AAS Research Mega Thread (not pro hormones)

[BeastFitness]

ANDROGEN RECEPTORS
OK so this is going to be fairly in depth and if your not up to par on androgen receptors, pathways, basic means of activation, it might be slightly hard to understand FULLY but you'll get the meaning!





Measurement of myostatin concentrations in human serum: Circulating concentrations in young and older men and effects of testosterone administration.

Abstract
Methodological problems, including binding of myostatin to plasma proteins and cross-reactivity of assay reagents with other proteins, have confounded myostatin measurements. Here we describe development of an accurate assay for measuring myostatin concentrations in humans. Monoclonal antibodies that bind to distinct regions of myostatin served as capture and detector antibodies in a sandwich ELISA that used acid treatment to dissociate myostatin from binding proteins. Serum from myostatin-deficient Belgian Blue cattle was used as matrix and recombinant human myostatin as standard. The quantitative range was 0.15-37.50 ng/mL. Intra- and inter-assay CVs in low, mid, and high range were 4.1%, 4.7%, and 7.2%, and 3.9%, 1.6%, and 5.2%, respectively. Myostatin protein was undetectable in sera of Belgian Blue cattle and myostatin knockout mice. Recovery in spiked sera approximated 100%. ActRIIB-Fc or anti-myostatin antibody MYO-029 had no effect on myostatin measurements when assayed at pH 2.5. Myostatin levels were higher in young than older men (mean+/-S.E.M. 8.0+/-0.3 ng/mL vs. 7.0+/-0.4 ng/mL, P=0.03). In men treated with graded doses of testosterone, myostatin levels were significantly higher on day 56 than baseline in both young and older men; changes in myostatin levels were significantly correlated with changes in total and free testosterone in young men. Myostatin levels were not significantly associated with lean body mass in either young or older men.
CONCLUSION:
Myostatin ELISA has the characteristics of a valid assay: nearly 100% recovery, excellent precision, accuracy, and sufficient sensitivity to enable measurement of myostatin concentrations in men and women.


Testosterone up-regulates androgen receptors and decreases differentiation of porcine myogenic satellite cells in vitro.

Abstract
Accumulation of DNA is essential for muscle growth, yet mechanisms of androgen-induced DNA accretion in skeletal muscle are unclear. The purpose of this study was to determine whether androgen receptors (AR) are present in cultured skeletal muscle satellite cells and myotubes and examine the effects of testosterone on satellite cell proliferation and differentiation. Immunoblot analysis using polyclonal AR antibodies (PG-21) revealed an immunoreactive AR protein of approximately 107 kDa in porcine satellite cells and myotubes. Immunocytochemical AR staining was confined to the nuclei of satellite cells, myotubes, and muscle-derived fibroblasts. Administration of 10(-7) M testosterone to satellite cells, myotubes, and muscle-derived fibroblasts increased immunoreactive AR. In satellite cells and myotubes, AR increased incrementally after 6, 12, and 24 h of exposure to testosterone. Testosterone (10(-10) - 10(-6) M), alone or in combination with insulin-like growth factor I, basic fibroblast growth factor, or platelet-derived growth factor-BB, had no effect (P > 0.01) on porcine satellite cell proliferation, and testosterone pretreatment for 24 h did not alter the subsequent responsiveness of cells to these growth factors. Satellite cell differentiation was depressed (20-30%) on days 2-4 of treatment with 10(-7) M testosterone. This effect was not reversible within 48 h after treatment withdrawal and replacement with control medium. These data indicate that satellite cells are direct targets for androgen action, and testosterone administration increases immunoreactive AR protein and reduces differentiation of porcine satellite cells in vitro.


Androgen receptor in rat skeletal muscle: characterization and physiological variations.

Abstract
Androgen binding has been studied in the quadriceps femoris of recently castrated adult and intact immature male and female rats using a variety of techniques for separating and measuring hormone-receptor complexes. [3H]Testosterone, [3H]androstanolone (or 5 alpha-dihydrotestosterone). [3H]methyltrienolone (a potent synthetic androgen), and [3H]estradiol bind to the androgen receptor. Affinities are identical for the first two hormones (Kd = approximately 70 pM) and lower for estradiol (Kd = approximately 0.2 nM), as determined by Scatchard plots of binding data. Competition experiments indicate that in addition to the nonradioactive steroids corresponding to the above-cited tritiated compounds, progesterone, cyproterone acetate (an antiandrogen), and spironolactone compete for [3H]androgen binding by the receptor, but diethylstilbestrol, moxestrol (a potent synthetic steroidal estrogen), and cortisol do not. 3 alpha- and 3 beta-androstanediols slightly inhibit testosterone binding. Therefore, striated muscle androgen receptor specificity is identical to that of all androgen receptors of target tissues which have been previously studied. Binding is abolished by pronase and heat treatment, and displays an approximate 7S sedimentation coefficient in low salt ultracentrifugation gradient analysis. Preliminary observations suggest hormone-induced receptor translocation into the nucleus. No evidence has been found for an independent estrogen receptor. In the course of the binding experiments, extensive metabolism of androstanoloe and testosterone was observed in muscle cytosol at 0-4 C, during the 2-h incubation period used for most binding studies. Metabolite formation can jeopardize the binding data, specifically altering the significance of competition experiments with relatively high concentrations of steroids approaching the Km of metabolizing enzymes. Therefore, most quantitative studies were performed in enzyme-free, receptor-containing cytosol preparations. In adult male rats castrated for 2 days, the concentration of receptor in the cytosol was of the order of 1 fmol/mg protein and corresponded to 72 fmol/mg tissue DNA (that is, 100 and 20 times less than that in corresponding prostatic cytosol, respectively). In the adult female rat 2 days after castration, the concentration of receptor in the cytosol was 0.34 fmol/mg protein. Treatment with testosterone pellets (20 mg for 15 days) increased androgen receptor concentration significantly. In spite of the relatively low concentration of androgen-binding sites, the typical binding specificity of the androgen receptor and the regulatory effects of androgens on their own receptor support the possibility that some effect(s) of androgens upon skeletal muscles may be initiated directly at the cellular level through this receptor, a concept which is also in agreement with recently demonstrated in vitro effects of androgens on cultured myoblasts.


