has ANYONE actually ran erdafitinib on this forum?

[reggina]

literally EVERYONE seems to be talking about it but no one gives a fuck about the side effects. Scoliosis, retinal detachment and kidney stones just to increase 2-3 inches of height does not seem worth it. Who here has actually taken erda lmao everyone seems to just be larping about it.

 

[Deleted member 341805]

literally EVERYONE seems to be talking about it but no one gives a fuck about the side effects. Scoliosis, retinal detachment and kidney stones just to increase 2-3 inches of height does not seem worth it. Who here has actually taken erda lmao everyone seems to just be larping about it.

Bunch of people I know run it, I just shipped erda out to someone a few days ago. It isn't larp lol.

Maybe from your shitty tiktok kids yeah.

Everything has "side effects". Compound usage doesn't end at, "Oh this thing has these potential bad side effects lets just end there" Side effect mitigation research is a thing for a reason.

 

[flowiza]

2-3 inches of height does not seem worth it.

way more if you add hgh tren abalo and shit also what?? how is 3 inches not worth it lmao

 

[flowiza]

Bunch of people I know run it, I just shipped erda out to someone a few days ago. It isn't larp lol.

Maybe from your shitty tiktok kids yeah.

Everything has "side effects". Compound usage doesn't end at, "Oh this thing has these potential bad side effects lets just end there" Side effect mitigation research is a thing for a reason.

yeah lmao like anyone has gotten alzheimers from tren or liver failure from halo

 

[cc000]

literally EVERYONE seems to be talking about it but no one gives a fuck about the side effects. Scoliosis, retinal detachment and kidney stones just to increase 2-3 inches of height does not seem worth it. Who here has actually taken erda lmao everyone seems to just be larping about it.

2-3 inches is alot

 

[Deleted member 341805]

yeah lmao like anyone has gotten alzheimers from tren or liver failure from halo

 

[reggina]

Bunch of people I know run it, I just shipped erda out to someone a few days ago. It isn't larp lol.

Maybe from your shitty tiktok kids yeah.

Everything has "side effects". Compound usage doesn't end at, "Oh this thing has these potential bad side effects lets just end there" Side effect mitigation research is a thing for a reason.

Well obviously everything has side effects but retinal detachment is a side effect experienced by 20%+ of the people taking it. Also what side effect mitigation compounds does one need to use with erda?

 

[Deleted member 341805]

2-3 inches is alot

way more if you add hgh tren abalo and shit also what?? how is 3 inches not worth it lmao

That's 5'9"-- 6'0", Or 6'1"-- 6'4"

Big gains

 

[Deleted member 341805]

Well obviously everything has side effects but retinal detachment is a side effect experienced by 20%+ of the people taking it. Also what side effect mitigation compounds does one need to use with erda?

Decreasing and monitoring phosphate, low dosing it.

 

[flowiza]

That's 5'9"-- 6'0", Or 6'1"-- 6'4"

Big gains

yes lmao like half a head above ur previous height isnt alot

 

[flowiza]

That's 5'9"-- 6'0", Or 6'1"-- 6'4"

Big gains

niggas think their height cycle would add 10 inches increased fah

 

[reggina]

Decreasing and monitoring phosphate, low dosing it.

whats the result how much can you realistically grow stacked with HGH and an AI?

 

[reggina]

niggas think their height cycle would add 10 inches increased fah

i'd even be grateful for half an inch, but some niggas dont get any results and all the side effects

 

[Deleted member 341805]

niggas think their height cycle would add 10 inches increased fah

Literally, i don't understand what people expect from height stacks or height stackers.

Do they really think people are saying "Yeah bro I'm gonna run this and go from a genetic potential of 5'6 -- 6'2 dewd"

Most average height stack being hgh and ai will probably add on like an inch or 2 at best, adding in erda will give you like 2-4 guaranteed inches. Other things like SERDs, nuking test using naaas' that also buffer igf-1 will give you even crazier gains. Potentially 4-6

Though, I'm making these estimates from if you ran it at an optimal time. A lot of people run it far too late like at 16 thinking they'll get anything over 2 inches with that plate status lmao

 

[Deleted member 341805]

i'd even be grateful for half an inch, but some niggas dont get any results and all the side effects

People don't get results because they run it too late. All the time.

