[Biomaxx]

Bone age, often discussed in association with Tanner stage, is how far your skeleton has progressed through the maturation process. In essence, it's a way of estimating how much growth potential someone has remaining. A bit of research has been done into whether this can be slowed down or even partly reversed, and one compound making appearances in the literature is tamoxifen. It's said to reduce the rate of skeletal maturation without interfering with typical sex-specific development, which may in turn raise predicted or eventual adult height. The idea derives from how estrogen works: at low levels, it can support bone mass, but at higher levels, it accelerates growth-plate closure. Because tamoxifen selectively modulates estrogen receptors rather than blocking them outright, researchers have proposed that it might slow skeletal maturity without shutting down estrogen's other functions entirely.

Animal data are less clear-cut. Rodent studies demonstrate that tamoxifen can increase cell death in the growth plates-particularly in the resting and hypertrophic zones-which, in fetal rats, has been associated with an arrest in lengthwise bone growth. Human clinical data, however, have demonstrated height-increasing potential, which suggests that the rodent findings reflect high-exposure scenarios that don't translate directly to humans. Given these mixed results, my conclusion is that tamoxifen isn't an ideal approach, particularly in comparison with established medical regimens such as growth hormone combined with aromatase inhibitors.

 

[Biomaxx]

Bone age, often discussed in association with Tanner stage, is how far your skeleton has progressed through the maturation process. In essence, it's a way of estimating how much growth potential someone has remaining. A bit of research has been done into whether this can be slowed down or even partly reversed, and one compound making appearances in the literature is tamoxifen. It's said to reduce the rate of skeletal maturation without interfering with typical sex-specific development, which may in turn raise predicted or eventual adult height. The idea derives from how estrogen works: at low levels, it can support bone mass, but at higher levels, it accelerates growth-plate closure. Because tamoxifen selectively modulates estrogen receptors rather than blocking them outright, researchers have proposed that it might slow skeletal maturity without shutting down estrogen's other functions entirely.

Animal data are less clear-cut. Rodent studies demonstrate that tamoxifen can increase cell death in the growth plates-particularly in the resting and hypertrophic zones-which, in fetal rats, has been associated with an arrest in lengthwise bone growth. Human clinical data, however, have demonstrated height-increasing potential, which suggests that the rodent findings reflect high-exposure scenarios that don't translate directly to humans. Given these mixed results, my conclusion is that tamoxifen isn't an ideal approach, particularly in comparison with established medical regimens such as growth hormone combined with aromatase inhibitors.

 

[Biomaxx]

Bone age, often discussed in association with Tanner stage, is how far your skeleton has progressed through the maturation process. In essence, it's a way of estimating how much growth potential someone has remaining. A bit of research has been done into whether this can be slowed down or even partly reversed, and one compound making appearances in the literature is tamoxifen. It's said to reduce the rate of skeletal maturation without interfering with typical sex-specific development, which may in turn raise predicted or eventual adult height. The idea derives from how estrogen works: at low levels, it can support bone mass, but at higher levels, it accelerates growth-plate closure. Because tamoxifen selectively modulates estrogen receptors rather than blocking them outright, researchers have proposed that it might slow skeletal maturity without shutting down estrogen's other functions entirely.

Animal data are less clear-cut. Rodent studies demonstrate that tamoxifen can increase cell death in the growth plates-particularly in the resting and hypertrophic zones-which, in fetal rats, has been associated with an arrest in lengthwise bone growth. Human clinical data, however, have demonstrated height-increasing potential, which suggests that the rodent findings reflect high-exposure scenarios that don't translate directly to humans. Given these mixed results, my conclusion is that tamoxifen isn't an ideal approach, particularly in comparison with established medical regimens such as growth hormone combined with aromatase inhibitors.

Fucking boost in put alot of effort into this js for fucking grey shitposter to cover it

 

[Biomaxx]

Bone age, often discussed in association with Tanner stage, is how far your skeleton has progressed through the maturation process. In essence, it's a way of estimating how much growth potential someone has remaining. A bit of research has been done into whether this can be slowed down or even partly reversed, and one compound making appearances in the literature is tamoxifen. It's said to reduce the rate of skeletal maturation without interfering with typical sex-specific development, which may in turn raise predicted or eventual adult height. The idea derives from how estrogen works: at low levels, it can support bone mass, but at higher levels, it accelerates growth-plate closure. Because tamoxifen selectively modulates estrogen receptors rather than blocking them outright, researchers have proposed that it might slow skeletal maturity without shutting down estrogen's other functions entirely.

Animal data are less clear-cut. Rodent studies demonstrate that tamoxifen can increase cell death in the growth plates-particularly in the resting and hypertrophic zones-which, in fetal rats, has been associated with an arrest in lengthwise bone growth. Human clinical data, however, have demonstrated height-increasing potential, which suggests that the rodent findings reflect high-exposure scenarios that don't translate directly to humans. Given these mixed results, my conclusion is that tamoxifen isn't an ideal approach, particularly in comparison with established medical regimens such as growth hormone combined with aromatase inhibitors.

Ffs Mandy dexter longhairedChad . Rep up and boost

 

[Circadex]

View attachment 4799

Probably because you use dashes a bit. Gbt loves to use them.

 

[Biomaxx]

Probably because you use dashes a bit. Gbt loves to use them.

Honestly think im smarter then gpt

 

[Dexter]

for something written so concisely, it's a great thread broski. almost all points are like 9.5/10 in accuracy but it'd be much better if you wrote more, I'd love to read it. (given you have free time to post that in the first place).

but srs it's really informative and it'll defo help someone out.

 

[Circadex]

Honestly think im smarter then gpt

Gbt is a LLM. I don't think you can really say it has "intelligence" because it's just a amalgamation of training data & reddit posts, so yeah you are
Or you're joking and im too aspie to understand...

 

[Mandy]

Good thread,tamoxifen is my favorite cycle support compound. And I have to say,it’s pretty much mixed. Raloxifene which is also a SERM and used for pubertal gynecomastia has been shown to the opposite and that is fuse the epiphyseal plates earlier than usual because it’s agonistic to the ER-ẞ receptor in the plate. The research on reducing the overall bone age and prolong the growth period with tamoxifen is mixed,more leaned towards prolonging and not fusing.