Heightmaxxing with Erdafinitib - summary of a study.

[Niebvll]

Your guess is just as good as mine mate

I dont have a guess
Its completely out of reason to believe that jump can be made naturally

 

[DominoDominus]

Paper: https://www.sciencedirect.com/science/article/pii/S2405844024069184#fig1

Will make this short, nothing fancy
Still rep because this is the greatest hopefuel you'll ever read.

These researchers have studied a causal relationship between the use of igf-1 and erdafinitibs inhibitory effects.
See this excerpt
Erdafinitib inhibits PI3K/AKT and MAPK/ERK signaling pathways.
During erdafinitib inhibition, IGF-1 can activate the PI3K/AKT pathway but not the MAPK/ERK pathway.

The researchers speculate this might be the cause for profound longitudinal growth seen in case studies of extreme growth spurts in cancer kids using erdafinitib.
This clearly suggests that the inhibition of MAPK/ERK and promotion of PI3K/AKT simultaneously causes rapid height gain / growth

Take a look at these figures.
Patient 1 started GH at 8yr to treat GHD (Growth hormone deficiency) And is treated with erdafinitib to treat a brain tumor. (mesencephalic glioma)
View attachment 5385363
So basically kid no. 1 only gets thick bones in his hand as a result.
pretty cheap for good height gains. (still sub 180 tho)

Another one:
Patient started 7mg/day erdafinitib at 15 yr and 4 months, Experienced many treatment pauses because of hyperphosphatemia and was using high doses of phosphate binding medicine to combat this.
5 months after treatment with erdafinitib starts, the dose is lowered to 5mg/day due to relocation and to lower treatment pauses.
Patient was on erdafinitib to treat cancer and has an "activating FGFR1 variant" (gene mutation that causes overexpression of FGFR1 gene)
View attachment 5385366
Kid goes from 10 cm/yr AGV, to 19 cm/yr AGV. Pretty insane.
However the consequences are concerning.



View attachment 5385398
Fig. 2. Abnormal rapid skeletal growth in a patient treated with erdafitinib, a pan-FGFR inhibitor.
A. X-ray of the cervical and thoracic spine before treatment (a, b, and c) and 9 months after treatment (d, e, f, g, h, and i) with erdafitinib showing the development of cervical lordosis and thoracic scoliosis.
B. MRI images (sagittal, T1 post- Contrast Fat saturation (FS) pulse sequences) of the cervical, thoracic, and lumbar spine demonstrating the development and progression of spinal deformities after commencing erdafitinib: a. Baseline; b. at 2 months; c. at 5 months; d. at 9 months; e. at 12 months which was 3 months after cessation of erdafitinib and after cervical deformity surgical correction.

In short: He needed surgery because his spine had crumpled into a C shape around the neck area.
You can see the spinal development if you look from left to right.

Bone analysis revealed that his bone density was equal to that of osteoporosis.
"0.6322 gm/sq.cm, which is −3.8 standard deviation below the mean value for the age-matched population and more than 2.5 standard deviations below the value for males at peak bone mass."
All hormonal markers (hgh, test, IGF-1 ETC..) Stayed within normal range during treatment. i.e. you don't need to blast gh when on ts.

It's pretty clear that erda is a potent and strong drug to increase height velocity. But the sideeffect profile is just as dire. Stick to a low dose and don't use it for longer than 6 months unless you want to look like a camel-necked freak...

I've got no more time saars. read the rest if you want to - it's a really interesting study.
Start from here: https://www.sciencedirect.com/science/article/pii/S2405844024069184#fig1:~:text=Bone age assessments had not been performed prior to or during erdafitinib therapy. At cessation of therapy, bone

dnr water

 

[Noriju]

I dont have a guess
Its completely out of reason to believe that jump can be made naturally

Could’ve been an outlier that keeps growing until 20, and has a high trailing AGV
You wouldn’t and couldn’t know.
Because we don’t have his identical twin to compare with.

 

[Niebvll]

Could’ve been an outlier that keeps growing until 20 and has a high trailing AGV

Comparing continue growing to jumping 50 percentiles at the end of your growth time frame

You wouldn’t and couldn’t know.

Im telling you the trajectory makes it obvious he wouldnt lmao

Because we don’t have his identical twin to compare with.

T

 

[Noriju]

Im telling you the trajectory makes it obvious he wouldnt lmao

No it definitely does. You’re acting like his trajectory would’ve just flatlined immediately if he didn’t take erda.
It’s a probability density function of outcomes.

 

[Niebvll]

No it definitely does. You’re acting like his trajectory would’ve just flatlined immediately if he didn’t take erda.

