Noahlooksmaxx
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This is not medical advice. This document is a theoretical and educational framework for research and educational purposes only. The compounds and methods discussed in this framework do not constitute a diagnosis, prognosis, prescription, or treatment recommendation. None of these compounds or methods are approved explicitly for the purposes of maximizing height, facial modification, or off-label use in humans without the presence of clinical oversight. The author assumes no liability for having written this document. You agree to hold harmless the author of this document, who expressly disclaims all responsibility for actions taken or not taken based on the information discussed herein.
Photo showcasing the difference between open and closed growth plates in the femurs.
In order to achieve a greater height velocity by way of exogenous HGH alone, your growth plates must be open. You can get an x-ray of the wrist and knee to confirm this, and have a doctor measure your bone age to see what potential height increase you have left. HGH increases chondrocyte proliferation in the growth plates, so if your growth plates have been exhausted, this growth pathway is closed to you for good. Your wrist growth plates fuse first, then knees, then spine, then finally in your 20s, your craniofacial sutures.
First high quality post so sorry if its not as good as its supposed to be. I hoped i found all the mistakes while checking for them jfl
Human growth hormone (somatropin) is a peptide hormone that stimulates growth in the body. Endogenous GH is produced by the pituitary gland in a pulsatile manner, converting to hepatic IGF-1. This production is highest during sleep. HGH binds to growth hormone receptors (GHR) which activates downstream genes responsible for growth. Both HGH and IGF-1 bind to osteogenic cell receptors and are directly responsible for osteoblast differentiation and the expression of genes such as collagen 1α1, OCN, ALP, BMP2, and BMP4 [1]. Locally produced IGF-1, not just hepatic, is responsible for skeletal remodeling through IGF binding proteins. In other words, higher levels of HGH leads to more skeletal remodeling and bone formation.
Photo showcasing the difference between open and closed growth plates in the femurs.
In order to achieve a greater height velocity by way of exogenous HGH alone, your growth plates must be open. You can get an x-ray of the wrist and knee to confirm this, and have a doctor measure your bone age to see what potential height increase you have left. HGH increases chondrocyte proliferation in the growth plates, so if your growth plates have been exhausted, this growth pathway is closed to you for good. Your wrist growth plates fuse first, then knees, then spine, then finally in your 20s, your craniofacial sutures.
Lipolysis: upregulates your body’s ability to hydrolyze lipid triglycerides, mobilizing stored fat cells into energy. HGH is very effective for targeting stubborn fat deposits and body recomposition
Bone formation: GH can increase linear growth velocity especially in the case of height. While studies focus on idiopathic short stature and GH deficiencies, there are countless anecdotes showing HGH can increase adult height even in non-GH deficient individuals.
Periosteal and appositional bone growth even after the fusion of facial sutures (think: jaw thickening and widening, brow ridge protrusion, extended zygomatic bones)
Longitudinal growth in open growth plates and facial sutures: forward maxillary growth, elongation of the mandibular ramus, and frontal/nasal bone projection
Sleep quality: HGH reduces sleep disturbances and thus improves sleep quality as confirmed by a 4 month rHGH replacement therapy study.
Lean muscle mass: while it doesn’t have a direct anabolic effect on skeletal muscle mass, there are other performance parameters influenced by HGH/IGF-1.
Bone formation: GH can increase linear growth velocity especially in the case of height. While studies focus on idiopathic short stature and GH deficiencies, there are countless anecdotes showing HGH can increase adult height even in non-GH deficient individuals.
Periosteal and appositional bone growth even after the fusion of facial sutures (think: jaw thickening and widening, brow ridge protrusion, extended zygomatic bones)
Longitudinal growth in open growth plates and facial sutures: forward maxillary growth, elongation of the mandibular ramus, and frontal/nasal bone projection
Sleep quality: HGH reduces sleep disturbances and thus improves sleep quality as confirmed by a 4 month rHGH replacement therapy study.
Lean muscle mass: while it doesn’t have a direct anabolic effect on skeletal muscle mass, there are other performance parameters influenced by HGH/IGF-1.
HGH is often fearmongered due to the risk of hyperglycemia, blunted insulin action, and insulin resistance. This is relatively easy to mitigate.
Checklist:
Blood glucose monitor: HGH increases gluconeogenesis and can simultaneously impair glucose tolerance. This makes it essential to monitor fasted glucose. This is not medical advice, but the off-label logic goes that you should monitor glucose levels to catch early dysglycemia.
