Estrogen/closure of growth plates/muscularity

[Sir Savage]

Here is something I've been thinking about for a while, and I'd like everyone's thoughts on this. First, a little background.



Men in my family, on the Savage side, share just about the same characteristics, particularly in height and muscularity. We are shorter, 5'5''-5'8'', and develop very muscular physiques without touching weights.



For example, when I was fourteen years old, I started a series of growth spurts, not so much in height, but in muscle growth. At one point, I was actually accused of using steroids, because I changed so much in such a short period time. Periodically, thoughout my teen years I would experience more of these spurts.



I noticed, however, that about the same time that these "muscle spurts" started happening, I was not experiencing as much height growth as I did before these spurts.



Now, these "muscle spurts" must have been induced by an "explosion" of testosterone, because, as I said, I did not touch a weight. And, as we all know, testosterone aromatizes into estrogen, which closes growth plates.



Now, enough background, to the questions. Is it possible that because of our increase in testosterone, and thus estrogen during our teen years, and NOT necessarily our genetics, that men in my family are shorter? Could the seemingly drastic increase in estrogen be responsible for it? If so, could an anti-estrogen be taken to block the estrogen, and increase height? Or, is there something else going on here?

[nightop]

Here is something I've been thinking about for a while, and I'd like everyone's thoughts on this. First, a little background.



Men in my family, on the Savage side, share just about the same characteristics, particularly in height and muscularity. We are shorter, 5'5''-5'8'', and develop very muscular physiques without touching weights.



For example, when I was fourteen years old, I started a series of growth spurts, not so much in height, but in muscle growth. At one point, I was actually accused of using steroids, because I changed so much in such a short period time. Periodically, thoughout my teen years I would experience more of these spurts.



I noticed, however, that about the same time that these "muscle spurts" started happening, I was not experiencing as much height growth as I did before these spurts.



Now, these "muscle spurts" must have been induced by an "explosion" of testosterone, because, as I said, I did not touch a weight. And, as we all know, testosterone aromatizes into estrogen, which closes growth plates.



Now, enough background, to the questions. Is it possible that because of our increase in testosterone, and thus estrogen during our teen years, and NOT necessarily our genetics, that men in my family are shorter? Could the seemingly drastic increase in estrogen be responsible for it? If so, could an anti-estrogen be taken to block the estrogen, and increase height? Or, is there something else going on here?

Good question (i've pondered about similiar before). This is just a guess:



First off, I would think that when people generically use the term "genetics" in such a case, it would *include* all of the factors which control height/growth... meaning, the genetic influences on height/growth involve a very complex group of aspects; gene expression (read *genetics*) controlling aromatase levels, T output, GH, SHBG, AR and ER counts/locations/densities, and a host of other hormones and factors to consider (with environmental and diet induced changes aside). Basically, "genetics" would encompass all such factors.



I would think (and have often wondered if I'm correct) that yes an estrogen control method (such as aromatase inhibitors) would indeed allow for further height beyond what height would have occurred naturally... However, one of the problems would be trying to figure out when to use the drug, at what dose, and for how long... personally, I wouldn't try it with a 13 year old... but the idea is interesting.



I believe the issues and mechanisms regarding growth/height are in fact very complicated, and it is hard to really delve into this issue without some basic studies regarding this. A graph of average male hormone levels plotted against a graph of average male height/growth spikes/values would possibly help.

[Yanick]

I don't think using an anti-E would be practical at all. I'm sure we all know the benefits of E even though they might not be great for muscularity and all that. Also i don't see how we could ever predict when these growth spurts are going to happen, so you would need to be running said anti-e for years at a time, in which time the acne, joint pain would probably be horrible for the teen.

[nightop]

I don't think using an anti-E would be practical at all. *I'm sure we all know the benefits of E even though they might not be great for muscularity and all that. *Also i don't see how we could ever predict when these growth spurts are going to happen, so you would need to be running said anti-e for years at a time, in which time the acne, joint pain would probably be horrible for the teen.

I agree... and would never suggest anyone try it. However, if a line could be found for an individual between necessary basal estrogen levels and still prevent plate closure, in terms of the anti-e dose, then it might not be as dangerous as say full dosed arimidex ED for years straight. However, at such a time in life there are alot of other processing occuring which one would not want to jeopardize in any matter.