Pharmacological doses of testosterone upregulated androgen receptor and 3-Beta-hydroxysteroid dehydrogenase/delta-5-delta-4 isomerase and impaired leydig cells steroidogenesis in adult rats.

Abstract
Anabolic androgenic steroids (AAS) are testosterone derivatives originally designed to enhance muscular mass and used for the treatment of many clinical conditions as well as in contraception. Despite popular interest and abuse, we still lack a broad understanding of effects of AAS on synthesis of steroid hormones on the molecular level. This study was designed to systematically analyze the effects of pharmacological/high doses of testosterone on steroidogenic machinery in Leydig cells. Two different experimental approaches were used: (1) In vivo experiment on groups of adult male rats treated with testosterone for 1 day, 2 weeks, and 2 months; (2) Direct in vitro testosterone treatment of Leydig cells isolated from intact rats. Result showed that prolonged in vivo treatment with testosterone decreased the expression of Scarb1 (scavenger receptor class B type 1), Tspo (translocator protein), Star (steroidogenic acute regulatory protein), Cyp11a1 (cholesterol side-chain cleavage enzyme), and Cyp17a1 (17α-hydroxylase/17, 20 lyase) in Leydig cells. Oppositely, the expression of Hsd3b (3-beta-hydroxysteroid dehydrogenase/delta-5-delta-4 isomerase), Ar (androgen receptor), and Pde4a/b (cyclic adenosine monophosphate-dependent phosphodiesterases) was increased. Androgenization for 2 weeks inhibited Cyp19 (aromatase) transcription, whereas 2-month exposure caused the opposite effect. Direct in vitro testosterone treatment also decreased the expression of Cyp11a1, Cyp17a1, and Cyp19a1, whereas Hsd3b was upregulated. The results of expression analysis were supported by declined steroidogenic capacity and activity of Leydig cells, although conversion of pregnenolone to progesterone was stimulated. The upregulation of AR and 3βHSD in testosterone-impaired Leydig cells steroidogenesis could be the possible mechanism that maintain and prevent loss of steroidogenic function.

Androgen receptor in human skeletal muscle and cultured muscle satellite cells: up-regulation by androgen treatment.

Abstract
Androgens stimulate myogenesis, but we do not know what cell types within human skeletal muscle express the androgen receptor (AR) protein and are the target of androgen action. Because testosterone promotes the commitment of pluripotent, mesenchymal cells into myogenic lineage, we hypothesized that AR would be expressed in mesenchymal precursor cells in the skeletal muscle. AR expression was evaluated by immunohistochemical staining, confocal immunofluorescence, and immunoelectron microscopy in sections of vastus lateralis from healthy men before and after treatment with a supraphysiological dose of testosterone enanthate. Satellite cell cultures from human skeletal muscle were also tested for AR expression. AR protein was expressed predominantly in satellite cells, identified by their location outside sarcolemma and inside basal lamina, and by CD34 and C-met staining. Many myonuclei in muscle fibers also demonstrated AR immunostaining. Additionally, CD34+ stem cells in the interstitium, fibroblasts, and mast cells expressed AR immunoreactivity. AR expression was also observed in vascular endothelial and smooth muscle cells. Immunoelectron microscopy revealed aggregation of immunogold particles in nucleoli of satellite cells and myonuclei; testosterone treatment increased nucleolar AR density. In enriched cultures of human satellite cells, more than 95% of cells stained for CD34 and C-met, confirming their identity as satellite cells, and expressed AR protein. AR mRNA and protein expression in satellite cell cultures was confirmed by RT-PCR, reverse transcription and real-time PCR, sequencing of RT-PCR product, and Western blot analysis. Incubation of satellite cell cultures with supraphysiological testosterone and dihydrotestosterone concentrations (100 nm testosterone and 30 nm dihydrotestosterone) modestly increased AR protein levels. We conclude that AR is expressed in several cell types in human skeletal muscle, including satellite cells, fibroblasts, CD34+ precursor cells, vascular endothelial, smooth muscle cells, and mast cells. Satellite cells are the predominant site of AR expression. These observations support the hypothesis that androgens increase muscle mass in part by acting on several cell types to regulate the differentiation of mesenchymal precursor cells in the skeletal muscle.





Ok so if you've read all of those studies, understand the material, and can connect the dots you can see that androgen receptor down regulation is extremely over exaggerated within our industry today. In the presence of androgen's (and supported by multiple other sources), the truth is that androgen receptors up-regulating increasing and CONTINUOUSLY expressing new androgen receptor sites systemically throughout the body and tissue.

When unattached to an androgen, the half life is approximately three hours which are then replaced with new ones.

When attached to an androgen, they become more sensitive and their half life doubles and the amount of new receptors increases.

Remember that androgen receptor-mediated effects are not the whole story when it comes to anabolic steroid activity in the body.

 

[Hyde]

The "short-cycling" dry short/esterless/oral article was an awesome read. Am I missing anything when I say it looks like a standard protocol was basically moderate tren ace and anavar for 2-3wks, 2 weeks of clomid, and 2 weeks neither AAS or SERM, and they never came off 2.5mg of letro daily??

Bump for discussion

Seems like staying on 2.5mg letro for years would be a pretty poor idea for longevity, which seemed to be a major concern of the protocol in the first place

 

[B5150]

Bump for discussion

Seems like staying on 2.5mg letro for years would be a pretty poor idea for longevity, which seemed to be a major concern of the protocol in the first place

i realize that I brought it up and it is worth discussion but I would prefer not to derail this thread off topic.

Please post up in here and we can carry on the discussion there. Thanks for understanding.

http://anabolicminds.com/forum/steroids/18318-short-cycles-some-7.html#post5244320

 

[Hyde]

i realize that I brought it up and it is worth discussion but I would prefer not to derail this thread off topic.

Please post up in here and we can carry on the discussion there. Thanks for understanding.

http://anabolicminds.com/forum/steroids/18318-short-cycles-some-7.html#post5244320

I was actually more focusing on long-term letrozole usage, as that would be really interesting to see health studies on larger dosages (if there are any). I realize this isn't actually AAS though and appreciate the link!

 

[B5150]

FWIW I used .5mg (1/2mg [1/5 of a 2.5mg dose]) while using 200mg of testosterone for 6 months (I'm on TRT for many years now). I figured it was so cheap and even cheaper when the effective dose was so minuscule. It destroyed my E2 to less than <5 (it was undetectable) and it slaughtered my HDL and elevated my LDL.

