Why HGH is cope and will NOT work for you!!!! (HGH USERS GTFIH!!!)

A lot of People continue to believe that healthy children who lack growth hormone deficiency will experience height increases through HGH injections.

It won’t.

Why?

Let’s get into this


1. How Growth Hormone Actually Works

Human growth hormone (HGH), also called somatotropin, is a hormone that the pituitary gland, which is about the size of a pea and found at the base of your brain, makes and releases

Its main job?

Human growth hormone triggers growth in almost every tissue and organ in your body. It’s mostly known for its growth-promoting effect on cartilage and bone, especially in puberty. Cells in cartilage called chondrocytes and cells in bones called osteoblasts, receive signals from HGH to increase replication and thus allow for growth in size.


2. What the Studies ACTUALLY Show

People often cite studies claiming “HGH increases height.” Let’s clarify what these studies actually studied.

Most research involves children who are GH-deficient children who cannot produce normal levels of GH due to medical conditions. Examples:




VERY Important: These studies are on children who are medically short due to GH deficiency, and do NOT produce enough HGH not normal kids. The effect is correcting a deficiency, not surpassing genetic potential.



Some other studies explore ISS (Idiopathic Short Stature):


B-B-But ISS Children Grew Taller why can’t i?

Let’s clarify: ISS children are not short simply because of genetics. ISS is defined as short stature without a known cause, that INCLUDES GENETICS and many children diagnosed as having ISS have partial GH insensitivity (Evidence: Idiopathic short stature)

Bottom line: if you are within normal growth ranges and are not diagnosed as ISS, these studies do NOT apply to you.


3. Why HGH does NOT work for healthy normal children with PROOF

For children with normal growth hormone (GH) levels, exogenous GH administration cannot increase final adult height. Here’s why:



  • GH does not create new growth potential.
    The growth plates in long bones experience linear growth through their epiphyseal plates. The genetic code determines both number and proliferative capacity of chondrocytes present at these growth plates. GH promotes the growth of chondrocytes and their development into mature cells, yet it cannot boost these cells' genetic-based growth capacity beyond their existing limits.
  • GH cannot override genetic determinants of stature.
    Height is a polygenic trait which multiple genetic loci control its development. The treatment of GH-sufficient children with GH therapy does not affect their gene expression or the genetic skeletal structure which their genome contains.
  • Endocrine feedback loops limit excessive growth signaling.
    The GH–IGF-1 axis is tightly regulated:
    • Elevated serum IGF-1 inhibits hypothalamic GHRH secretion and stimulates somatostatin release, reducing endogenous GH production.
    • Peripheral tissues exhibit receptor-mediated resistance to supra-physiologic GH and IGF-1 concentrations, limiting further cellular proliferation.
  • Physiologic ceiling effect.
    In GH-sufficient children, endogenous GH already saturates IGF-1 production and downstream growth plate signaling. Exogenous GH cannot enhance this process; the system is operating at maximal physiological capacity. Clinical evidence and studies supports these claims: children with normal GH levels do not achieve increased adult height despite high-dose GH administration
EVIDENCE AND STUDIES ON NORMAL KIDS:

Final height after growth hormone therapy in non-growth-hormone-deficient children with short stature - PubMed

No Improvement of Adult Height in Non-growth Hormone (GH) Deficient Short Children with GH Treatment - PMC

https://www.sciencedirect.com/science/article/abs/pii/S002234769470192X

No Improvement of Adult Height in Non-growth Hormone (GH) Deficient Short Children with GH Treatment - PubMed



Analogy (for conceptual clarity): Imagine a plant with genetically fixed maximum height. Adequate water and nutrients allow it to reach its potential. Adding more water beyond what it can physiologically use does not make it grow taller; it may even disrupt normal growth processes.

Summary: GH in healthy, non-deficient children simply optimizes a process that is already at capacity. There is no latent or “hidden” height to unlock the endocrine system and growth plates are already functioning at their maximum biological limits.


4. Why people think it works!!!!!!

This is where most people get fooled and start to think it’s working.

HGH can TEMPORARILY increase growth rate (as seen in the studies). You grow faster for a period, but it does NOT increase final adult height. Your genetic height ceiling remains THE SAME. In the end you will grow the same without HGH.


5. What you actually get and are paying for: Side Effects

Injecting ratpiss HGH from Chinese labs is retarded and will NOT work all you are paying for are potential risks including:

  • Insulin resistance
  • Increased risk of type 2 diabetes
  • Fluid retention and edema
  • Joint pain
  • Carpal tunnel syndrome
  • Hip growth plate injury
  • Benign intracranial hypertension (severe headaches and vision changes)
  • Abnormal IGF‑1 elevations
  • Theoretical increased cancer risk due to chronic IGF‑1 stimulation
​

6. Summary

HGH only works in:

  • Documented GH deficiency
  • Select ISS cases


HGH does NOT:

  • Make normal kids taller than their genetics allow
  • Extend growth plates
  • Increase final adult height
  • Create height out of nowhere
If you do not have a diagnosed condition, you will not gain any adult height you will only get side effects.

The truth?: There is no hack around genetics. Injecting Chinese ratpiss HGH is expensive, unnecessary, and retarded.



Biology does not care about your retarded cope.
 
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urs said:
^ if thats true (according to you) if your pairing it with an ai theres no doubt your gonna grow taller
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No, ive explained this multiple times in this thread, e2 is needed for growth
 
Ahmed88 said:
No, ive explained this multiple times in this thread, e2 is needed for growth
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Then how u explain aromatase deficiency? And again, how do you explain gigantism? Literally like none of ur arguments in this entire post and all of ur replies here are valid, provide some arguments that prove before u claim shit please
 
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megapro981 said:
Then how u explain aromatase deficiency? And again, how do you explain gigantism? Literally like none of ur arguments in this entire post and all of ur replies here are valid, provide some arguments that prove before u claim shit please
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GH may accelerate growth and allow attainment of the upper end of genetically predetermined height, but it does not and cannot surpass the hard ceiling set by polygenic skeletal architecture. Aromatase inhibitors extend the duration of epiphyseal closure because they decrease estrogen levels, yet estrogen remains vital for chondrocyte development and growth together with the control of essential genes which include CTX5, Sox9, Runx2, and extracellular matrix modulators. Blocking estrogen disrupts these gene networks and cartilage maturation, producing at best a marginal temporal extension of growth, not a fundamental increase in growth potential.
 
Ahmed88 said:
GH may accelerate growth and allow attainment of the upper end of genetically predetermined height, but it does not and cannot surpass the hard ceiling set by polygenic skeletal architecture. Aromatase inhibitors extend the duration of epiphyseal closure because they decrease estrogen levels, yet estrogen remains vital for chondrocyte development and growth together with the control of essential genes which include CTX5, Sox9, Runx2, and extracellular matrix modulators. Blocking estrogen disrupts these gene networks and cartilage maturation, producing at best a marginal temporal extension of growth, not a fundamental increase in growth potential.
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Yet again I see 0 actual reason provided as to why it wouldnt work, and 0 reason as to why gigantism and aromatase deficiency work but not achieving almost the exact same conditions but with exogenous compounds instead.

Sure height is polygenic but there is still 0 reason why additional gh wouldnt increase final height. Theres many mechanisms gh/igf1 has directly on the growth plate tissue that would easily lead to not only higher growth velocity but also higher net final growth. Even though the differentiation and division potential of the resting zone is generally considered predetermined by genetics it doesnt mean at all that what happens in the other zones of the plate wouldnt affect final height as what happens there isnt as close to predetermined at all. To prove me wrong that gigantism from a pituitary tumor isnt proof of my claims u need to provide proof or at least some strong mechanistic link to why that tumor would override this "polygenic hard ceiling" ur talking about and why exogenously injected highly dosed rhgh wouldnt do the same.

And yes ofc estrogen affects a lot in the plates, thats just a general fact not an argument against my point in the slightest. Its still clear that having less or even extremely low levels of estrogen as seen in aromatase deficiency does in fact lead to a higher final adult height. And people with aromatase deficiency have far lower levels of e2 than what people would reach with ais yet their cartilage remains intact and functional. Lower levels of estrogen wouldnt only delay closure of the plates but also delay senescence of the resting zone progenitors. Ur arguments are flawed and ur dodging my points.
 
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megapro981 said:
Sure height is polygenic but there is still 0 reason why additional gh wouldnt increase final height. Theres many mechanisms gh/igf1 has directly on the growth plate tissue that would easily lead to not only higher growth velocity but also higher net final growth. Even though the differentiation and division potential of the resting zone is generally considered predetermined by genetics it doesnt mean at all that what happens in the other zones of the plate wouldnt affect final height as what happens there isnt as close to predetermined at all. To prove me wrong that gigantism from a pituitary tumor isnt proof of my claims u need to provide proof or at least some strong mechanistic link to why that tumor would override this "polygenic hard ceiling" ur talking about and why exogenously injected highly dosed rhgh wouldnt do the same
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Pharmacologic administration of exogenous Growth hormone in pediatric individuals with an intact somatotropic axis does not produce a meaningful increase in attained adult stature. Although GH augments both hepatic and autocrine/paracrine synthesis of Insulin-like growth factor 1, which acts on the epiphyseal growth plate to enhance chondrocyte mitotic activity, hypertrophic enlargement, and extracellular matrix deposition, these actions primarily modify the kinetics of longitudinal growth rather than the total amount of growth achievable before physeal involution.

The epiphyseal cartilage is governed by an intrinsic developmental program in which the pool of resting zone progenitor chondrocytes progressively declines through replicative exhaustion and functional maturation. This process, commonly described as Growth plate senescence, establishes an upper limit on cumulative longitudinal expansion independent of short-term hormonal stimulation. Supraphysiologic GH–IGF-1 signaling can transiently increase proliferative throughput within the proliferative zone; however, such acceleration simultaneously advances the temporal progression of growth plate maturation and depletion of progenitor reserves. Consequently, increases in childhood growth velocity are offset by earlier exhaustion of the proliferative capacity of the physis, resulting in no substantive change in final adult height.

Endocrine disorders characterized by sustained GH hypersecretion, represent pathologic states involving continuous and markedly elevated circulating GH and IGF-1 concentrations, frequently accompanied by broader disturbances in pituitary regulation. These conditions therefore do not reflect the physiologic response to exogenous GH exposure in otherwise healthy children.

Moreover, hormone concentrations required to meaningfully perturb intrinsic growth plate regulatory dynamics would necessitate prolonged supraphysiologic exposure, a scenario that creates multiple side effects (such as mentioned above).

Accordingly, in children with normal endocrine function, exogenous GH administration does not increase the ultimate adult height attained, but instead alters the temporal dynamics of growth, producing transient increases in growth velocity without expanding the genetically and developmentally constrained total longitudinal growth potential of the skeleton. (this is backed by scientific studies not someone called megapro981)

Rep me
 
doesnt it affect facial bones???
 
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Ahmed88 said:
No, ive explained this multiple times in this thread, e2 is needed for growth
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e2 is needed but too much or normal amounts lead to your plates being closed sooner nigga, thats why you lower your e2 to a certain range. with a ai
 
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Ahmed88 said:
Pharmacologic administration of exogenous Growth hormone in pediatric individuals with an intact somatotropic axis does not produce a meaningful increase in attained adult stature. Although GH augments both hepatic and autocrine/paracrine synthesis of Insulin-like growth factor 1, which acts on the epiphyseal growth plate to enhance chondrocyte mitotic activity, hypertrophic enlargement, and extracellular matrix deposition, these actions primarily modify the kinetics of longitudinal growth rather than the total amount of growth achievable before physeal involution.

The epiphyseal cartilage is governed by an intrinsic developmental program in which the pool of resting zone progenitor chondrocytes progressively declines through replicative exhaustion and functional maturation. This process, commonly described as Growth plate senescence, establishes an upper limit on cumulative longitudinal expansion independent of short-term hormonal stimulation. Supraphysiologic GH–IGF-1 signaling can transiently increase proliferative throughput within the proliferative zone; however, such acceleration simultaneously advances the temporal progression of growth plate maturation and depletion of progenitor reserves. Consequently, increases in childhood growth velocity are offset by earlier exhaustion of the proliferative capacity of the physis, resulting in no substantive change in final adult height.

Endocrine disorders characterized by sustained GH hypersecretion, represent pathologic states involving continuous and markedly elevated circulating GH and IGF-1 concentrations, frequently accompanied by broader disturbances in pituitary regulation. These conditions therefore do not reflect the physiologic response to exogenous GH exposure in otherwise healthy children.

Moreover, hormone concentrations required to meaningfully perturb intrinsic growth plate regulatory dynamics would necessitate prolonged supraphysiologic exposure, a scenario that creates multiple side effects (such as mentioned above).

Accordingly, in children with normal endocrine function, exogenous GH administration does not increase the ultimate adult height attained, but instead alters the temporal dynamics of growth, producing transient increases in growth velocity without expanding the genetically and developmentally constrained total longitudinal growth potential of the skeleton. (this is backed by scientific studies not someone called megapro981)

Rep me
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My name on a looksmaxxing forum is completely irrelevant to what im saying ahmed88, Im trying to have a productive argument with u and thats it. Nothing im saying is contradicted by studies, much of it is supported, and some of it have no direct studies on it but we can draw easy and very strong mechanical links enough to be seen as proof. Ur using studies on ghd or iss which almost always uses very insufficient dosages to mimic gigantism. Both ISS and GHD studies shouldnt be perfectly used as a proxy for healthy people when it comes to taking exogenous rhgh for height, gigantism is a better proxy as they are healthy and a normal height a lot of times and a lot of times the gigantism is only caused by a pituitary adenoma secreting gh and has no effect on any other pituitary axis. And since u mentioned that in children with normal endocrine function meaning ISS studies, these obviously cant be used for loads of reasons, they clearly have genetic traits limiting growth, and sometimes even directly on ghr and its downstream effects, as seen here where some ISS patient had to receive 346mcg/kg/day of rhgh just to get into +2 SDS igf1 levels, upper range of normal.