Glucose control agents:
➢ Berberine: activates AMPK, mimicking metformin to a lesser degree, but oftentimes without the side effects. It’s non-prescription so you can get it from trusted sellers OTC. Suppresses gluconeogenesis in the liver and increases sensitivity to insulin (which HGH can reduce.)
➢ Ceylon cinnamon: often paired with berberine. Improves autophosphorylation of insulin receptors. Modest glucose and HbA1c improvement. Cheap and great safety profile. Pretty weak to take on its own.
➢ Bitter melon: promotes glucose uptake. Inconsistent data in humans. Not reliable, especially on its own, but often combined with berberine.
➢ Metformin: strongest of the pack. Very high evidence in humans for controlling fasted glucose. Favorable lipid profile and potent antioxidant. Can cause side effects in the GI tract and requires a prescription. This is more of a “last resort”. Take B12 with it to avoid deficiency.
➢ Retatrutide: pairs well with HGH in experimental protocols. Due to the glucagon receptor agonism, it can reverse dysglycemia and improve the action of insulin. The real use case here is that if you’re already taking retatrutide, it may be sufficient to manage glucose levels without the need for other agents, but it wouldn’t be recommended to rely on it as a substitute unless needed for weightloss/maintenance.
Checklist:
Blood glucose monitor: HGH increases gluconeogenesis and can simultaneously impair glucose tolerance. This makes it essential to monitor fasted glucose. This is not medical advice, but the off-label logic goes that you should monitor glucose levels to catch early dysglycemia.
Glucose control agents:
➢ Berberine: activates AMPK, mimicking metformin to a lesser degree, but oftentimes without the side effects. It’s non-prescription so you can get it from trusted sellers OTC. Suppresses gluconeogenesis in the liver and increases sensitivity to insulin (which HGH can reduce.)
➢ Ceylon cinnamon: often paired with berberine. Improves autophosphorylation of insulin receptors. Modest glucose and HbA1c improvement. Cheap and great safety profile. Pretty weak to take on its own.
➢ Bitter melon: promotes glucose uptake. Inconsistent data in humans. Not reliable, especially on its own, but often combined with berberine.
➢ Metformin: strongest of the pack. Very high evidence in humans for controlling fasted glucose. Favorable lipid profile and potent antioxidant. Can cause side effects in the GI tract and requires a prescription. This is more of a “last resort”. Take B12 with it to avoid deficiency.
➢ Retatrutide: pairs well with HGH in experimental protocols. Due to the glucagon receptor agonism, it can reverse dysglycemia and improve the action of insulin. The real use case here is that if you’re already taking retatrutide, it may be sufficient to manage glucose levels without the need for other agents, but it wouldn’t be recommended to rely on it as a substitute unless needed for weightloss/maintenance.
This is the most controversial and theoretical part of the guide. How long you run HGH for, and what dosage you use, is not a clear and exact science. Most, if not all, people in this community recommending dosage and cycle length for HGH are speculating heavily. So let’s look at the science and use logic to dictate our decision.
Low Dose
If we use a low dose (e.g. 1-2 iu daily) of exogenous HGH, this will mimic natural GH pulsatile release. This is a fairly typical dose used in GH replacement therapy. Growth rate may improve slightly, while preventing over-calcification of the hypertrophic zones in growth plates. Marginal improvements in craniofacial structure are possible. However, the effect is likely going to be quite minimal.
High Dose
By utilizing a high dose (12iu+ daily) of exogenous HGH, there is a high potential for unintended complications.
❖ Bone age: In studies using high dose HGH replacement therapy on children, the growth velocity increased significantly (increase of ~1.3 SD vs. controls), however, their bone age (rate of skeletal maturation) increased by a factor of 1.8 [8]. This was NOT present in lower dose HGH replacement therapy, which was considered “clinically acceptable”. This tells us that it is indeed true that HGH can increase height velocity dramatically, but is contraindicated by the rate of skeletal maturation.
➢ A huge caveat here is that this is relevant to GH deficient children. Those cases only really need a low clinical dose of GH to replace what their bodies lack, and they would grow normally. In a theoretical case of normal GH production, utilizing exogenous HGH to push growth beyond physiological predictions is not backed by clinical research. However, we have utterly countless anecdotes that HGH works.
➢ The main factor limiting final height is senescence of mesenchymal stem cells and chondrocytes in the growth plates, which is regulated by the hormone estradiol (e2). Essentially, the proliferative zone in the growth plate becomes exhausted. By suppressing e2, we can delay this process and keep growth plates open longer. Anastrozole has clinical research confirming this is effective to grow taller during puberty, and is paired with growth hormone replacement therapy. Using a high dose of HGH makes controlling e2 a critical step, or the growth plate hypertrophic zone can become exhausted early.