They never get xrays they just assume they're still growing which they probably are but you need to examine the plate through an xray, you can tell what state of fusion it's at

 

[Deleted member 341805]

whats the result how much can you realistically grow stacked with HGH and an AI?

Probably 1-2 inches, especially if you high dose the fuck out of hgh and nuke your e2 to 0 with 2.5mg letrozole daily at like 14 in the peak growth phase. More than 2 inches wouldn't be too much of a stretch honestly

 

[reggina]

People don't get results because they run it too late. All the time.

They never get xrays they just assume they're still growing which they probably are but you need to examine the plate through an xray, you can tell what state of fusion it's at

i've planned to get a wrist xray to check out my growth plate status soon.
currently 15 and 4 months and my genetic potential is around 5'10 and im 5'6.5, dad is 6'0 and mom is 5'4.5.

IF you're talking about 2 inches of guaranteed height growth over my potiential then i think its worth the risk of being blind. Anything to escape hell

 

[reggina]

Probably 1-2 inches, especially if you high dose the fuck out of hgh and nuke your e2 to 0 with 2.5mg letrozole daily at like 14 in the peak growth phase. More than 2 inches wouldn't be too much of a stretch honestly

if im correct 0 e2 is worse for your growth, best to stay at very low e2 levels to not nuke your brain development.

 

[Deleted member 341805]

i've planned to get a wrist xray to check out my growth plate status soon.
currently 15 and 4 months and my genetic potential is around 5'10 and im 5'6.5, dad is 6'0 and mom is 5'4.5.

IF you're talking about 2 inches of guaranteed height growth over my potiential then i think its worth the risk of being blind. Anything to escape hell

The 2 inches is in reference to hgh and ai. Every 14-15 year old should be on a hgh and ai stack regardless.

Erda is if you're greedy, just do your own research.

If you're even more greedy, use roids like anavar halo or tren to buffer igf-1 and help with chondrocyte proliferation. And leave your test at a low-normal amount.

You probably won't though, just putting things on the table for you.

Also come back in around 2 years, I'll bet you any money you will get 6'0" natty. My brother is 15 and 5'6.5, he's projected to be 6'1. But obviously we have better height genes.

 

[Deleted member 341805]

if im correct 0 e2 is worse for your growth, best to stay at very low e2 levels to not nuke your brain development.

This is a tiktok sensation lol E2 is just a neuroprotective neurosteroid and can help with cognitive function a bit, though nuking e2 literally has not been shown to impair cognition in a letrozole group vs placebo.

Spoiler: Study for you my brother

Cognitive effects of aromatase inhibitor therapy in peripubertal boys - PubMed

Our results suggest that blockade of oestrogen biosynthesis with an aromatase inhibitor does not influence cognitive performance in peripubertal males.

pubmed.ncbi.nlm.nih.gov

 

[reggina]

The 2 inches is in reference to hgh and ai. Every 14-15 year old should be on a hgh and ai stack regardless.

Erda is if you're greedy, just do your own research.

If you're even more greedy, use roids like anavar halo or tren to buffer igf-1 and help with chondrocyte proliferation. And leave your test at a low-normal amount.

You probably won't though, just putting things on the table for you.

Also come back in around 2 years, I'll bet you any money you will get 6'0" natty. My brother is 15 and 5'6.5, he's projected to be 6'1. But obviously we have better height genes.

I would definitely run HGH and AI if i could. Im broke and even if i wasn't my jew parents wont let me grow to 6'1 and slay. No parent would want their kid to be pinning chinese HGH every night.

My father was also 5'7 at my age so at the minimum i hope to atleast grow to 5'10. Also wanted to ask if you think mk677 is a good idea to waste my money on? Its cheap and will probably also help my gymcel as a bonus but does it have any meaningful effect on growth?

 

[Deleted member 341805]

I would definitely run HGH and AI if i could. Im broke and even if i wasn't my jew parents wont let me grow to 6'1 and slay. No parent would want their kid to be pinning chinese HGH every night.