It has the potential to adversely effect bone minerals and bone density and can cause early onset of osteoporosis. It also has a detrimental effect on lipids. I cannot imagine the issues woman have when using it at 2.5mg/d for the treatment of breast cancer .

Invalid Link Removed
Invalid Link Removed

Edit: please note that the article linked above and that I posted was old and was dated "2002"

 

[brofessorx]

I prefer to use letro in pct as my ai, at 1/4 the dosage .625mg e/d for the first 3 weeks.
very easy to destroy your estrogen using letrozole.

 

[B5150]

I prefer to use letro in pct as my ai, at 1/4 the dosage .625mg e/d for the first 3 weeks.
very easy to destroy your estrogen using letrozole.

Used in that fashion and that duration it is great. The first few weeks using it with "androgenic hormones" I was sliced and diced but long term it was detrimental.

 

[BeastFitness]

Sorry for the delay guys! The weekend really got away from me and I got slammed with work!

Bump for discussion

Seems like staying on 2.5mg letro for years would be a pretty poor idea for longevity, which seemed to be a major concern of the protocol in the first place

i realize that I brought it up and it is worth discussion but I would prefer not to derail this thread off topic.

Please post up in here and we can carry on the discussion there. Thanks for understanding.

http://anabolicminds.com/forum/steroids/18318-short-cycles-some-7.html#post5244320

I was actually more focusing on long-term letrozole usage, as that would be really interesting to see health studies on larger dosages (if there are any). I realize this isn't actually AAS though and appreciate the link!

FWIW I used .5mg (1/2mg [1/5 of a 2.5mg dose]) while using 200mg of testosterone for 6 months (I'm on TRT for many years now). I figured it was so cheap and even cheaper when the effective dose was so minuscule. It destroyed my E2 to less than <5 (it was undetectable) and it slaughtered my HDL and elevated my LDL.

It has the potential to adversely effect bone minerals and bone density and can cause early onset of osteoporosis. It also has a detrimental effect on lipids. I cannot imagine the issues woman have when using it at 2.5mg/d for the treatment of breast cancer .

Invalid Link Removed
Invalid Link Removed

Edit: please note that the article linked above and that I posted was old and was dated "2002"

I prefer to use letro in pct as my ai, at 1/4 the dosage .625mg e/d for the first 3 weeks.
very easy to destroy your estrogen using letrozole.

Used in that fashion and that duration it is great. The first few weeks using it with "androgenic hormones" I was sliced and diced but long term it was detrimental.

So in terms of letro let's look at the research first (which mostly deals with breast cancer patients)

Long-term efficacy and safety of letrozole for the adjuvant treatment of early breast cancer in postmenopausal women: a review

Abstract
Aromatase inhibitors (AIs) are becoming more widely used than tamoxifen as adjuvant hormonal therapy for postmenopausal women (PMW) with early breast cancer (EBC). It is clear that these drugs offer important efficacy benefits over tamoxifen and differ from tamoxifen in their safety profile. The accepted strategies for adjuvant AI therapy include initial adjuvant treatment following surgery, switching and/or sequencing from prior tamoxifen, and extended adjuvant therapy following the full 5 years of tamoxifen treatment. Among the available AIs, letrozole has been evaluated in large, well-controlled, double-blind clinical trials in the initial adjuvant, extended adjuvant, and more recently, the sequential adjuvant settings. Letrozole is the most potent of the AIs and provides near complete suppression of plasma estrogens in PMW. Letrozole also significantly reduces the occurrence of early distant metastases, the most lethal type of recurrence event, which can lead to improved survival. Clinical comparisons of letrozole with both tamoxifen and placebo have also provided important long-term safety data on the use of AIs as adjuvant therapy in PMW with EBC. The weight of clinical evidence indicates that letrozole is a safe and effective option for adjuvant hormonal therapy across all three AI treatment settings.

Long-term safety of aromatase inhibitors in the treatment of breast cancer

Abstract
Following promising data for metastatic breast cancer in terms of efficacy and safety profile, third-generation aromatase inhibitors (AI), anastrozole, letrozole, and exemestane, underwent a full development in early setting. If recent results consistently show the superiority of these agents over tamoxifen, the therapeutic strategies of AIs in adjuvant setting are still debated. Beyond the choice of clinical strategy, the long duration of exposure to AI in adjuvant setting required a full determination of the long-term toxicity profile of these agents. While all three AIs have either favorable (decreased incidence of hot flashes, gynecologic and thromboembolic side-effects) or unfavorable (skeletal complications, arthralgia, musculoskeletal pain, sexual dysfunction) class adverse events, some variability between AIs has been reported in side-effects as well as gastrointestinal, urogenital, neurologic, and visual disturbances, confirming the lack of interchangeability between the three AIs. The overall therapeutic index of AIs appears today superior to that of tamoxifen with proven improved efficacy and better toxicity profile. This review will explore the results from the available adjuvant AIs trials with a particular emphasis on safety profiles, quality of life, and therapeutic index, helping to define the present role of AIs in the adjuvant management of postmenopausal patients with breast cancer.

Letrozole versus testosterone. a single-center pilot study of HIV-infected men who have sex with men on highly active anti-retroviral therapy (HAART) with hypoactive sexual desire disorder and raised estradiol levels.

Abstract
Since the advent of Highly Active Anti-Retroviral Therapy (HAART), men with HIV experience good quality of life and expect to have normal sexual function. However, it appears that men infected with HIV commonly complain of sexual problems. There is evidence that men on HAART develop low sexual desire that is associated with raised estradiol levels. It has been postulated that abnormal metabolism seen in this group of men increases the aromatization of testosterone to estradiol. We hypothesized that letrozole, an aromatase inhibitor that inhibits the conversion of testosterone to estradiol, would be beneficial in these men.
AIM: The aim of this study was to compare the effects of testosterone vs. an aromatase inhibitor, letrazole, in HIV-infected men with raised estradiol and low sexual desire.
METHODS: Thirteen men who have sex with men on HAART with low sexual desire as well as raised estradiol levels (>120 pmol/L) were randomly allocated to receive either parenteral testosterone (Sustanon 250 intramuscular injection) (N = 6) or letrozole 2.5 mg orally daily (N = 7) for 6 weeks.
MAIN OUTCOME MEASURES: Sex steroid hormone assays, sex hormone-binding globulin, virological, hematological, and biochemical parameters were measured before and after treatment. Each subject was given the Spector Sexual Desire Inventory and the Depression/Anxiety Stress Scale before and immediately after treatment. Subjects were also asked to estimate the number of actual sexual acts before and after treatment. Results. Inventory data showed a rise in dyadic desire in both treatment arms. Mean actual sexual acts rose from 0.33 to 1.5 in the testosterone group and from 0.43 to 1.29 for the letrozole group. Luteinizing hormone increased in seven of seven men on letrozole. Serum testosterone increased in seven of seven men on letrozole. There were no adverse events from either medication.
CONCLUSION: Letrozole may be useful in the management of men on HAART who have low sexual desire.

