Quick caution for all FGFR-inhibitor users, high risk of deformity

Well originally I was only taking GH and realised it was mainly cope so I added test so now my main goal is a body halo lmao
I love roshidere tho w pfp :ogre:
Yeah body halo is fine. Height it’s over
 
  • +1
Reactions: Sub5kang and ICL
Yeah body halo is fine.
I figured
Height it’s over
Why so? Test aromatisation into estrogen? I'm getting my 4th week bloodwork and will take ai if needed
My plates are still open I've grown an inch three months on GH but it might just be my natural growth since it never really slowed down
 
  • +1
  • Love it
Reactions: Paul.jnxy and ICL
Why so? Test aromatisation into estrogen? I'm getting my 4th week bloodwork and will take ai if needed
Prolly talking about local growth plate estrogen synthesis discourse @Paul.jnxy can you confirm?
 
  • +1
Reactions: Paul.jnxy and Sub5kang
Impressively, one individual went from 170cm to 200cm in just 150 weeks, which is notable.
Come On What GIF by MOODMAN
 
  • JFL
Reactions: ICL and Paul.jnxy
Prolly talking about local growth plate estrogen synthesis discourse @Paul.jnxy can you confirm?
Can't really lower local E2 only serum so it's inevitable on a test base
 
  • +1
Reactions: ICL
Reta does not have any negative effects on Growth hormone at the receptor or JAK2/STAT5 but it can blunt some growth promoting effects. Mainly by reducing appetite (sorry my teacher walked in on my group) Im not gonna explain how Reta works. It’s pretty self explanatory. I won’t go into the pathways in depth as the only real thing I wanted to say is that it reduces nutrient availability by nuking appetite. Yet it can have positive effects such as The glucagon receptor agonism which may mildly help hepatic IGF1 production. That’s why I recommend low dosing at 1-2 mg max a week. Becouse Reta keeps BG in much healthier levels and reducing metabolic stress. I prefer it over straight insulin firstly becouse I’m not that informed on lantus or trebisa plus body builders health problems are almost always a result of exo insulin.
 
  • +1
Reactions: ICL
Prolly talking about local growth plate estrogen synthesis discourse @Paul.jnxy can you confirm?
Yes exactly. :feelshah:
 
  • +1
Reactions: ICL
I figured

Why so? Test aromatisation into estrogen? I'm getting my 4th week bloodwork and will take ai if needed
My plates are still open I've grown an inch three months on GH but it might just be my natural growth since it never really slowed down
@ICL said it perfectly
 
  • +1
Reactions: Sub5kang and ICL
Reta does not have any negative effects on Growth hormone at the receptor or JAK2/STAT5 but it can blunt some growth promoting effects. Mainly by reducing appetite (sorry my teacher walked in on my group) Im not gonna explain how Reta works. It’s pretty self explanatory. I won’t go into the pathways in depth as the only real thing I wanted to say is that it reduces nutrient availability by nuking appetite. Yet it can have positive effects such as The glucagon receptor agonism which may mildly help hepatic IGF1 production. That’s why I recommend low dosing at 1-2 mg max a week. Becouse Reta keeps BG in much healthier levels and reducing metabolic stress. I prefer it over straight insulin firstly becouse I’m not that informed on lantus or trebisa plus body builders health problems are almost always a result of exo insulin.
Lmk what you think. I feel like I rambled a bunch of nothing :forcedsmile:
 
  • +1
Reactions: ICL
Prolly talking about local growth plate estrogen synthesis discourse @Paul.jnxy can you confirm?
Can you elaborate
 
  • +1
Reactions: Paul.jnxy and ICL
Can you elaborate
so as we all know

cholestrol is the main molecule used for steroidegenisis. for instance, the testosterone in your body is synthesized from testosterone, the rest such as estrogen and DHT are metabolites that require enzymes for conversion.