My father was also 5'7 at my age so at the minimum i hope to atleast grow to 5'10. Also wanted to ask if you think mk677 is a good idea to waste my money on? Its cheap and will probably also help my gymcel as a bonus but does it have any meaningful effect on growth?

To some degree

 

[jakon]

Literally, i don't understand what people expect from height stacks or height stackers.

Do they really think people are saying "Yeah bro I'm gonna run this and go from a genetic potential of 5'6 -- 6'2 dewd"

Most average height stack being hgh and ai will probably add on like an inch or 2 at best, adding in erda will give you like 2-4 guaranteed inches. Other things like SERDs, nuking test using naaas' that also buffer igf-1 will give you even crazier gains. Potentially 4-6

Though, I'm making these estimates from if you ran it at an optimal time. A lot of people run it far too late like at 16 thinking they'll get anything over 2 inches with that plate status lmao

@Niebvll

 

[Niebvll]

Literally, i don't understand what people expect from height stacks or height stackers.

Do they really think people are saying "Yeah bro I'm gonna run this and go from a genetic potential of 5'6 -- 6'2 dewd"

Genetic potential is a myth
And technically that height increase would be possible

Most average height stack being hgh and ai will probably add on like an inch or 2 at best

i agree

adding in erda will give you like 2-4 guaranteed inches

Depending on when you start, even more

Other things like SERDs, nuking test using naaas' that also buffer igf-1 will give you even crazier gains. Potentially 4-6

Definetely not

Though, I'm making these estimates from if you ran it at an optimal time. A lot of people run it far too late like at 16 thinking they'll get anything over 2 inches with that plate status lmao

Definetely possible with running other compounds instead of the bullshit you just mentioned (excl erda)

 

[Deleted member 341805]

Genetic potential is a myth

This is a retard statement lmfao genetics definitely largely predetermine height given no pharmaceutical intervention is involved

Depending on when you start, even more

Applies to every heightmaxxing protocol

Definetely not

Definitely if started at a good time period* If you're on 0 test 0 e2 with estrogen receptor degraders you're effectively like males who have CYP19A1 mutations and never stop growing. Your plate quite literally cannot fuse with 0 e2 and 0 estrogen receptor activity

Definetely possible with running other compounds instead of the bullshit you just mentioned (excl erda)

rhGH and ai's aren't bullshit, neither are serds or naaas lol I'd rather take those 4 over erda, overrated compound

 

[Niebvll]

This is a retard statement lmfao genetics definitely largely predetermine height given no pharmaceutical intervention is involved

1. Where did I say genetics dont matter for height? I said there is no such thing as "genetic potential"
3. The "largely" before the predetermination completely erases the meaning of predetermination. Nothing is determined yet, theres only influence.
2. You added a prerequisite which didnt exist before and doesnt even make sense considering you were actually talking about a "genetic potential" being uninfluenced by pharmaceutical intervention (in this case erda)

Applies to every heightmaxxing protocol

Did I say otherwise?
Just dodging my point

Definitely if started at a good time period* If you're on 0 test 0 e2 with estrogen receptor degraders you're effectively like males who have CYP19A1 mutations and never stop growing. Your plate quite literally cannot fuse with 0 e2 and 0 estrogen receptor activity

intrinsic senescence exists lol of course they can still fuse
I agree that this would in theory work but definetely not "crazier gains than fgfr3i"
As you said yourself, extremely growth plate maturation dependent

rhGH and ai's aren't bullshit, neither are serds or naaas lol

They are for heightmaxing because 1 most people use them wrong and 2 a handful of cms are not saving you lmao

I'd rather take those 4 over erda, overrated compound

Not overrated but definitely overhyped

 

[Deleted member 341805]

1. Where did I say genetics dont matter for height? I said there is no such thing as "genetic potential"

I'm not saying that you said they don't matter, the point of "there's no such thing as genetic potential" is probably you attacking me from the iqlet points people make like "You could've been 6'5 bruh" idiots or the "you're stuck here and can't fix it".

When I say genetic potential I'm referring to a large predetermination of how your body functions to produce a certain amount of bone growth without any intervention. Like pfah through khamis roche

3. The "largely" before the predetermination completely erases the meaning of predetermination. Nothing is determined yet, theres only influence.

