shao2niche
Iron
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hello, i am a creator on TT, and this is an old file within my vault, icba to recitify whatever small mistake i've made, but enjoy. icba either to find the images/figures of which it is
Vocab Sheet
Growth Plates -> if you dont know what this is please gtfo
Endocrine Axis -> System of Feedback
HPS Axis -> Hypothalamic-Pituitary-Somatotropic Axis -> GH/IGF-1 Axis
GHRH -> Growth-Hormone-Releasing-Hormone
Somatotrophs -> Pituitary Cells that make and release GH
Ghrelin -> Hunger Hormone that also stimulates GH via a separate receptor, GHSR, and drives appetite, why shi like MK increased GH and also hunger
Somatostatin -> Hypothalamic inhibitor of GH secretion, opposite of GHRH/ghrelin
GH/HGH/Somatropin -> self-explanatory -> Growth Hormone, Somatropin is the name for rhGH -> Recombinant-Human-Growth-Hormone
GHR/Growth Hormone Receptor -> the receptor GH binds to (primarily within liver) to trigger IGF-1 production as well as its direct effects
Endogenous -> "natural" production
Exogenous -> "unnatural" production
Longitudinal -> Linear, in the case of growth it would mean bone lengthening -> height
Epiphyseal Fusion/Closure -> premature growth plate fusion/closure
Endochondral Ossification -> process of cartilage being replaced by bone in which the lengthening of skeleton occurs
Bone Age -> done using an X-ray, primarily of the hand/wrist -> helps to estimate bone age, and how close plates are to closing
Growth Velocity -> growth speed, (measured in cm/year)
Mid-Parental Height/MPH -> genetic estimation from parents height, essentially just guessing based off of genes
Predicted Adult Height/PAH -> projected height using current height and bone age of the person of discussion
Final Adult Height/FAH -> self explanatory, final adult height once plates are 100% closed
Idiopathic Short Stature/ISS -> short stature with no reason/justification -> the population that WE will be learning about regarding HGH/HGH + AI usage
Other Useful LINGOOOOO:
Estradiol/E2 -> primary estrogen, also primary driver of premature growth plate closure, high e2 -> close faster, low e2 -> open longer
Aromatase (CYP19A1) -> enzyme that converts testosterone into E2, why most people express concerns regarding test during puberty as well as why mfs are running TRT dosing w other compound that make up a gram or two of gear
Aromatase Inhibitor/AI -> used to block the enzyme, separated into 2 different kinds reversible, and suicide/irreversible
Selective Estrogen Receptor Modulator/SERM -> different from an AI, blocks estrogen at the receptor, whereas the AI blocks the enzyme, although different tool often used for the same goal (heightmaxxing JFL)
now... onto the GOOD stuff hehe
okay, this is going to be a fun read/write - some of the topics have already been covered minorly within previous topics, but we're going in-depth for this one... how fun
Endocrine System Analysis -> HPS Axis
although this topic has been briefly covered within 01 - The Endocrine System -> 4 Axis
the most important takeaways is the following:
Hypothalamus (brain, which tells your body to release hormones)
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Pituitary (responsible for stimulating hormone)
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Target Gland (whichever gland is required targeting: responsible for the differing hormones, for)
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Effects on the Body:
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-> This causes your body to send signals (regarding the amount thats further needed, e.g. more or less)
also keynote, the original hypothesis regarding HGH was the following
GH -> liver -> circulation of IGF-1 -> growth
-> this model was via somatomedin hypothesis, Salmon & Daughaday 1957 (1957!!! THATS hella long ago, 69 years ago to be specific)
however now the corrected model is as follows
GH acts DIRECTLY on the growth plate, not only via IGF-1 via liver, -> stimulating resting/precursor chondrocytes
-> GH primes the cell, then local IGF-1 drives its clonal expansion
TLDR: regarding height liver IGF-1 doesn't matter for height, whats important is local IGF-1 within the actual growth plates
-> GH directly affects growth plates, and causes local IGF-1
-> study within mice -> lost ~75% of circulating IGF-1
-> still grew to normal height
-> Yakar et al. 1999
also another important side note:
your body can't differentiate between "natural" (endogenous) and "unnatural" (exogenous) production
-> your body has no way to tell if something is "natural vs injected", it reads the level for GH, or essentially the IGF-1/GH signal, and if you have a high enough total GH -> Somatostatin (essentially inhibits the secretion//release of HGH)
-> the reason that your body blunts/decreases the natural HGH production, is because the threshold is reached, given a set point,
- if (GH levels) rise above, Somatostatin will occur
- if (GH levels) lower under, GHRH/Ghrelin will occur
now given that, the real question is:
How can we OPTIMIZE HGH Secretion?