I literally already debunked what u said about progenitor cells running out, u dont need to have more progenitor cells to achieve more growth, gh/igf achieves it through multiple direct pathways like PI3K/Akt and MAPK/ERK, it increases the profileration rate as well as keeps them profilerating longer in the profilerative zone, as well as decreasing apoptosis and hypertrophic cell size, it also increases production of ecm components such as collagen X, aggrecan and other proteoglycans in the hypertrophic zones, all of means that the progenitor cells doesnt determine a hard ceiling on growth. Amount of chondrocyte cells, size of chondrocyte cells, and how much space the ecm takes up before the cells transdifferentiate or die and get converted to bone cells all can be changed after the resting zone in the other zones and that part is highly respondent to factors like gh/igf1 for example. Also when it comes to senescence the main driver of this is estrogen signaling, which is where aromatase inhibitors come in, they would directly delay senescence. Sure periods of extremely high gh and igf1 may speed up the velocity by a lot and cause quicker senescence maybe, resting zone progenitor exhaustion and closure but that doesnt mean that the growth cant outpace the closure or through these other effects I talked about still yield a higher final adult height, and again gigantism is proof of this idk what u dont understand about gigantism. Maybe I need to make it clearer? Gigantism in a lot of cases is caused ONLY by the changes in gh release, increasing gh release by an very big amount and changing the secretion patterns. So if this works for height which it does, then it must also be true that injecting high amounts of rhgh exogenously which would achieve the exact same conditions will produce the same effect, aka a lot of height gains.

I already sent this but ig u didnt see? It very clearly shows that in a very big amount of gigantism cases the gh secreting adenoma solely affects gh release and has 0 noticable effect on any other pituitary hormone, therefore the claim on broader pituitary disturbances is irrelevant. And no shit that someone will get side effects doing this, thats up to the person if they would want to risk the side effects as with any other compound, Im simply arguing that it works, especially if u know how to do it right which isnt hard at all. Ill go over every other claim u made for why gigantism wouldnt work the same as well. U claimed once that the feedback mechanisms prevent this, very easily no they dont. The only 2 relevant feedback mechanisms are the hpg axis which we will obv ignore as we rely on exogenous rhgh, and the other one is the peripheral tissues cells feedback mechanisms like socs proteins, these are also not valid as they are as strong as in gigantism cases as if were injecting exogenous gh, the pituitary tumor wouldnt affect those peripheral tissue feedback mechanisms at all and in gigantism they arent powerful enough to completely block the downstream signal at all, only blunt it a bit. And u also claimed that gigantism leads to states where gh levels are constantly very elevated, which is literally easily replicated by using rhgh, just split dosage if u want to make it more continous than it already is. Now all ur arguments on why gigantism wouldnt be the same as exogenous rhgh are debunked? Any more I didnt mention?

Stop circling ur arguments and points all the time, even when theyre irrelevant and have already been debunked.

It has to be clear ur just copy pasting chatgpt atp right?
 
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just a chud said:
doesnt it affect facial bones???
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Yes, its almost the exact same thing Im arguing with him for but with acromegaly instead of gigantism, as its proven that it has that effect in acromegaly its also proven it would have that same effect in someone injecting highly dosed exogenous rhgh. Whether the aesthetic changes on facial bones and soft tissue will benefit u is subjective and is dependent on a lot of factors like genetics and baseline for example.
 
megapro981 said:
My name on a looksmaxxing forum is completely irrelevant to what im saying ahmed88, Im trying to have a productive argument with u and thats it. Nothing im saying is contradicted by studies, much of it is supported, and some of it have no direct studies on it but we can draw easy and very strong mechanical links enough to be seen as proof. Ur using studies on ghd or iss which almost always uses very insufficient dosages to mimic gigantism. Both ISS and GHD studies shouldnt be perfectly used as a proxy for healthy people when it comes to taking exogenous rhgh for height, gigantism is a better proxy as they are healthy and a normal height a lot of times and a lot of times the gigantism is only caused by a pituitary adenoma secreting gh and has no effect on any other pituitary axis. And since u mentioned that in children with normal endocrine function meaning ISS studies, these obviously cant be used for loads of reasons, they clearly have genetic traits limiting growth, and sometimes even directly on ghr and its downstream effects, as seen here where some ISS patient had to receive 346mcg/kg/day of rhgh just to get into +2 SDS igf1 levels, upper range of normal.

I literally already debunked what u said about progenitor cells running out, u dont need to have more progenitor cells to achieve more growth, gh/igf achieves it through multiple direct pathways like PI3K/Akt and MAPK/ERK, it increases the profileration rate as well as keeps them profilerating longer in the profilerative zone, as well as decreasing apoptosis and hypertrophic cell size, it also increases production of ecm components such as collagen X, aggrecan and other proteoglycans in the hypertrophic zones, all of means that the progenitor cells doesnt determine a hard ceiling on growth. Amount of chondrocyte cells, size of chondrocyte cells, and how much space the ecm takes up before the cells transdifferentiate or die and get converted to bone cells all can be changed after the resting zone in the other zones and that part is highly respondent to factors like gh/igf1 for example. Also when it comes to senescence the main driver of this is estrogen signaling, which is where aromatase inhibitors come in, they would directly delay senescence. Sure periods of extremely high gh and igf1 may speed up the velocity by a lot and cause quicker senescence maybe, resting zone progenitor exhaustion and closure but that doesnt mean that the growth cant outpace the closure or through these other effects I talked about still yield a higher final adult height, and again gigantism is proof of this idk what u dont understand about gigantism. Maybe I need to make it clearer? Gigantism in a lot of cases is caused ONLY by the changes in gh release, increasing gh release by an very big amount and changing the secretion patterns. So if this works for height which it does, then it must also be true that injecting high amounts of rhgh exogenously which would achieve the exact same conditions will produce the same effect, aka a lot of height gains.

I already sent this but ig u didnt see? It very clearly shows that in a very big amount of gigantism cases the gh secreting adenoma solely affects gh release and has 0 noticable effect on any other pituitary hormone, therefore the claim on broader pituitary disturbances is irrelevant. And no shit that someone will get side effects doing this, thats up to the person if they would want to risk the side effects as with any other compound, Im simply arguing that it works, especially if u know how to do it right which isnt hard at all. Ill go over every other claim u made for why gigantism wouldnt work the same as well. U claimed once that the feedback mechanisms prevent this, very easily no they dont. The only 2 relevant feedback mechanisms are the hpg axis which we will obv ignore as we rely on exogenous rhgh, and the other one is the peripheral tissues cells feedback mechanisms like socs proteins, these are also not valid as they are as strong as in gigantism cases as if were injecting exogenous gh, the pituitary tumor wouldnt affect those peripheral tissue feedback mechanisms at all and in gigantism they arent powerful enough to completely block the downstream signal at all, only blunt it a bit. And u also claimed that gigantism leads to states where gh levels are constantly very elevated, which is literally easily replicated by using rhgh, just split dosage if u want to make it more continous than it already is. Now all ur arguments on why gigantism wouldnt be the same as exogenous rhgh are debunked? Any more I didnt mention?

Stop circling ur arguments and points all the time, even when theyre irrelevant and have already been debunked.

It has to be clear ur just copy pasting chatgpt atp right?
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You didn't debunk any of my arguments, why are you trying to mimic gigantism? You claim that ,,you can safely mimic gigantism if you know what ur doing" is just utterly wrong and ridiculous.

Your proposition assumes that increasing systemic concentration of growth hormone inevitably produces proportional enhancement of terminal skeletal length. This interpretation reflects a mechanistic reduction of developmental endocrinology. Although signaling downstream of Growth hormone and its effector mediator Insulin-like growth factor 1 promotes mitotic activation of chondrocytes within epiphyseal cartilage, macroscopic growth is not governed exclusively by signaling amplitude. Skeletal development is regulated through coordinated temporal programming, genetic architecture, and microenvironmental niche stability rather than isolated intracellular cascade intensity.

The growth plate functions as a stratified cellular production interface in which longitudinal bone extension depends upon lineage propagation originating from a relatively dormant progenitor compartment situated in the resting zone. This region demonstrates biological characteristics analogous to stem-cell maintenance systems, where cumulative replicative stress and molecular aging progressively diminish functional output across developmental progression. The phenomenon designated as Growth plate senescence describes the gradual decline of proliferative competence within physeal cartilage. While excessive GH/IGF signaling may transiently elevate chondrocyte division frequency inside proliferative columns, such acceleration tends to advance maturation kinetics, promoting premature hypertrophic transition and subsequent ossification rather than expanding total osteochondral elongation capacity.

The argument that progenitor cell abundance is not a fundamental constraint on longitudinal growth fails to account for hierarchical lineage dependency inherent in endochondral ossification. Even if signaling pathways including PI3K/Akt and MAPK/ERK enhance cellular survival probability, mitotic activation, and extracellular matrix deposition, these molecular effects operate primarily on cells already committed to differentiation pathways. Structural bone elongation requires continuous recruitment of undifferentiated precursor populations capable of generating additional chondrocyte columns. Modulation of hypertrophic cellular volume, collagen X synthesis, aggrecan distribution, or matrix spatial occupancy cannot generate new developmental lineages once upstream progenitor reservoirs experience attrition.

The comparison with Pituitary gigantism is not scientifically valid as definitive proof of pharmacologic growth hormone efficacy in normative physiology. Gigantism represents a pathological endocrine state characterized by persistent dysregulated somatotroph hormone secretion during critical developmental intervals. The substantial variability of final stature among gigantism patients indicates that GH concentration alone does not determine skeletal endpoint length, as genomic determinants regulating morphogenesis, physeal maturation timing, and systemic endocrine integration remain dominant modulators of height phenotype.

The hypothesis that recombinant GH administration can replicate tumor-mediated hormone exposure through dosage escalation or injection frequency modification neglects nonlinear endocrine pharmacokinetics. Receptor regulatory desensitization, intracellular inhibitory mediators such as suppressor of cytokine signaling proteins, and multi-axis hormonal feedback networks impose adaptive constraints on somatotropic signaling. Biological regulatory systems function under complex homeostatic modulation rather than simple linear amplification relationships.

Moreover, longitudinal clinical evidence does not demonstrate substantial augmentation of adult stature in individuals possessing intact somatotropic axis function who receive recombinant GH therapy. Investigations involving treatment outcomes in Idiopathic short stature and related non-deficient pediatric populations reveal only marginal modification of final skeletal height despite prolonged pharmacological exposure. These observations indicate that enhancement of growth velocity does not necessarily translate into expansion of developmental endpoint size.

The conjecture that accelerated proliferative activity can consistently exceed physeal maturation progression is unsupported by histomorphological developmental data. In many biological growth systems, increased mitogenic signaling is accompanied by proportional acceleration of differentiation and tissue maturation, thereby preserving overall developmental trajectory rather than extending ultimate structural dimensions.

Im not the one repeating myself, its quite the opposite actually.


(Rep me back nigga 😢)
 
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Ahmed88 said:
A lot of People continue to believe that healthy children who lack growth hormone deficiency will experience height increases through HGH injections.

It won’t.

Why?

Let’s get into this


1. How Growth Hormone Actually Works

Human growth hormone (HGH), also called somatotropin, is a hormone that the pituitary gland, which is about the size of a pea and found at the base of your brain, makes and releases

Its main job?

Human growth hormone triggers growth in almost every tissue and organ in your body. It’s mostly known for its growth-promoting effect on cartilage and bone, especially in puberty. Cells in cartilage called chondrocytes and cells in bones called osteoblasts, receive signals from HGH to increase replication and thus allow for growth in size.


2. What the Studies ACTUALLY Show

People often cite studies claiming “HGH increases height.” Let’s clarify what these studies actually studied.

Most research involves children who are GH-deficient children who cannot produce normal levels of GH due to medical conditions. Examples:




VERY Important: These studies are on children who are medically short due to GH deficiency, and do NOT produce enough HGH not normal kids. The effect is correcting a deficiency, not surpassing genetic potential.



Some other studies explore ISS (Idiopathic Short Stature):


B-B-But ISS Children Grew Taller why can’t i?

Let’s clarify: ISS children are not short simply because of genetics. ISS is defined as short stature without a known cause, that INCLUDES GENETICS and many children diagnosed as having ISS have partial GH insensitivity (Evidence: Idiopathic short stature)

Bottom line: if you are within normal growth ranges and are not diagnosed as ISS, these studies do NOT apply to you.


