RXT and growth.. *pic inside*

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  1. Quote Originally Posted by cry0smate
    It is my understanding (I just recently learned this) that estrogens increase IGF-1 circulation and production in the body which stunts growth.
    Just to clarify I know estrogen affects growth plates but I was concerned that it was implied that test didn't. I imagine the response in males is different than in females for obvious reasons.

  2. Actually they have not been able to isolate a difference in the mode of action of growth plate closure in the sexes:

    By itself, E2 stimulated maturation of all subpopulations only in pharmacologic doses (10(-7) M). Physiologic E2 concentrations were no different than negative controls treated with ITS (insulin, transferrin, and selenite). Regardless of E2 concentrations, the addition of E2 to 1 nM T3 did not appreciably affect the response to T3 alone, which stimulates maturation of the phenotype. All effects were comparable in both male and female chondrocytes, in all cell subpopulations (maturation stages) and fetuses of varying gestational age.
    Calcif Tissue Int. 2004 Sep;75(3):214-24

    This is a very recent study. It appears chondrocytes conversion to calcified bone material works the same for both sexes.

    Further, we know estrogen is important, but it's more of a signaler:

    ...Estrogen does not induce growth plate ossification directly; instead, estrogen accelerates the programmed senescence of the growth plate, thus causing earlier proliferative exhaustion and consequently earlier fusion.
    Proc Natl Acad Sci U S A. 2001 Jun 5;98(12):6871-6. Epub 2001 May 29.

    This study is 4 years old, and was performed on rabbits. We have since begun to develop working theories on exactly what other things are present to CAUSE the rapid closure. If estrogen were the only casuative factor, then every girl would stop growing at puberty, and this is not how it works.

    HOWEVER-->while the process is the same for male and female, our production of these hormones is different. About five years ago a paper was published entitled:
    Estrogen, bone growth and sex: a sea change in conventional wisdom

    This is significant, b/c it studied a HUMAN male with "a homozygous mutation in the estrogen receptor alpha gene, which results in estrogen-receptor alpha resistance, and of males and females with autosomal recessive mutations in the CYP19 gene encoding aromatase, which leads to a failure to synthesize estrogens."

    The results are fascinating:

    For example, in the male, estrogen (not androgen) derived from direct testicular secretion (approximately 20%) and from extragonadal aromatization of testosterone and androstenedione (approximately 80%), is the critical sex hormone in the pubertal growth spurt, skeletal maturation, accrual of peak bone mass, and the maintenance of bone mass in the adult. Estrogen stimulates chondrogenesis in the epiphyseal growth plate increasing pubertal linear growth. At puberty, estrogen promotes skeletal maturation and the gradual, progressive closure of the epiphyseal growth plate, possibly as a consequence of both estrogen-induced vascular and osteoblastic invasion and the termination of chondrogenesis. In addition, during puberty and into the third decade, estrogen has an anabolic effect on the osteoblast and an apoptotic effect on the osteoclast, increasing bone mineral acquisition in axial and appendicular bone. In the adult, estrogen is important in maintaining the constancy of bone mass through its effects on remodeling and bone turnover. Establishing a role for estrogen does not exclude a direct action of testosterone on bone in the human male (especially on cortical bone), but this action is less characterized than thought in the past and is relatively minor in comparison with the major effect of estrogen in the male.
    J Pediatr Endocrinol Metab. 2000;13 Suppl 6:1439-55.

    So we know estrogen is very important, but we know other factors are at work, too.

    Bottom line--it's a bad idea to play around with your hormones while you're growing.

  3. very interesting. Thanks for the info!

  4. bump!

  5. if your growth plates close will you just stop growing in height and width or will you not get a beard not look older etc...

  6. Not to sound like a flaming teen here but doesnt this happen anyways? What I mean atleast for me at the age of I guess 15ish I can remember my hormones going crazy by themselfs. That might explain why I stopped growing at the age of ****ing 16-17. But I can specifically remember occurances of sides you commonly get from being "on." Another thing just to help my facts was I can vivdly remember getting gyno when I was young. Puffy, itchy, witha lump behind my nips. All of this happened naturally.

    I guess what I am trying to say is how can my growth plates still be open after that? Sounds a lot worse than a short 4 weeker in terms of sides. Again im not arguing with the fact that young use is just stupid, I just like to learn.

  7. Quote Originally Posted by showrmshldrs230
    Isn't estrogen responsible for closing growth plates?
    To answer your question, yes it is the primary trigger. But that could mean having high testosterone and higher estrogen levels, or low testosterone and high estrogen levels. There's the absolute levels of each hormone, the free levels, the biologically active levels, the ratio of each to each, etc.