Precogged this response, and this isn't true. You can have a quantification of predetermination it doesn't have to be absolute. Predetermination and influence are synergistic terms lmao

2. You added a prerequisite which didnt exist before and doesnt even make sense considering you were actually talking about a "genetic potential" being uninfluenced by pharmaceutical intervention (in this case erda)

You're misinterpreting the switch, when I said pharmaceutical intervention won't push you 8 inches above your pfah, and you responded there's no such thing as "genetic potential" I switched to purely talking about genetics. Genetics and pharmaceutical intervention are still synergistic

Did I say otherwise?
Just dodging my point

I'm not saying you said otherwise, and I'm not dodging your point lol. What age you start is legitimately an intuitive presupposition in heightmaxxing

intrinsic senescence exists lol of course they can still fuse
I agree that this would in theory work but definetely not "crazier gains than fgfr3i"
As you said yourself, extremely growth plate maturation dependent

I've already made posts and threads about this, intrinsic senescence is just chondrocyte apoptosis which doesn't happen until later in life.

As seen with cyp19a1 mutations they usually stop growing in the late 20s-30s. The point of e2 is that it simply accelerates this chondrocyte lifespan beyond what it actually would be through programmed cell death (as all cells obviously go through cell death at

They are for heightmaxing because 1 most people use them wrong and 2 a handful of cms are not saving you lmao

Most people using them wrong is a fallacious argument for saying it doesn't work

A handful of cms will save you, these have been shown to give up to 8cm with a moderate dosage of rhGH in iss kids. That's 3.2 inches, literally going from manletism to tall (5'9-6'0") running other things alongside rhGH is bound to give you additional height gains.

Not overrated but definitely overhyped

I can agree to that

 

[Niebvll]

I'm not saying that you said they don't matter, the point of "there's no such thing as genetic potential" is probably you attacking me from the iqlet points people make like "You could've been 6'5 bruh" idiots or the "you're stuck here and can't fix it".

When I say genetic potential I'm referring to a large predetermination of how your body functions to produce a certain amount of bone growth without any intervention. Like pfah through khamis roche

I can agree to the last part but any attempt to define genetic potential will always meet issues
You could argue that one's body's response to pharmaceutical intervention is also largely your genetics and that such an intervention doesnt go against it, the potential would then have to include all positively affecting pharmaceutical procedures possible, reaching this would then be near impossible.

Precogged this response, and this isn't true. You can have a quantification of predetermination it doesn't have to be absolute. Predetermination and influence are synergistic terms lmao

No theyre not without dividing the object of predetermination into parts (not physically), that cant be done with "genetic potential" as its an undefined term even
You could argue certain aspects of xyz are genetically predetermined and others arent, which would then leave room for influence to take place in the parts not predetermined but nothing like that has been done
In my understanding of english, predetermination by definition asserts that an outcome is already fixed by prior causes, any influence would have to be a part of the predetermined causes, though not necessarily directly.

You're misinterpreting the switch, when I said pharmaceutical intervention won't push you 8 inches above your pfah, and you responded there's no such thing as "genetic potential" I switched to purely talking about genetics. Genetics and pharmaceutical intervention are still synergistic

Reply 1 for this

I've already made posts and threads about this, intrinsic senescence is just chondrocyte apoptosis which doesn't happen until later in life.

Yes it is and chondrocyte apoptosis (after hyperthropy) still happens, just delayed
"Later in life" sounds like a decade or so
Every study trial with aromatisation inhibition showed that while the result was a widened growth plate, maturation continued and that not in a super slowed down way that equals you to

As seen with cyp19a1 mutations they usually stop growing in the late 20s-30s.

they have their deficiency since theyre children, if you start during puberty you will definitely not experience the same delay
I'm willing to look into this more though I'd appreciate a thread recommendation

Most people using them wrong is a fallacious argument for saying it doesn't work

Not saying they dont work, I never did and even agreed that they do (https://looksmax.org/threads/has-anyone-actually-ran-erdafitinib-on-this-forum.2180724/post-30278835). Im saying theyre bullshit to promote for Heightmaxing

A handful of cms will save you, these have been shown to give up to 8cm with a moderate dosage of rhGH in iss kids.