Natural Methods:
okie starting off with natural methods, most of this is well known and effectively water
Sleep -> major stimulus for GH release (occurs in pulses)
Exercise -> stimulates release
Stress -> stimulates release
Fasting -> stimulates release
-> science behind is this is that GH is a counter regulatory fuel hormone -> meaning its job is to raise blood glucose and mobilize fat, so when you're low blood sugar, it stimulates GH
-> this is also why supraphysiological exogenous GH is insulin resistance
Now what to AVOID?
Hyperglycaemia -> suppresses release
-> mentioned above within fasting (essentially hypoglycaemia -> given low bloodsugar)
Obesity -> Estrogen -> Estradiol -> Premature Growth Plate Closure
... now that the water is covered, time to cover what PM suggests about height growth
Unnatural Methods (HGH after this in-depth)
Direct Exogenous GH
-> rhGH, just straight HGH LOL
GHRH and GHRH analogs
-> Sermorelin
-> CJC-1295 w and wo Dac
-> Tesamorelin
GHS
-> GHRPs
-> Hexarelin
-> Ipamorelin
-> MK-677
-> Ghrelin
ofc theres more and a large science behind this given the GHRHR and the GHSR and how it acts via the cAMP/PKA as to the Calcium/PKC, but essentially a mix of these, GHRH + GHS would be ideal
Pubmed & HGH/HGH + AI Usage:
okay, so what exactly do we know about rhGH (exogenous HGH) usage and its effects on developing people?
-> GH increases growth velocity, but can cause premature growth plate closure (in directly)
-> causes earlier puberty, leading it higher e2, leading to growth plate closure
Hochberg et al., found that given 3.3-9 yos 4-6 IUs of HGH, it caused them to be from -1.3 to -2.6 cm shorter than what they would have been
some background information about this study,
-> they took rhGH for 3 years
-> the researchers hypothesized that growth deceleration was due to a tolerance at the target organ level
keep in mind that the average IU secretion during that age was ~2 IU of GH per day (as in avg within adolescence), with prepubertal children on avg to be secreting ~1.8 IUs of GH per day Martha et al.,
so given this information what does this suggest?
- no HGH is not going to magically make you grow taller, you need to know the proper dosing and science behind it
so what exactly is the science behind it and what do we know?
- HGH causes quicker skeletal maturation
- bone age is extremely important
so does this mean that all hope is lost? NO you just need to know how to dose properly as mentioned prior
so what are some aspects to consider?
Martha et al., suggests that the avg person in late puberty (given tanner ages 4-5) produces ~5.4 +- 0.75 IUs every day, given a 24 hour period as HGH is secreted in pulses.
now you might be thinking, doesn't this just mean that i can run ~6ish IUs daily then?
no we JUST went over this....
it causes premature growth plate closure (indirectly), so you may just end up cooking yourself LOL
so now what is actually the proper dosing suggested via PM?
DNR THIS SECTION IF YOU'RE A YOUNG JIT JUST RUN AN AI + HGH, THE MORE THE BETTER LOL
there are several studies regarding this, e.g. Wit et al., Kamp et al., for example, Wit et al.,suggests that for a 0.24 mg/kg/wk dose vs a 0.37 mg/kg/wk resulted in +5.4 cm and a +7.2 cm in overall growth
-> WOW thats great a minor difference of 1.8 cm difference given an increase of 54% GH!