Like I said before... I believe there are many complications and factors which we are not taking into account.

[Supnut]

and remember, regardless its too late for you by now. you've stop growing up period.

[Sir Savage]

nightop, well, when I said genetics, I meant the actual height genes themselves, and not other factors that influence height, such as various hormones. However, you're right, it is all genetic.



Yanick, I'm not talking about the practicality of it, I'm talking about the theory of it. In other words, is it theoretically possible, if estrogen is the problem.



Supnut, hehe, I'm not talking about NOW, you silly ass. You are correct, I am well past the age. I wouldn't have tried it, anyway. I would not trade my muscularity for additional height, if indeed that would be the trade-off.



Thanks for the responses, guys. Anyone else?

[Par Deus]

Duchaine talked about this in his FLAVONE X article (aka chrysin)



It should work.



Something else I think is interesting -- I had the partially the opposite experience as savage. I got much bigger and taller during my growth spurt -- went from 5'6 130 (14) to 5'11' 180 (16) in two years. # in () is both my age and bicep measurment, at the time.



Why I think this is interesting is that, while you are growing quickly, you are probably stretching the muscle fibers, thus recreating to some extent, those bird and cat studies where they hang a weight of of a limb for a month, and they get crazy hypertrophy and HYPERPLASIA.



Would be very cool to add 3" and have the "filling out" come with it. One, of course, has to comes to terms with the dangers and morality, but there is a big fucking difference between a 6' 200lb QB and a 6'3" 225lb one.

[Dio]

I'm pretty sure it would work. I can't find it now, but I have a study that talks about the relationship of height to aromatase deficiency. While boys that had this problem ended up taller, they also had much weaker bones. I'll post the study when I find it. I'm guessing that any treatment that was long enough to create effects would have some negative repercussions.



As far as the rapid growth causing fascia stretching and hyperplasia -- my personal experience does not coincide with this. I grew 6" in one year and did not get any muscle out of it. So in that instance hyperplasia is out.



Finally I have a couple of studies that might be of interest dealing with estrogen and TE and nolva and growth hormone:



The Journal of Clinical Endocrinology & Metabolism Vol. 87, No. 4 1634-1639

Copyright © 2002 by The Endocrine Society



--------------------------------------------------------------------------------



Endocrine Care



Combined Treatment with Testosterone (T) and Ethinylestradiol (EE2) in Constitutionally Tall Boys: Is Treatment with T Plus EE2 More Effective in Reducing Final Height in Tall Boys than T Alone?

Ralph Decker, Carl-Joachim Partsch and Wolfgang G. Sippell

Division of Pediatric Endocrinology, Department of Pediatrics, Christian-Albrechts University, Kiel 24105, Germany



Address all correspondence and requests for reprints to: Prof. Dr. Wolfgang G. Sippell, Department of Pediatrics, Schwanenweg 20, D-24105 Kiel, Germany. E-mail: . sippell@pediatrics.uni-kiel.de



Abstract



Estrogens have been shown to rapidly inhibit longitudinal growth in tall boys. To antagonize the initial growth accelerating effect of T, 41 boys with an initial height prediction in excess of 203 cm were treated prospectively with either T enanthate (TE) 250 mg/wk im in combination with ethinylestradiol (EE2) 0.1 mg/d taken orally for the first 5.8 ± 0.47 wk (mean ± SE) of treatment (group 1, n = 20) or with TE alone (group 2, n = 21). Patients were randomized to one or the other treatment regimen. Mean (±SE) predicted adult height was 206.8 ± 0.7 cm in group 1 and 206.4 ± 0.8 cm in group 2. Total duration of treatment was 16.1 ± 0.8 months and 14.0 ± 1.2 months in group 1 and 2, respectively (NS). EE2-induced side effects in group 1 (gynecomastia) were limited and fully reversible. No negative long-term sequelae were found at final height with respect to hypothalamic-pituitary-gonadal axis activity and to testis volumes. Although there was a tendency to a lower initial growth velocity measured by knemometry in group 1 (0.30 ± 0.05 vs. 0.38 ± 0.05 mm/wk, NS), final height did not differ in both study groups (195.0 ± 0.8 cm in group 1, 194.6 ± 0.8 cm in group 2). Similarly, height reduction (initial predicted adult height minus final height) was not significantly different between the two groups (12.0 ± 0.9 cm in group 1, 11.7 ± 0.9 cm in group 2). In conclusion, the addition of EE2 during the initial treatment phase to high-dose T in tall boys has no significant effect on height reduction. The results of this clinical trial suggest that the initial growth inhibiting effect of EE2 on the epiphyseal growth plates is overridden by the long-term administration of high dose TE.