3. Why HGH does NOT work for healthy normal children with PROOF

For children with normal growth hormone (GH) levels, exogenous GH administration cannot increase final adult height. Here’s why:



  • GH does not create new growth potential.
    The growth plates in long bones experience linear growth through their epiphyseal plates. The genetic code determines both number and proliferative capacity of chondrocytes present at these growth plates. GH promotes the growth of chondrocytes and their development into mature cells, yet it cannot boost these cells' genetic-based growth capacity beyond their existing limits.
  • GH cannot override genetic determinants of stature.
    Height is a polygenic trait which multiple genetic loci control its development. The treatment of GH-sufficient children with GH therapy does not affect their gene expression or the genetic skeletal structure which their genome contains.
  • Endocrine feedback loops limit excessive growth signaling.
    The GH–IGF-1 axis is tightly regulated:
    • Elevated serum IGF-1 inhibits hypothalamic GHRH secretion and stimulates somatostatin release, reducing endogenous GH production.
    • Peripheral tissues exhibit receptor-mediated resistance to supra-physiologic GH and IGF-1 concentrations, limiting further cellular proliferation.
  • Physiologic ceiling effect.
    In GH-sufficient children, endogenous GH already saturates IGF-1 production and downstream growth plate signaling. Exogenous GH cannot enhance this process; the system is operating at maximal physiological capacity. Clinical evidence and studies supports these claims: children with normal GH levels do not achieve increased adult height despite high-dose GH administration
EVIDENCE AND STUDIES ON NORMAL KIDS:

Final height after growth hormone therapy in non-growth-hormone-deficient children with short stature - PubMed

No Improvement of Adult Height in Non-growth Hormone (GH) Deficient Short Children with GH Treatment - PMC

https://www.sciencedirect.com/science/article/abs/pii/S002234769470192X

No Improvement of Adult Height in Non-growth Hormone (GH) Deficient Short Children with GH Treatment - PubMed



Analogy (for conceptual clarity): Imagine a plant with genetically fixed maximum height. Adequate water and nutrients allow it to reach its potential. Adding more water beyond what it can physiologically use does not make it grow taller; it may even disrupt normal growth processes.

Summary: GH in healthy, non-deficient children simply optimizes a process that is already at capacity. There is no latent or “hidden” height to unlock the endocrine system and growth plates are already functioning at their maximum biological limits.


4. Why people think it works!!!!!!

This is where most people get fooled and start to think it’s working.

HGH can TEMPORARILY increase growth rate (as seen in the studies). You grow faster for a period, but it does NOT increase final adult height. Your genetic height ceiling remains THE SAME. In the end you will grow the same without HGH.


5. What you actually get and are paying for: Side Effects

Injecting ratpiss HGH from Chinese labs is retarded and will NOT work all you are paying for are potential risks including:

  • Insulin resistance
  • Increased risk of type 2 diabetes
  • Fluid retention and edema
  • Joint pain
  • Carpal tunnel syndrome
  • Hip growth plate injury
  • Benign intracranial hypertension (severe headaches and vision changes)
  • Abnormal IGF‑1 elevations
  • Theoretical increased cancer risk due to chronic IGF‑1 stimulation
​

6. Summary

HGH only works in:

  • Documented GH deficiency
  • Select ISS cases


HGH does NOT:

  • Make normal kids taller than their genetics allow
  • Extend growth plates
  • Increase final adult height
  • Create height out of nowhere
If you do not have a diagnosed condition, you will not gain any adult height you will only get side effects.

The truth?: There is no hack around genetics. Injecting Chinese ratpiss HGH is expensive, unnecessary, and retarded.



Biology does not care about your retarded cope.
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DNR faggot im still going to pin my 12iu nightly:lul:
 
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AtrophicPyra said:
dont listen to this guy human "GROWTH" hormone works. just take ais bec it can prematurely close ur growth plates from the estrogen.
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i'll preface this by saying I know very little on the subject. But wouldn't ais just elongate the period of openness for growth plates due to the lowered estrogen? Ik it comes with its side effects, but would ais overall (with hgh ofc) allow for longer and therefore larger growth?
 
sokilix said:
i'll preface this by saying I know very little on the subject. But wouldn't ais just elongate the period of openness for growth plates due to the lowered estrogen? Ik it comes with its side effects, but would ais overall (with hgh ofc) allow for longer and therefore larger growth?
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i was retarded writing these types of posts trying to answerfarm, chrondokryte proliferation through fgfr3 inhibition is how you grow taller

take smth like vosoritide is my recommendaiton not an fgfr3 inhibitor but does the job
^
its a cnp analog
 
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AtrophicPyra said:
i was retarded writing these types of posts trying to answerfarm, chrondokryte proliferation through fgfr3 inhibition is how you grow taller

take smth like vosoritide is my recommendaiton not an fgfr3 inhibitor but does the job
^
its a cnp analog
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You just turn more retarded by the minute huh, not even gonna bother explaining this one just research
 
Ahmed88 said:
You just turn more retarded by the minute huh, not even gonna bother explaining this one just research
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how do u have more reps than me AHMED88 ur the most hated user on the forum
 
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Reactions: Ahmed88
megapro981 said:
Yes, its almost the exact same thing Im arguing with him for but with acromegaly instead of gigantism, as its proven that it has that effect in acromegaly its also proven it would have that same effect in someone injecting highly dosed exogenous rhgh. Whether the aesthetic changes on facial bones and soft tissue will benefit u is subjective and is dependent on a lot of factors like genetics and baseline for example.
Click to expand...
but u cant control how much and where the bone grows right?
 
Ahmed88 said:
You didn't debunk any of my arguments, why are you trying to mimic gigantism? You claim that ,,you can safely mimic gigantism if you know what ur doing" is just utterly wrong and ridiculous.

Your proposition assumes that increasing systemic concentration of growth hormone inevitably produces proportional enhancement of terminal skeletal length. This interpretation reflects a mechanistic reduction of developmental endocrinology. Although signaling downstream of Growth hormone and its effector mediator Insulin-like growth factor 1 promotes mitotic activation of chondrocytes within epiphyseal cartilage, macroscopic growth is not governed exclusively by signaling amplitude. Skeletal development is regulated through coordinated temporal programming, genetic architecture, and microenvironmental niche stability rather than isolated intracellular cascade intensity.

The growth plate functions as a stratified cellular production interface in which longitudinal bone extension depends upon lineage propagation originating from a relatively dormant progenitor compartment situated in the resting zone. This region demonstrates biological characteristics analogous to stem-cell maintenance systems, where cumulative replicative stress and molecular aging progressively diminish functional output across developmental progression. The phenomenon designated as Growth plate senescence describes the gradual decline of proliferative competence within physeal cartilage. While excessive GH/IGF signaling may transiently elevate chondrocyte division frequency inside proliferative columns, such acceleration tends to advance maturation kinetics, promoting premature hypertrophic transition and subsequent ossification rather than expanding total osteochondral elongation capacity.

The argument that progenitor cell abundance is not a fundamental constraint on longitudinal growth fails to account for hierarchical lineage dependency inherent in endochondral ossification. Even if signaling pathways including PI3K/Akt and MAPK/ERK enhance cellular survival probability, mitotic activation, and extracellular matrix deposition, these molecular effects operate primarily on cells already committed to differentiation pathways. Structural bone elongation requires continuous recruitment of undifferentiated precursor populations capable of generating additional chondrocyte columns. Modulation of hypertrophic cellular volume, collagen X synthesis, aggrecan distribution, or matrix spatial occupancy cannot generate new developmental lineages once upstream progenitor reservoirs experience attrition.

The comparison with Pituitary gigantism is not scientifically valid as definitive proof of pharmacologic growth hormone efficacy in normative physiology. Gigantism represents a pathological endocrine state characterized by persistent dysregulated somatotroph hormone secretion during critical developmental intervals. The substantial variability of final stature among gigantism patients indicates that GH concentration alone does not determine skeletal endpoint length, as genomic determinants regulating morphogenesis, physeal maturation timing, and systemic endocrine integration remain dominant modulators of height phenotype.

The hypothesis that recombinant GH administration can replicate tumor-mediated hormone exposure through dosage escalation or injection frequency modification neglects nonlinear endocrine pharmacokinetics. Receptor regulatory desensitization, intracellular inhibitory mediators such as suppressor of cytokine signaling proteins, and multi-axis hormonal feedback networks impose adaptive constraints on somatotropic signaling. Biological regulatory systems function under complex homeostatic modulation rather than simple linear amplification relationships.

Moreover, longitudinal clinical evidence does not demonstrate substantial augmentation of adult stature in individuals possessing intact somatotropic axis function who receive recombinant GH therapy. Investigations involving treatment outcomes in Idiopathic short stature and related non-deficient pediatric populations reveal only marginal modification of final skeletal height despite prolonged pharmacological exposure. These observations indicate that enhancement of growth velocity does not necessarily translate into expansion of developmental endpoint size.

The conjecture that accelerated proliferative activity can consistently exceed physeal maturation progression is unsupported by histomorphological developmental data. In many biological growth systems, increased mitogenic signaling is accompanied by proportional acceleration of differentiation and tissue maturation, thereby preserving overall developmental trajectory rather than extending ultimate structural dimensions.

Im not the one repeating myself, its quite the opposite actually.


(Rep me back nigga 😢)
Click to expand...

I kinda did debunk them imo. I feel like u just make general statements instead of trying to directly argue against what I claim on the most part. Im repeating my arguments because u just dont seem to get them. Ive explained the fact that socs proteins and that the effects arent linear to gh and igf1 levels are irrelevant as the growth plate wouldnt be able to tell if the gh is coming exogenously or from a pituitary adenoma secreting it already but u keep making that point still, thats why. And u make the point again that fast maturation of the plate might be bad, but thats exactly what happens again, in gigantism, and in gigantism it does still lead to a lot of growth. U also seem to for whatever reason be 100% certain that the height velocity and growth in the plates will be 1:1 proportional to how much it would accelerate closure in high gh conditions, how can u be so sure of that, especially when again, gigantism proves thats not true. Almost everything ur saying can be countered with gigantism if u understand what gigantism is in its nature.

The fact that height in gigantism has a wide range still doesnt refute that it increases height by a lot as the average height of that big range is also very much so above average. Were talking about an average of maybe 200cm for men, thats far above average.

Again u brung up ISS studies which again, arent that good of a proxy to healthy people. Saying that in gigantism it happens during critical developement years doesnt need to be said, thats for taken and with my claim too, if they want this to work they would need to take it during times where growth plates are open, that goes without saying.

I did claim that u can mimic gigantism conditions in the "eyes" of the growth plates yes, didnt say anything about safety though, obv theres side effects.

Lets imagine 2 scenarios, first scenario is where a person has gigantism from a pituitary adenoma, this adenoma secretes nothing but gh, no effect on other pituitary hormones, the growth plates sees a massive amount of continous gh and systemic igf1 exposure and responds by whatever it does downstream of this. The second scenario is where a person injects exogenous rhgh subq to reach the same gh levels seen in the first scenario and as continous as the first scenario too, the growth plate here also sees a massive amount of continous gh and systemic igf1 exposure and responds by whatever it does downstream of this. In both of these scenarios, the growth plate responds the exact same, there is no other change in the growth plate tissue that depends on if it comes from endogenously or if it comes exogenously, it wont be able to tell and it wont be able to respond in a different way by for example feedback mechanisms reducing downstream signaling with for example socs proteins in either scenario, assuming all other parameters line up like genetics and age etc. Gigantism is direct proof that it works. If u want to prove that it doesnt work u need to as I said already, tell me how the plate would tell which scenario is which and how the response would change cause of it and how.

I dont think this will go anywhere so idk Ima agree to disagree ig
 
  • +1
Reactions: Ahmed88
I take it for skin and sleep. Doubt itll do anything for height and bone growth at 3 or 4 IUs but idrc. Maybe after 2-3 years taken daily it might make a noticeable difference
 
  • So Sad
Reactions: Ahmed88
Ahmed88 said:
So get side effects and waste money, to get your already future planned height 2 years sooner?
Click to expand...
omd:lul: ima rather be 6'2 at 16 than 6'3 at nineteen
 
  • JFL
Reactions: Ahmed88
Ahmed88 said:
B-B-But ISS Children Grew Taller why can’t i?

Let’s clarify: ISS children are not short simply because of genetics. ISS is defined as short stature without a known cause, that INCLUDES GENETICS and many children diagnosed as having ISS have partial GH insensitivity (Evidence: Idiopathic short stature)
Click to expand...
Yes, many children with Idiopathic Short Stature (ISS) have underlying genetic causes for their short stature. While defined as having no known cause, advanced genetic testing has shown that ISS often involves genetic defects related to growth hormone, bone development, or polygenic factors, rather than just being a random occurrence.
 
thinking of doing 3-4 ius for 6-8 weeks then up to 6-8 ius then leave it there for a while just for the skin/sleep
 
  • +1
Reactions: Ahmed88
mtnuglyboy said:
thinking of doing 3-4 ius for 6-8 weeks then up to 6-8 ius then leave it there for a while just for the skin/sleep
Click to expand...
Yeah but why not dsip or ghkcu for half the price
 
copingcoper said:
Yes, many children with Idiopathic Short Stature (ISS) have underlying genetic causes for their short stature. While defined as having no known cause, advanced genetic testing has shown that ISS often involves genetic defects related to growth hormone, bone development, or polygenic factors, rather than just being a random occurrence.
Click to expand...
You're thinking abt passed down defects not family genetics
 
ghkcu takes hella long for effects and dsip is kinda mid + i want to experiment bonesmashing my chin and zygos with hgh to see if anything will happen cause im kinda bonesless:feelswah:
 
  • JFL
Reactions: Ahmed88
mtnuglyboy said:
ghkcu takes hella long for effects and dsip is kinda mid + i want to experiment bonesmashing my chin and zygos with hgh to see if anything will happen cause im kinda bonesless:feelswah:
Click to expand...
Do accutane for acne, tret or taz for retinol
And Dsip or even melatonin works better then HGH for sleep
Bonesmashing is cope and is going to ruin you in the long term, you're 193cm honestly i wouldnt play with my hormones like that at that height
 
Ahmed88 said:
A lot of People continue to believe that healthy children who lack growth hormone deficiency will experience height increases through HGH injections.