(as in 0.37-0.24 = 0.13 -> 0.13/0.24 = 0.5417, 0.54147 x 100 = ~54%)
okay, minor issue though... this was ran for 2 years.. most of us are close to closing..
so this is useless?
-> not exactly, atleast we have confirmation that essentially says more rhGH = more growth
alright so whats next?
-> We need a group that applies specifically to us, with a growth plates near closure, they also need to have ISS, as a group with GHD doesn't apply to us,
enter Rothenbühler et al., <3
the subjects were 15 boys, each aged 15.5 +- 1 yos, a mean 72.5 ± 9 (0.0725 mg/kg-w) μg dose of rhGH/kg/d was given for 11 +- 4.8 months
how did this affect the boys? adult height reached -1.8 +- 0.9 SDS, while predicted height was -2.9 +- 0.6 SDS
now how does this actually translate? ~7 cm! massive, for near growth plate closure in only a ~year's time thats massive, for context the 7 cm (2.76 inches) is what they had on top of their natural growth.
_assuming a standard deviation (SD) of 6.5 cm.
original PAH
-2.9 × 6.5 = -18.85 cm
_actual FAH
-1.8 × 6.5 = -11.7 cm
gain in height
18.85 - 11.7 = 7.15 cm gain
okay that wraps up the HGH section, now what do we know about AI usage in pair with HGH?
figure A1
Pasted image 20260718222830.png
figure A2
Pasted image 20260718222855.png
AI Usage and in combination with rhGH
the studies that will be examined will be the following:
Mauras et al., (2x because shes the GOAT haha) and Wickman et al.,
now what exactly did these two studies analyze?
Mauras et al.,
"Anastrozole increases predicted adult height of short adolescent males treated with growth hormone: a randomized, placebo-controlled, multicenter trial for one to three years"
-> 52 adolescent males with GH deficiency treated with GH were randomized with either anastrozole or placebo for up to 36 months
-> "Fifty subjects completed 12 months, 41 completed 24 months, and 28 completed 36 months."
-> "Linear growth was comparable between groups; however, there was a significantly slower increase in bone age advancement from baseline in the anastrozole group vs. placebo group after 2 yr (+1.8+/-0.1 vs. +2.7+/-0.1 yr, P<0.0001) and after 3 yr (+2.5+/-0.2 vs. +4.1+/-0.1 yr, P<0.0001)."
->"This resulted in a net increase in predicted adult height of +4.5+/-1.2 cm in the anastrozole group at 24 months and +6.7+/-1.4 cm at 36 months as compared with a 1-cm gain at both time points in the placebo group."
figure B1
Pasted image 20260719171747.png
figure B2
Pasted image 20260719173536.png
TLDR:
study for GHD adolescents ran over a period of 3 years resulted in the following:
-> delayed growth plate closure was very prominent as shown by figure B1
-> there was a massive difference in height -> could possibly show that rhGH alone is useless
- take this with a caveat, as i was unable to access the dosages (extract read only, IM NOT PAYING $60 FOR A LIL SECTION)
alright now you might be asking, ouu shi why did the group with only rhGH show such little gain in PAH?
-> could possibly be a result of premature growth plate closure as we know that rhGH speeds up skeletal speed up
-> resulted in a 4.5 +- 1.2 cm at the 2 year mark, and 6.7 +- 1.4 cm at the 3 year mark, so pretty major differences than just rhGH
but shaonuttt these are people with GHD and unknown AI dosages .. 
(
SAY LESS HOMIE
onto the next study!
Mauras et al.,
"Randomized Trial of Aromatase Inhibitors, Growth Hormone, or Combination in Pubertal Boys with Idiopathic, Short Stature"
-> study done with 76 boys w an average age of 14
-> they were subject to HGH, AI, or HGH + AI
-> dosing was 1 mg Anastrozole ED, or 2.5 mg Letrozole ED, with ~0.42 mg/kg-wk of HGH
side note: the conversion rate between mg and iu is 1:3, so 0.42/7 = 0.06 mg/kg-d
so ~0.18 IU/kg-d, similar to the 0.07 mg/kg-d figure mentioned earlier within Rothenbühler et al.,
->period of study was 24-36 MONTHS
->"Height gain, mean (SE), at 24 months was: AI, +14.0 (0.8) cm; GH, +17.1 (0.9) cm; AI/GH, +18.9 (0.8) cm (P < .0006, analysis of covariance)."