    Basically it's a delicate balance, your body relies on triggers from this system to properly regulate your growth and this can go on until your mid twenties and sometimes later before you hit a state of homeostasis, where things generally aren't changing anymore.

    So, anything that messes with these levels, whether it raises testosterone or lowers estrogen or frees some of each, has the potential to harm you permanently at your age. So the best thing is stay away completely from hormone or hormone modulating products. Stick with creatine and such things for now. A handy way to deal with gyno is bulk up a little so it's less noticable, but that would mean not being as lean as you could be. The other answer is to go see a doctor who will probably tell you surgery is the best option, and he'd be right.

  8. So tired of seeing everyone say that you grow will you are 21, you have the POSSIBILITY of growing until 21. My father is a Doctor and has been for over 20 years and my Mother is an X-Ray Tech. There are grow plates all over the human body and it is not all that difficult to tell when one has closed. If you all that worried about it, goto your doc and get an xray. My father says most kids growth plates close around 17-18 and it is grossly overexagerated how much of a factor stunted growth actually is.

    Personally I would worry more about my endocrine system at a younf age and not my height, unless of course you think you may have mroe in you

  9. I would be equally concerned with both. You don't want to do anything that could jeopardize either. Just wait till the recommended age of 21 before taking anything. You can always add mass later on in life but you can't change your height.

    It would be interesting to see if moderate doses of an AI could allow one to grow taller than they moight normally. But the potential hazards just aren't worth it.

  10. J Pediatr Endocrinol Metab. 2005 Mar;18(3):285-93. Related Articles, Links

    The effect of letrozole on bone age progression, predicted adult height, and adrenal gland function.

    Karmazin A, Moore WV, Popovic J, Jacobson JD.

    Section of Endocrinology, Department of Pediatrics, Children's Mercy Hospitals, Kansas City, MO 64108, USA.

    A common problem in pediatric endocrinology is limited growth potential resulting from advancing skeletal maturation. We determined the efficacy of letrozole, an aromatase inhibitor, on delaying bone age advancement in adolescent males with limited growth potential. Twenty-four patients met the study inclusion criteria. Six patients treated with androgen were analyzed separately. Low-dose ACTH stimulation tests were performed to ascertain the effect of letrozole on adrenal gland function. In patients not on androgen, bone age progression decelerated from 1.51+/-0.57 (deltabone age/deltachronological age) before treatment to 0.68+/-0.66 on therapy (mean duration 12.4 months; p <0.0005). Predicted adult height standard deviation scores (SDS) increased from -1.41+/-0.54 to -0.64+/-0.65 on treatment (p <0.0005). Similar results were noted in androgen-treated patients. Approximately one-fourth of patients displayed subnormal responsiveness to ACTH. In summary: 1) letrozole decelerates skeletal maturation, resulting in significant increases in predicted adult height, and 2) letrozole causes mild adrenal suppression.

    PMID: 15813607 [PubMed - in process]


    J Endocrinol. 2004 Jul;182(1):165-72. Related Articles, Links

    The aromatase inhibitor letrozole increases epiphyseal growth plate height and tibial length in peripubertal male mice.

    Eshet R, Maor G, Ben Ari T, Ben Eliezer M, Gat-Yablonski G, Phillip M.

    Felsenstein Medical Research Center and Institute of Endocrinology and Diabetes, Schneider Children's Medical Center of Israel, Petah Tikva, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.

    Sex hormones may influence longitudinal growth, either indirectly, by affecting the growth-hormone-insulin-like growth factor I (IGF-I) axis, or directly, by affecting changes within the epiphyseal growth plate (EGP). The aim of the present study was to investigate the effects of letrozole, an aromatase inhibitor, on longitudinal growth and changes in the EGP in vivo. Eighteen peripubertal male mice were divided into three groups. The first group was killed at baseline, the second was injected with letrozole (Femara) s.c., 2 mg/kg body weight/day, for 10 days, and the third was injected with the vehicle alone. Serum testosterone levels were found to be significantly higher in the treated group than in the controls. Letrozole induced a significant increase in body weight, tail length and serum growth hormone level, but had no significant effect on the level of serum IGF-I. On histomorphometric study, there was a significant increase (12%) in EGP height in the treated animals compared with controls. Immunohistochemistry showed a 3.4-fold letrozole-induced increase in the proliferation of the EGP chondrocytes, as estimated by the number of proliferation cell nuclear antigen-stained cells, and a decrease in the differentiation of the EGP chondrocytes, as estimated by type X collagen staining. Letrozole did not interfere with type II collagen levels. The study group also showed a twofold increase in the number of IGF-I receptor-positive cells compared with controls. In conclusion, the aromatase inhibitor, letrozole, appears to increase the linear growth potential of the EGP in mice.