No Im not?
His trajectory was <25th pct, even with much luck it wouldve only gotten around the 25th pct maybe 30th as end result
It wouldve NEVER went to the 75th pct
How is that acting like it wouldve flatlined

It’s a probability density function of outcomes.

Gpt slop
Obvious shit that this never happens

 

[Noriju]

Gpt slop
Obvious shit that this never happens

No just finance wisdom nigga.
But allright. Lets just settle cause we obv cant agree and more discussion is fruitless

 

[Ahmed88]

I literally sent several below

Those weren't even remotely close to the claims, you made...

Yeah and I specifically said that this ISNT scientific discussion
It wasnt atleast
Because I discussion with you always leads to you being like muh gpt find me a way to stay right in this

Oh my god, nigga.

First of all, do you even know what a scientific discussion or debate is?

The MOMENT two people disagree over a factual scientific claim and argue about what the evidence shows, that’s a scientific discussion.

Even minor disagreements between researchers are considered scientific debates, we’re already welllllll beyond that.


Second, dismissing my arguments as gpt is just pussy behavior you’re still making claims completely out of your ass with no evidence.

If my arguments are supposedly just GPT and you still can’t refute them, doesn’t that make it even worse for you?


Either address the evidence or don’t.

“Muh u don't debate cause u use GPT” isn’t an excuse to run away from a debate.

The point is that I never acted like anyone has to accept it
I noted that it is logical and nothing more

That makes even less sense nigga????


If you’re not presenting it as evidence, then it’s just your personal inference not a fact.

So stop stating it as if those cohorts exist until you actually provide the data.


Plenty of things sound logically plausible in biology and turn out to be wrong once they’re tested. That’s exactly why we rely on empirical data instead of intuition, and that's thw reason why society exists and isn't governed by people who say, "muh logical".

Sure they could THEORETICALLY magically all have had some weird growth plate thing going on
And MAGICALLY only during the time of treatment, thats why they didnt have abnormal effects outside of the treatment
And all studies just completely ignored it and didnt note it
Or they just were completely normal growth plate wise.

Oh my fucking god NIGGER.


I NEVER said they had some mysterious growth plate disorder. I literally said they HAVE FUCKING GROWTH IMPAIRMENT SO THEY ARENT NORMAL?!?!?!


That’s LITTERALLY stated in YOUR OWN BULLSHIT PAPER


So in simple 3 year old terms= no, you can not remove a sickness and replace it with another, growth impairment means they are not normal healthy kids!!!

Already talked about this
Classifying that as catch up growth is completely retarded, the growth velocity is a result of the inctease in proliferating chondrocytes, which also increases the differentiating ones and its a cycle like that
The only way that this wasnt an addition in FAH would be if Erda depleted the rz like HGH does when adding velocity
But Erda doesnt do this and instead make chondrocytes proliferate beyond their natural limit. So on the baseline of natural growth, you get the addition of growth caused by delayed senescence
How do you not see that this is FAH increase

WHAT IS IT WITH YOU, AND SAYING RANDOM BULLSHIT WITHOUT EVIDENCE


Everything you just said about reserve zone depletion, delayed senescence, bla bla, is NOT clinical evidence that final genetic adult height increases (and even more funny, is the fact that most of what you said, is still random bullshit, without evidence)


The only endpoint these papers actually measured is growth velocity during treatment. They did not measure adult height, they did not compare achieved height to genetic target height, and they DIDN'T EVEN show that patients ultimately exceeded the height they would have reached without treatment.

The point is that FGFR1 doesnt affect growth

What????

Lmao nigga, what the fuck is this stupid ass claim, did you just forget the thousands of growth diseases, linked to FGFR1, like
osteoglophonic dysplasia?????

Genuinely, had enough of this shit.

Alredy showed an example with completely normal levels otherwise
Correlation of "prior brain surgery" to the growth plate?

No, you didn't

 

[Niebvll]

Those weren't even remotely close to the claims, you made...

Oh my god, nigga.

First of all, do you even know what a scientific discussion or debate is?

The MOMENT two people disagree over a factual scientific claim and argue about what the evidence shows, that’s a scientific discussion.

Even minor disagreements between researchers are considered scientific debates, we’re already welllllll beyond that.


Second, dismissing my arguments as gpt is just pussy behavior you’re still making claims completely out of your ass with no evidence.

If my arguments are supposedly just GPT and you still can’t refute them, doesn’t that make it even worse for you?


Either address the evidence or don’t.

“Muh u don't debate cause u use GPT” isn’t an excuse to run away from a debate.




