clavicel
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Been looking into the effects of SERMs on growth plate closure, and I keep finding conflicting info. Here I have linked some studies about the effects of tamoxifen (nolvadex) on bone growth that appear to have opposite conclusions.
"[Tamoxifen] caused a dose-dependent growth retardation of cultured metatarsal bones. No catch-up growth was observed after [tamoxifen] was removed from the culture medium. Detailed analysis of sectioned growth plate cartilage revealed increased apoptosis of chondrocytes within the resting and hypertrophic zones." - https://pubmed.ncbi.nlm.nih.gov/17293177/
And here's an in vivo follow-up confirming the results: https://www.researchgate.net/publication/5503175
"As expected, E2 was found to suppress longitudinal bone growth, but in contrast, this parameter was stimulated by tamoxifen. We conclude that tamoxifen acts as an agonist with respect to estrogen’s stimulatory action on bone formation but as an antagonist in terms of estrogen’s inhibition of longitudinal growth, suggesting that the protective effect of SERMs on the skeleton is partly mediated by stimulation of osteoblast activity." - https://academic.oup.com/endo/article/146/3/1060/2500135
Here's another one (which I don't fully understand) that seems to describe the same effect: https://pubmed.ncbi.nlm.nih.gov/11983487/
This one done on actual boys in puberty says it has no effect: https://www.degruyter.com/view/journals/jpem/29/1/article-p77.xml
So which is it? This is quite important for any pubertymaxxers wanting to cycle as they will have to PCT somehow.
"[Tamoxifen] caused a dose-dependent growth retardation of cultured metatarsal bones. No catch-up growth was observed after [tamoxifen] was removed from the culture medium. Detailed analysis of sectioned growth plate cartilage revealed increased apoptosis of chondrocytes within the resting and hypertrophic zones." - https://pubmed.ncbi.nlm.nih.gov/17293177/
And here's an in vivo follow-up confirming the results: https://www.researchgate.net/publication/5503175
"As expected, E2 was found to suppress longitudinal bone growth, but in contrast, this parameter was stimulated by tamoxifen. We conclude that tamoxifen acts as an agonist with respect to estrogen’s stimulatory action on bone formation but as an antagonist in terms of estrogen’s inhibition of longitudinal growth, suggesting that the protective effect of SERMs on the skeleton is partly mediated by stimulation of osteoblast activity." - https://academic.oup.com/endo/article/146/3/1060/2500135
Here's another one (which I don't fully understand) that seems to describe the same effect: https://pubmed.ncbi.nlm.nih.gov/11983487/
This one done on actual boys in puberty says it has no effect: https://www.degruyter.com/view/journals/jpem/29/1/article-p77.xml
So which is it? This is quite important for any pubertymaxxers wanting to cycle as they will have to PCT somehow.