Now here's where it gets a bit trickier, as the growth plates have their own steroidegenisis mechanism, in which it has aromatase, testosterone, it's metabolites, etc. These cannot be inhibited as they are inside the growth plate, not the bloodstream, where the body absorbs the aromatase inhibitors, hence you cannot inhibit them; this is due to the fact that growth plate's
 
  • +1
Reactions: Kojo, Paul.jnxy and Sub5kang
Reta does not have any negative effects on Growth hormone at the receptor or JAK2/STAT5 but it can blunt some growth promoting effects. Mainly by reducing appetite (sorry my teacher walked in on my group) Im not gonna explain how Reta works. It’s pretty self explanatory. I won’t go into the pathways in depth as the only real thing I wanted to say is that it reduces nutrient availability by nuking appetite. Yet it can have positive effects such as The glucagon receptor agonism which may mildly help hepatic IGF1 production. That’s why I recommend low dosing at 1-2 mg max a week. Becouse Reta keeps BG in much healthier levels and reducing metabolic stress. I prefer it over straight insulin firstly becouse I’m not that informed on lantus or trebisa plus body builders health problems are almost always a result of exo insulin.
Wouldnt you inhibit growth due to lack of caloric intake as well as macronutrient intake, that would be suboptimal. Using insulin or reta is also not gonna fix your insulin desensitivity, only the blood glucose, since GH directly affects sensitivity and slin will just make your cells more resistant.
 
  • +1
Reactions: Paul.jnxy
I've been noticing many threads on taking FGFR(3) inhibitors recently, and I think many of these users have barely done any research;

At first, I felt like there are only studies and case studies for those with fgfr3 over-expression to inhibit it to normal (hence taller height), I'm not sure how making it underexpressed would yield a beneficial effect on height (an "worth it" effect) which is desirable or significant

Besides, FGFR3 is a brake for growth, it exists for a reason as it stops cartilage from becoming into bone. Inhibiting it to lower-than-normal makes me skeptic about possible deformation, or side effects. You'd be growing uncontrollably, unideal to your cells which are not perfect and will easily mess up.


Just look at children who used FGFR3 inhibitors, 42% of them develop SCFE, considered a medical emergency.

Erdafitinib had to be discontinued due to the patient's unusual rapid growth over the 9 months of therapy, severe kyphoscoliosis, and spinal cord compression with cervical myelopathy. The patient grew a total of 14.3 cm, or at an annualized growth of 19.06 cm (normal growth is ∼10 cm per year for a 15-year-old male).
https://pmc.ncbi.nlm.nih.gov/articles/PMC11152661/#:~:text=e-,rdafitinib had to be,15-year-old male).,-Growth
View attachment 5196212
You may argue that this was a small group size of 7 patients, but, SCFE is an extremely rare condition, 3/7 which means this cannot be coincidence.

Impressively, one individual went from 170cm to 200cm in just 150 weeks, which is notable.

I assume you will not be using these in short cycles, as we've seen 50 weeks resulting in SCFE yet achieving 13cm of height

Another instance, those with congenital FGFR UNDERexpression usually grow tall but have deformities such as kyphosis, permanently bent fingers, etc; this is called CATSHL syndrome which makes you unusually tall while causing loss of function and making bones too long.

Is it really worth the height growth it gives you?

They also look similar to those who are marfanoid;
View attachment 5196227
so i'm not sure how practical it would be inhibiting it and if the stature gained from this is beneficial or desirable.

I'd like to see anyone that makes an FGFR3 thread countering these questions, which I'm looking forward to see if he'll bring something new to the table and address the dilemma's, especially the fact that some users contemplate Pan-FGFR inhibitors which would be egregious (case studies show fgfr1/2/3/4 inhibited yet caused a deformity, what would a pan-fgfr inhibitor do?)

@Vireon @anondude @N1kolai @81xa @chang cypionate
haha have you even looked at what people are dosing for heightmaxxing vs oncology?? That should debunk this entire thread
 
  • Hmm...
Reactions: Paul.jnxy
haha have you even looked at what people are dosing for heightmaxxing vs oncology?? That should debunk this entire thread
5 month of fgfr inhibitiom caused multiple complications for 2 of the individuals.

I don't think dose is far off, it was not mentioned
 
Wouldnt you inhibit growth due to lack of caloric intake as well as macronutrient intake, that would be suboptimal. Using insulin or reta is also not gonna fix your insulin desensitivity, only the blood glucose, since GH directly affects sensitivity and slin will just make your cells more resistant.
Yes this is the biggest issue (nutrient intake) yet you mentioned a dose of 1.mg/kg/ per week which is ridiculously high. Such a hugh dose their is no point in Reta. Even tho at a reasonably high dose (12 ius ed) I still noticed a hugeee apetite increase like atleast double then before.

https://pubmed.ncbi.nlm.nih.gov/37326322/

reta significantly improved markers of insulin sensitivity. Plus like you said exo insulin doesent cover the issue either (insulin sensitivity) you are just adding more insulin which can work temporarily but not long term.

