theladarer2000
Gold
- Joined
- Jan 16, 2026
- Posts
- 751
- Reputation
- 789
Why hgh is cope for height:
Exogenous hGH is not some magic drug for height growth unless you are truly growth-hormone deficient and treated early. In normal or near-normal adolescents, hGH increases short-term growth velocity, but not final adult height. What determines final height is how long the growth plates stay open and how fast they senesce, which is driven by estrogen signaling, not GH itself. Even in prepubertal treatment, the average adult height gain is often only a few centimeters (3-6cm) and much of the apparent “growth” is just pulling growth forward in time rather than increasing the final endpoint. Another common cope however, is “let me just take an AI with it”, while this might sound good on paper, low estrogen comes with many side effects and only gives meaningful impact if you have had low estrogen for an extended period of time.
Why hgh is cope for facial bone growth:
hGH is also cope for facial bone growth, and a big reason is remodeling biology. Most craniofacial bones have low osteoblast turnover rates compared to long bones during growth, especially after early adolescence. Outside of early developmental windows, these bones primarily undergo slow surface remodeling and density changes, not robust appositional growth. GH can stimulate IGF-1 and osteoblast activity systemically, but if the baseline remodeling rate is low, there is nothing meaningful to amplify. Data show that even in GH-deficient patients, facial changes are modest and inconsistent, usually limited to slight mandibular length changes or altered proportions, not real widening of the zygomas or forward midface expansion. In non-deficient individuals, GH mainly affects soft tissue thickness, cartilage, and bone density. (BONE DENSITY IS INTERNAL, NOTHING TO DO WITH WIDTH)Also, we need to understand that exogenous GH is not localized. GH and downstream IGF-1 act systemically, and their skeletal effects are preferentially allocated to bones with high turnover and mechanical demand, not to bones you wish would grow. The bones that “need it most” are long bones during active growth, vertebrae, and weight-bearing structures where remodeling rates and strain-induced signaling are highest. Craniofacial bones, especially the zygomas and maxilla, sit at the opposite end of that spectrum.
(If you have a contention to this please let me know since I’m always interested in gaining new information.
Exogenous hGH is not some magic drug for height growth unless you are truly growth-hormone deficient and treated early. In normal or near-normal adolescents, hGH increases short-term growth velocity, but not final adult height. What determines final height is how long the growth plates stay open and how fast they senesce, which is driven by estrogen signaling, not GH itself. Even in prepubertal treatment, the average adult height gain is often only a few centimeters (3-6cm) and much of the apparent “growth” is just pulling growth forward in time rather than increasing the final endpoint. Another common cope however, is “let me just take an AI with it”, while this might sound good on paper, low estrogen comes with many side effects and only gives meaningful impact if you have had low estrogen for an extended period of time.
Why hgh is cope for facial bone growth:
hGH is also cope for facial bone growth, and a big reason is remodeling biology. Most craniofacial bones have low osteoblast turnover rates compared to long bones during growth, especially after early adolescence. Outside of early developmental windows, these bones primarily undergo slow surface remodeling and density changes, not robust appositional growth. GH can stimulate IGF-1 and osteoblast activity systemically, but if the baseline remodeling rate is low, there is nothing meaningful to amplify. Data show that even in GH-deficient patients, facial changes are modest and inconsistent, usually limited to slight mandibular length changes or altered proportions, not real widening of the zygomas or forward midface expansion. In non-deficient individuals, GH mainly affects soft tissue thickness, cartilage, and bone density. (BONE DENSITY IS INTERNAL, NOTHING TO DO WITH WIDTH)Also, we need to understand that exogenous GH is not localized. GH and downstream IGF-1 act systemically, and their skeletal effects are preferentially allocated to bones with high turnover and mechanical demand, not to bones you wish would grow. The bones that “need it most” are long bones during active growth, vertebrae, and weight-bearing structures where remodeling rates and strain-induced signaling are highest. Craniofacial bones, especially the zygomas and maxilla, sit at the opposite end of that spectrum.
(If you have a contention to this please let me know since I’m always interested in gaining new information.