Short-term aromatase inhibition: effects on glucose metabolism and serum leptin levels in young and elderly men

Abstract
Objective To assess and compare the effects of short-term aromatase inhibition on glucose metabolism, lipid profile, and adipocytokine levels in young and elderly men.
Design and methods Ten elderly and nine young healthy men were randomized to receive letrozole 2.5 mg daily or placebo for 28 days in a crossover design.
Results Both in young and elderly men, active treatment significantly increased serum testosterone (+128 and +99%, respectively) and decreased estradiol levels (−41 and −62%, respectively). Fasting glucose and insulin levels decreased in young men after active intervention (−7 and −37%, respectively) compared with placebo. Leptin levels fell markedly in both age groups (−24 and −25%, respectively), while adiponectin levels were not affected by the intervention. Lipid profile was slightly impaired in both groups, with increasing low density lipoprotein-cholesterol levels (+14%) in the younger age group and 10% lower levels of APOA1 in the elderly. A decline in IGF1 levels (−15%) was observed in the younger age group. No changes in weight or body mass index were observed in either young or old men.
Conclusions Short-term aromatase inhibition appears to affect glucose metabolism in young men, and lipid metabolism, including leptin secretion, in young and elderly men. Furthermore, the short period of exposure suggests that these changes might be mediated by direct effects of sex steroids rather than by changes in body composition.

Aromatase inhibitors (AI) have been used in males in idiopathic short stature, constitutional delay of puberty, precocious puberty, gynecomastia, oligospermia, hypogonadism related to obesity and ageing.

Introduction
Aromatase inhibitors (AI) have been used in the treatment of idiopathic short stature (ISS), constitutional delay of puberty (CDP) and precocious puberty in boys to increase adult height. Moreover, it has been used in the management of gynecomastia, oligospermia and male hypogonadism related to obesity and ageing.[1,2,3] This retrospective study was carried out to assess the efficacy of letrozole, an AI, in varied conditions in Indian males.
Go to:
Case Reports
Case A
A 15-year-old male presented with macromastia. He had delayed puberty.
Wt - 62.7 kg; Ht - 155 cm; Sexual Maturation Rate (SMR) - G1P1, testes - 3 ml, stretched penile length (SPL) - 5 cm.
LH - 6.3 IU/L, follicle-stimulating hormone (FSH) - 2.9 IU/L, prolactin (PRL) - 5.1 ng/ml, normal thyroid-stimulating hormone (TSH) and T4.
Testosterone (T) - 43.8 ng/dl and estradiol (E2) - 9.79 pg/ml. T/E2 = 4.4:1. He was prescribed letrozole 2.5 mg - 3 times/week.
After 6 months of AI therapy:
Wt - 68.8 kg; Ht - 158.5 cm; SMR - G3P3, testes 10 ml, SPL - 6 cm. There was insignificant change in breast enlargement.
T - 331.62 ng/dl; E2-8.05 pg/ml. T/E2 = 41.2.
There was 650% increase in T and 17.9% decrease in E2.
Case B
A 14-year-old male was referred for obesity. He had delayed puberty.
Wt - 66.6 kg; Ht - 158 cm; SMR - G1P1, SPL - 4 cm.
LH - 3.59 IU/L; FSH - 2.48 IU/L; PRL - 13.8 ng/ml, normal TSH and T4.
T - 25.81 ng/dl; E2 - 141.3 pg/ml; T/E2 = 0.18:1.
He was prescribed injection T - 100 mg monthly and letrozole 2.5 mg - 3 times/week for 4 months. After 3 weeks of last dose of injection T and 3 days of last dose of letrozlole: Wt - 68.9 kg; Ht - 159.5 cm; SMR-G2P2, SPL ~5 cm.
T - 310.6 ng/dl; E2 - 13.15 pg/ml; T/E2 = 23.6:1.
There was ~1100% increase in T and 90% decrease in E2.
Case C
A 23-year-old male was referred for management of hypogonadism.
Wt - 55.9 kg; Ht - 161 cm; body mass index - 21.6; no anosmia; SMR - G1P1, SPL - 4 cm. LH <0.07 IU/L, FSH - 0.032 IU/L, PRL - 4.93 ng/ml, T - 13 ng/dl.
He was prescribed injection T - 100 mg every 3 weeks along with letrozole 2.5 mg - 2 times/week. After 3 weeks of last (4th) injection T and 3 days of last letrozole dose: T - 74 ng/dl.
There was 469% increase in T.
Case D
A 27-year-old male was referred for poor semen quality. His total functional sperm fraction (TFSF), denoted by sperm count (×106) by normal morphology (%) by normal motility (%), was 70 × 106/ml × 30% × 30% =6.3.
T - 257.9 ng/dl; E2 - 35.8 pg/ml; T/E2 = 7.2:1.
He was prescribed letrozole - 2.5 mg - 2 times/week.
After 1 month of therapy: T - 754.9 ng/dl; E2 - 28.5 pg/ml; T/E2 = 26.5:1.
There was 200% increase in T and 20% decrease in E2.
TFSF - 80 × 106 × 70% × 30% =16.8.
Go to:
Discussion
AI have been used in boys with ISS and CDP to increase adult height.[1,4,5] Boys with ISS with a mean age of 11 years were treated with letrozole 2.5 mg once daily or placebo for 2 years. There was a gain of 5.9 cm in predicted adult height in the letrozole treated group.[4] A significant increase in predicted adult height has also been observed in boys with CDP who were treated with a combination of T and letrozole.[5] AI slow down epiphyseal maturation by lowering E2 levels. This approach proved successful in other conditions, too, viz. aromatase excess syndrome, sertoli cell tumors and testotoxicosis (along with antiandrogen).[1] AI have limited efficacy in the treatment of gynecomastia; hence, they are not recommended as a first line treatment for gynecomastia.[1] Significant improvement in SMR was observed in CDP cases (Case A and B). There was marked improvement in SMR in case A with “sole” therapy with letrozole, but insignificant response in gynecomastia. Case B was treated with a “combination” of T and letrozole.
AI therapy is associated with a sustained increase in FSH and a positive effect on sperm concentration and motility.[1] Case D (T <300 ng/dl; T/E <10:1) showed improvement in semen quantity and quality with letrozole even though sperm count was normal. Some men with severe oligospermia (<5 × 106/ml), low T levels (<300 ng/dl), T (ng/dl) to E2 (pg/ml) ratio <10 and normal gonadotropins concentration may have a treatable endocrinopathy. AI have been successfully used in this subset of patients.[1,3,6] 2.5 mg/d letrozole for 6 months has been shown to improve seminal parameters (denoted by TFSF).[3]
AI have been used in the treatment of hypogonadism related with obesity and ageing. Letrozole 2.5 mg once a week produced sustained normalization of serum total T in males with obesity related hypogonadism; however, free T rose to supraphysiological levels emphasizing the need for estimation of free T during AI treatment.[2]
It has been suggested that aromatase is less suppressed in the testis compared with adipocytes and muscle tissue. It is questionable whether AI are able to stimulate T production sufficiently in men with truly low T levels.[1] There was a marked increase in T with combination treatment with T and letrozole in CDP (Case B) as compared with Idiopathic Hypogonadotropic Hypogonadism (IHH) (Case C) where there was lesser response with the same combination therapy. The marked increased in T with letrozole in CDP as compared to lesser response in IHH can aid in distinguishing the two conditions with the use of AI.
Most of the recent studies with AI in boys and adult men do not show a major detrimental effects (including bone).[1] The harmful effects are unlikely if the dose is carefully adjusted (even weekly) based on T and E2 levels.[3]
This retrospective study in Indian males showed insignificant effect of AI in gynecomastia and IHH, significant effect in CDP and some benefit in improving seminal parameters. Moreover, this study highlights the importance of estimating E2 (along with T and gonadotropins) in various endocrinopathies, which can be benefitted by reducing E2 by AI.
Further prospective, randomized, blinded, placebo-controlled, long-term studies are needed to clarify the role of AI in the management of growth impairment, male infertility and hypogonadism.