Exactly
in ISS kids
Not in healthy kids

That's 3.2 inches, literally going from manletism to tall (5'9-6'0") running other things alongside rhGH is bound to give you additional height gains.

Yes but as a more or less healthy person youre not going to see the same result as someone in the bottom 2.3%, even if their cause is not hormone related

 

[darklooktriad]

Yes, 0 side effects, honestly I got smarter and better eye sight after my 3 year cycle

 

[Niebvll]

Yes, 0 side effects, honestly I got smarter and better eye sight after my 3 year cycle

I love your shitposts

 

[Deleted member 341805]

I can agree to the last part but any attempt to define genetic potential will always meet issues
You could argue that one's body's response to pharmaceutical intervention is also largely your genetics and that such an intervention doesnt go against it, the potential would then have to include all positively affecting pharmaceutical procedures possible, reaching this would then be near impossible.

I don't think this requires a response really, there's no dissonance here

No theyre not without dividing the object of predetermination into parts (not physically), that cant be done with "genetic potential" as its an undefined term even
You could argue certain aspects of xyz are genetically predetermined and others arent, which would then leave room for influence to take place in the parts not predetermined but nothing like that has been done
In my understanding of english, predetermination by definition asserts that an outcome is already fixed by prior causes, any influence would have to be a part of the predetermined causes, though not necessarily directly.

Predetermination as an analytical term can have different presups applied to, insofar as you hold to a compatibilist view of determination. For example you can say something is determined to happen, but there also can be influence affecting the conclusion of prior causes.

Example being, a car is driving from point a-b. This is determined to happen as long as there's no causal interference with the determined process.

Another example is putting marbles down a slide. The ending path that the marble is predetermined to come out of is predetermined as it's already there, however there can be interferences with the pathway. This still applies under your definition of of a fixed outcome.

Yes it is and chondrocyte apoptosis (after hyperthropy) still happens, just delayed
"Later in life" sounds like a decade or so
Every study trial with aromatisation inhibition showed that while the result was a widened growth plate, maturation continued and that not in a super slowed down way that equals you to

Also addressed this in the same thread, chondrocyte death after hypertrophy is not the same as resting zone apoptosis. Resting zones chons are reserve chondrocytes that are supposed to be used to continue future growth. Estrogen matures the lifespan of these cells and makes them undergo early cell death. Apoptosis post hypertrophy and apoptosis that makes your plates fuse are 2 different things.

Post Hypertrophy apoptosis induces growth, Resting zone apoptosis (Plate fusion) hastens fusion and halts growth.

Yes aromatase inhibition isn't enough because aromatase inhibitors induce negative feedback loops that increase estrogen by almost tripling testosterone, and their estrogen receptors are still active. They also don't downregulate the extra test in the study patients.

they have their deficiency since theyre children, if you start during puberty you will definitely not experience the same delay
I'm willing to look into this more though I'd appreciate a thread recommendation

This is true, but plate fusion doesn't really start at all for anyone until early puberty simply due to there not being enough hormones to supply the growth plate with either rapid growth or fusion. If they grow for a decade or so after us normal people, I'd expect us that missed out on a few years of low e2 to still be able to prolong our growth for a few more years. And yeah I'll send you stuff

Not saying they dont work, I never did and even agreed that they do (https://looksmax.org/threads/has-anyone-actually-ran-erdafitinib-on-this-forum.2180724/post-30278835). Im saying theyre bullshit to promote for Heightmaxing

But then what does it mean for it to be bullshit? If it works in what way is it bullshit?

Exactly
in ISS kids
Not in healthy kids

Yes but as a more or less healthy person youre not going to see the same result as someone in the bottom 2.3%, even if their cause is not hormone related

Idiopathy analytically entails that the kids are healthy though, the point of idiopathy is that these kids are just short for no examined reason at all. They don't have growth hormone receptor insensitivity as that'd contradict being ISS.