    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. [email protected]

    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.
    Novel treatment of delayed male puberty with aromatase inhibitors.

    Dunkel L, Wickman S.

    University of Helsinki, Hospital for Children and Adolescents, Finland. [email protected]

    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
    Lakartidningen. 2002 Jan 17;99(3):165-8. Related Articles, Links

    [Growth rate can be manipulated. Estrogen production in pubertal boys can be blocked by an aromatase inhibitor]

    [Article in Swedish]

    Hagenas L.

    Barnendokrinologiska enheten, Astrid Lindgrens barnklinik, Karolinska sjukhuset, Stockholm. [email protected]

    A review of a twelve month clinical trial [1] using a new, effective aromatase inhibitor treatment in boys with delayed puberty shows that the pubertal increase in estrogen levels can be blocked, with concomitant preserved pubertal growth rate. Circulating testosterone levels are greatly enhanced during treatment due to increased gonadotrophin secretion. Despite this, bone age maturation is slow leading to an increased final height prognosis (mean 5.1 cm) for the boys treated with aromatase inhibitor.

    : J Endocrinol Invest. 2000 Dec;23(11):721-3. Related Articles, Links

    Delayed closure of epiphyseal cartilages induced by the aromatase inhibitor anastrozole. Would it help short children grow up?

    ***lia G, Arosio M, Porretti S.

    Institute of Endocrine Sciences, Ospedale Maggiore IRCCS, University of Milan, Italy. giovanni.***[email protected]

    Estrogens locally generated from androgen precursors due to the action of aromatase play a main role in epiphyseal cartilage fusion. Treatment with an aromatase inhibitor (anastrozole, 1 mg/day for 3 yr) in a boy previously operated on for a hamartoma causing precocious puberty and presenting with advanced bone maturation and nearly fused epiphyseal cartilages, slowed cartilage fusion consenting a higher final stature than expected (164.4 cm vs 158.4 cm). It is suggested that treatment with aromatase inhibitors, alone or in combination with rh-GH, may also be useful in children with constitutional short stature in order to delay epiphyseal closure and improve the final height.
    Estrogen suppression in males: metabolic effects.

    Mauras N, O'Brien KO, Klein KO, Hayes V.

    Nemours Research Programs at the Nemours Children's Clinic, Jacksonville, Florida 32207, USA. [email protected]

    We have shown that testosterone (T) deficiency per se is associated with marked catabolic effects on protein, calcium metabolism, and body composition in men independent of changes in GH or insulin-like growth factor I production. It is not clear,,however, whether estrogens have a major role in whole body anabolism in males. We investigated the metabolic effects of selective estrogen suppression in the male using a potent aromatase inhibitor, Arimidex (Anastrozole). First, a dose-response study of 12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at baseline and after 10 days of oral Arimidex given as two different doses (either 0.5 or 1 mg) in random order with a 14-day washout in between. A sensitive estradiol (E2) assay showed an approximately 50% decrease in E2 concentrations with either of the two doses; hence, a 1-mg dose was selected for other studies. Subsequently, eight males (aged 15-22 yr; four adults and four late pubertal) had isotopic infusions of [(13)C]leucine and (42)Ca/(44)Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex. Contrary to the effects of T withdrawal, there were no significant changes in body composition (body mass index, fat mass, and fat-free mass) after estrogen suppression or in rates of protein synthesis or degradation; carbohydrate, lipid, or protein oxidation; muscle strength; calcium kinetics; or bone growth factors concentrations. However, E2 concentrations decreased 48% (P = 0.006), with no significant change in mean and peak GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations. There was a 58% increase in serum T (P = 0.0001), sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and rates of bone calcium deposition and resorption did not change. In conclusion, these data suggest that in the male 1) estrogens do not contribute significantly to the changes in body composition and protein synthesis observed with changing androgen levels; 2) estrogen is a main regulator of the gonadal-pituitary feedback for the gonadotropin axis; and 3) this level of aromatase inhibition does not negatively impact either kinetically measured rates of bone calcium turnover or indirect markers of bone calcium turnover, at least in the short term. Further studies will provide valuable information on whether timed aromatase inhibition can be useful in increasing the height potential of pubertal boys with profound growth retardation without the confounding negative effects of gonadal androgen suppression.

  11. The full texts of some of these are good reads if you can get them.

    and if I were younger I would consider taking a mild aromatase inhibitor that wasn't so harsh as to lower IGF but strong enough to signifigantly lower estrogen and raise T.

  12. Liltwisted.. explain how you, at 14, not 22 would have any clue what you are talking about?


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