Estrogen receptor blockade with tamoxifen diminishes growth hormone secretion in boys: evidence for a stimulatory role of endogenous estrogens during male adolescence

DL Metzger and JR Kerrigan

Department of Pediatrics, University of Virginia Health Sciences Center, Charlottesville 22908.



The increase in GH production during the male adolescent growth spurt has been attributed to both androgen and estrogen receptor-mediated processes. To evaluate the role of endogenous estrogens in the control of GH secretion, we administered the estrogen receptor antagonist tamoxifen to 10 late pubertal males. Blood samples were obtained for GH determination at 10-min intervals on 2 occasions during the last 24 h of a 4-day course of either tamoxifen or placebo. Waveform-specific, multiple parameter deconvolution analysis was employed to assess GH secretory and elimination dynamics. Estrogen receptor blockade resulted in a significant (P < 0.05) diminution in mean 24-h serum GH concentrations, from 3.9 +/- 1.0 (placebo; mean +/- SEM) to 2.7 +/- 0.6 micrograms/L (tamoxifen). This was associated with a significant (P < 0.01) decline in the GH production rate [237 +/- 55 vs. 155 +/- 33 micrograms/L GH distribution volume (Lv).24 h]. Furthermore, this reduction in GH secretion was the result of significant decreases in both the maximal GH secretory rate (0.46 +/- 0.08 vs. 0.34 +/- 0.06 microgram/Lv.min; P < 0.01) and, to a smaller degree, GH secretory burst number (16 +/- 1 vs. 14 +/- 1/24 h; P < 0.05). There was also a trend toward reduced mass of GH secreted per burst (13.3 +/- 2.5 vs. 10.3 +/- 2.0 micrograms/Lv; P = 0.06). No significant alterations in either GH elimination t1/2 or GH secretory burst half-duration were observed during estrogen receptor antagonism. Tamoxifen treatment was associated with a significant (P < 0.05) decrease in plasma insulin- like growth factor-I concentrations. However, total and free testosterone, 17 beta-estradiol, insulin-like growth factor-binding protein-3, and pooled 24-h LH concentrations were not significantly changed by short term blockade of estrogen action. We postulate that endogenous estrogens play a facilitatory role in neuroendocrine control of the somatotropic axis during puberty in boys. Tamoxifen blocks this estrogen-dependent stimulation of GH secretion without altering the hormone elimination t1/2. Furthermore, we speculate that any stimulatory role of androgens on GH secretion is exerted primarily through the estrogen receptor after aromatization.

[virtualcyber]

Does anyone know if our height growth involves cells with short telomere?



The number of self-replication each cell can go through is partially controlled by telomere (which is a basically the tail of a DNA strand), which gets shorter after each replication. Some of cells we have stop replicating, because the telomere length becomes zero.

[Sir Savage]

Good stuff, fellas.



Dio, interesting that the boys in the study you mentioned had weaker bones. I know that estrogen deficiency can lead to bone loss, as is evident in females that overtrain (ammenhoria sp?) and in post-menopausal women.



And, it appears that the first study you posted throws my theory out the window.



Am I correct in my interpretation that they are saying testosterone leads to growth in height? If so, how does that explain my very rapid muscle gain, without increasing in height much?

[Dio]

I found that study but strangely it does not have an abstract. I have it in pdf form; if anyone is interested I will e-mail it to them.



Savage,



I don't think it means that test would stimulate growth (although it has been used for that purpose) in this study, the conclusion is that the addition of test will counter the effects of estrogen on the bone plates so height is not effected.

[Sir Savage]

I read too fast, as is often the case.