They legitimately do not have any medical issues yet they are just short. This can be accounted for genes like simply being super unlucky and inheriting all of the short polygenic traits. So they're identical to us

 

[Niebvll]

I don't think this requires a response really, there's no dissonance here

Predetermination as an analytical term can have different presups applied to, insofar as you hold to a compatibilist view of determination. For example you can say something is determined to happen, but there also can be influence affecting the conclusion of prior causes.

Example being, a car is driving from point a-b. This is determined to happen as long as there's no causal interference with the determined process.

Another example is putting marbles down a slide. The ending path that the marble is predetermined to come out of is predetermined as it's already there, however there can be interferences with the pathway. This still applies under your definition of of a fixed outcome.

Also addressed this in the same thread, chondrocyte death after hypertrophy is not the same as resting zone apoptosis. Resting zones chons are reserve chondrocytes that are supposed to be used to continue future growth. Estrogen matures the lifespan of these cells and makes them undergo early cell death. Apoptosis post hypertrophy and apoptosis that makes your plates fuse are 2 different things.

Estrogen speeds up the maturation which leads to undergoing proliferation, hypertrophy and then apoptosis
I havent heard of estrogen causing stemlike chondrocytes to undergo cell death directly

Yes aromatase inhibition isn't enough because aromatase inhibitors induce negative feedback loops that increase estrogen by almost tripling testosterone, and their estrogen receptors are still active.

There's no increase in estrogen even with extra testosterone because the inhibitor is still active
Estrogen receptoes of people with CYP19A1 mutation are normal as well. You didnt really mention ESRalpha mutations

This is true, but plate fusion doesn't really start at all for anyone until early puberty simply due to there not being enough hormones to supply the growth plate with either rapid growth or fusion. If they grow for a decade or so after us normal people, I'd expect us that missed out on a few years of low e2 to still be able to prolong our growth for a few more years.

Yeah a few more years, but not until late 20s or even 30s maybe early 20s

And yeah I'll send you stuff

But then what does it mean for it to be bullshit? If it works in what way is it bullshit?

Its bullshit to concentrate on that when there's far more effective methods
Cba going that pathway for 5cms if lucky

Idiopathy analytically entails that the kids are healthy though, the point of idiopathy is that these kids are just short for no examined reason at all.

There is something off with them, we just dont know what yet
If they were exactly normaly they would not suffer short stature

They don't have growth hormone receptor insensitivity as that'd contradict being ISS.

Didnt say they did

They legitimately do not have any medical issues yet they are just short.

They dont have any we know of

This can be accounted for genes like simply being super unlucky and inheriting all of the short polygenic traits. So they're identical to us

The idiopathy excludes genetic causes

 

[Deleted member 341805]

Estrogen speeds up the maturation which leads to undergoing proliferation, hypertrophy and then apoptosis
I havent heard of estrogen causing stemlike chondrocytes to undergo cell death directly

Estrogen doesn't speed up the maturation of hypertrophied cells, cells that hypertrophy swell and have a genetically determined size for how much they grow before apoptosis. This programmed cell death is mediated through indian hedgehog and runx2 genes.

The entire point of estrogen is that it gets rid of the cells that cause you to grow in the first place which are the reserve cells lmao

This is also why scientists are trying to discover how to reopen growth plates with stem cells as that's the foundation of cartilage and growth.

There's no increase in estrogen even with extra testosterone because the inhibitor is still active
Estrogen receptoes of people with CYP19A1 mutation are normal as well. You didnt really mention ESRalpha mutations

I was talking about the negative feedback loop that triggers more estrogen, i wasn't saying the estrogen actually increases.

The estrogen stays low but the test skyrockets into supraphysiological test and the remaining small trace amounts of intracrine estrogen hypersensitise the estrogen receptors since that also is another negative feedback loop the body produces.

When there's a low amount of something, it upregulates other things to maintain homeostasis and vice versa. It's the same reason synthetic androgens shut off your hpga because your brain says there's already enough as opposed to not enough like what happens with ai's.

So this increased test interacting with trace aromatase that then converts this test into e2 that then binds with stronger affinity to er's just doesn't make a difference in your growth.