It won’t.

Why?

Let’s get into this


1. How Growth Hormone Actually Works

Human growth hormone (HGH), also called somatotropin, is a hormone that the pituitary gland, which is about the size of a pea and found at the base of your brain, makes and releases

Its main job?

Human growth hormone triggers growth in almost every tissue and organ in your body. It’s mostly known for its growth-promoting effect on cartilage and bone, especially in puberty. Cells in cartilage called chondrocytes and cells in bones called osteoblasts, receive signals from HGH to increase replication and thus allow for growth in size.


2. What the Studies ACTUALLY Show

People often cite studies claiming “HGH increases height.” Let’s clarify what these studies actually studied.

Most research involves children who are GH-deficient children who cannot produce normal levels of GH due to medical conditions. Examples:




VERY Important: These studies are on children who are medically short due to GH deficiency, and do NOT produce enough HGH not normal kids. The effect is correcting a deficiency, not surpassing genetic potential.



Some other studies explore ISS (Idiopathic Short Stature):


B-B-But ISS Children Grew Taller why can’t i?

Let’s clarify: ISS children are not short simply because of genetics. ISS is defined as short stature without a known cause, that INCLUDES GENETICS and many children diagnosed as having ISS have partial GH insensitivity (Evidence: Idiopathic short stature)

Bottom line: if you are within normal growth ranges and are not diagnosed as ISS, these studies do NOT apply to you.


3. Why HGH does NOT work for healthy normal children with PROOF

For children with normal growth hormone (GH) levels, exogenous GH administration cannot increase final adult height. Here’s why:



  • GH does not create new growth potential.
    The growth plates in long bones experience linear growth through their epiphyseal plates. The genetic code determines both number and proliferative capacity of chondrocytes present at these growth plates. GH promotes the growth of chondrocytes and their development into mature cells, yet it cannot boost these cells' genetic-based growth capacity beyond their existing limits.
  • GH cannot override genetic determinants of stature.
    Height is a polygenic trait which multiple genetic loci control its development. The treatment of GH-sufficient children with GH therapy does not affect their gene expression or the genetic skeletal structure which their genome contains.
  • Endocrine feedback loops limit excessive growth signaling.
    The GH–IGF-1 axis is tightly regulated:
    • Elevated serum IGF-1 inhibits hypothalamic GHRH secretion and stimulates somatostatin release, reducing endogenous GH production.
    • Peripheral tissues exhibit receptor-mediated resistance to supra-physiologic GH and IGF-1 concentrations, limiting further cellular proliferation.
  • Physiologic ceiling effect.
    In GH-sufficient children, endogenous GH already saturates IGF-1 production and downstream growth plate signaling. Exogenous GH cannot enhance this process; the system is operating at maximal physiological capacity. Clinical evidence and studies supports these claims: children with normal GH levels do not achieve increased adult height despite high-dose GH administration
EVIDENCE AND STUDIES ON NORMAL KIDS:

Final height after growth hormone therapy in non-growth-hormone-deficient children with short stature - PubMed

No Improvement of Adult Height in Non-growth Hormone (GH) Deficient Short Children with GH Treatment - PMC

https://www.sciencedirect.com/science/article/abs/pii/S002234769470192X

No Improvement of Adult Height in Non-growth Hormone (GH) Deficient Short Children with GH Treatment - PubMed



Analogy (for conceptual clarity): Imagine a plant with genetically fixed maximum height. Adequate water and nutrients allow it to reach its potential. Adding more water beyond what it can physiologically use does not make it grow taller; it may even disrupt normal growth processes.

Summary: GH in healthy, non-deficient children simply optimizes a process that is already at capacity. There is no latent or “hidden” height to unlock the endocrine system and growth plates are already functioning at their maximum biological limits.


4. Why people think it works!!!!!!

This is where most people get fooled and start to think it’s working.

HGH can TEMPORARILY increase growth rate (as seen in the studies). You grow faster for a period, but it does NOT increase final adult height. Your genetic height ceiling remains THE SAME. In the end you will grow the same without HGH.


5. What you actually get and are paying for: Side Effects

Injecting ratpiss HGH from Chinese labs is retarded and will NOT work all you are paying for are potential risks including:

  • Insulin resistance
  • Increased risk of type 2 diabetes
  • Fluid retention and edema
  • Joint pain
  • Carpal tunnel syndrome
  • Hip growth plate injury
  • Benign intracranial hypertension (severe headaches and vision changes)
  • Abnormal IGF‑1 elevations
  • Theoretical increased cancer risk due to chronic IGF‑1 stimulation
​

6. Summary

HGH only works in:

  • Documented GH deficiency
  • Select ISS cases


HGH does NOT:

  • Make normal kids taller than their genetics allow
  • Extend growth plates
  • Increase final adult height
  • Create height out of nowhere
If you do not have a diagnosed condition, you will not gain any adult height you will only get side effects.

The truth?: There is no hack around genetics. Injecting Chinese ratpiss HGH is expensive, unnecessary, and retarded.



Biology does not care about your retarded cope.
Click to expand...
True.

HGH is pretty much shit for everything including muscle and chronically high systemic igf1 isn't good for you.

It's only real use case is during a steep deficit due to its extreme anti catabolic effects.
 
  • +1
Reactions: Ahmed88
ICANNOTBECONTAINED said:
True.

HGH is pretty much shit for everything including muscle and chronically high systemic igf1 isn't good for you.

It's only real use case is during a steep deficit due to its extreme anti catabolic effects.
Click to expand...
Mirin finally someone with high iq
 
  • +1
Reactions: ICANNOTBECONTAINED
Ahmed88 said:
Do accutane for acne, tret or taz for retinol
And Dsip or even melatonin works better then HGH for sleep
Bonesmashing is cope and is going to ruin you in the long term, you're 193cm honestly i wouldnt play with my hormones like that at that height
Click to expand...
if i take hgh once i run out can i just hop off no pct aand bs ?
 
  • +1
Reactions: Ahmed88
mtnuglyboy said:
if i take hgh once i run out can i just hop off no pct aand bs ?
Click to expand...
Yeah i guess, although it takes some time for your body to recover your natural gh levels

Rep me nigga
 
  • +1
Reactions: mtnuglyboy
Ahmed88 said:
Yeah i guess, although it takes some time for your body to recover your natural gh levels

Rep me nigga
Click to expand...
stop calling me a nigga before i use my ebonics language on u and start hiring crackhead niggers on u lurking around kfc at 2am to switch u down with a draco with a extended mag
 
  • JFL
Reactions: Ahmed88
Ahmed88 said:
A lot of People continue to believe that healthy children who lack growth hormone deficiency will experience height increases through HGH injections.

It won’t.

Why?

Let’s get into this


1. How Growth Hormone Actually Works

Human growth hormone (HGH), also called somatotropin, is a hormone that the pituitary gland, which is about the size of a pea and found at the base of your brain, makes and releases

Its main job?

Human growth hormone triggers growth in almost every tissue and organ in your body. It’s mostly known for its growth-promoting effect on cartilage and bone, especially in puberty. Cells in cartilage called chondrocytes and cells in bones called osteoblasts, receive signals from HGH to increase replication and thus allow for growth in size.


2. What the Studies ACTUALLY Show

People often cite studies claiming “HGH increases height.” Let’s clarify what these studies actually studied.

Most research involves children who are GH-deficient children who cannot produce normal levels of GH due to medical conditions. Examples:




VERY Important: These studies are on children who are medically short due to GH deficiency, and do NOT produce enough HGH not normal kids. The effect is correcting a deficiency, not surpassing genetic potential.



Some other studies explore ISS (Idiopathic Short Stature):


B-B-But ISS Children Grew Taller why can’t i?

Let’s clarify: ISS children are not short simply because of genetics. ISS is defined as short stature without a known cause, that INCLUDES GENETICS and many children diagnosed as having ISS have partial GH insensitivity (Evidence: Idiopathic short stature)

Bottom line: if you are within normal growth ranges and are not diagnosed as ISS, these studies do NOT apply to you.


3. Why HGH does NOT work for healthy normal children with PROOF

For children with normal growth hormone (GH) levels, exogenous GH administration cannot increase final adult height. Here’s why:



  • GH does not create new growth potential.
    The growth plates in long bones experience linear growth through their epiphyseal plates. The genetic code determines both number and proliferative capacity of chondrocytes present at these growth plates. GH promotes the growth of chondrocytes and their development into mature cells, yet it cannot boost these cells' genetic-based growth capacity beyond their existing limits.
  • GH cannot override genetic determinants of stature.
    Height is a polygenic trait which multiple genetic loci control its development. The treatment of GH-sufficient children with GH therapy does not affect their gene expression or the genetic skeletal structure which their genome contains.
  • Endocrine feedback loops limit excessive growth signaling.
    The GH–IGF-1 axis is tightly regulated:
    • Elevated serum IGF-1 inhibits hypothalamic GHRH secretion and stimulates somatostatin release, reducing endogenous GH production.
    • Peripheral tissues exhibit receptor-mediated resistance to supra-physiologic GH and IGF-1 concentrations, limiting further cellular proliferation.
  • Physiologic ceiling effect.
    In GH-sufficient children, endogenous GH already saturates IGF-1 production and downstream growth plate signaling. Exogenous GH cannot enhance this process; the system is operating at maximal physiological capacity. Clinical evidence and studies supports these claims: children with normal GH levels do not achieve increased adult height despite high-dose GH administration
EVIDENCE AND STUDIES ON NORMAL KIDS:

Final height after growth hormone therapy in non-growth-hormone-deficient children with short stature - PubMed

No Improvement of Adult Height in Non-growth Hormone (GH) Deficient Short Children with GH Treatment - PMC

https://www.sciencedirect.com/science/article/abs/pii/S002234769470192X

No Improvement of Adult Height in Non-growth Hormone (GH) Deficient Short Children with GH Treatment - PubMed



Analogy (for conceptual clarity): Imagine a plant with genetically fixed maximum height. Adequate water and nutrients allow it to reach its potential. Adding more water beyond what it can physiologically use does not make it grow taller; it may even disrupt normal growth processes.

Summary: GH in healthy, non-deficient children simply optimizes a process that is already at capacity. There is no latent or “hidden” height to unlock the endocrine system and growth plates are already functioning at their maximum biological limits.


4. Why people think it works!!!!!!

This is where most people get fooled and start to think it’s working.

HGH can TEMPORARILY increase growth rate (as seen in the studies). You grow faster for a period, but it does NOT increase final adult height. Your genetic height ceiling remains THE SAME. In the end you will grow the same without HGH.


5. What you actually get and are paying for: Side Effects

Injecting ratpiss HGH from Chinese labs is retarded and will NOT work all you are paying for are potential risks including:

  • Insulin resistance
  • Increased risk of type 2 diabetes
  • Fluid retention and edema
  • Joint pain
  • Carpal tunnel syndrome
  • Hip growth plate injury
  • Benign intracranial hypertension (severe headaches and vision changes)
  • Abnormal IGF‑1 elevations
  • Theoretical increased cancer risk due to chronic IGF‑1 stimulation
​

6. Summary

HGH only works in:

  • Documented GH deficiency
  • Select ISS cases


HGH does NOT:

  • Make normal kids taller than their genetics allow
  • Extend growth plates
  • Increase final adult height
  • Create height out of nowhere
If you do not have a diagnosed condition, you will not gain any adult height you will only get side effects.

The truth?: There is no hack around genetics. Injecting Chinese ratpiss HGH is expensive, unnecessary, and retarded.



Biology does not care about your retarded cope.
Click to expand...
will return to this thread when I'm not deliriously tired so I can verbally smite you, you are the sperm to my original posts and that is why you do not grasp the basic logic of this fucking topic, SILENCE.

he looks at the far fetched efforts of those who claim to be truecell, "HighIQ" they whisper to themselves gathered around him around him, but they are riddled with botched lefort 3s, frozen facial muscles and fascia from layers of Botox and bonesmashing, I stand alone on the pinnacle of HPTA axis control, with my divine technique, curse against nature, I can bend the wills and whims of the laws of human form to my desire, unaffected by those flocked by the Norwood reaper beneath me, with MK677 as my shield and Letrozole as my sword, I am the alchemist who looms in the woods of heightmaxxing, you will not see me, only hear the crackle of branches under my Sasquatch sized feet, smell the sickly sweet scent of letrozole in my sweat, I will be there, follow the empty vials of CJCDAC, follow the trail,
Aromasin pills spilled on the Forrest floor like a gnomes pathway open only to those who stop to see where it leads, follow the flowers overgrown with growth hormone piss, I will be there, an acromegalic monstrosity, like Zarathustra he watches from the mountains and weeps at the idiocy of those underneath him.

jfl at the quality of posts here nowadays, I weep for the ones who roped years before now unable to bare the weight of the Letrozoles languish, for they would have screamed statistics in their glass high chairs crafted from a wasted decades hgh bottles and thrown ACID down on the flocks of disengaged PEPTIDE PIGLETS that infest this forum
🧙‍♂️
 
  • Woah
Reactions: Ahmed88
TakaTeo said:
will return to this thread when I'm not deliriously tired so I can verbally smite you, you are the sperm to my original posts and that is why you do not grasp the basic logic of this fucking topic, SILENCE.

he looks at the far fetched efforts of those who claim to be truecell, "HighIQ" they whisper to themselves gathered around him around him, but they are riddled with botched lefort 3s, frozen facial muscles and fascia from layers of Botox and bonesmashing, I stand alone on the pinnacle of HPTA axis control, with my divine technique, curse against nature, I can bend the wills and whims of the laws of human form to my desire, unaffected by those flocked by the Norwood reaper beneath me, with MK677 as my shield and Letrozole as my sword, I am the alchemist who looms in the woods of heightmaxxing, you will not see me, only hear the crackle of branches under my Sasquatch sized feet, smell the sickly sweet scent of letrozole in my sweat, I will be there, follow the empty vials of CJCDAC, follow the trail,
Aromasin pills spilled on the Forrest floor like a gnomes pathway open only to those who stop to see where it leads, follow the flowers overgrown with growth hormone piss, I will be there, an acromegalic monstrosity, like Zarathustra he watches from the mountains and weeps at the idiocy of those underneath him.

jfl at the quality of posts here nowadays, I weep for the ones who roped years before now unable to bare the weight of the Letrozoles languish, for they would have screamed statistics in their glass high chairs crafted from a wasted decades hgh bottles and thrown ACID down on the flocks of disengaged PEPTIDE PIGLETS that infest this forum
🧙‍♂️
Click to expand...
He's a troll
 
  • +1
Reactions: wannabemogger
Zagro said:
He's a troll
Click to expand...
gtfo my thread faggot,
has me on ignore+ left the discussion 3 times yet always comes back
thanks for the bump tho :lul:
 
Last edited:
Instead of taking HGH I recommend Lactopontin with probiotics and a lot of fiber intake, such a formula increase GH along with IGF1
 
  • +1
Reactions: Ahmed88
Ahmed88 said:
A lot of People continue to believe that healthy children who lack growth hormone deficiency will experience height increases through HGH injections.

