framepilled
@hightierchad on tt
- Joined
- Nov 6, 2025
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holy cope nigga keep injecting your shitty peptides and pray to gandy youll grow from 5ft1 manlet to 6´7 jfl how does that retard have 1k posts- 3'11 indian
I’m laughing so hard I’m actually cryingnigga tryna click bait on the forums:kek:
im already 7'2holy cope nigga keep injecting your shitty peptides and pray to gandy youll grow from 5ft1 manlet to 6´7 jfl how does that retard have 1k posts
start posting youtube videos and make titles like those and give very surface level information thats a fuckin money glitchI’m laughing so hard I’m actually crying
Thanks
I used to do it actually I got a video with a good amount of views once on some Roblox thingy when I was like 12start posting youtube videos and make titles like those and give very surface level information thats a fuckin money glitch
I used to do it actually I got a video with a good amount of views once on some Roblox thingy when I was like 12
But nowadays it would be like “INJECTING PEPTIDES AT 3 AM *GONE WRONG* *GONE SEXUAL* *GONE PARANORMAL* *COPS CALLED* *MUST WATCH* *HEIGHT GAINED*”





growing above genetic boundaries is impossible in every single aspect.the ONLY way to grow past your genetic boundaries is too prolong your height growth window.
Its more like a distance to a brick wall, if u remove that wall u can go further. Obviusly most ways to prolong the epiphyseal plate ossification are experimental and unstudied by scientist. But through my personal research I belive there are ways to exceed the genetic hieght capgrowing above genetic boundaries is impossible in every single aspect.
you can see it as the genetic boundary being 100% thus meaning you cant achieve more than 100% because thats not possible in the genetic aspect.
But very good thread for the rest, we need more people like you![]()
thats not exceeding genetic potential tho but yeah that is correct for gaining height.Its more like a distance to a brick wall, if u remove that wall u can go further
im not as educated in thyroid hormones but wouldnt supplementing t4 be a bit to overkill since the other compounds + life style changes result in higher thyroid levels in general?t4-
Thyroid hormone primes tissues to respond to GH. It increases the expression of GH receptors and boosts the liver's ability to produce IGF-1-the real growth driver downstream of GH. If thyroid hormone is low, GH may be released normally, but the body is basically deaf to it. When T4 is too high, GH and IGF-1 can be high, but the system burns so hot that the net effect becomes chaotic: growth plate exhaustion, acceleration of bone turnover, and metabolic frenzy.
T4 is ideally used later in a cycle as over time hgh can damage the thyroid. Mb for not specifyingim not as educated in thyroid hormones but wouldnt supplementing t4 be a bit to overkill since the other compounds + life style changes result in higher thyroid levels in general?
thus to much thyroid hormones could lead to sooner epiphyseal closure by speeding up bone age.
again im not to educated in the topic of thyroid hormones but still.
+ thread idea: How to optimize bone age.
faster bone maturation = faster fusion = less longitudal growth
slower bone maturation = slower fusion = more longitudal growth
https://looksmax.gg/threads/tamoxifen-semi-advanced.9192/im not as educated in thyroid hormones but wouldnt supplementing t4 be a bit to overkill since the other compounds + life style changes result in higher thyroid levels in general?
thus to much thyroid hormones could lead to sooner epiphyseal closure by speeding up bone age.
again im not to educated in the topic of thyroid hormones but still.
+ thread idea: How to optimize bone age.
faster bone maturation = faster fusion = less longitudal growth
slower bone maturation = slower fusion = more longitudal growth
good threadFirst of all, the ONLY way to grow past your genetic boundaries is too prolong your height growth window. The way to do this is to delay you epiphyseal plates from ossificating (the procces of cartilage turning into bone) the way this happens is when chondrocytes ( the main cell in cartilage) proliferate, they then hypertrophy causing the calcification of the area. This lays down a foundation for the drivers of that ossifcation (osteoclast and osteoblast) to start working.
But daddy ? How can i stop this?
dont worry my child, these stacks ive formulated will include compunds that do just that and ill explain how
This first stack is comprised of four compund
Hgh
aromasin
abaloparatide
t4
hgh-
everyone knows abt hgh so i wont do much explaing. Exougenous hgh follows the bodies natural process (also why it mogs gh secretagogues and increlex). The main takeaway is that it follows the process of igf signaling also producing adequate igfpb and other important allies.
aromasin-
aromasin is the absolute best aromatase inhibitor. Its not harsh so it doest immediatly crash levels. CRUCIAL- never take high dose ai. It may seem like a good idea, less e2= less fusure . But at the cost of mental retardation and stunted deveolpment and a high potential of plate fractures. Micro dosing 6.25mg eod should be taken
abaloparatide (DYOR)-
Ive included abaloparatide here for two reason.