Testosterone boost from letrozole
· 0.02 mg of Letrozole increased testosterone by 45% after 2 days
· 0.1 mg of Letrozole increased testosterone by 49% after 2 days
· 0.5 mg of Letrozole increased testosterone by 48% after 2 days
· 1 mg of Letrozole increased testosterone by 41% after 2 days
· 2.5 mg of Letrozole increased testosterone by 74% after 3 days
· 10 mg of Letrozole increased testosterone by 97% after 2 days
· 30 mg of Letrozole increased testosterone by 113% after 3 days


At the end of the day, I feel letro (like many compounds) has its place BUT it needs to be used within the proper cycle with the correct dosage and length. I am personally not a fan of taking ANYTHING extremely long term without any breaks.

 

[datsthat]

I love this thread. Lots to read and digest.

 

[hamdysayed]

Well damn so much info that It got me 100% overwhelmed... like tons of info.
I'll try to keep up, one question
if one is scared of side effects of tren how would u go by trying it, u start at low dose or how can u know it will mess u up or not ?
Since some can tolerate it n some cant!

 

[BamBam0319]

Well damn so much info that It got me 100% overwhelmed... like tons of info.
I'll try to keep up, one question
if one is scared of side effects of tren how would u go by trying it, u start at low dose or how can u know it will mess u up or not ?
Since some can tolerate it n some cant!

Interested to know more along these lines as well. I plan on starting tren a week from today, 50mg EOD for the first 4 pins and then 100mg EOD until I run out, provided everything goes well the first week. I have 19mL on hand.

 

[B5150]

Use acetate and start low. Increase as tolerated. If you cannot tolerate it stop or reduce until the unwanted sides diminish. With acetate you will know pretty quickly if it is or isn't for you.

 

[BeastFitness]

I love this thread. Lots to read and digest.

Glad you like it!!!

Well damn so much info that It got me 100% overwhelmed... like tons of info.
I'll try to keep up, one question
if one is scared of side effects of tren how would u go by trying it, u start at low dose or how can u know it will mess u up or not ?
Since some can tolerate it n some cant!

Interested to know more along these lines as well. I plan on starting tren a week from today, 50mg EOD for the first 4 pins and then 100mg EOD until I run out, provided everything goes well the first week. I have 19mL on hand.

Use acetate and start low. Increase as tolerated. If you cannot tolerate it stop or reduce until the unwanted sides diminish. With acetate you will know pretty quickly if it is or isn't for you.

Agreed with David. I would start with a low dose of 50-100mgs per week of tren ace. Remember, it's a good idea to use a shorter ester when trying a new compound so you can control the sides quicker



Pharmacological and endocrinological studies on anabolic agents.