It won’t.

Why?

Let’s get into this


1. How Growth Hormone Actually Works

Human growth hormone (HGH), also called somatotropin, is a hormone that the pituitary gland, which is about the size of a pea and found at the base of your brain, makes and releases

Its main job?

Human growth hormone triggers growth in almost every tissue and organ in your body. It’s mostly known for its growth-promoting effect on cartilage and bone, especially in puberty. Cells in cartilage called chondrocytes and cells in bones called osteoblasts, receive signals from HGH to increase replication and thus allow for growth in size.


2. What the Studies ACTUALLY Show

People often cite studies claiming “HGH increases height.” Let’s clarify what these studies actually studied.

Most research involves children who are GH-deficient children who cannot produce normal levels of GH due to medical conditions. Examples:




VERY Important: These studies are on children who are medically short due to GH deficiency, and do NOT produce enough HGH not normal kids. The effect is correcting a deficiency, not surpassing genetic potential.



Some other studies explore ISS (Idiopathic Short Stature):


B-B-But ISS Children Grew Taller why can’t i?

Let’s clarify: ISS children are not short simply because of genetics. ISS is defined as short stature without a known cause, that INCLUDES GENETICS and many children diagnosed as having ISS have partial GH insensitivity (Evidence: Idiopathic short stature)

Bottom line: if you are within normal growth ranges and are not diagnosed as ISS, these studies do NOT apply to you.


3. Why HGH does NOT work for healthy normal children with PROOF

For children with normal growth hormone (GH) levels, exogenous GH administration cannot increase final adult height. Here’s why:



  • GH does not create new growth potential.
    The growth plates in long bones experience linear growth through their epiphyseal plates. The genetic code determines both number and proliferative capacity of chondrocytes present at these growth plates. GH promotes the growth of chondrocytes and their development into mature cells, yet it cannot boost these cells' genetic-based growth capacity beyond their existing limits.
  • GH cannot override genetic determinants of stature.
    Height is a polygenic trait which multiple genetic loci control its development. The treatment of GH-sufficient children with GH therapy does not affect their gene expression or the genetic skeletal structure which their genome contains.
  • Endocrine feedback loops limit excessive growth signaling.
    The GH–IGF-1 axis is tightly regulated:
    • Elevated serum IGF-1 inhibits hypothalamic GHRH secretion and stimulates somatostatin release, reducing endogenous GH production.
    • Peripheral tissues exhibit receptor-mediated resistance to supra-physiologic GH and IGF-1 concentrations, limiting further cellular proliferation.
  • Physiologic ceiling effect.
    In GH-sufficient children, endogenous GH already saturates IGF-1 production and downstream growth plate signaling. Exogenous GH cannot enhance this process; the system is operating at maximal physiological capacity. Clinical evidence and studies supports these claims: children with normal GH levels do not achieve increased adult height despite high-dose GH administration
EVIDENCE AND STUDIES ON NORMAL KIDS:

Final height after growth hormone therapy in non-growth-hormone-deficient children with short stature - PubMed

No Improvement of Adult Height in Non-growth Hormone (GH) Deficient Short Children with GH Treatment - PMC

https://www.sciencedirect.com/science/article/abs/pii/S002234769470192X

No Improvement of Adult Height in Non-growth Hormone (GH) Deficient Short Children with GH Treatment - PubMed



Analogy (for conceptual clarity): Imagine a plant with genetically fixed maximum height. Adequate water and nutrients allow it to reach its potential. Adding more water beyond what it can physiologically use does not make it grow taller; it may even disrupt normal growth processes.

Summary: GH in healthy, non-deficient children simply optimizes a process that is already at capacity. There is no latent or “hidden” height to unlock the endocrine system and growth plates are already functioning at their maximum biological limits.


4. Why people think it works!!!!!!

This is where most people get fooled and start to think it’s working.

HGH can TEMPORARILY increase growth rate (as seen in the studies). You grow faster for a period, but it does NOT increase final adult height. Your genetic height ceiling remains THE SAME. In the end you will grow the same without HGH.


5. What you actually get and are paying for: Side Effects

Injecting ratpiss HGH from Chinese labs is retarded and will NOT work all you are paying for are potential risks including:

  • Insulin resistance
  • Increased risk of type 2 diabetes
  • Fluid retention and edema
  • Joint pain
  • Carpal tunnel syndrome
  • Hip growth plate injury
  • Benign intracranial hypertension (severe headaches and vision changes)
  • Abnormal IGF‑1 elevations
  • Theoretical increased cancer risk due to chronic IGF‑1 stimulation
​

6. Summary

HGH only works in:

  • Documented GH deficiency
  • Select ISS cases


HGH does NOT:

  • Make normal kids taller than their genetics allow
  • Extend growth plates
  • Increase final adult height
  • Create height out of nowhere
If you do not have a diagnosed condition, you will not gain any adult height you will only get side effects.

The truth?: There is no hack around genetics. Injecting Chinese ratpiss HGH is expensive, unnecessary, and retarded.



Biology does not care about your retarded cope.
Click to expand...
saying this to gatekeep brother
 
  • WTF
Reactions: Ahmed88
people who say this lack critical thinking.
 
Ahmed88 said:
Just read my fucking explanation nigga it takes one search to find out iss children arent short cause of genetics, yes they are healthy medically because there is no explanation for their short stature (so basically they dont know whats wrong) stop saying the same thing over and over again
Click to expand...
i think it's bcz of IGF1 receptors sensitivity
 
  • +1
Reactions: xqBandit and Ahmed88
Ahmed88 said:
A lot of People continue to believe that healthy children who lack growth hormone deficiency will experience height increases through HGH injections.

It won’t.

Why?

Let’s get into this


1. How Growth Hormone Actually Works

Human growth hormone (HGH), also called somatotropin, is a hormone that the pituitary gland, which is about the size of a pea and found at the base of your brain, makes and releases

Its main job?

Human growth hormone triggers growth in almost every tissue and organ in your body. It’s mostly known for its growth-promoting effect on cartilage and bone, especially in puberty. Cells in cartilage called chondrocytes and cells in bones called osteoblasts, receive signals from HGH to increase replication and thus allow for growth in size.


2. What the Studies ACTUALLY Show

People often cite studies claiming “HGH increases height.” Let’s clarify what these studies actually studied.

Most research involves children who are GH-deficient children who cannot produce normal levels of GH due to medical conditions. Examples:




VERY Important: These studies are on children who are medically short due to GH deficiency, and do NOT produce enough HGH not normal kids. The effect is correcting a deficiency, not surpassing genetic potential.



Some other studies explore ISS (Idiopathic Short Stature):


B-B-But ISS Children Grew Taller why can’t i?

Let’s clarify: ISS children are not short simply because of genetics. ISS is defined as short stature without a known cause, that INCLUDES GENETICS and many children diagnosed as having ISS have partial GH insensitivity (Evidence: Idiopathic short stature)

Bottom line: if you are within normal growth ranges and are not diagnosed as ISS, these studies do NOT apply to you.


3. Why HGH does NOT work for healthy normal children with PROOF

For children with normal growth hormone (GH) levels, exogenous GH administration cannot increase final adult height. Here’s why:



  • GH does not create new growth potential.
    The growth plates in long bones experience linear growth through their epiphyseal plates. The genetic code determines both number and proliferative capacity of chondrocytes present at these growth plates. GH promotes the growth of chondrocytes and their development into mature cells, yet it cannot boost these cells' genetic-based growth capacity beyond their existing limits.
  • GH cannot override genetic determinants of stature.
    Height is a polygenic trait which multiple genetic loci control its development. The treatment of GH-sufficient children with GH therapy does not affect their gene expression or the genetic skeletal structure which their genome contains.
  • Endocrine feedback loops limit excessive growth signaling.
    The GH–IGF-1 axis is tightly regulated:
    • Elevated serum IGF-1 inhibits hypothalamic GHRH secretion and stimulates somatostatin release, reducing endogenous GH production.
    • Peripheral tissues exhibit receptor-mediated resistance to supra-physiologic GH and IGF-1 concentrations, limiting further cellular proliferation.
  • Physiologic ceiling effect.
    In GH-sufficient children, endogenous GH already saturates IGF-1 production and downstream growth plate signaling. Exogenous GH cannot enhance this process; the system is operating at maximal physiological capacity. Clinical evidence and studies supports these claims: children with normal GH levels do not achieve increased adult height despite high-dose GH administration
EVIDENCE AND STUDIES ON NORMAL KIDS:

Final height after growth hormone therapy in non-growth-hormone-deficient children with short stature - PubMed

No Improvement of Adult Height in Non-growth Hormone (GH) Deficient Short Children with GH Treatment - PMC

https://www.sciencedirect.com/science/article/abs/pii/S002234769470192X

No Improvement of Adult Height in Non-growth Hormone (GH) Deficient Short Children with GH Treatment - PubMed



Analogy (for conceptual clarity): Imagine a plant with genetically fixed maximum height. Adequate water and nutrients allow it to reach its potential. Adding more water beyond what it can physiologically use does not make it grow taller; it may even disrupt normal growth processes.

Summary: GH in healthy, non-deficient children simply optimizes a process that is already at capacity. There is no latent or “hidden” height to unlock the endocrine system and growth plates are already functioning at their maximum biological limits.


4. Why people think it works!!!!!!

This is where most people get fooled and start to think it’s working.

HGH can TEMPORARILY increase growth rate (as seen in the studies). You grow faster for a period, but it does NOT increase final adult height. Your genetic height ceiling remains THE SAME. In the end you will grow the same without HGH.


5. What you actually get and are paying for: Side Effects

Injecting ratpiss HGH from Chinese labs is retarded and will NOT work all you are paying for are potential risks including:

  • Insulin resistance
  • Increased risk of type 2 diabetes
  • Fluid retention and edema
  • Joint pain
  • Carpal tunnel syndrome
  • Hip growth plate injury
  • Benign intracranial hypertension (severe headaches and vision changes)
  • Abnormal IGF‑1 elevations
  • Theoretical increased cancer risk due to chronic IGF‑1 stimulation
​

6. Summary

HGH only works in:

  • Documented GH deficiency
  • Select ISS cases


HGH does NOT:

  • Make normal kids taller than their genetics allow
  • Extend growth plates
  • Increase final adult height
  • Create height out of nowhere
If you do not have a diagnosed condition, you will not gain any adult height you will only get side effects.

The truth?: There is no hack around genetics. Injecting Chinese ratpiss HGH is expensive, unnecessary, and retarded.