It grows bone- as its a pthrp its main goal is to grow bone (prescribed for osteoporosis) meaning a couple extra cm could be expected
It can delay plate fusure (unproven) - theoretically it can
Slow proliferating chondrocyte maturation
Slow the chondrocytes reaching that hypertrophic state (only if taken early in puberty)
t4-
Thyroid hormone primes tissues to respond to GH. It increases the expression of GH receptors and boosts the liver's ability to produce IGF-1-the real growth driver downstream of GH. If thyroid hormone is low, GH may be released normally, but the body is basically deaf to it. When T4 is too high, GH and IGF-1 can be high, but the system burns so hot that the net effect becomes chaotic: growth plate exhaustion, acceleration of bone turnover, and metabolic frenzy.Hgh
aromasin
insulin
CNP analogs
Hgh and aromsin explained
insulin-
It’s one of the strongest IGF-1 supporters because the liver needs adequate insulin signaling to make IGF-1 in response to GH. Low insulin states (fasting, uncontrolled diabetes) mean GH goes up, but IGF-1 goes down. lots of signal but no growth. High insulin states (post-meal, insulin therapy) make IGF-1 output more robust, which is one reason puberty, when insulin is often tr higher, becomes a prime time for growth spurts
Cnp analogs-
CNP maintains the functionality of the growth plate by keeping chondrocytes in their proliferative state and acting against FGFR3 signalling, which normally limits the growth of the bone. The CNP analogues, like vosoritide, extend this effect by having a longer half-life. In achondroplasia, such analogues increase the velocity of growth by strengthening the proliferative signals in the growth plate. They do not directly delay the normal epiphyseal closure but are theoretically discussed since they are capable of prolonging the proliferative phase of chondrocytes.
I could probably come up with more but I cba and I have work in an hour.
Gonna do some more research into calcium blockades but I didn't include them bc they seem stupid asf
Much love bhais please correct me of im wrong and leave your own suggestions
Obv these can be swapped around js listing the conpounds really
9Dino
Mandy
Ogre_cel
where's fgfr3 inhibitors?First of all, the ONLY way to grow past your genetic boundaries is too prolong your height growth window. The way to do this is to delay you epiphyseal plates from ossificating (the procces of cartilage turning into bone) the way this happens is when chondrocytes ( the main cell in cartilage) proliferate, they then hypertrophy causing the calcification of the area. This lays down a foundation for the drivers of that ossifcation (osteoclast and osteoblast) to start working.
But daddy ? How can i stop this?
dont worry my child, these stacks ive formulated will include compunds that do just that and ill explain how
This first stack is comprised of four compund
Hgh
aromasin
abaloparatide
t4
hgh-
everyone knows abt hgh so i wont do much explaing. Exougenous hgh follows the bodies natural process (also why it mogs gh secretagogues and increlex). The main takeaway is that it follows the process of igf signaling also producing adequate igfpb and other important allies.
aromasin-
aromasin is the absolute best aromatase inhibitor. Its not harsh so it doest immediatly crash levels. CRUCIAL- never take high dose ai. It may seem like a good idea, less e2= less fusure . But at the cost of mental retardation and stunted deveolpment and a high potential of plate fractures. Micro dosing 6.25mg eod should be taken
abaloparatide (DYOR)-
Ive included abaloparatide here for two reason.
It grows bone- as its a pthrp its main goal is to grow bone (prescribed for osteoporosis) meaning a couple extra cm could be expected
It can delay plate fusure (unproven) - theoretically it can
Slow proliferating chondrocyte maturation
Slow the chondrocytes reaching that hypertrophic state (only if taken early in puberty)
t4-
Thyroid hormone primes tissues to respond to GH. It increases the expression of GH receptors and boosts the liver's ability to produce IGF-1-the real growth driver downstream of GH. If thyroid hormone is low, GH may be released normally, but the body is basically deaf to it. When T4 is too high, GH and IGF-1 can be high, but the system burns so hot that the net effect becomes chaotic: growth plate exhaustion, acceleration of bone turnover, and metabolic frenzy.Hgh
aromasin
insulin
CNP analogs
Hgh and aromsin explained
insulin-
It’s one of the strongest IGF-1 supporters because the liver needs adequate insulin signaling to make IGF-1 in response to GH. Low insulin states (fasting, uncontrolled diabetes) mean GH goes up, but IGF-1 goes down. lots of signal but no growth. High insulin states (post-meal, insulin therapy) make IGF-1 output more robust, which is one reason puberty, when insulin is often tr higher, becomes a prime time for growth spurts
Cnp analogs-
CNP maintains the functionality of the growth plate by keeping chondrocytes in their proliferative state and acting against FGFR3 signalling, which normally limits the growth of the bone. The CNP analogues, like vosoritide, extend this effect by having a longer half-life. In achondroplasia, such analogues increase the velocity of growth by strengthening the proliferative signals in the growth plate. They do not directly delay the normal epiphyseal closure but are theoretically discussed since they are capable of prolonging the proliferative phase of chondrocytes.
I could probably come up with more but I cba and I have work in an hour.
Gonna do some more research into calcium blockades but I didn't include them bc they seem stupid asf
Much love bhais please correct me of im wrong and leave your own suggestions
Obv these can be swapped around js listing the conpounds really
9Dino
Mandy
Ogre_cel
Gonna redo this soon with morewhere's fgfr3 inhibitors?