-> "Those treated through 36 months grew more. Regardless of treatment duration, height SDS at near-final height, n = 71; age, 17.4 (0.2) years; bone age, 15.3 (0.1) years; height achieved, ∼97.6%, was: AI, -1.4 (0.1); GH, -1.4 (0.2); AI/GH, -1.0 (0.1) (P = .06). Absolute height change was: AI, +18.2 (1.6) cm; GH, +20.6 (1.5) cm; AI/GH, +22.5 (1.4) cm (P = .01) (expected height gain at -2.0 height SDS, +13.0 cm)."
-> "Combination therapy with AI/GH increases height potential in pubertal boys with ISS more than GH and AI alone treated for 24–36 months with a strong safety profile."
alright so what exactly does this mean?
TLDR: HGH + AI is the most effective by far
AI only prolongs growth plate closure but does nothing for growth velocity
HGH increases growth velocity but can negatively affect growth plate closure (indirectly)
HGH + AI = effects of prolonged growth plate closure, but also the effects of increase growth velocity,
-> some interesting figures from the studies
figure C1
it is evident that AI + HGH is the best, and that fact that HGH ended up with the highest bone age reinforces the idea that it speeds up skeletal maturation and growth plate closure
Screenshot 2026-07-20 at 10.54.39 PM.png
figure C2
once again HGH + AI is the best
Pasted image 20260720225738.png
figure C3
actually interesting graph, FFM = Fat Free Mass, I thought that HGH would yield greater results, but HGH actually turns out to be marginally worse than an AI, so to anyone saying "take HGH for muscle" just take an AI IG LOL
and of course by a significant margin, HGH + AI is the best
Screenshot 2026-07-20 at 10.56.03 PM.png
figure C4
imo the most interesting by far within this entire massive section
regarding the first graph, what happens is the system that has been mentioned prior, AI -> Low E2, body sees that E2 is low and wishes to regulate to a normal amount again, so produces more T to compensate for it, but the aromatase inhibitor keeps inhibiting it, consistent cycle
regarding the second graph, it is crushed in both AI and AI/HGH models, with AI + HGH being slightly higher, now why exactly is E2 so high for the HGH only group? As covered at an earlier time, HGH causes earlier/faster puberty with supraphysiological doses, meaning Test as well as E2 by default would be higher
regarding the third slide, it follows the trend that we've been seeing throughout the last, however with a minor extremely important detail, Estrogen actually induces hepatic GH resistance, you'd think that "oh wow why does that occur? how would Estrogen affect IGF-1? arent they in different axes?", this will be covered at a later date
okay, so ultimately what did we learn from the following 3 graphs? first of all, that HGH + AI is indisputably the best for its job, causing height growth. second of all, it also shows that the different HP axes are interconnected, otherwise it wouldn't explain why HGH + AI is better in some cases and worse in other cases
-> if they didnt interact with each other, for things such as E2, the HGH/AI group would yield the same results as the AI group, however it did not, the same applies for IGF-1
Pasted image 20260720225714.png
"After 4-8 years of GH treatment, Hintz et al. have found a 5-6 cm increase in final height compared to the predicted adult height before beginning therapy, but most patients did not reach their target heights. Other studies, however, have found no improvement in final height and Kawai et al. even suggests that GH therapy diminishes the final height of treated children due to an earlier puberty and a shorter pubertal growth spurt."