Yeah but there's no aromatase at all in people with cyp19a1 mutations, it literally does not exist in our body. It'll always exist in small trace amounts in our bodies. So we have to shut off our receptors to the small trace amounts to even get the same effect as them that actually stops growth. Though, I think nuking e2 and test is enough for DELAY

Yeah a few more years, but not until late 20s or even 30s maybe early 20s

I don't disagree, I wasn't saying to 20s and 30s but I was saying prolonging it later than normal. Of course those guys are superior to us in that regard

Its bullshit to concentrate on that when there's far more effective methods
Cba going that pathway for 5cms if lucky

I don't disagree here, but gh is the foundation of any heightmaxxing protocol. GHR agonism is very necessary for growth. Also 5cm is common not lucky

There is something off with them, we just dont know what yet
If they were exactly normaly they would not suffer short stature

There isn't, they have no aetiology. This kind of reasoning is also fallacious because you're affirming the consequent.

"If they were normal they wouldn't have short stature" But you're affirming your consequent of saying they're abnormal because they're short when the claim that ought to be proven is whether that short stature is caused by an abnormality.

Didnt say they did

But that's the point, they have no verifiable medical issues

They dont have any we know of

Yes? We already know all possible issues that lead to shortened height. Natural Gene inheritance (Not a medical issue, completely natural just unlucky), Gene mutations (Which are a medical issue that is verifiable) and Environmental causes like getting a tumor or something like that

The idiopathy excludes genetic causes

That's the point, genetic causes aren't a medical issue it's just being unlucky. There's a difference between your natural genetic inheritance causing you to be short vs a gene mutation which scientists can easily verify by simply finding any issue in your body related to growth pathways.

You do know that height is polygenic right? Which also explains why siblings can have completely different heights. I'm 6'2.5 but my brother is projected to be 6ft. It simply means out of the millions of genes in the gene pool I inherited more genes that stimulate height growth than my brother did. This also explains why people with short parents can be tall and vice versa. Though, pretty rare of course

People with ISS simply didn't get the genetic makeup for height growth and that's the entire point of it being iss because there's no medical issue at hand. Pure gene inheritance bad luck. It is very very rare tho

 

[Niebvll]

Estrogen doesn't speed up the maturation of hypertrophied cells, cells that hypertrophy swell and have a genetically determined size for how much they grow before apoptosis.

i didnt even say that
estrogen speeds up general cell maturation which leads to hypertrophy before cell death

This programmed cell death is mediated through indian hedgehog and runx2 genes.

Ok interesting to know what pathways exactly are responsible

The entire point of estrogen is that it gets rid of the cells that cause you to grow in the first place which are the reserve cells lmao

not by direct cell death but by tipping them over from progenitors to normal chondrocytes and preventing progenitor renewal

I was talking about the negative feedback loop that triggers more estrogen, i wasn't saying the estrogen actually increases.

The estrogen stays low but the test skyrockets into supraphysiological test and the remaining small trace amounts of intracrine estrogen hypersensitise the estrogen receptors since that also is another negative feedback loop the body produces.

Lmao local aromatisation isnt unknown lol but ais can overturn it regardless if you nuke enough
"Skyrockets" is such an exaggeration as well, usually a 50-100% increase
Do you have any studies on the hypersensitisation? I highly doubt that this is a major thing, the body doesnt adjust estrogen receptors like that

So this increased test interacting with trace aromatase that then converts this test into e2 that then binds with stronger affinity to er's just doesn't make a difference in your growth.

Yeah but there's no aromatase at all in people with cyp19a1 mutations, it literally does not exist in our body. It'll always exist in small trace amounts in our bodies. So we have to shut off our receptors to the small trace amounts to even get the same effect as them that actually stops growth. Though, I think nuking e2 and test is enough for DELAY

Ais literally widen the growth plate thus more bone growth potential, taking them is not a "no difference" thing
I dont get your point rn but I also forgot the original point

I don't disagree, I wasn't saying to 20s and 30s but I was saying prolonging it later than normal. Of course those guys are superior to us in that regard

I don't disagree here, but gh is the foundation of any heightmaxxing protocol. GHR agonism is very necessary for growth. Also 5cm is common not lucky

5cm is definetely lucky, most will not get above 3cm. The biggest part is that you have to start early enough which you cant just put as presumption, we gotta be staying realistic for this community and not just some ideal theoretical scenario

There isn't, they have no aetiology. This kind of reasoning is also fallacious because you're affirming the consequent.
"If they were normal they wouldn't have short stature" But you're affirming your consequent of saying they're abnormal because they're short when the claim that ought to be proven is whether that short stature is caused by an abnormality.