[Par Deus]

Prolly by increasing GH/IGF-1

[Mischievous]

From a theoretical perspective I think it is possible that estrogen might play a role in the "exact" height a person end up at ... perhaps whether one is 5'10" or 5'10.75"; but, I think other "genetic" factors pretty much determine one's ultimate height ... that is ... the DNA programming we receive from our parents ... for myself I would consider one's diet while growing up as possibly at least as responsible for how close one gets to their ultimate "height potential" as any aromatase issue ...



Unless I mistaken, the original conception of the principle of statistical regression was made by observing the heights of people and their offsprings ...



Basically ... the idea was that ... if you put two tall people together ... you should see very tall offsprings ... and two very short people ... would yield shorter offsprings. However, what they found was that people tend to "regress towards the mean" with their offsprings ... that is ... two tall people mostly had slightly shorter kids and two short people tended to have slightly taller offsprings ... and ... overtime ... "humanity as a whole" might trend towards taller offsprings; but, the regression towards the mean remained constant ... something in the genetic programming ...



Now, I bet all of us can think of tons of examples in our own lives that seem to contridict this (though I myself had a 5'10" dad and a 5'6" mother and ended up 6'0") ...



For example, one of the families that lived close to me growing up was very tall ... I think the dad was 6'5" and the mother was 6'1" ... they had three children ... 3 boys and a girl ... the boys were (by ages): 6'4", 6'9", and 6'3" and the girl was probably about: 5'10. So, the theory tends to hold, except maybe for the 6'9" kid ... which doesn't fit in at all. Could it be due to strange estrogenic properties in him during growth spurts? Perhaps? But, could it just be the roll of the dice in differences in genetic make-up? That would be my first guess for most of the explaination ...



I say this while still pointing out that there are cases where sever deficiencies can cause very strange outcomes ... for example ... I think I remember that the disease that causes overproduction of GH sometimes resulted in people well over 7 feet tall ... so ... one factor seems to have the potential to really effect height ... but ... as far as I know ... this still is a factor that is "written in the genetic code" ...

[MMA]

Here is something I've been thinking about for a while, and I'd like everyone's thoughts on this. First, a little background.



Men in my family, on the Savage side, share just about the same characteristics, particularly in height and muscularity. We are shorter, 5'5''-5'8'', and develop very muscular physiques without touching weights.



For example, when I was fourteen years old, I started a series of growth spurts, not so much in height, but in muscle growth. At one point, I was actually accused of using steroids, because I changed so much in such a short period time. Periodically, thoughout my teen years I would experience more of these spurts.



I noticed, however, that about the same time that these "muscle spurts" started happening, I was not experiencing as much height growth as I did before these spurts.



Now, these "muscle spurts" must have been induced by an "explosion" of testosterone, because, as I said, I did not touch a weight. And, as we all know, testosterone aromatizes into estrogen, which closes growth plates.



Now, enough background, to the questions. Is it possible that because of our increase in testosterone, and thus estrogen during our teen years, and NOT necessarily our genetics, that men in my family are shorter? Could the seemingly drastic increase in estrogen be responsible for it? If so, could an anti-estrogen be taken to block the estrogen, and increase height? Or, is there something else going on here?

very possible. also, one form of gigantism is caused by a lack of aromitase, the people just keep growing and growing. several people on the anabolic boards are experimenting with this, with arimidex and femara.



one of the foremost height enhancement experts on the boards is our very own Anabolics.

[MMA]

Here is something I've been thinking about for a while, and I'd like everyone's thoughts on this. First, a little background.



Men in my family, on the Savage side, share just about the same characteristics, particularly in height and muscularity. We are shorter, 5'5''-5'8'', and develop very muscular physiques without touching weights.



For example, when I was fourteen years old, I started a series of growth spurts, not so much in height, but in muscle growth. At one point, I was actually accused of using steroids, because I changed so much in such a short period time. Periodically, thoughout my teen years I would experience more of these spurts.



I noticed, however, that about the same time that these "muscle spurts" started happening, I was not experiencing as much height growth as I did before these spurts.



Now, these "muscle spurts" must have been induced by an "explosion" of testosterone, because, as I said, I did not touch a weight. And, as we all know, testosterone aromatizes into estrogen, which closes growth plates.