That makes even less sense nigga????


If you’re not presenting it as evidence, then it’s just your personal inference not a fact.

So stop stating it as if those cohorts exist until you actually provide the data.


Plenty of things sound logically plausible in biology and turn out to be wrong once they’re tested. That’s exactly why we rely on empirical data instead of intuition, and that's thw reason why society exists and isn't governed by people who say, "muh logical".



Oh my fucking god NIGGER.


I NEVER said they had some mysterious growth plate disorder. I literally said they HAVE FUCKING GROWTH IMPAIRMENT SO THEY ARENT NORMAL?!?!?!


That’s LITTERALLY stated in YOUR OWN BULLSHIT PAPER


So in simple 3 year old terms= no, you can not remove a sickness and replace it with another, growth impairment means they are not normal healthy kids!!!






WHAT IS IT WITH YOU, AND SAYING RANDOM BULLSHIT WITHOUT EVIDENCE


Everything you just said about reserve zone depletion, delayed senescence, bla bla, is NOT clinical evidence that final genetic adult height increases (and even more funny, is the fact that most of what you said, is still random bullshit, without evidence)


The only endpoint these papers actually measured is growth velocity during treatment. They did not measure adult height, they did not compare achieved height to genetic target height, and they DIDN'T EVEN show that patients ultimately exceeded the height they would have reached without treatment.



What????

Lmao nigga, what the fuck is this stupid ass claim, did you just forget the thousands of growth diseases, linked to FGFR1, like
osteoglophonic dysplasia?????

Genuinely, had enough of this shit.




No, you didn't

DNR might read later

 

[Ahmed88]

The evidence presented in the study is all you need.
The growth velocity increase in patient 2 increased his FAH. Though not explicitly stated by the researchers, this is definitively true.

Lets take a hypothetical example:
A boy, 15 years old, with a bone age equal to 15 years old.
At 15 y and all the way to 18y we’ll give him an AGV of 3cm/yr cause he’s deficient or something.
At 18y we’ll say that his bones fuse and all growth stops permanantly (still hypothetical)

Now under normal circumstances our patient would grow to have +9 cm of height. (In our thought experiment)

Let’s say that for his last year of growth he receives a growth boosting drig that increases his growth up to 6cm/yr.
Under these circumstances he would then have gained +12cm of height.

our thought experiment is unrealistic and doesn’t really mean anything.
But when you look at patient 2 in the study provided by me and Niebvll you’ll see that he has the exact same parametres applied to him as the patient in our thought experiment. (Albeit with different AGV and Height and age. Different numbers, same situation)

How could this not have increased FAH?
Patient 2 was however very young and it could’ve been puberty…

Yeah, but that’s exactly the issue????

The patient was DEFICIENT so restoring normal growth conditions will OBVIOUSLY allow him to catch up toward his genetic potential.

That does not prove that the treatment increased genetic height beyond what a normal non deficient person would have reached. A deficient child has "missing" growth to recover, so giving a treatment that corrects the deficit can OBVIOUSLY increase final height compared to the untreated deficient state.


But if you take a child who is already growing normally with normal growth plate function and give the same treatment, does it add extra height beyond their natural potential?

No.
We simply do not have the evidence for that, and even theoretically increased velocity alone would not demonstrate increased final height.

A normal child already has functioning growth shit. And the body has alot of regulatory limits.

DNR might read later

 

[Niebvll]

Yeah, but that’s exactly the issue????

The patient was DEFICIENT so restoring normal growth conditions will OBVIOUSLY allow him to catch up toward his genetic potential.

That does not prove that the treatment increased genetic height beyond what a normal non deficient person would have reached. A deficient child has "missing" growth to recover, so giving a treatment that corrects the deficit can OBVIOUSLY increase final height compared to the untreated deficient state.


But if you take a child who is already growing normally with normal growth plate function and give the same treatment, does it add extra height beyond their natural potential?

No.
We simply do not have the evidence for that, and even theoretically increased velocity alone would not demonstrate increased final height.

A normal child already has functioning growth shit. And the body has alot of regulatory limits.

Again DNR
I just dont have the time to answer

 

[Niebvll]

Those weren't even remotely close to the claims, you made...

Oh my god, nigga.

First of all, do you even know what a scientific discussion or debate is?

The MOMENT two people disagree over a factual scientific claim and argue about what the evidence shows, that’s a scientific discussion.

Which is why I wanted to pull out you dumbass

Even minor disagreements between researchers are considered scientific debates, we’re already welllllll beyond that.