Biology does not care about your retarded cope.
Click to expand...
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pubmed.ncbi.nlm.nih.gov

Final height of short normal children treated with growth hormone - PubMed

Long-term therapy in this group of children appears safe but the small increment in final height, approximately 2.8 cm in boys and 2.5 cm in girls, does not justify the widespread use of r-hGH for short normal children.
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov

Effect of growth hormone therapy on height in children with idiopathic short stature: a meta-analysis - PubMed

Treatment with GH results in short-term increases in growth for children with idiopathic short stature, and long-term GH can increase adult height. These results are fundamental to decisions about GH use and raise questions about the goals of treatment. Use of GH for idiopathic short stature in...
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov

Recombinant growth hormone for idiopathic short stature in children and adolescents - PubMed

Results suggest that growth hormone therapy can increase short-term growth and improve (near) final height. Increases in height are such that treated individuals remain relatively short when compared with peers of normal stature. Further research in the form of large, multicentre RCTs are...
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
 
xqBandit said:
pubmed.ncbi.nlm.nih.gov

Final height of short normal children treated with growth hormone - PubMed

Long-term therapy in this group of children appears safe but the small increment in final height, approximately 2.8 cm in boys and 2.5 cm in girls, does not justify the widespread use of r-hGH for short normal children.
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov

Effect of growth hormone therapy on height in children with idiopathic short stature: a meta-analysis - PubMed

Treatment with GH results in short-term increases in growth for children with idiopathic short stature, and long-term GH can increase adult height. These results are fundamental to decisions about GH use and raise questions about the goals of treatment. Use of GH for idiopathic short stature in...
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov

Recombinant growth hormone for idiopathic short stature in children and adolescents - PubMed

Results suggest that growth hormone therapy can increase short-term growth and improve (near) final height. Increases in height are such that treated individuals remain relatively short when compared with peers of normal stature. Further research in the form of large, multicentre RCTs are...
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
Click to expand...
@Ahmed88 very cope for height man, very cope 😂
 
xqBandit said:
pubmed.ncbi.nlm.nih.gov

Final height of short normal children treated with growth hormone - PubMed

Long-term therapy in this group of children appears safe but the small increment in final height, approximately 2.8 cm in boys and 2.5 cm in girls, does not justify the widespread use of r-hGH for short normal children.
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov

Effect of growth hormone therapy on height in children with idiopathic short stature: a meta-analysis - PubMed

Treatment with GH results in short-term increases in growth for children with idiopathic short stature, and long-term GH can increase adult height. These results are fundamental to decisions about GH use and raise questions about the goals of treatment. Use of GH for idiopathic short stature in...
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov

Recombinant growth hormone for idiopathic short stature in children and adolescents - PubMed

Results suggest that growth hormone therapy can increase short-term growth and improve (near) final height. Increases in height are such that treated individuals remain relatively short when compared with peers of normal stature. Further research in the form of large, multicentre RCTs are...
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
Click to expand...
1st Study: 1996, AND 3 UNTREATED KIDS THE REST WERE ,,LOST" :feelskek::feelskek::feelskek::feelskek::feelskek::feelskek::feelskek::feelskek::feelskek: :feelskek::feelskek::feelskek::feelskek::feelskek:

2,3: ISS STUDIES :feelskek::feelskek:



:feelskek::feelskek:
 
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Ahmed88 said:
Cells in cartilage called chondrocytes and cells in bones called osteoblasts, receive signals from HGH to increase replication and thus allow for growth in size.
Click to expand...
More nuanced than just that. GH also increases IGF-1 which is the majority of the signal. IGF-1 largely dominates GH. Also, "thus allow for growth in size" can be very misleading, the chondrocytes grow about 5x in the hypertrophic phase regardless and mass amounts of GH only slightly make it bigger. The growth is due to the increased replication amount. The IGF-1 signals the cell to keep duplicating before its life runs out.

Ahmed88 said:
Cells in cartilage called chondrocytes
Click to expand...
Oversimplified.

Ahmed88 said:
cells in bones called osteoblasts
Click to expand...
Incorrect and conceptually wrong.

Ahmed88 said:
The growth plates in long bones experience linear growth through their epiphyseal plates. The genetic code determines both number and proliferative capacity of chondrocytes present at these growth plates. GH promotes the growth of chondrocytes and their development into mature cells, yet it cannot boost these cells' genetic-based growth capacity beyond their existing limits.
Click to expand...
I'm concerned this entire thread was written by AI at this point. GH promotes chondrocytes duplicating. This is good as the entire reason the average person is nowhere near the average patient with gigantism is due to them duplicating insane amounts. People with gigantism showcase we are not near our genetic potential in any regard. Increased GH will cause height to increase. It's just that the ratio isn't 1:1 and rather logarithmic or so.

The cells' "genetic-based growth capacity" isn't even an argument as we aren't at our genetic potential like I stated. Chondrocytes don't get "tired" or "exhausted" like how GPT might make it seem like. The PTHrP loop demonstrates that the main thing that matters is SOX9 upregulation.

Ahmed88 said:
GH cannot override genetic determinants of stature.
Height is a polygenic trait which multiple genetic loci control its development. The treatment of GH-sufficient children with GH therapy does not affect their gene expression or the genetic skeletal structure which their genome contains.
Click to expand...
This is the same point as before..?

Ahmed88 said:
Endocrine feedback loops limit excessive growth signaling.
The GH–IGF-1 axis is tightly regulated:
  • Elevated serum IGF-1 inhibits hypothalamic GHRH secretion and stimulates somatostatin release, reducing endogenous GH production.
  • Peripheral tissues exhibit receptor-mediated resistance to supra-physiologic GH and IGF-1 concentrations, limiting further cellular proliferation.
Click to expand...
Over simplification which is implying a false narrative. The effect would be blunted, not eliminated.

Ahmed88 said:
Physiologic ceiling effect.
In GH-sufficient children, endogenous GH already saturates IGF-1 production and downstream growth plate signaling. Exogenous GH cannot enhance this process; the system is operating at maximal physiological capacity. Clinical evidence and studies supports these claims: children with normal GH levels do not achieve increased adult height despite high-dose GH administration
Click to expand...
IGF-1 levels could be pushed higher with endogenous GH... This is seen in studies.. Gigantism proves this.. Did you just pull this out GPT..?????


Ahmed88 said:
Analogy (for conceptual clarity): Imagine a plant with genetically fixed maximum height. Adequate water and nutrients allow it to reach its potential. Adding more water beyond what it can physiologically use does not make it grow taller; it may even disrupt normal growth processes.
Click to expand...
Except it's nothing like that at all..? We are nowhere near our genetic potential. I'd love for you to justify how gigantism patients work then.


Ahmed88 said:
HGH can TEMPORARILY increase growth rate (as seen in the studies). You grow faster for a period, but it does NOT increase final adult height. Your genetic height ceiling remains THE SAME. In the end you will grow the same without HGH.
Click to expand...
You don't know what you're talking about.. They replicate faster but it does not necessarily mean they also go from proliferation -> pre hypertrophic faster. Therefore, you will be taller.


Ahmed88 said:
HGH only works in:

  • Documented GH deficiency
  • Select ISS cases


HGH does NOT:

  • Make normal kids taller than their genetics allow
  • Extend growth plates
  • Increase final adult height
  • Create height out of nowhere
Click to expand...
Gigantism just doesn't exist, I guess...

Ahmed88 said:
Robert wadlow had a tumour, we do not, his tumour supressed his natural feedback system extremely
Click to expand...
That's not even an argument. You made the broad claim that hgh will not work for users here. It will if you inject enough. The feedback system can be bypassed via doing more no matter what, it will just be blunted like I stated. Gigantism/tumor patients don't have anything else unique. This shows that GH is what truly matters.


Ahmed88 said:
andwe need e2 for growth since it enhances hgh and igf1 signaling in growth plates and supports chondrocyte , supressing e2 would likely have negative effects on your health and height
Click to expand...
Slightly lower E2 & increase PTHrP and lower IHH. There you go. That's fixed now!

And before "you would need crazy amounts to grow, it's not realistic," you made a general claim that is very misleading, it doesn't matter if an unhealthy treatment is there.

cometohaunted said:
people with higher gh levels than others would analytically have to be taller
Click to expand...
Good one.. Except the normal range is within a narrow margin. It's like comparing SOX9 levels and thinking it's irrelevant because they're not taller solely off it.

cometohaunted said:
gigantism is caused by pituitary tumours that is a stupid response lmfao
Click to expand...
No..? It's not..? It shows the feedback loop is a major factor and we're nowhere close to genetic limits. The loop can be bypassed. You know nothing about height. Go ahead and explain to me the growth plate structure and how chondrocytes are even made, bub. You know nothing.

cometohaunted said:
Still disagree w this, plate proliferation being catalysed by estradiol doesn't ignore the fact that genes still control to activity and rate, so even if you inhibit a large portion of your estradiol (which if you don't know what you're doing or what your levels are you could cause hormonal balance which does the exact opposite of growing you anyways) your cxxc5 and wnt/b-catenin pathways are still active. There's no evidence suggesting that these pathways or gene expressions decline with estradiol blockage jfl
Click to expand...
E2 does regulate growth plate activity.
SOX9 overrides wnt/b-catenin pathways. Estrogen makes the levels go higher. Wnt/b-catenin cannot force cells to exit proliferation immediately. SOX9 “overrides” the differentiation signal.
Lower E2 and increase PTHrP. There you go, it's fixed.

cometohaunted said:
That's not all pituitary tumors do that's the entire point.. Jesus Christ, a pituitary tumor wouldn't ONLY affect gh as pituitary issues would give you issues with all hormones and feedback since it's the master gland that controls the entire endocrine system.. read op again he already refuted this jfl
Click to expand...
Gigantism proves that isolated GH excess can drive extreme height. You do not need "all pituitary hormones disrupted" to explain gigantism. The claim confuses potential effects with typical functional outcome.

Ahmed88 said:
CTX5, Sox9, Runx2, and extracellular matrix modulators. Blocking estrogen disrupts these gene networks and cartilage maturation, producing at best a marginal temporal extension of growth, not a fundamental increase in growth potential.
Click to expand...
@StyIix @Fridx @sergdying


This is what I mean when I say people don't know what they're talking about. This guy said blocking E2 disrupts SOX9 + RUNX2.. E2 HIGHERS SOX9 WHICH MAKES CELLS REPLICATE MORE BEFORE MOVING ONTO THE PRE HYPERTROPHIC STAGE. SOX9 IS ALSO DIRECTLY LINKED TO INHIBITING RUNX2. RUNX2 SHOULD BE INHIBITED. HE ASKED CHATGPT FOR ARGUMENTS. HE HAS NO SHAME AND NO MERIT. THESE PEOPLE ARE MORONS.

Ahmed88 said:
Pharmacologic administration of exogenous Growth hormone in pediatric individuals with an intact somatotropic axis does not produce a meaningful increase in attained adult stature.
Click to expand...
Going off what exactly..? NO STUDY HAS BEEN DONE ON THE AMOUNTS NEEDED. You made claims on this all being speculation and then say this.. Yikes..

Ahmed88 said:
Skeletal development is regulated through coordinated temporal programming, genetic architecture, and microenvironmental niche stability rather than isolated intracellular cascade intensity.
Click to expand...
Go ahead and tell me what changes with gigantism. Scientists have ruled growth hormone works for height off that. Get a grip.

Ahmed88 said:
such acceleration tends to advance maturation kinetics, promoting premature hypertrophic transition and subsequent ossification rather than expanding total osteochondral elongation capacity.
Click to expand...
Are you joking at this point..? You claim e2 would disrupt the hypertrophic transition when it would help and then say this..?

This isn't even correct either. The PTHrP loop is responsible for the cell going to the next phase. The levels are based upon a gradient. This is based upon how far up/down they are in their journey. The majority of the "exhaustion" comes from time. One dividing at 1 unit per second vs another dividing at 3 units per second wouldn't cause a major difference in when they transition. The SOX9 levels are untouched.

Ahmed88 said:
The argument that progenitor cell abundance is not a fundamental constraint on longitudinal growth fails to account for hierarchical lineage dependency inherent in endochondral ossification. Even if signaling pathways including PI3K/Akt and MAPK/ERK enhance cellular survival probability, mitotic activation, and extracellular matrix deposition, these molecular effects operate primarily on cells already committed to differentiation pathways. Structural bone elongation requires continuous recruitment of undifferentiated precursor populations capable of generating additional chondrocyte columns. Modulation of hypertrophic cellular volume, collagen X synthesis, aggrecan distribution, or matrix spatial occupancy cannot generate new developmental lineages once upstream progenitor reservoirs experience attrition.
Click to expand...
GPT slop once again. Collagen X, RUNX2, MEF2C/MEF2D are all idealized with what I said.

Also, WE'RE NOT EVEN CLOSE TO THE LIMIT. WE HAVE AT MOST .01% EFFIECNY. THERE COULD BE MAGNITUDES OF ORDERS OF MORE DIVISON. WE WOULD RUN INTO ATP/OXYGEN PROBLEMS BEFORE ANY OF THAT.

Ahmed88 said:
The comparison with Pituitary gigantism is not scientifically valid as definitive proof of pharmacologic growth hormone efficacy in normative physiology. Gigantism represents a pathological endocrine state characterized by persistent dysregulated somatotroph hormone secretion during critical developmental intervals. The substantial variability of final stature among gigantism patients indicates that GH concentration alone does not determine skeletal endpoint length, as genomic determinants regulating morphogenesis, physeal maturation timing, and systemic endocrine integration remain dominant modulators of height phenotype.
Click to expand...
Gigantism demonstrates that GH is sufficient to increase height when growth plates are open. The fact that GH is chronically elevated in a pathological state does not change the underlying biology. Variability in final height among patients reflects genetics, nutrition, and hormonal timing, but does not negate the causal role of GH in stimulating growth plate proliferation. Therefore, gigantism provides clear proof that GH can increase skeletal length under the right conditions.


Ahmed88 said:
The hypothesis that recombinant GH administration can replicate tumor-mediated hormone exposure through dosage escalation or injection frequency modification neglects nonlinear endocrine pharmacokinetics. Receptor regulatory desensitization, intracellular inhibitory mediators such as suppressor of cytokine signaling proteins, and multi-axis hormonal feedback networks impose adaptive constraints on somatotropic signaling. Biological regulatory systems function under complex homeostatic modulation rather than simple linear amplification relationships.

Moreover, longitudinal clinical evidence does not demonstrate substantial augmentation of adult stature in individuals possessing intact somatotropic axis function who receive recombinant GH therapy. Investigations involving treatment outcomes in Idiopathic short stature and related non-deficient pediatric populations reveal only marginal modification of final skeletal height despite prolonged pharmacological exposure. These observations indicate that enhancement of growth velocity does not necessarily translate into expansion of developmental endpoint size.