Now, enough background, to the questions. Is it possible that because of our increase in testosterone, and thus estrogen during our teen years, and NOT necessarily our genetics, that men in my family are shorter? Could the seemingly drastic increase in estrogen be responsible for it? If so, could an anti-estrogen be taken to block the estrogen, and increase height? Or, is there something else going on here?

J Steroid Biochem Mol Biol. 2003 Sep;86(3-5):345-56. Related Articles, Links





Novel treatment of short stature with aromatase inhibitors.



Dunkel L, Wickman S.



Hospital for Children and Adolescents, University of Helsinki, PO Box 281, Helsinki 00029 HUS, Finland. leo.dunkel@hus.fi



Estrogens have an essential role in the regulation of bone maturation and importantly in the closure of growth plates in both sexes. This prospective, randomized, placebo-controlled study was undertaken to evaluate whether suppression of estrogen synthesis in pubertal boys delays bone maturation and ultimately results in increased adult height. A total of 23 boys with constitutional delay of puberty (CDP) received a conventional, low-dose testosterone treatment for inducing progression of puberty. Eleven of these 23 boys were randomized to receive a specific and potent P450-aromatase inhibitor, letrozole, for suppression of estrogen action, and 12 boys were randomized to receive placebo. Estradiol concentrations in the letrozole-treated boys remained at the pretreatment level during the administration of letrozole, whereas the concentrations increased during the treatment with testosterone alone and during spontaneous progression of puberty. Testosterone concentrations increased in all groups, but during the letrozole treatment, the increase was more than fivefold higher than in the group treated with testosterone alone. The inhibition of estrogen synthesis delayed bone maturation. The slower bone maturation in the boys treated with testosterone and letrozole, despite higher androgen concentrations, than in the boys treated with testosterone indicate that estrogens are more important than androgens in regulation of bone maturation in pubertal boys. During the 18 months follow-up, an increase of 5.1 cm in predicted adult height was observed in the boys who received testosterone and letrozole, but no change was seen in the boys who received testosterone alone or in the untreated boys. This finding indicates that an increase in adult height can be attained in growing adolescent boys by inhibiting of estrogen action.

Publication Types:

Clinical Trial

Randomized Controlled Trial



PMID: 14623531 [PubMed - indexed for MEDLINE]

[Ex_banana-eater]

"Genetix" at this board has done extensive research on this subject, specifically on recreating a hormonal milleau similar to puberty before epiphysial closure. Maybe he'll chime in.



The best way to do it would be to include testosterone, IGF-1, and GH into the equation. Keep in mind testosterone alone without aromatase inhibitors has been found to increase predicted height in adolescents with abnormally tall stature. A mix of testosterone and an AI would be for a more cautious person.



Also, in this thread, we have to determine exactly what we mean by "genetics." Genetics is often to do with the level of hormones or times they kick in during growth stages.

[Josh]

@ExBE:

"Genetix" at this board has done extensive research on this subject, specifically on recreating a hormonal milleau similar to puberty before epiphysial closure.

I did a search on genetix puberty but came up with zip. Any chance you could give refs to any of his posts/work.



Cheers bud,



J

[lynx]

The best way to do it would be to include testosterone, IGF-1, and GH into the equation. Keep in mind testosterone alone without aromatase inhibitors has been found to increase predicted height in adolescents with abnormally tall stature. A mix of testosterone and an AI would be for a more cautious person.

I think that to attempt this kind of change with an aromatase inhibitor, it is especially important to include real testosterone, because neuronal estrogen/test/dht are vital to proper development of the nervous system.

[My Lord]

Does anyone know if our height growth involves cells with short telomere?



The number of self-replication each cell can go through is partially controlled by telomere (which is a basically the tail of a DNA strand), which gets shorter after each replication.* Some of cells we have stop replicating, because the telomere length becomes zero.

The normal senescent slowing of plate growth has been shown to be dependent on the total number or sum of replications that the chondrocytes have cycled through. This is in contrast to the dogma that age was the main controlling factor. The study I am recalling, did a really neat thing to show this. They gave dexamethasone to block linear growth for a certain period of time. When the block was removed a significant increase in growth (less senescence) was observed. It was termed "catch-up growth". And certainly, as the model of senescence has strong correlation to telomere activity and cleaveage, the link is appreciable. Let me see if I can find the study.