Yeah body halo is fine. Height it’s overWell 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
I read it, just didn't have anything relevant to add to it
I figured
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?
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.
@ICL said it perfectly
Lmk what you think. I feel like I rambled a bunch of nothing
Zargo made a good thread on this. il see if I can find it
Tag me when you find it
so as we all know
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.
haha have you even looked at what people are dosing for heightmaxxing vs oncology?? That should debunk this entire threadI'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).Slipped capital femoral epiphyses: a major on target adverse event associated with FGFR tyrosine kinase inhibitors in pediatric patients - PMC
FGFR tyrosine kinase inhibitors (TKIs) are increasingly being used off label in pediatrics. Long term safety data is limited, and serious toxicities unique to pediatrics may emerge. In a retrospective analysis of patients<18 years of age with ...pmc.ncbi.nlm.nih.gov
https://pmc.ncbi.nlm.nih.gov/articles/PMC11152661/#:~:text=e-,rdafitinib had to be,15-year-old male).,-Growth
View attachment 5196212Infigratinib, a Selective FGFR1-3 Tyrosine Kinase Inhibitor, Alters Dentoalveolar Development at High Doses - PMC
Fibroblast Growth Factor Receptor-3 (FGFR3) gain-of-function mutations are linked to achondroplasia. Infigratinib, a FGFR1-3 tyrosine kinase inhibitor, improves skeletal growth in an achondroplasia mouse model. FGFs and their receptors have critical ...
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
5 month of fgfr inhibitiom caused multiple complications for 2 of the individuals.
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.
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
Partially right I will make A thread about this.
Nigha stop stealing what I was gonna say in my thread
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
This is js about bodyweight, nothin about h1bac, blood glucose tho
Good point. Here is another one for diabetes.
The preference should be to look into health, personally, since I am tall I do not need these compounds.
Will assess in a momentGood 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.
Likely tho
cscf and skeletal kyphosis is bone health brah
3/7 is still a very high chance