The conjecture that accelerated proliferative activity can consistently exceed physeal maturation progression is unsupported by histomorphological developmental data. In many biological growth systems, increased mitogenic signaling is accompanied by proportional acceleration of differentiation and tissue maturation, thereby preserving overall developmental trajectory rather than extending ultimate structural dimensions.
Click to expand...
While normal-dose GH therapy in GH-sufficient children produces modest height gains due to homeostatic feedback, this does not negate the fundamental biology. GH drives growth plate proliferation through IGF-1, and gigantism demonstrates that chronic, high-level GH exposure can substantially increase height. Regulatory mechanisms like receptor desensitization or SOCS proteins modulate the effect but do not abolish it. Acceleration of proliferation may sometimes advance hypertrophy, yet the growth plate is far from maximal efficiency in typical humans, leaving room for increased chondrocyte output and skeletal elongation under elevated GH conditions.


--

TLDR: OP uses GPT for his arguments and knows nothing about the specific important pathways. He has demonstrated 0 knowledge of the growth plate, proper logic, PTHrP loop, etc. GH DOES increase height. That is observed in many ways.

@Ghost Philosophy can we get this user banned..? This is GPT slop that is misinformation. Nothing about this was at all correct.
 
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topology said:
More nuanced than just that. GH also increases IGF-1 which is the majority of the signal. IGF-1 largely dominates GH. Also, "thus allow for growth in size" can be very misleading, the chondrocytes grow about 5x in the hypertrophic phase regardless and mass amounts of GH only slightly make it bigger. The growth is due to the increased replication amount. The IGF-1 signals the cell to keep duplicating before its life runs out.


Oversimplified.


Incorrect and conceptually wrong.


I'm concerned this entire thread was written by AI at this point. GH promotes chondrocytes duplicating. This is good as the entire reason the average person is nowhere near the average patient with gigantism is due to them duplicating insane amounts. People with gigantism showcase we are not near our genetic potential in any regard. Increased GH will cause height to increase. It's just that the ratio isn't 1:1 and rather logarithmic or so.

The cells' "genetic-based growth capacity" isn't even an argument as we aren't at our genetic potential like I stated. Chondrocytes don't get "tired" or "exhausted" like how GPT might make it seem like. The PTHrP loop demonstrates that the main thing that matters is SOX9 upregulation.


This is the same point as before..?


Over simplification which is implying a false narrative. The effect would be blunted, not eliminated.


IGF-1 levels could be pushed higher with endogenous GH... This is seen in studies.. Gigantism proves this.. Did you just pull this out GPT..?????



Except it's nothing like that at all..? We are nowhere near our genetic potential. I'd love for you to justify how gigantism patients work then.



You don't know what you're talking about.. They replicate faster but it does not necessarily mean they also go from proliferation -> pre hypertrophic faster. Therefore, you will be taller.



Gigantism just doesn't exist, I guess...


That's not even an argument. You made the broad claim that hgh will not work for users here. It will if you inject enough. The feedback system can be bypassed via doing more no matter what, it will just be blunted like I stated. Gigantism/tumor patients don't have anything else unique. This shows that GH is what truly matters.



Slightly lower E2 & increase PTHrP and lower IHH. There you go. That's fixed now!

And before "you would need crazy amounts to grow, it's not realistic," you made a general claim that is very misleading, it doesn't matter if an unhealthy treatment is there.


Good one.. Except the normal range is within a narrow margin. It's like comparing SOX9 levels and thinking it's irrelevant because they're not taller solely off it.


No..? It's not..? It shows the feedback loop is a major factor and we're nowhere close to genetic limits. The loop can be bypassed. You know nothing about height. Go ahead and explain to me the growth plate structure and how chondrocytes are even made, bub. You know nothing.


E2 does regulate growth plate activity.
SOX9 overrides wnt/b-catenin pathways. Estrogen makes the levels go higher. Wnt/b-catenin cannot force cells to exit proliferation immediately. SOX9 “overrides” the differentiation signal.
Lower E2 and increase PTHrP. There you go, it's fixed.


Gigantism proves that isolated GH excess can drive extreme height. You do not need "all pituitary hormones disrupted" to explain gigantism. The claim confuses potential effects with typical functional outcome.


@StyIix @Fridx @sergdying


This is what I mean when I say people don't know what they're talking about. This guy said blocking E2 disrupts SOX9 + RUNX2.. E2 HIGHERS SOX9 WHICH MAKES CELLS REPLICATE MORE BEFORE MOVING ONTO THE PRE HYPERTROPHIC STAGE. SOX9 IS ALSO DIRECTLY LINKED TO INHIBITING RUNX2. RUNX2 SHOULD BE INHIBITED. HE ASKED CHATGPT FOR ARGUMENTS. HE HAS NO SHAME AND NO MERIT. THESE PEOPLE ARE MORONS.


Going off what exactly..? NO STUDY HAS BEEN DONE ON THE AMOUNTS NEEDED. You made claims on this all being speculation and then say this.. Yikes..


Go ahead and tell me what changes with gigantism. Scientists have ruled growth hormone works for height off that. Get a grip.


Are you joking at this point..? You claim e2 would disrupt the hypertrophic transition when it would help and then say this..?

This isn't even correct either. The PTHrP loop is responsible for the cell going to the next phase. The levels are based upon a gradient. This is based upon how far up/down they are in their journey. The majority of the "exhaustion" comes from time. One dividing at 1 unit per second vs another dividing at 3 units per second wouldn't cause a major difference in when they transition. The SOX9 levels are untouched.


GPT slop once again. Collagen X, RUNX2, MEF2C/MEF2D are all idealized with what I said.

Also, WE'RE NOT EVEN CLOSE TO THE LIMIT. WE HAVE AT MOST .01% EFFIECNY. THERE COULD BE MAGNITUDES OF ORDERS OF MORE DIVISON. WE WOULD RUN INTO ATP/OXYGEN PROBLEMS BEFORE ANY OF THAT.


Gigantism demonstrates that GH is sufficient to increase height when growth plates are open. The fact that GH is chronically elevated in a pathological state does not change the underlying biology. Variability in final height among patients reflects genetics, nutrition, and hormonal timing, but does not negate the causal role of GH in stimulating growth plate proliferation. Therefore, gigantism provides clear proof that GH can increase skeletal length under the right conditions.



While normal-dose GH therapy in GH-sufficient children produces modest height gains due to homeostatic feedback, this does not negate the fundamental biology. GH drives growth plate proliferation through IGF-1, and gigantism demonstrates that chronic, high-level GH exposure can substantially increase height. Regulatory mechanisms like receptor desensitization or SOCS proteins modulate the effect but do not abolish it. Acceleration of proliferation may sometimes advance hypertrophy, yet the growth plate is far from maximal efficiency in typical humans, leaving room for increased chondrocyte output and skeletal elongation under elevated GH conditions.


--

TLDR: OP uses GPT for his arguments and knows nothing about the specific important pathways. He has demonstrated 0 knowledge of the growth plate, proper logic, PTHrP loop, etc. GH DOES increase height. That is observed in many ways.

@Ghost Philosophy can we get this user banned..? This is GPT slop that is misinformation. Nothing about this was at all correct.
Click to expand...
High iq
 
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Holy shit, i shouldn't have pressed the ,,show ignored content button"
topology said:
More nuanced than just that. GH also increases IGF-1 which is the majority of the signal. IGF-1 largely dominates GH. Also, "thus allow for growth in size" can be very misleading, the chondrocytes grow about 5x in the hypertrophic phase regardless and mass amounts of GH only slightly make it bigger. The growth is due to the increased replication amount. The IGF-1 signals the cell to keep duplicating before its life runs out.
Click to expand...
Mostly correct, the presence of IGF-1 doesn't invalidate my point.

topology said:
Oversimplified.
Click to expand...
Conceptually sound.

topology said:
Incorrect and conceptually wrong.
Click to expand...
Not wrong.
topology said:
This is the same point as before..?
Click to expand...
Sounds better.

topology said:
Over simplification which is implying a false narrative. The effect would be blunted, not eliminated.
Click to expand...
Also conceptually sound. I am implying nothing but the truth.

topology said:
IGF-1 levels could be pushed higher with endogenous GH... This is seen in studies.. Gigantism proves this.. Did you just pull this out GPT..?????
Click to expand...
I debated this with the other users, u can read it urself, ( in short: its medically wrong to compare normal children with a tumour, even if it was possible (with continous 24/7 hugh amounts of HGH, you're essentially mimicking a DISEASE)
topology said:
Except it's nothing like that at all..? We are nowhere near our genetic potential. I'd love for you to justify how gigantism patients work then
Click to expand...
,,nowhere near our genetic potential" yeah im lost for words, are we just pulling shit out of our ass???
topology said:
You don't know what you're talking about.. They replicate faster but it does not necessarily mean they also go from proliferation -> pre hypertrophic faster. Therefore, you will be taller.
Click to expand...
You're treating them them as if they're independent knobs, you can tweak separately, they're NOT. In the growth plates they are tightly coupled processes.

topology said:
Gigantism just doesn't exist, I guess...
Click to expand...
Im talking about exogenous HGH :feelsuhh:

topology said:
That's not even an argument. You made the broad claim that hgh will not work for users here. It will if you inject enough. The feedback system can be bypassed via doing more no matter what, it will just be blunted like I stated. Gigantism/tumor patients don't have anything else unique. This shows that GH is what truly matters.
Click to expand...
Do you even read other arguments? I clearly specified why it doesn't work MULTIPLE times, atp you're ragebaiting
topology said:
Slightly lower E2 & increase PTHrP and lower IHH. There you go. That's fixed now!

And before "you would need crazy amounts to grow, it's not realistic," you made a general claim that is very misleading, it doesn't matter if an unhealthy treatment is there.
Click to expand...
Medically wrong. You can not achieve optimal levels. You're acting like u have a control panel infront of you ,,yeah lets lower a little E2, tune a but of PTHrP and some of IHH" Thats just not how biology works
topology said:
Good one.. Except the normal range is within a narrow margin. It's like comparing SOX9 levels and thinking it's irrelevant because they're not taller solely off it.
Click to expand...
Nope, just wrong.

topology said:
No..? It's not..? It shows the feedback loop is a major factor and we're nowhere close to genetic limits. The loop can be bypassed. You know nothing about height. Go ahead and explain to me the growth plate structure and how chondrocytes are even made, bub. You know nothing.
Click to expand...
Are you like fucking mentally retarded? I had enough of this
topology said:
E2 does regulate growth plate activity.
SOX9 overrides wnt/b-catenin pathways. Estrogen makes the levels go higher. Wnt/b-catenin cannot force cells to exit proliferation immediately. SOX9 “overrides” the differentiation signal.
Lower E2 and increase PTHrP. There you go, it's fixed.
Click to expand...
Lmao, you're going in circles, You’re taking individual pieces of signaling biology (SOX9, Wnt/β-catenin, E2, PTHrP) and treating them like isolated switches with a clear “override hierarchy.” That’s not how the growth plate works.

I won't even bother going into detail on this one since its easy to understand, and just useless
topology said:
Gigantism proves that isolated GH excess can drive extreme height. You do not need "all pituitary hormones disrupted" to explain gigantism. The claim confuses potential effects with typical functional outcome.
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Medically wrong once again. Stop going in circles and read the fucking replies i sent to other people
topology said:
This is what I mean when I say people don't know what they're talking about. This guy said blocking E2 disrupts SOX9 + RUNX2.. E2 HIGHERS SOX9 WHICH MAKES CELLS REPLICATE MORE BEFORE MOVING ONTO THE PRE HYPERTROPHIC STAGE. SOX9 IS ALSO DIRECTLY LINKED TO INHIBITING RUNX2. RUNX2 SHOULD BE INHIBITED. HE ASKED CHATGPT FOR ARGUMENTS. HE HAS NO SHAME AND NO MERIT. THESE PEOPLE ARE MORONS.
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Yeah i had enough, you’re oversimplifying the growth plate biology so hard it’s not even funny Yes E2 affects SOX9 and RUNX2, and SOX9 delays RUNX2-mediated hypertrophy, but it’s not some magic “override switch” you can just flip Estradiol is essential for proper GH/IGF-1 signaling, chondrocyte proliferation, matrix production, and overall growth plate organization. Lowering it doesn’t “extend proliferation” it destabilizes the fucking system.



topology said:
Going off what exactly..? NO STUDY HAS BEEN DONE ON THE AMOUNTS NEEDED. You made claims on this all being speculation and then say this.. Yikes.
Click to expand...
The studies i linked? Are u mentally challenged, or dylexic?

topology said:
Go ahead and tell me what changes with gigantism. Scientists have ruled growth hormone works for height off that. Get a grip.
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Once again, i and cometohaunted explained this multiple times, Scientists have ruled growth hormone doesn't work for normal children
topology said:
Are you joking at this point..? You claim e2 would disrupt the hypertrophic transition when it would help and then say this..?

This isn't even correct either. The PTHrP loop is responsible for the cell going to the next phase. The levels are based upon a gradient. This is based upon how far up/down they are in their journey. The majority of the "exhaustion" comes from time. One dividing at 1 unit per second vs another dividing at 3 units per second wouldn't cause a major difference in when they transition. The SOX9 levels are untouched.
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Are you serious? You’re totally misrepresenting how growth plate biology works. I never said E2 would disrupt the system, E2 doesn’t “disrupt” hypertrophic transition, it actually supports it by coordinating proliferation and differentiation properly The PTHrP IHH loop is what controls the timing of when chondrocytes move from proliferation to pre-hypertrophy, and it’s gradient-based depending on cell position, not how fast they’re dividingSo saying that faster replication from higher SOX9 or GH somehow makes them transition sooner is wrong the majority of timing is set by developmental programming, not replication speed. One cell dividing faster than another doesn’t suddenly bypass the PTHrP IHH gradient. SOX9 levels stay the same, and the transition to hypertrophy is still governed by positional cues and intrinsic timing. You can speed up proliferation briefly, but that doesn’t extend growth plate lifespan or final height.

topology said:
GPT slop once again. Collagen X, RUNX2, MEF2C/MEF2D are all idealized with what I said.