➢ There are severe risks of organ enlargement, dysglycemia, acromegaly, blunted insulin response, prediabetic symptoms, left ventricular hypertrophy, and much more. User’s discretion is highly advised at doses exceeding this.
What would be the "Ideal Dose"?
We really have no idea what the ideal dose is for craniofacial development and heightmaxxing. There are no clinical studies with healthy participants with normal GH levels for these purposes. The reason is clear: why would they test a drug on healthy individuals that don’t “need” it? This is because the health industry doesn’t perceive short stature as a flaw, provided it follows their predicted adult height. They certainly don’t consider recessed craniofacial bones as a flaw unless it impairs your breathing or you have a malocclusion. Otherwise, all cosmetic surgeries would be covered by insurance.
So what do we do? We can logically deduce that a dose of 1-2iu daily will lead to very little changes in bone development, and that high doses exceeding 12iu daily will lead to adverse effects and could exhaust the hypertrophic zones in growth plates. So, the ideal likely falls somewhere in the middle. If we were to take 5-6iu daily, we can mitigate side effects while still getting the advantages of greatly increasing bone development. Due to local estrogenic activity, we still have the potential to speed up bone age and lead to relatively early growth plate fusion, so managing this is still important. At this dose, IGF-1 will typically rise to 2-3x serum concentrations in a few weeks. Sustaining this for several months will lead to enhanced skeletal remodeling.
How long is the Cycle?
The ideal cycle is anywhere from 3-9 months. Any less and you get very limited results, since there isn’t enough time for true skeletal remodeling. This is just when your growth velocity starts to increase. Any more and you risk IGF-1 receptor desensitization, diminishing returns, and hypertrophic zone exhaustion. This of course is all dependent on your genetics and anatomy. Some people will benefit more from a longer cycle, and some people will benefit a lot from a short blast. Do your own research, get your blood work done, and take your support meds.
Example Cycle: 8 months
❖ 6iu HGH daily, pinned at night
❖ 1,200mg berberine HCI daily
❖ 200mg ceylon cinnamon daily❖ 1mg anastrozole every other day
❖ 5,000iu vitamin D3 daily
❖ 100mcg vitamin K2 daily
❖ 1g calcium daily
❖ 250mg magnesium glycinate daily
❖ 30mg zinc glycinate daily
❖ 3mg boron daily
❖ 1g MSM 2x daily
❖ Omega 3 fatty acids (2-4g EPA + DHA) daily
❖ Pure Encapsulations Men’s Nutrients daily
❖ 500mg nicotinamide mononucleotide daily
Low Dose
If we use a low dose (e.g. 1-2 iu daily) of exogenous HGH, this will mimic natural GH pulsatile release. This is a fairly typical dose used in GH replacement therapy. Growth rate may improve slightly, while preventing over-calcification of the hypertrophic zones in growth plates. Marginal improvements in craniofacial structure are possible. However, the effect is likely going to be quite minimal.
High Dose
By utilizing a high dose (12iu+ daily) of exogenous HGH, there is a high potential for unintended complications.
❖ Bone age: In studies using high dose HGH replacement therapy on children, the growth velocity increased significantly (increase of ~1.3 SD vs. controls), however, their bone age (rate of skeletal maturation) increased by a factor of 1.8 [8]. This was NOT present in lower dose HGH replacement therapy, which was considered “clinically acceptable”. This tells us that it is indeed true that HGH can increase height velocity dramatically, but is contraindicated by the rate of skeletal maturation.
➢ A huge caveat here is that this is relevant to GH deficient children. Those cases only really need a low clinical dose of GH to replace what their bodies lack, and they would grow normally. In a theoretical case of normal GH production, utilizing exogenous HGH to push growth beyond physiological predictions is not backed by clinical research. However, we have utterly countless anecdotes that HGH works.
➢ The main factor limiting final height is senescence of mesenchymal stem cells and chondrocytes in the growth plates, which is regulated by the hormone estradiol (e2). Essentially, the proliferative zone in the growth plate becomes exhausted. By suppressing e2, we can delay this process and keep growth plates open longer. Anastrozole has clinical research confirming this is effective to grow taller during puberty, and is paired with growth hormone replacement therapy. Using a high dose of HGH makes controlling e2 a critical step, or the growth plate hypertrophic zone can become exhausted early.
➢ There are severe risks of organ enlargement, dysglycemia, acromegaly, blunted insulin response, prediabetic symptoms, left ventricular hypertrophy, and much more. User’s discretion is highly advised at doses exceeding this.