Im not a researcher
Neither are you I would suppose
Not in the sense as we'd know it from actually qualified people

Second, dismissing my arguments as gpt is just pussy behavior you’re still making claims completely out of your ass with no evidence.

I didnt dismiss anything, I didnt even mention any of your arguments
I told you why I dont like talking to you

If my arguments are supposedly just GPT and you still can’t refute them, doesn’t that make it even worse for you?

Again never even said that
You like to put words in my mouth huh

That makes even less sense nigga????


If you’re not presenting it as evidence, then it’s just your personal inference not a fact.

Yeah exactly
I was just NOTING it

So stop stating it as if those cohorts exist until you actually provide the data.

This isnt about the cohorts lol i presented those your point was that me noting something was "just logical" wasnt enough for you
Not about the cohorts

Plenty of things sound logically plausible in biology and turn out to be wrong once they’re tested. That’s exactly why we rely on empirical data instead of intuition, and that's thw reason why society exists and isn't governed by people who say, "muh logical".

Yeah thats why I DIDNT use it as evidence for anything you dumbfuck

Oh my fucking god NIGGER.

I NEVER said they had some mysterious growth plate disorder. I literally said they HAVE FUCKING GROWTH IMPAIRMENT SO THEY ARENT NORMAL?!?!?!

They dont

That’s LITTERALLY stated in YOUR OWN BULLSHIT PAPER

Only in one and that was just to prove the cohorts exist lol

So in simple 3 year old terms= no, you can not remove a sickness and replace it with another, growth impairment means they are not normal healthy kids!!!

Never said that

WHAT IS IT WITH YOU, AND SAYING RANDOM BULLSHIT WITHOUT EVIDENCE

Everything you just said about reserve zone depletion, delayed senescence, bla bla, is NOT clinical evidence that final genetic adult height increases (and even more funny, is the fact that most of what you said, is still random bullshit, without evidence)

The only endpoint these papers actually measured is growth velocity during treatment. They did not measure adult height, they did not compare achieved height to genetic target height, and they DIDN'T EVEN show that patients ultimately exceeded the height they would have reached without treatment.

Oh my fucking God allah strike you down
OBVIOUSLY theyre not gonna count chondrocyte levels in a cancer study
Its LITERALLY how FGFR3 inhibition works biochemically
"Muh no empirical evidence its just talk" is so fucking retarded
Yes theres no evidence as in a study but again its fucking obvious
You didnt even try to refute it, of course you dont have to but it wouldve been interesting

What????

Lmao nigga, what the fuck is this stupid ass claim, did you just forget the thousands of growth diseases, linked to FGFR1, like
osteoglophonic dysplasia?????

Dont act like thats something everyone knows and "forgets", i know exactly you had to look growth impairment up
My point was that the alterations og fgfr1 in the cohorts didnt matter for growth and didn impair it
YET AGAIN you ignored the case study just saying "no you didnt" when its right there

 

[Ahmed88]

Which is why I wanted to pull out you dumbass

Could of worded it, less homosexually.

Im not a researcher
Neither are you I would suppose
Not in the sense as we'd know it from actually qualified people

"Researcher” is a broad term.

I didnt dismiss anything, I didnt even mention any of your arguments
I told you why I dont like talking to you

You sound like my fucking ex,

"Muh muh i don't like talking to you"

Again never even said that
You like to put words in my mouth huh

It's a fucking question, dumbass geez.

Yeah exactly
I was just NOTING it

Are you on your period?

This isnt about the cohorts lol i presented those your point was that me noting something was "just logical" wasnt enough for you
Not about the cohorts

It's about both.

Yeah thats why I DIDNT use it as evidence for anything you dumbfuck

Never claimed you did...

They dont

Let me fucking get this straight, you think the kids in YOUR paper don't have growth impairments?

Are you like clinically retarded?

Only in one and that was just to prove the cohorts exist lol

Your studies consisted of, a retarded stidy on growth impaired kids, a paywalled study and a broken link.

Never said that

Never claimed you did, just wanted to explain it to you, because you have the understanding of a autistic 3 year old.

Oh my fucking God allah strike you down
OBVIOUSLY theyre not gonna count chondrocyte levels in a cancer study
Its LITERALLY how FGFR3 inhibition works biochemically
"Muh no empirical evidence its just talk" is so fucking retarded
Yes theres no evidence as in a study but again its fucking obvious
You didnt even try to refute it, of course you dont have to but it wouldve been interesting

Then don't use it as fucking evidence?

Jesus christ

Dont act like thats something everyone knows and "forgets", i know exactly you had to look growth impairment up

No, i didn't

My point was that the alterations og fgfr1 in the cohorts didnt matter for growth and didn impair it

It did?