Also, WE'RE NOT EVEN CLOSE TO THE LIMIT. WE HAVE AT MOST .01% EFFIECNY. THERE COULD BE MAGNITUDES OF ORDERS OF MORE DIVISON. WE WOULD RUN INTO ATP/OXYGEN PROBLEMS BEFORE ANY OF THAT.
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Yeah man this is the most retarded shit, i've read, pulling shit out ur ass, i don't even know what to say ,,.01%"? Fucking hell bro
topology said:
Gigantism demonstrates that GH is sufficient to increase height when growth plates are open. The fact that GH is chronically elevated in a pathological state does not change the underlying biology. Variability in final height among patients reflects genetics, nutrition, and hormonal timing, but does not negate the causal role of GH in stimulating growth plate proliferation. Therefore, gigantism provides clear proof that GH can increase skeletal length under the right conditions.
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Muhhhhhhhh Gigantism brooooooo gigantism brooo muhhhhh, this whole reply is filled with your muh gigantism, stop fucking repeating arguments nigga
topology said:
While normal-dose GH therapy in GH-sufficient children produces modest height gains due to homeostatic feedback, this does not negate the fundamental biology. GH drives growth plate proliferation through IGF-1, and gigantism demonstrates that chronic, high-level GH exposure can substantially increase height. Regulatory mechanisms like receptor desensitization or SOCS proteins modulate the effect but do not abolish it. Acceleration of proliferation may sometimes advance hypertrophy, yet the growth plate is far from maximal efficiency in typical humans, leaving room for increased chondrocyte output and skeletal elongation under elevated GH conditions.
Click to expand...
holy shit nigga is gigantism all you say?gigantism is not a normal model for GH effects it’s caused by pituitary tumors that chronically flood the body with GH, bypassing all feedback loops and exposing growth plates to unregulated IGF1 over years. In healthy kids, feedback mechanisms, receptor regulation, genetics and growth plate programming immediately limit excess GH, so you can’t replicate that. Growth plates aren’t underutilized “factories proliferation, hypertrophy, and ossification are tightly timed and position-dependent. Gigantism shows what happens when the system is broken; it does not prove you can safely or effectively increase adult height in normal humans and tbh, we don’t even fully understand tumor biology, secretion patterns, or how exactly it interacts with the rest of the endocrine system.

Which once again proves how flawed and stupid and retarded you are to compare a unhealthy tumor, with normal kids
 
Ahmed88 said:
Conceptually sound.
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Not at all..? It's over simplified and not actually representative of the truth.

Ahmed88 said:
Not wrong.
Click to expand...
There are 3 types of bone types. It doesn't paint the full picture.

Ahmed88 said:
Also conceptually sound. I am implying nothing but the truth.
Click to expand...
Endocrine feedback and receptor desensitization cause diminishing returns on GH/IGF-1 signaling, but they do not eliminate supraphysiologic effects, only blunts them. What you stated is very misleading to make your point sound like it has more merit than it actually does.

Ahmed88 said:
Mostly correct, the presence of IGF-1 doesn't invalidate my point.
Click to expand...
The point is you have many gaps in what you say. It's obvious it's from ChatGPT. You try to explain everything but fail to explain the actual logical gaps.

Ahmed88 said:
I debated this with the other users, u can read it urself, ( in short: its medically wrong to compare normal children with a tumour, even if it was possible (with continous 24/7 hugh amounts of HGH, you're essentially mimicking a DISEASE)
Click to expand...
No, you didn't. Your argument holds no merit. No doctor would agree with you.

Ahmed88 said:
,,nowhere near our genetic potential" yeah im lost for words, are we just pulling shit out of our ass???
Click to expand...
Gigantism proves that..?

:lul::lul::lul::lul:

The average replications done by progenitors is orders of magnitudes smaller than the genetic celling. The progenitors can replicate about 10-100x more depending on the person. The limit is NEVER things like SHOX, FGFR3, etc.

Gigantism proves this, bub. And before "The loop is ruined!!!" It doesn't matter, the loop can be bypassed via inputting more largely, the increase is also logarithmic, we wouldn't need gigantism levels to be much taller. The current limit is due to the PTHrP levels. Go and do some research.

Ahmed88 said:
You're treating them them as if they're independent knobs, you can tweak separately, they're NOT. In the growth plates they are tightly coupled processes.
Click to expand...
Go ahead and link sources showing how using growth hormone to up the replication will cause them to progress faster and not get a net gain. I do not want a link to the replication limit.

You literally debunked this point below. You're using GPT and not realizing you contradict yourself.

Ahmed88 said:
Im talking about exogenous HGH :feelsuhh:
Click to expand...
Doesn't matter..?

Ahmed88 said:
Do you even read other arguments? I clearly specified why it doesn't work MULTIPLE times, atp you're ragebaiting
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The arguments have no merit. The things you stated are incorrect and/or misleading. Go ahead and debunk me.

Ahmed88 said:
Medically wrong. You can not achieve optimal levels. You're acting like u have a control panel infront of you ,,yeah lets lower a little E2, tune a but of PTHrP and some of IHH" Thats just not how biology works
Click to expand...
You can..?

PTHrP can be injected near the growth plate and it would work upon it..
E2 being lowered would increase efficiency. This one is obviously the easiest to accomplish.
Vismodegib for example would decrease IHH.

The argument here isn't even to encourage that but rather to show you're wrong biologically.

Ahmed88 said:
Nope, just wrong.
Click to expand...
How is that wrong.? Height is polygenetic like you mentioned. Hormone levels are only outside the normal range when a condition occurs. It's not like you can be between 1 unit - 100,000 units naturally.. The normal range is irrelevant. The conditions even prove my point more. It shows more/less GH will cause height differences.

Ahmed88 said:
Are you like fucking mentally retarded? I had enough of this
Click to expand...
Not an argument..? What I stated is the truth. Doesn't matter if it's unhealthy by any standard.

Ahmed88 said:
Lmao, you're going in circles, You’re taking individual pieces of signaling biology (SOX9, Wnt/β-catenin, E2, PTHrP) and treating them like isolated switches with a clear “override hierarchy.” That’s not how the growth plate works.

I won't even bother going into detail on this one since its easy to understand, and just useless
Click to expand...
wnt/B-catenin only is able to override SOX9 assuming it has high levels for long enough.. The current limitations is the PTHrP levels. wnt/b-catenin does not cause the main transition currently. There is a clear hierarchy when talking about SOX9, you moron. It directly inhibits the job of Wnt/B-catenin. Also, you're acting like the pathway isn't easily fixable. You can make it self destruct via axins.


There was no point being made. E2 only lowers predicted height as it impacts PTHrP. SOX9 is a result of the PTHrP loop. Do you know anything about this subject..? Wnt/B-catenin makes the transcription factors within the nucleus.. SOX9 inhibits it.. See the link..? It's all connected, it's not individualized.

Ahmed88 said:
Medically wrong once again. Stop going in circles and read the fucking replies i sent to other people
Click to expand...
Gigantism is driven by excess GH acting through the GH–IGF-1 axis, which increases chondrocyte proliferation and slightly increases hypertrophic expansion at the growth plate. That is sufficient on its own to produce extreme growth, and pretending otherwise just shows how much of a moron you are.

Growth plate closure is primarily regulated by Estrogen, not GH, which is why conditions with impaired estrogen signaling continue growing despite normal or even low GH.

GH/IGF-1 does not inherently accelerate senescence, it amplifies growth velocity, while closure depends on estrogen-mediated depletion of the progenitor pool and differentiation dynamics.

Yes, feedback loops and receptor desensitization exist, but they impose diminishing returns, not a hard stop, otherwise disorders like Gigantism wouldn’t reach extreme heights.

Claiming that “all hormones/pathways must be disrupted” conflicts secondary tumor effects with the primary mechanism. Isolated GH excess is both clinically and mechanistically sufficient. This is proven.

Ahmed88 said:
Yeah i had enough, you’re oversimplifying the growth plate biology so hard it’s not even funny Yes E2 affects SOX9 and RUNX2, and SOX9 delays RUNX2-mediated hypertrophy, but it’s not some magic “override switch” you can just flip Estradiol is essential for proper GH/IGF-1 signaling, chondrocyte proliferation, matrix production, and overall growth plate organization. Lowering it doesn’t “extend proliferation” it destabilizes the fucking system.
Click to expand...
You're overstating it. E2 modulates the GH/IGF-1 axis, it's not the depending factor. Also, this is IRRELEVANT as we're assuming it's synthetic hormones. Low E2 levels largely don't affect the chondrocyte proliferative zone receptors. Your argument doesn't have any merit. They would continue dividing and only IF E2 is too low would it cause in issue in later stages, not the proliferation. Increasing SOX9 would actually improve growth plate organization too :lul::lul::lul: It would cause more ECM to be made which causes the pre hypertrophic phase to go more smoothly. The structural issues as a result wouldn't occur until much later.


Ahmed88 said:
The studies i linked? Are u mentally challenged, or dylexic?
Click to expand...
The "studies" don't administer anything to healthy children and even if they did, it wouldn't be enough...? You linked no studies showing what I was asking for..


Ahmed88 said:
Once again, i and cometohaunted explained this multiple times, Scientists have ruled growth hormone doesn't work for normal children
Click to expand...
This is factually false. Go ahead and provide your source. Growth hormone therapy is given to anyone who is short enough, you don't require a condition.


Ahmed88 said:
and it’s gradient-based depending on cell position, not how fast they’re dividingSo saying that faster replication from higher SOX9 or GH somehow makes them transition sooner is wrong the majority of timing is set by developmental programming, not replication speed.
Click to expand...
The thing that makes them turn is going down the PTHrP gradient like you said.. This literally works against your argument. You said GH makes your cells transition sooner. The genetic limits are nowhere near what natural humans are at. Therefore, increasing SOX9 would increase replication and make you taller. The structural issues would not arise until much later as I stated before more SOX9 means more ECM.


Ahmed88 said:
One cell dividing faster than another doesn’t suddenly bypass the PTHrP IHH gradient. SOX9 levels stay the same, and the transition to hypertrophy is still governed by positional cues and intrinsic timing. You can speed up proliferation briefly, but that doesn’t extend growth plate lifespan or final height.
Click to expand...
You can increase proliferation.. That means more cells.. That means more height.. The limit currently is not the genetic celling you're talking about.. That's the issue within your argument.. No argument was made for plate lifespan..

The final height would be higher as you make more cells. Follow the logic..?

Also, I'm not even sure what you're trying to get at. This debunks your whole HGH makes transitioning happens faster argument.

Ahmed88 said:
One cell dividing faster than another doesn’t suddenly bypass the PTHrP IHH gradient. SOX9 levels stay the same
Click to expand...

I'd like to make a comment specifically on this.

This is my entire point..?

More cells = more height. Nothing negative is affected.. Yikes.


Ahmed88 said:
Yeah man this is the most retarded shit, i've read, pulling shit out ur ass, i don't even know what to say ,,.01%"? Fucking hell bro
Click to expand...
SHOX, FGFR3, etc are not the celling. I don't know where you got that idea from. Gigantism proves this as it doesn't impact the genetic code..


Ahmed88 said:
Muhhhhhhhh Gigantism brooooooo gigantism brooo muhhhhh, this whole reply is filled with your muh gigantism, stop fucking repeating arguments nigga
Click to expand...
Maybe because it debunks everything you said..?



Ahmed88 said:
holy shit nigga is gigantism all you say?gigantism is not a normal model for GH effects it’s caused by pituitary tumors that chronically flood the body with GH, bypassing all feedback loops and exposing growth plates to unregulated IGF1 over years.
Click to expand...
And that can be replicated..? It would once again only blunt it but still allow you to climb levels.. Yikes.


Ahmed88 said:
In healthy kids, feedback mechanisms, receptor regulation, genetics and growth plate programming immediately limit excess GH, so you can’t replicate that.
Click to expand...
You're using normal genetics to try and explain a synthetic hormonal approach..? :lul::lul::lul::lul::lul::lul::lul: All the loops can be bypassed, get a grip.

Ahmed88 said:
Growth plates aren’t underutilized “factories proliferation, hypertrophy, and ossification are tightly timed and position-dependent.
Click to expand...
The proliferative stage would be optimized with SOX9.

Guess what..? SOX9 makes more ECM. ECM is what is needed for the pre hypertrophic phase.

You could easily combine it with a bone stack to manage the bone issues/terminal differentiation issue too. Not sure what argument this even is.


Ahmed88 said:
Gigantism shows what happens when the system is broken; it does not prove you can safely or effectively increase adult height in normal humans and tbh, we don’t even fully understand tumor biology, secretion patterns, or how exactly it interacts with the rest of the endocrine system.
Click to expand...
Gigantism shows that more IGF-1 and GH means being taller. If I can prove you can raise levels way above the normal would you concede..? You wouldn't, that's the issue. The tumor doesn't impact anything major, it would be obvious if it had.


Ahmed88 said:
Which once again proves how flawed and stupid and retarded you are to compare a unhealthy tumor, with normal kids
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You didn't even provide an argument. You said "Gigantism = not normal so not applied to normal kids. We also don't know what gigantism is. Growth plates aren't something you can program."

Literal GPT arguments. This is exactly what GPT pushes back on when you provide an argument to it. Get a grip, it's so obvious what you're doing.
 
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