Tbf I’d be willing to trade being slightly sub optimal then being diabetic
 
  • +1
Reactions: ICL
5 month of fgfr inhibitiom caused multiple complications for 2 of the individuals.

I don't think dose is far off, it was not mentioned
But yeah your thread is pretty good, thats why i want more people to look into CNP analogs which offer a much safer inhibition of fgfr3

The only thing i have to say is there is a window where you can partially inhibit FGFR3 without taking it out, and get extra growth without hitting CATSHL which is what i assume most users try to due. Ofc its only speculative as you can't get the data exactly

But from my own anecdotes and others experience it's good, many users still take the trade off of being partly paralyzed for 4+ inches
 
  • +1
  • Hmm...
Reactions: ICL and Paul.jnxy
haha have you even looked at what people are dosing for heightmaxxing vs oncology?? That should debunk this entire thread
Partially right I will make A thread about this.
 
But yeah your thread is pretty good, thats why i want more people to look into CNP analogs which offer a much safer inhibition of fgfr3

The only thing i have to say is there is a window where you can partially inhibit FGFR3 without taking it out, and get extra growth without hitting CATSHL which is what i assume most users try to due. Ofc its only speculative as you can't get the data exactly

But from my own anecdotes and others experience it's good, many users still take the trade off of being partly paralyzed for 4+ inches
Nigha stop stealing what I was gonna say in my thread :forcedsmile:
 
  • +1
  • JFL
Reactions: ICL and alexbrown8384
Yes this is the biggest issue (nutrient intake) yet you mentioned a dose of 1.mg/kg/ per week which is ridiculously high. Such a hugh dose their is no point in Reta. Even tho at a reasonably high dose (12 ius ed) I still noticed a hugeee apetite increase like atleast double then before.

https://pubmed.ncbi.nlm.nih.gov/37326322/

reta significantly improved markers of insulin sensitivity. Plus like you said exo insulin doesent cover the issue either (insulin sensitivity) you are just adding more insulin which can work temporarily but not long term.

Tbf I’d be willing to trade being slightly sub optimal then being diabetic
I linked the wrong paper https://pubmed.ncbi.nlm.nih.gov/37366315/

This should be it mb
 
  • +1
Reactions: ICL
Yes this is the biggest issue (nutrient intake) yet you mentioned a dose of 1.mg/kg/ per week which is ridiculously high. Such a hugh dose their is no point in Reta. Even tho at a reasonably high dose (12 ius ed) I still noticed a hugeee apetite increase like atleast double then before.

https://pubmed.ncbi.nlm.nih.gov/37326322/

reta significantly improved markers of insulin sensitivity. Plus like you said exo insulin doesent cover the issue either (insulin sensitivity) you are just adding more insulin which can work temporarily but not long term.

Tbf I’d be willing to trade being slightly sub optimal then being diabetic
It's insulin sensitivity markers, which is h1bac and blood glucose, these don't really say anything as you can still have good markers with less sensitivity (i.e. low carb diet, though the cells are still getting more resistant as the liver doesnt stop peoducing glucose and the kidneys must produce more) plus that study is irrelevant, it talks about TRT
 
  • +1
Reactions: Paul.jnxy
It's insulin sensitivity markers, which is h1bac and blood glucose, these don't really say anything as you can still have good markers with less sensitivity (i.e. low carb diet, though the cells are still getting more resistant as the liver doesnt stop peoducing glucose and the kidneys must produce more) plus that study is irrelevant, it talks about TRT
I linked the wrong trial nigha mb check my replies. Yes you are right but what else are you gonna do?
 
  • +1
Reactions: ICL
so as we all know

cholestrol is the main molecule used for steroidegenisis. for instance, the testosterone in your body is synthesized from testosterone, the rest such as estrogen and DHT are metabolites that require enzymes for conversion.

Now here's where it gets a bit trickier, as the growth plates have their own steroidegenisis mechanism, in which it has aromatase, testosterone, it's metabolites, etc. These cannot be inhibited as they are inside the growth plate, not the bloodstream, where the body absorbs the aromatase inhibitors, hence you cannot inhibit them; this is due to the fact that growth plate's
Yeah true
The only way to mitigate this is to go to a trt dose or lower though neither of which I want to do :Comfy:
185cm isn't enough but Ill bank on a miracle here
 
Last edited:
  • +1
Reactions: ICL
This is js about bodyweight, nothin about h1bac, blood glucose tho
Good point. Here is another one for diabetes.