SIDE EFFECTS WILL BE COVERED WITHIN 03 - B - HGH with Other Compounds + Side Effects
(ignore this, i use obisidan as a vault for all of my knowledge, so it just links to another file, just wanted to remain authetic, though i may upload it at a later day)abstract from
https://wellesu.com/10.2174/1389201003378997
https://academic.oup.com/jcem/article-abstract/87/8/3573/2846550?redirectedFrom=fulltext&login=false
Meir Lampit, Ze’ev Hochberg, Prevention of Growth Deceleration after Withdrawal of Growth Hormone Therapy in Idiopathic Short Stature, The Journal of Clinical Endocrinology & Metabolism, Volume 87, Issue 8, 1 August 2002, Pages 3573–3577, https://doi.org/10.1210/jcem.87.8.8721
https://pubmed.ncbi.nlm.nih.gov/12193430/
Kamp GA, Waelkens JJ, de Muinck Keizer-Schrama SM, Delemarre-Van de Waal HA, Verhoeven-Wind L, Zwinderman AH, Wit JM. High dose growth hormone treatment induces acceleration of skeletal maturation and an earlier onset of puberty in children with idiopathic short stature. Arch Dis Child. 2002 Sep;87(3):215-20. doi: 10.1136/adc.87.3.215. PMID: 12193430; PMCID: PMC1719235.
https://pubmed.ncbi.nlm.nih.gov/7634503/
Barton JS, Gardineri HM, Cullen S, Hindmarsh PC, Brook CG, Preece MA. The growth and cardiovascular effects of high dose growth hormone therapy in idiopathic short stature. Clin Endocrinol (Oxf). 1995 Jun;42(6):619-26. doi: 10.1111/j.1365-2265.1995.tb02689.x. PMID: 7634503.
https://pubmed.ncbi.nlm.nih.gov/12460321/
Lanes R, Gunczler P, Esaa S, Weisinger JR. The effect of short- and long-term growth hormone treatment on bone mineral density and bone metabolism of prepubertal children with idiopathic short stature: a 3-year study. Clin Endocrinol (Oxf). 2002 Dec;57(6):725-30. doi: 10.1046/j.1365-2265.2002.01614.x. PMID: 12460321.
https://pubmed.ncbi.nlm.nih.gov/15644821/
Wit JM, Rekers-Mombarg LT, Cutler GB, Crowe B, Beck TJ, Roberts K, Gill A, Chaussain JL, Frisch H, Yturriaga R, Attanasio AF. Growth hormone (GH) treatment to final height in children with idiopathic short stature: evidence for a dose effect. J Pediatr. 2005 Jan;146(1):45-53. doi: 10.1016/j.jpeds.2004.08.055. PMID: 15644821.
https://www.sciencedirect.com/science/article/abs/pii/S1096637415000040
Rothenbühler et al.,
https://pubmed.ncbi.nlm.nih.gov/18165285/
Mauras N, Gonzalez de Pijem L, Hsiang HY, Desrosiers P, Rapaport R, Schwartz ID, Klein KO, Singh RJ, Miyamoto A, Bishop K. Anastrozole increases predicted adult height of short adolescent males treated with growth hormone: a randomized, placebo-controlled, multicenter trial for one to three years. J Clin Endocrinol Metab. 2008 Mar;93(3):823-31. doi: 10.1210/jc.2007-1559. Epub 2007 Dec 28. PMID: 18165285; PMCID: PMC2266949.
https://pmc.ncbi.nlm.nih.gov/articles/PMC5155684/
Mauras N, Ross JL, Gagliardi P, Yu YM, Hossain J, Permuy J, Damaso L, Merinbaum D, Singh RJ, Gaete X, Mericq V. Randomized Trial of Aromatase Inhibitors, Growth Hormone, or Combination in Pubertal Boys with Idiopathic, Short Stature. J Clin Endocrinol Metab. 2016 Dec;101(12):4984-4993. doi: 10.1210/jc.2016-2891. Epub 2016 Oct 6. PMID: 27710241; PMCID: PMC5155684.
https://pubmed.ncbi.nlm.nih.gov/11403810/
Wickman S, Sipilä I, Ankarberg-Lindgren C, Norjavaara E, Dunkel L. A specific aromatase inhibitor and potential increase in adult height in boys with delayed puberty: a randomised controlled trial. Lancet. 2001 Jun 2;357(9270):1743-8. doi: 10.1016/S0140-6736(00)04895-9. PMID: 11403810.