Abstract
When used in connection with animal production the term "anabolic agents" covers a wide range. Ther steroidal male and female sex hormones are included in this list, as are the nonsteroidal estrogens. For the clinician and for the endocrinologist, anabolics are only steroids chemically related to testosterone and 19-nortestosterone. Estrogens, though possessing anabolic properties, too, do not belong to this class. This paper will deal with anabolic agents in in the stricter sense of which mainly trenbolone acetate combined with hexestrol has been recommended for bull and heifer fattening. To consider possible consumer injury from ingestion of meat from anabolic agent treated animals, it is necessary to know the pharmacological properties of the agents, the doses producing certain effects or might produce, and the levels of residues in the meat. Trenbolone acetate will be compared with the following anabolic agents: methenolone acetate, methandrostenolone, nandrone, androstanazole, and 19-nortestosterone. The activity spectrum of trenbolone acetate is similar to that of 19-nortestosterone or those anabolics that are derived from 19-nortestosterone. The compound has about three times stronger androgenic effect than testosterone propionate. Its index of dissociation between anabolic/androgenic activity is 2--3. This index is 3--10 for the other anabolic agents. As regards the virilizing potency, trenbolone acetate is also on the top of the list. It seems that androgenicity and degree of virilization run paralle. The antigonadotropic activity (inhibition of ovulation and testicular growth) of trenbolone acetate exceeds that of testosterone propionate by the factor 3. The compound is not estrogenic and seemingly not or only weakly progestationally active. In principle, the androgenic activity (symptoms of virilization) as well as the antigonadotropic effect (disturbances of the menstrual cycle in women, inhibition of spermiogenesis in men) of trenbolone acetate might be noted. This risk, however, can be excluded by mere calculation. In rats, 0.1 mg/kg trenbolone acetate have an antigonadotropic effect. This corresponds to a daily dose of 5--7 mg in humans. By the same extrapolation, a daily human dose of 100 mg can be calculated for androgenic activity. Such factors of conversion are, of course, not precise because rats are much less sensitive to androgens and anabolics than humans. Thus, testosterone propionate is active only in daily doses of 10--20 mg. If in humans trenbolone acetate also has three times the activity of testosterone propionate, effects in man had to be counted with not less than a daily intake of 3--5 mg trenbolone acetate. The dose which is recommended for livestock fattening is 300 mg. IT can, therefore, be excluded almost with certainty that the meat would contain such large amounts of hormone residues.

 

[BamBam0319]

Use acetate and start low. Increase as tolerated. If you cannot tolerate it stop or reduce until the unwanted sides diminish. With acetate you will know pretty quickly if it is or isn't for you.

Yep that's what I've got!

 

[BamBam0319]

Agreed with David. I would start with a low dose of 50-100mgs per week of tren ace. Remember, it's a good idea to use a shorter ester when trying a new compound so you can control the sides quicker

50-100 mg per week? So what, like 25mg per injection EOD to start?

 

[B5150]

You'd likely be fine a bit higher but some people cannot appreciate how trenbolone makes you feel until they use it and find its not for them.

EOD 25mg x 7 / 2 = 87.5mg/w
EOD 30mg x 7 / 2 = 105mg/w
EOD 35mg x 7 / 2 = 122.5mg/w
EOD 40mg x 7 / 2 = 140mg/w
EOD 45mg x 7 / 2 = 157.5mg/w
EOD 50mg x 7 / 2 = 175mg/w

 

[BamBam0319]

You'd likely be fine a bit higher but some people cannot appreciate how trenbolone makes you feel until they use it and find its not for them.

EOD 25mg x 7 / 2 = 87.5mg/w
EOD 30mg x 7 / 2 = 105mg/w
EOD 35mg x 7 / 2 = 122.5mg/w
EOD 40mg x 7 / 2 = 140mg/w
EOD 45mg x 7 / 2 = 157.5mg/w
EOD 50mg x 7 / 2 = 175mg/w

What if I did:
Week 1: 25mg Sun,Tues,Thurs,Sat 100mg total
Week 2: 50mg Sun,Tues,Thurs,Sat 200mg total
Week 3: 100mg Mon,Wed,Fri 300mg total
Week 4: 100mg Sun,Tues,Thurs,Sat 400mg total
Week 5: 100mg Mon,Wed,Fri 300mg total
Week 6: 100mg Sun,Tues,Thurs,Sat 400mg total
Week 7: 100mg Mon,Wed then I will run out.
Do you think that would be an acceptable way to assess how I react to tren?

 

[B5150]

Acceptable? I don't know. Advisable? Not sure. The thing is even though it's s short Ester it still needs to achieve peak and reasonably stable plasma levels. I don't believe IMHO that protocol will achieve that. I'm not saying no. I'm just Sharing my opinion on that plan. Maybe start a trenbolone thread so as not to derail FitnessBeast research thread.

 

[BamBam0319]

Acceptable? I don't know. Advisable? Not sure. The thing is even though it's s short Ester it still needs to achieve peak and reasonably stable plasma levels. I don't believe IMHO that protocol will achieve that. I'm not saying no. I'm just Sharing my wire on that plan. Maybe start a trenbolone thread so as not to derail FitnessBeast data thread.

I think a more fitting word would be "reasonable" not "acceptable." But good idea. I'll do that. Thank you

 

[Dma378]

Well damn so much info that It got me 100% overwhelmed... like tons of info.
I'll try to keep up, one question
if one is scared of side effects of tren how would u go by trying it, u start at low dose or how can u know it will mess u up or not ?
Since some can tolerate it n some cant!

This was my, and I'm sure many people's concern too. The Tren ph gave me pretty bad sides with epi, so I was nervous. So much so that my first pin of Tren ace gave me anxiety and I had to go sit on the couch and calm down!!

Turns out I handled it far better than oral. But started low as advised. 50mg EOD is a good number. Also as said with a short ester you'll know what works quick and adjustments take effect quick. 2 weeks at 50-75 EOD and assess.

As I increased my Tren I lowered my Cyp until I found what felt good which was around 250 Cyp/week and up to 150 EOD Ace. Around week 4 I had it dialed in and ran it for a total of 8 weeks.

Had sides but they were manageable. Was also running Mast at 500mg/week, Caber .5mg e5d, Adex .5mg e3-4d. Once or twice a week sleep like crap, sweaty all the damn time, kind of tense. But man the gym....

 

[hamdysayed]

This was my, and I'm sure many people's concern too. The Tren ph gave me pretty bad sides with epi, so I was nervous. So much so that my first pin of Tren ace gave me anxiety and I had to go sit on the couch and calm down!!

Turns out I handled it far better than oral. But started low as advised. 50mg EOD is a good number. Also as said with a short ester you'll know what works quick and adjustments take effect quick. 2 weeks at 50-75 EOD and assess.

As I increased my Tren I lowered my Cyp until I found what felt good which was around 250 Cyp/week and up to 150 EOD Ace. Around week 4 I had it dialed in and ran it for a total of 8 weeks.

Had sides but they were manageable. Was also running Mast at 500mg/week, Caber .5mg e5d, Adex .5mg e3-4d. Once or twice a week sleep like crap, sweaty all the damn time, kind of tense. But man the gym....

Thanks bro for the help and the info.
There is so much to learn..