YET AGAIN you ignored the case study just saying "no you didnt" when its right there

Broken link, mate for the 100th time


Almost burned my chicken because of you.

 

[Niebvll]

Could of worded it, less homosexually.

Enemies to lovers yaoi?

You sound like my fucking ex,

Maybe I am

Are you on your period?

Yes

Let me fucking get this straight, you think the kids in YOUR paper don't have growth impairments?

In one

Your studies consisted of, a retarded stidy on growth impaired kids, a paywalled study and a broken link.

The link worked fine for me

Broken link, mate for the 100th time

Its not fucking broken I literally checked it out right before sending to make sure i got the right one

Almost burned my chicken because of you.

Im gonna burn your balls nigga

 

[Noriju]

Maybe I am

Yes

In one

The link worked fine for me

Its not fucking broken I literally checked it out right before sending to make sure i got the right one


Im gonna burn your balls nigga

Could of worded it, less homosexually.

"Researcher” is a broad term.

You sound like my fucking ex,

"Muh muh i don't like talking to you"

It's a fucking question, dumbass geez.

Are you on your period?

It's about both.


Never claimed you did...


Let me fucking get this straight, you think the kids in YOUR paper don't have growth impairments?

Are you like clinically retarded?


Your studies consisted of, a retarded stidy on growth impaired kids, a paywalled study and a broken link.


Never claimed you did, just wanted to explain it to you, because you have the understanding of a autistic 3 year old.

Then don't use it as fucking evidence?

Jesus christ

No, i didn't

It did?

Broken link, mate for the 100th time


Almost burned my chicken because of you.

Listen you fucking faggots if you’re gonna argue like a married couple go get a room

let’s stick to the matter at hand and stop the para-argument.

Both patients in this study which is the same study in my original post – have conditions that could impair regular growth.
Patient N° 1. Has a mesencephalic glioma. Which is located at the “midbrain portion of the brainstem”
ChatGPT (paid model) says:

I think it would be reasonable to discount the glioma having an effect on patient 1’s growth axis as it is explicitly cited to be unlikely.
The direct cause is however likely to be due to the cancer therapy they received between 5-8 years of age. Which is also what the researchers’ paper attributes it to.

Patient N° 2. Has a “FGFR3-overexpressing ependymoma”.
An ependymoma is a rare type of tumor that starts in the cells of the brain or the spinal cord.
Needless to say the kid has an overexpression of his FGFR3 kinase.

It is hard to dispute @Ahmed88 ‘s claims in both cases because he is objectively correct.


I’d like to however say that — with all the knowledge we have about growth pathways, it should be a walk in the park to keep plates open.

What i mean is that we know what causes the plates to close, how to keep them open and how to accelerate the growth, we have absolute control over the height of a person (provided rz cells aren’t depleted)
Even in the study they stopped gh + erda treatment and used test to close the plates.
It is self evident from this passage alone that they could’ve decided to keep the plates open and let him grow taller.

What do you think?
@Niebvll @Ahmed88

 

[Niebvll]

Listen you fucking faggots if you’re gonna argue like a married couple go get a room

let’s stick to the matter at hand and stop the para-argument.

Both patients in this study which is the same study in my original post – have conditions that could impair regular growth.
Patient N° 1. Has a mesencephalic glioma. Which is located at the “midbrain portion of the brainstem”
ChatGPT (paid model) says:
View attachment 5453684
I think it would be reasonable to discount the glioma having an effect on patient 1’s growth axis as it is explicitly cited to be unlikely.
The direct cause is however likely to be due to the cancer therapy they received between 5-8 years of age. Which is also what the researchers’ paper attributes it to.

Patient N° 2. Has a “FGFR3-overexpressing ependymoma”.
An ependymoma is a rare type of tumor that starts in the cells of the brain or the spinal cord.
Needless to say the kid has an overexpression of his FGFR3 kinase.

It is hard to dispute @Ahmed88 ‘s claims in both cases because he is objectively correct.


I’d like to however say that — with all the knowledge we have about growth pathways, it should be a walk in the park to keep plates open.

What i mean is that we know what causes the plates to close, how to keep them open and how to accelerate the growth, we have absolute control over the height of a person (provided rz cells aren’t depleted)
Even in the study they stopped gh + erda treatment and used test to close the plates.
It is self evident from this passage alone that they could’ve decided to keep the plates open and let him grow taller.

What do you think?
@Niebvll @Ahmed88

DNR
@Ahmed88 lets get a room bae