us for coaching