 

[BeastFitness]

In terms of the tren questions, if you want you can shoot me a pm OR start a tren based thread so like David said, we can keep this all research based and not a specific cycle thread…I'd be more than happy to help out in anyway!


NOW RESEARCH TIME

Today I wanna talk a little bit about anadrol

Effects of an oral androgen on muscle and metabolism in older, community-dwelling men

To determine whether oxymetholone increases lean body mass (LBM) and skeletal muscle strength in older persons, 31 men 65–80 yr of age were randomized to placebo (group 1) or 50 mg (group 2) or 100 mg (group 3) daily for 12 wk. For the three groups, total LBM increased by 0.0 ± 0.6, 3.3 ± 1.2 (P < 0.001), and 4.2 ± 2.4 kg (P < 0.001), respectively. Trunk fat decreased by 0.2 ± 0.4, 1.7 ± 1.0 (P = 0.018), and 2.2 ± 0.9 kg (P= 0.005) in groups 1, 2, and 3, respectively. Relative increases in 1-repetition maximum (1-RM) strength for biaxial chest press of 8.2 ± 9.2 and 13.9 ± 8.1% in the two active treatment groups were significantly different from the change (−0.8 ± 4.3%) for the placebo group (P < 0.03). For lat pull-down, 1-RM changed by −0.6 ± 8.3, 8.8 ± 15.1, and 18.4 ± 21.0% for the groups, respectively (1-way ANOVA, P = 0.019). The pattern of changes among the groups for LBM and upper-body strength suggested that changes might be related to dose. Alanine aminotransferase increased by 72 ± 67 U/l in group 3 (P < 0.001), and HDL-cholesterol decreased by −19 ± 9 and −23 ± 18 mg/dl in groups 2 and 3, respectively (P = 0.04 and P = 0.008). Thus oxymetholone improved LBM and maximal voluntary muscle strength and decreased fat mass in older men.


Oxymetholone for the treatment of HIV-wasting: a double-blind, randomized, placebo-controlled phase III trial in eugonadal men and women.

Abstract
BACKGROUND:
Despite highly active antiretroviral therapy (HAART), chronic involuntary weight loss still remains a serious problem in the care of HIV patients due to various alterations in energy metabolism and endocrine regulation. Previous studies in HIV-positive men undergoing androgen replacement therapy or treatment with recombinant growth hormone (rGH) have shown partial restoration of lean body mass (LBM), but these treatments have largely not been sufficiently studied in eugonadal individuals.
METHOD:
A double-blind, randomized, placebo-controlled trial of 89 HIV-positive eugonadal women and men with wasting assigned to the anabolic steroid oxymetholone (50 mg bid or tid) or placebo for 16 weeks was performed. Body weight, bioimpedance measurements, quality of life parameters, and appetite were analyzed.
RESULTS:
Oxymetholone led to a significant weight gain of 3.0 +/- 0.5 and 3.5 +/- 0.7 kg in the tid and bid groups, respectively (p <.05 for each treatment versus placebo), while individuals in the placebo group gained an average of 1.0 +/- 0.7 kg. Body cell mass (BCM) increased in the oxymetholone bid group (3.8 +/- 0.4 kg; p <.0001) and in the oxymetholone tid group (2.1 +/- 0.6 kg; p <.005). Significant improvements were noted in appetite and food intake, increased wellbeing, and reduced weakness by self-examination. The most important adverse event was liver-associated toxicity. Overall, 43% of patients in the tid group, 25% of patients in the bid oxymetholone group, and 8% in the placebo group had a greater than 5 times baseline increase for ALT, AST, or gamma GT, while other adverse events were not increased over placebo.
CONCLUSION:
Oxymetholone can be considered an effective anabolic steroid in eugonadal male and female patients with AIDS-associated wasting. The bid (100 mg/day) regimen appeared to be equally effective to the tid (150 mg/day) regimen in terms of weight gain, LBM, and BCM and was associated with less liver toxicity.


The efficacy of oxymetholone in combination with erythropoietin on hematologic parameters and muscle mass in CAPD patients.

OBJECTIVES: To determine the efficacy of oxymetholone, an androgenic steroid, in combination with rHuEPO on hematologic and muscle mass in CAPD patients. METHODS: A double-blinded, placebo-controlled experimental study was conducted for 6 months and 24 CAPD patients were divided into two groups. The treatment group (n = 11) received rHuEPO plus oral oxymetholone (50 mg/tablet twice daily). The placebo group (n = 13) received rHuEPO plus a placebo twice daily. The evolution of the patients' hematologic parameters and the impact of the drugs on their muscle mass were evaluated. RESULTS: After 6 months of therapy, hematocrit and hemoglobin values of the treatment group were significantly different from those of the placebo group (38.1 +/- 1.0% and 32.8 +/- 0.9%, p = 0.001; 12.9 +/- 0.3 g/dl and 11.0 +/- 0.3 g/dl, p = 0.001 for hematocrit and hemoglobin, respectively). The increase in hematocrit and hemoglobin values observed in treatment group was statistically greater than those of the placebo group (p < 0.01). After 6 months, none of anthropometric parameters, albumin, protein or lean body mass levels, were significantly different from baseline in the placebo group. Conversely, most of the anthropometric parameters, albumin and lean body mass levels were significantly increased in the oxymetholone group (p < 0.05). The mean weight of subjects in the oxymetholone group changed from 63.82 +/- 2.71 to 67.02 +/- 3.26 kg (p = 0.001). The subjective global assessment score for 7 patients in the treatment group (63.6%) changed in a positive manner. A rise in liver enzymes was the main side effect observed in the treatment group. CONCLUSIONS: Oxymetholone significantly enhances the erythropoietic effects of rHuEPO and improves the nutritional status of CAPD patients. However, significant increases in liver enzymes need to be monitored closely.


Oxymetholone ameliorates insulin sensitivity in maintenance hemodialysis patients: a randomized controlled trial.