Rosenstock J, et al.
Retatrutide, a GIP, GLP-1 and glucagon receptor agonist, for people with type 2 diabetes: a randomised, double-blind, placebo- and active-controlled, parallel-group, phase 2 trial

If I recall correctly
In people with type 2 diabetes, reta produced dose-dependent reductions in HA1c of up to −2.02% at 24 weeks (12 mg dose).
Plus It also significantly lowered fasting plasma glucose.
 
Last edited:
  • +1
Reactions: ICL
But yeah your thread is pretty good, thats why i want more people to look into CNP analogs which offer a much safer inhibition of fgfr3

The only thing i have to say is there is a window where you can partially inhibit FGFR3 without taking it out, and get extra growth without hitting CATSHL which is what i assume most users try to due. Ofc its only speculative as you can't get the data exactly

But from my own anecdotes and others experience it's good, many users still take the trade off of being partly paralyzed for 4+ inches
The preference should be to look into health, personally, since I am tall I do not need these compounds.

Besides, many individuals on this forum neglect health. But you'll keep neglecting health until it neglects you and you either die an excrutiating death or require assistance to take a shit
 
Good point. Here is another one for diabetes.


Rosenstock J, et al.
Retatrutide, a GIP, GLP-1 and glucagon receptor agonist, for people with type 2 diabetes: a randomised, double-blind, placebo- and active-controlled, parallel-group, phase 2 trial

If I recall correctly
In people with type 2 diabetes, reta produced dose-dependent reductions in HA1c of up to −2.02% at 24 weeks (12 mg dose).
Plus It also significantly lowered fasting plasma glucose.
Will assess in a moment
 
  • +1
Reactions: Paul.jnxy
dnr can be taken safely if youre not sub 100iq
 
  • +1
  • JFL
Reactions: Paul.jnxy, alexbrown8384 and ICL
The preference should be to look into health, personally, since I am tall I do not need these compounds.

Besides, many individuals on this forum neglect health. But you'll keep neglecting health until it neglects you and you either die an excrutiating death or require assistance to take a shit
Okay but the sides of fgfr3 that are hard to avoid are mostly aesthethics based, not really anything health
 
  • +1
Reactions: ICL and Paul.jnxy
so as we all know

cholestrol is the main molecule used for steroidegenisis. for instance, the testosterone in your body is synthesized from testosterone, the rest such as estrogen and DHT are metabolites that require enzymes for conversion.

Now here's where it gets a bit trickier, as the growth plates have their own steroidegenisis mechanism, in which it has aromatase, testosterone, it's metabolites, etc. These cannot be inhibited as they are inside the growth plate, not the bloodstream, where the body absorbs the aromatase inhibitors, hence you cannot inhibit them; this is due to the fact that growth plate's
Well said.
 
  • +1
Reactions: ICL
main molecule used for steroidegenisis. for instance, the testosterone in your body is synthesized from
Testosterone is synthesised from cholesteol* not itself
 
read every atom. Mirin :love:
 
  • +1
Reactions: ICL
Testosterone is synthesised from cholesteol* not itself
I dont know why it cut off.

Theres lots of cartillage before you reach bone so most likely the blood (endocrine) aromatase inhibitors wont reach it and I believe the same with selective local agonists like tomafexine/raloxefine/endofexine

@Sub5kang
 
  • +1
Reactions: Sub5kang
Okay but the sides of fgfr3 that are hard to avoid are mostly aesthethics based, not really anything health
cscf and skeletal kyphosis is bone health brah :feelsokman:
Plus I doubt you wanna look marfanoid lol
 
  • +1
Reactions: alexbrown8384
3/7 is still a very high chance
Just because that was the outcome in one study or wtv doesnt mean thats the chance for all ways of taking it
Sybau with your fear mongering bro its natural selection either way
 
  • So Sad
Reactions: ICL
I dont know why it cut off.

Theres lots of cartillage before you reach bone so most likely the blood (endocrine) aromatase inhibitors wont reach it and I believe the same with selective local agonists like tomafexine/raloxefine/endofexine

@Sub5kang
What do you recommend fo linear vertical height growth then? My plates are open however I'm 18
 
  • +1
Reactions: ICL

Similar threads

victor801
Replies
2
Views
22
stnr74
stnr74
nwed
Replies
12
Views
145
nwed
nwed
Mathikxksss
Replies
2
Views
22
Mathikxksss
Mathikxksss
bratex2213
Replies
0
Views
51
bratex2213
bratex2213
Orka
Replies
16
Views
115
Starborn
Starborn

Users who are viewing this thread

  • Heyychico
Back
Top