Short stature itself is an abnormality, its safe to assume there is an abnormal cause behind abnormal results

But that's the point, they have no verifiable medical issues

Not yet, that doesnt mean they dont in general lol

Yes? We already know all possible issues that lead to shortened height. Natural Gene inheritance (Not a medical issue, completely natural just unlucky), Gene mutations (Which are a medical issue that is verifiable) and Environmental causes like getting a tumor or something like that

We obviously dont in detail, it can just as likely be undiscovered causes.

That's the point, genetic causes aren't a medical issue it's just being unlucky. There's a difference between your natural genetic inheritance causing you to be short vs a gene mutation which scientists can easily verify by simply finding any issue in your body related to growth pathways.

You do know that height is polygenic right? Which also explains why siblings can have completely different heights. I'm 6'2.5 but my brother is projected to be 6ft. It simply means out of the millions of genes in the gene pool I inherited more genes that stimulate height growth than my brother did. This also explains why people with short parents can be tall and vice versa. Though, pretty rare of course

Never questioned how genetics work, it is just fully unreasonable to assume ISS is purely due to bad genetic combination and thats it
Theres already been reclassifications of up to over 50% of cases in ISS categories from ISS to a new, previously undiscovered cause, just taking an exclusion diagnosis as explanation is not acceptable for me

People with ISS simply didn't get the genetic makeup for height growth and that's the entire point of it being iss because there's no medical issue at hand. Pure gene inheritance bad luck. It is very very rare tho

I cut this off before replying, same thing as above

 

[darodiddler]

im too broke to afford erda bro do they ship to iraq

 

[Deleted member 341805]

i didnt even say that
estrogen speeds up general cell maturation which leads to hypertrophy before cell death

Ok interesting to know what pathways exactly are responsible

not by direct cell death but by tipping them over from progenitors to normal chondrocytes and preventing progenitor renewal

Not true, this is called differentiation. This is mediated by genes we've spoken about before in a previous convo, not e2. E2 just shortens the actual lifespan leading up to apoptosis in rz cells

Lmao local aromatisation isnt unknown lol but ais can overturn it regardless if you nuke enough
"Skyrockets" is such an exaggeration as well, usually a 50-100% increase
Do you have any studies on the hypersensitisation? I highly doubt that this is a major thing, the body doesnt adjust estrogen receptors like that

Ais literally widen the growth plate thus more bone growth potential, taking them is not a "no difference" thing
I dont get your point rn but I also forgot the original point

It's usually 60%+ increase. the variation is anastrozole that doesn't affect the nfl as much as letrozole

Hypersensitisation is just a normal physiological process lmao it's not a specific growth plate mechanic, denervation supersensitivity is an example of this

Can't really be bothered to respond to the rest brother I'm so tired

 

[Niebvll]

Not true, this is called differentiation. This is mediated by genes we've spoken about before in a previous convo, not e2. E2 just shortens the actual lifespan leading up to apoptosis in rz cells

Oh my God
Estrogen affects msc and progenitor differentiation thats the whole point
No its not 100% gene driven, transcription factors are also regulated by estrogen. Estrogen exposure also pushes cell-cycle exit even through teminal differentiation in proliferating chondrocytes. Most important is that it moves proliferating chondrocytes to their hyperthropic stage which is accompanied by matrix marker expression

It's usually 60%+ increase. the variation is anastrozole that doesn't affect the nfl as much as letrozole

Hypersensitisation is just a normal physiological process lmao it's not a specific growth plate mechanic, denervation supersensitivity is an example of this

Talking about specifically estrogen receptor hypersensitisation
Do you have anything to back that up in particular

Cant really be bothered to respond to the rest brother I'm so tired

Ok
Its 2am here I understand you