What would be the "Ideal Dose"?
We really have no idea what the ideal dose is for craniofacial development and heightmaxxing. There are no clinical studies with healthy participants with normal GH levels for these purposes. The reason is clear: why would they test a drug on healthy individuals that don’t “need” it? This is because the health industry doesn’t perceive short stature as a flaw, provided it follows their predicted adult height. They certainly don’t consider recessed craniofacial bones as a flaw unless it impairs your breathing or you have a malocclusion. Otherwise, all cosmetic surgeries would be covered by insurance.
So what do we do? We can logically deduce that a dose of 1-2iu daily will lead to very little changes in bone development, and that high doses exceeding 12iu daily will lead to adverse effects and could exhaust the hypertrophic zones in growth plates. So, the ideal likely falls somewhere in the middle. If we were to take 5-6iu daily, we can mitigate side effects while still getting the advantages of greatly increasing bone development. Due to local estrogenic activity, we still have the potential to speed up bone age and lead to relatively early growth plate fusion, so managing this is still important. At this dose, IGF-1 will typically rise to 2-3x serum concentrations in a few weeks. Sustaining this for several months will lead to enhanced skeletal remodeling.
How long is the Cycle?
The ideal cycle is anywhere from 3-9 months. Any less and you get very limited results, since there isn’t enough time for true skeletal remodeling. This is just when your growth velocity starts to increase. Any more and you risk IGF-1 receptor desensitization, diminishing returns, and hypertrophic zone exhaustion. This of course is all dependent on your genetics and anatomy. Some people will benefit more from a longer cycle, and some people will benefit a lot from a short blast. Do your own research, get your blood work done, and take your support meds.
Example Cycle: 8 months
❖ 6iu HGH daily, pinned at night
❖ 1,200mg berberine HCI daily
❖ 200mg ceylon cinnamon daily❖ 1mg anastrozole every other day
❖ 5,000iu vitamin D3 daily
❖ 100mcg vitamin K2 daily
❖ 1g calcium daily
❖ 250mg magnesium glycinate daily
❖ 30mg zinc glycinate daily
❖ 3mg boron daily
❖ 1g MSM 2x daily
❖ Omega 3 fatty acids (2-4g EPA + DHA) daily
❖ Pure Encapsulations Men’s Nutrients daily
❖ 500mg nicotinamide mononucleotide daily
In summary, exogenous human growth hormone has a huge potential to induce lipolysis, sleep benefits, enhanced recovery, and real skeletal remodeling and thickening. However, the results of usage of this compound depends entirely on dosage, timing, and managing side effects effectively. If growth plates and facial sutures remain open, HGH exposure can increase chondrocyte proliferation and suture remodeling, leading to steady increases in height velocity and longitudinal growth.
Sources:
1. https://pmc.ncbi.nlm.nih.gov/articles/PMC8150312/
2. https://pmc.ncbi.nlm.nih.gov/articles/PMC7352659/
3. https://pmc.ncbi.nlm.nih.gov/articles/PMC11872712/
4. https://www.ncbi.nlm.nih.gov/books/NBK598214/table/t04/
5. pmc.ncbi.nlm.nih.gov/articles/PMC3832204/#S16
6. https://pmc.ncbi.nlm.nih.gov/articles/PMC2439518/#sec11
7. https://pubmed.ncbi.nlm.nih.gov/18347346/
8. https://pmc.ncbi.nlm.nih.gov/articles/PMC1719235/
9. https://pmc.ncbi.nlm.nih.gov/articles/PMC2266949/
Sources:
1. https://pmc.ncbi.nlm.nih.gov/articles/PMC8150312/
2. https://pmc.ncbi.nlm.nih.gov/articles/PMC7352659/
3. https://pmc.ncbi.nlm.nih.gov/articles/PMC11872712/
4. https://www.ncbi.nlm.nih.gov/books/NBK598214/table/t04/
5. pmc.ncbi.nlm.nih.gov/articles/PMC3832204/#S16
6. https://pmc.ncbi.nlm.nih.gov/articles/PMC2439518/#sec11
7. https://pubmed.ncbi.nlm.nih.gov/18347346/
8. https://pmc.ncbi.nlm.nih.gov/articles/PMC1719235/
9. https://pmc.ncbi.nlm.nih.gov/articles/PMC2266949/
IF YOU CANT FIND IT YOURSELF:
THIS ISNT SOMETHING FOR YOU BOYO
THIS ISNT SOMETHING FOR YOU BOYO
First high quality post so sorry if its not as good as its supposed to be. I hoped i found all the mistakes while checking for them jfl
