Any studies about growth plate closure?

not2friendly

New member
Any studies about growth plate closure?

Ok, I know steroids cause growth plate closure (GPC), in immature users (by immature I mean age wise, not in the sense of guys 35 year olds still watching "PowerPufF Girls:The Movie"), but I have always been under the impression that all gear does, not just gear that aromatizes into estrogen. Recently I have read posts saying that only the estrogen causes GPC, not the androgenic or anabolic hormones themselves. So in theory something like say Halo would not cause GPC. Is there scientific proof (in the form of therum), that any of you guys know about, and have a link to? This is a general question I'm an old man so I don't have to worry about it, my GP have been fused for years. Thanks and any info would be great.

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Die young...Die strong...Dianabol!!
 
I dont think they have done any human studies, it would probably be hard to get approval or a large enough subject group.
 
Here's a study you might be interested in.

Novel treatment of delayed male puberty with aromatase inhibitors.

Dunkel L, Wickman S.

University of Helsinki, Hospital for Children and Adolescents, Finland. leo.dunkel@hus.fi

BACKGROUND: As the evidence for the role of oestrogens in epiphyseal closure appears unequivocal, we hypothesized that boys with constitutional delay of puberty would attain greater adult height if oestrogen action was suppressed.

METHODS: We conducted a randomized, double-blind, placebo-controlled study in which we treated boys with constitutional delay of puberty with testosterone plus placebo or testosterone plus a potent fourth-generation aromatase inhibitor, letrozole.

FINDINGS: Letrozole effectively inhibited oestrogen synthesis. The 17beta-oestradiol concentrations increased in the untreated group and in the testosterone/placebo-treated group, but in the testosterone/letrozole-treated group no such increase was observed until letrozole treatment was discontinued. Testosterone concentrations were threefold higher in the testosterone/letrozole-treated group than in the other groups. Within 18 months, bone age had advanced by 1.1 +/- 0.3 years in the untreated group and by 1.7 +/- 0.3 years in the testosterone/placebo-treated group, but only by 0.9 +/- 0.2 years in the testosterone/letrozole-treated group (p = 0.02 between treatment groups). Predicted adult height did not change significantly in the untreated group and in the testosterone/placebo-treated group, whereas in the testosterone/letrozole-treated group the increase was 5.1 +/- 1.2 cm (p = 0.004).

CONCLUSIONS: Our findings suggest that, if oestrogen action is inhibited in growing adolescents, adult height will increase. This observation provides a rationale for studies aimed at delaying bone maturation in several growth disorders. Copyright 2002 S. Karger AG, Basel

JohnnyB
 
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