bruce410 said:
it is a horrible idea, you are going to shut your growth plates. i grew 3 more inches at 22. you should not juice till your 23-25 minimum bro.
actually as long as you run an AI, the growth plates WONT close. Estrogenic agonism is what causes premature closure.
(though agree that otherwise that would be true)
as a note- they are using AI's and ER blockers to extend height
: Pediatr Endocrinol Rev. 2006 Apr;3 Suppl 2:301-5. Links
Mechanisms for delaying epiphyseal fusion and improving adult height in pubertal patients with hypopituitarism.Eugster EA.
Section of Pediatric Endocrinology, Department of Pediatrics, James Whitcomb Riley Hospital for Children, Indiana University School of Medicine, Indianapolis, Indiana.
The preservation of linear growth potential is an important goal for many patients presenting to the pediatric endocrine clinic. This is particularly true for pubertal adolescents with growth hormone deficiency who are diagnosed late and for short children with hypopituitarism and central precocious puberty, a combination that confers a poor prognosis for adult stature. In this review, currently available and promising new strategies for delaying epiphyseal fusion and increasing adult height in pubertal patients are discussed. While GnRH analogues are the standard of care for treating central precocious puberty, concerns exist regarding adverse metabolic effects of these agents when used in adolescence. Alternate approaches that diminish epiphyseal estrogen exposure yet allow pubertal development to progress in boys include antiestrogens in the form of aromatase inhibitors and estrogen receptor antagonists. Data from clinical trials using these compounds in a variety of pediatric conditions are summarized, and future directions are identified.
Clin Endocrinol (Oxf). 2006 May;64(5):510-3. Links
Treatment with the aromatase inhibitor letrozole during adolescence increases near-final height in boys with constitutional delay of puberty.Hero M, Wickman S, Dunkel L.
Hospital for Children and Adolescents, Helsinki University Central Hospital, Helsinki, Finland.
OBJECTIVE: We investigated whether inhibition of oestrogen biosynthesis with the aromatase inhibitor, letrozole, during adolescence improves near-final height in boys with constitutional delay of puberty. PATIENTS AND METHODS: Seventeen boys with constitutional delay of puberty were randomized to receive testosterone (T) enanthate (1 mg/kg i.m.) every 4 weeks for 6 months in combination with placebo (Pl, n = 8), or the aromatase inhibitor letrozole (Lz, 2.5 mg/day orally) (n = 9), for 12 months. After treatment, patients were followed up until near-final height. Height discrepancy was calculated as near-final height minus mid-parental target height. MEASUREMENTS: The primary end point was the difference in near-final height between the groups treated either with T + Pl or T + Lz. Secondarily, height discrepancy and gain in height standard deviation score (SDS) were analysed in both groups. RESULTS: Boys treated with T + Lz reached a higher mean near-final height than did boys on T + Pl (175.8 vs. 169.1 cm, respectively, P = 0.04). In T + Lz-treated boys, mean near-final height did not differ from their mid-parental target height (175.8 vs. 177.1 cm, P = 0.38), whereas in T + Pl-treated boys, mean near-final height was lower than mid-parental target height (169.1 vs. 173.9 cm, P = 0.007). T + Lz-treated boys had a greater increment in height SDS over the pretreatment height SDS than T + Pl-treated boys (+1.4 SDS vs.+0.8 SDS, P = 0.03). CONCLUSIONS: Our findings indicate that in adolescent boys an increase in adult height can be attained by use of aromatase inhibitors.
1: J Clin Endocrinol Metab. 2005 Dec;90(12):6396-402. Epub 2005 Sep 27. Links
Inhibition of estrogen biosynthesis with a potent aromatase inhibitor increases predicted adult height in boys with idiopathic short stature: a randomized controlled trial.Hero M, Norjavaara E, Dunkel L.
Hospital for Children and Adolescents, University of Helsinki, Finland.
CONTEXT: In males as well as in females, estrogen is an essential regulator of bone maturation, growth plate fusion, and cessation of longitudinal growth. Therefore, an increase in predicted adult height (PAH) may be achieved in short boys by blocking estrogen biosynthesis. OBJECTIVE: We tested the hypothesis that a decrease in the rate of bone maturation and an increase in PAH can be achieved in boys with idiopathic short stature (ISS) by the method of blocking estrogen biosynthesis with an aromatase inhibitor. Secondarily, we investigated the effects of aromatase inhibition on bone mineralization. DESIGN: This was a prospective, double-blind, randomized, placebo (Pl)-controlled clinical study. SETTING: The study was performed at a university hospital out-patient clinic. PATIENTS: Thirty-one boys, aged 9.0-14.5 yr, with ISS were studied. INTERVENTION: The boys were treated with the aromatase inhibitor letrozole (Lz; 2.5 mg/d) or Pl for 2 yr. MAIN OUTCOME MEASURE: The main outcome measure was the change in PAH after 24 months of treatment. RESULTS: PAH increased by 5.9 cm (P < 0.0001), and height SD score for bone age increased by 0.7 SD score (P < 0.0001) in the Lz-treated boys, whereas no changes occurred in the respective measures in Pl-treated boys. Areal bone mineral density of the lumbar spine and femoral neck, assessed by dual-energy x-ray absorptiometry, increased in a similar fashion in both groups during the treatment, whereas bone mineral apparent density increased only in those taking Lz (median increase, 4.3%; P = 0.009). CONCLUSIONS: Treatment with the aromatase inhibitor Lz delays bone maturation and improves PAH in boys with ISS. No adverse effects on bone mineralization were evident after 2 yr of treatment.
Mol Cell Endocrinol. 2006 Jun 9; [Epub ahead of print] Links
Use of aromatase inhibitors to increase final height.Dunkel L.
Kuopio University Hospital, Kuopio, Finland.
During puberty in both sexes, the mechanism involved in epiphyseal fusion is mediated by the action of estrogen through a cascade of events including proliferation, differentiation, and apoptosis of chondrocytes. The enzyme P450 aromatase catalyzes the aromatization of C(19) androgens (androstenedione and testosterone) to C(18) estrogens (estrone and estradiol). Inhibition of estrogen action by aromatase inhibitors (AIs) appears to decelerate the process of growth plate fusion, and thus AIs may be used therapeutically to increase adult height. The clinical experience with AIs in the pediatric setting is limited to testolactone, fadrozole, letrozole, and anastrozole. Testolactone, a nonselective steroidal AI, has been used successfully as an adjunct to antiandrogen and gonadotropin-releasing hormone analogue (GnRHa), therapy for children with familial male-limited precocious puberty (FMPP) and congenital adrenal hyperplasia (CAH), and with some success in girls with McCune-Albright syndrome. The limitations of testolactone include its relatively low potency and the need for frequent dosing. Results of a randomized placebo-controlled trial in boys with delayed puberty treated with letrozole, a selective nonsteroidal AI, found that boys treated with letrozole+testosterone experienced delayed bone maturation and good growth response and achieved an increase in predicted adult height. In this study, only minor differences in bone density were seen between the placebo and letrozole treatment groups, both of which were receiving concomitant testosterone therapy. No adverse effects on testis size or inhibin B concentration were noted. The therapeutic value of AIs in growth promotion now remains to be substantiated in future controlled clinical trials.
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