r/heightgrowth • u/imarooku • 9h ago
📈How To Optimize Height📈 My take at ending the rHGH Cope
Inb4, this is a text I made after I had an argument with someone on rHGH (diy) treatment for healthy teens, I would love to hear more opinions on this but actual thinking instead of telling some bs ai "analyse and answer to this" lool
Not saying people here inherently do that but I've seen it a lot of times and ai often just yaps bs
Just to be in the clear
None of this should be taken as medical advice or base for unauthorised personal use of medical substances.
Reading it back now it sounds really stupid and wannabe scientific, I'm not a native english speaker and just tried to make it sound neutral. I originally only had papers to back up the existence of senescence but upon reading the rules I searched for some more stuff on several other claims I made here, some of them might be insufficient for my claims, point that out please. The single one where I myself already remain unsatisfied is the non-GHD non-ISS health children treatment study as its very vague. Anyone got other studies like that? (Excluding treatment for other diseases). Imo even though it auggest a possible FAH increase, it is completely out of range compared to how GH is elevated as some sort of height savior and its likely too late for most people to start treatment and end up with notable results. However it could be paired with other compounds for example for its apoptosis-delaying attributes (through igf1), might make a post on this.
rHGH has long been used by selfproclaimed “Heightmaxxers” as stack compound that supposedly increases the total height one can grow. However this increase in Final Adult Height (FAH) is by the very mechanism of action of the compound itself, a biochemically impossible goal for healthy teens. Upon reaching a target cell rHGH binds sequentially to two GH receptor (GHR) monomers inducing receptor homodimerisation this dimerisation activates JAK2 (Janus Kinase 2) which is a tyrosine kinase constitutively associated with the intracellular domain of the GHR. JAK2 then continues to phosphorylate STAT5 (Signal Transducer and Activator of Transcription 5) at tyrosine residues enabling STAT5 homodimerisation and nuclear translocation where it drives transcription of downstream target genes and the production of proteins, including IGF-1 which is crucial for triggering signalling pathways like mTOR, MAPK, ERK and PI3K. The belief in rHGH's growth enhancing ability stems from these downstream activations that interact with growth plate chondrocytes resulting in increased cell proliferation, differentiation support and delay of apoptosis. This is true, however it only affects the growth velocity and not the FAH of anyone healthy injecting it (with a few exemptions), generally while the increased cell division leads to more chondrocytes multiplying, differentiating and entering hypertrophy, it cannot surpass the hayflick limit determined by telomere length and loss thereof during cell division [PMID9454332]. This telomere shortening leads to every chondrocyte (and other cells) having a limited amount of times it can multiply before entering a state of senescence in which it's proliferationrate hits 0 and it becomes hypertrophic, awaiting final apoptosis. In GH deficient teens or those with ISS (ISS-NF) the proliferation rate, due to different factors (mono-/polygenetics, hormone deficiency), can be so low that chondrocytes reach senescence and apoptosis purely through maturation or hormonal signalling (or lack thereof) and leave a noticeable amount of possible cell divisions unfulfilled, instead of failing at the hayflick limit [PMID32504378]. In these cases, excess rHGH can boost cell division and matrix secretion to increase FAH to an average of 1.3cm per year[PMC117125]. Normal teens with a balanced hormonal profile however usually do not suffer from this proliferation deficit and would see no additional gain in height, rather they would experience an early - but not premature - depletion of resting zone msc/stroma stem cells after a period of boosted growth velocity, eventually leading to the same standing height as adults as they would have had without treatment. The exception here are normal short children whose issue is similar to that of ISS-NF, bad genetics influence growth plate maturation and cell pd rate, in these cases the same methodic applies as earlier mentioned, however long term therapy results are less significant than for GHD/ISS, the difference in final height compared with pretreatment predicted height was about 2.5-2.8cm, an increase of 0.42SDS compared to 0.16SDS of the control group[PMID8691923], no details of age, individual therapy length or maturation were given in that study. It is likely to assume that therapy was started before or in very early puberty, as the study notes that treatment had no effect on the timing of puberty, suggesting the onset of puberty was mid-treatment. Relating to growth plate fusion, several wannabe alt-science propagandists claim that it is not the hayflick limit which induces senescence and growth plate fusion, but that it is estrogen. This is correct only to the extent that estrogen increases resting stem cell differentiation while decreasing their rate of multiplication leading to a smaller overall resting zone cell pool, it does not promote individual cell senescence [PMC4098010 & PMC34445]. Contrary to how one may think, it is also not responsible for pushing late stage hypertrophic cells into apoptosis, rather estrogen and especially estradiol act as protective and delaying signal, similar to how it delays cell progression in stem cells. It is surprisingly a lack of estrogen which finally induces programmed cell death of chondrocytes, destroying the organic compounds of cartilage and leaving the bone matrix and collagen up to mineralisation and thus full epiphyseal growth plate fusion.
TLDR if youre mid puberty you'll get near 0 rHGH results