AIMS: To investigate the beneficial effects of oral oxymetholone on IR in hemodialysis (HD) patients by increasing skeletal muscle function and stimulating myocyte glucose uptake and metabolism. METHODS: In a randomized, controlled double-blind study, 44 patients were randomly assigned to one of two groups: a treatment group that received oxymetholone 50 mg orally twice daily and a control group that received placebo twice daily for 24 weeks. IR was calculated by using HOMA, and dual-energy X-ray absorptiometry was used to determine body composition. All patients were encouraged to walk at least one kilometer daily and were monitored by the Barthel index activity score. RESULTS: 25 men (57%) and 19 women (43%) were studied. 23 subjects were in the control group, and 21 subjects were in the treatment group. The mean age of patients and the duration of dialysis were 43.5 +/- 9.9 years and 92.8 +/- 37.8 months, respectively. After treatment, the HOMA index and body fat mass (FM) were significantly decreased in the treatment group compared to those in the control group (10.8 +/- 16.4 vs. 3.1 +/- 4.5; p < 0.05 and 1.73 +/- 2.77 vs. 0.40 +/- 1.12 kg; p < 0.05, respectively). Concurrently, the mean change of fat free mass (FFM) in the treatment group was higher than that in the control group (3.24 +/- 1.74 vs. 0.65 +/- 1.21 kg, p < 0.05). Two patients in the treatment group experienced an elevation in serum liver enzymes (9.52%). CONCLUSION: HD patients treated with short-term oral oxymetholone showed an increase in insulin sensitivity when compared to the placebo group, and this effect depended on changes in FFM and FM.


Overall anadrol can be a tremendous oral when looking to increase anabolism via increased protein synthesis as well as increasing intramuscular water retention and truly hardened up. The biggest drawback I see via the research and anecdotal evidence is people make 1 of 2 mistakes:
1. They take it in the offseason and it kills their appetite which means they cannot eat enough calories they need to grow (defeating the purpose)
OR
2. They dose it too high for too long

Anadrol has its place and IMHO, should be reserved for a dieting phase IF you experience the "lack of appetite" side effect.

 

[Dma378]

In terms of the tren questions, if you want you can shoot me a pm OR start a tren based thread so like David said, we can keep this all research based and not a specific cycle thread…I'd be more than happy to help out in anyway![/B]

Sorry bro. Makes sense.

 

[BeastFitness]

Sorry bro. Makes sense.

Oh its not a problem at all man! Just like David said earlier, we don't want it turning into a "Critique my Cycle" thread…BUT if the demand is there I wouldn't mind opening up something similar in a different thread!

The researcher inside of me likes to keep details in order haha

 

[Joedoubledose]

Sorry for the delay guys! The weekend really got away from me and I got slammed with work!















So in terms of letro let's look at the research first (which mostly deals with breast cancer patients)

Long-term efficacy and safety of letrozole for the adjuvant treatment of early breast cancer in postmenopausal women: a review

Abstract
Aromatase inhibitors (AIs) are becoming more widely used than tamoxifen as adjuvant hormonal therapy for postmenopausal women (PMW) with early breast cancer (EBC). It is clear that these drugs offer important efficacy benefits over tamoxifen and differ from tamoxifen in their safety profile. The accepted strategies for adjuvant AI therapy include initial adjuvant treatment following surgery, switching and/or sequencing from prior tamoxifen, and extended adjuvant therapy following the full 5 years of tamoxifen treatment. Among the available AIs, letrozole has been evaluated in large, well-controlled, double-blind clinical trials in the initial adjuvant, extended adjuvant, and more recently, the sequential adjuvant settings. Letrozole is the most potent of the AIs and provides near complete suppression of plasma estrogens in PMW. Letrozole also significantly reduces the occurrence of early distant metastases, the most lethal type of recurrence event, which can lead to improved survival. Clinical comparisons of letrozole with both tamoxifen and placebo have also provided important long-term safety data on the use of AIs as adjuvant therapy in PMW with EBC. The weight of clinical evidence indicates that letrozole is a safe and effective option for adjuvant hormonal therapy across all three AI treatment settings.

Long-term safety of aromatase inhibitors in the treatment of breast cancer

Abstract
Following promising data for metastatic breast cancer in terms of efficacy and safety profile, third-generation aromatase inhibitors (AI), anastrozole, letrozole, and exemestane, underwent a full development in early setting. If recent results consistently show the superiority of these agents over tamoxifen, the therapeutic strategies of AIs in adjuvant setting are still debated. Beyond the choice of clinical strategy, the long duration of exposure to AI in adjuvant setting required a full determination of the long-term toxicity profile of these agents. While all three AIs have either favorable (decreased incidence of hot flashes, gynecologic and thromboembolic side-effects) or unfavorable (skeletal complications, arthralgia, musculoskeletal pain, sexual dysfunction) class adverse events, some variability between AIs has been reported in side-effects as well as gastrointestinal, urogenital, neurologic, and visual disturbances, confirming the lack of interchangeability between the three AIs. The overall therapeutic index of AIs appears today superior to that of tamoxifen with proven improved efficacy and better toxicity profile. This review will explore the results from the available adjuvant AIs trials with a particular emphasis on safety profiles, quality of life, and therapeutic index, helping to define the present role of AIs in the adjuvant management of postmenopausal patients with breast cancer.

Letrozole versus testosterone. a single-center pilot study of HIV-infected men who have sex with men on highly active anti-retroviral therapy (HAART) with hypoactive sexual desire disorder and raised estradiol levels.

Abstract
Since the advent of Highly Active Anti-Retroviral Therapy (HAART), men with HIV experience good quality of life and expect to have normal sexual function. However, it appears that men infected with HIV commonly complain of sexual problems. There is evidence that men on HAART develop low sexual desire that is associated with raised estradiol levels. It has been postulated that abnormal metabolism seen in this group of men increases the aromatization of testosterone to estradiol. We hypothesized that letrozole, an aromatase inhibitor that inhibits the conversion of testosterone to estradiol, would be beneficial in these men.
AIM: The aim of this study was to compare the effects of testosterone vs. an aromatase inhibitor, letrazole, in HIV-infected men with raised estradiol and low sexual desire.
METHODS: Thirteen men who have sex with men on HAART with low sexual desire as well as raised estradiol levels (>120 pmol/L) were randomly allocated to receive either parenteral testosterone (Sustanon 250 intramuscular injection) (N = 6) or letrozole 2.5 mg orally daily (N = 7) for 6 weeks.
MAIN OUTCOME MEASURES: Sex steroid hormone assays, sex hormone-binding globulin, virological, hematological, and biochemical parameters were measured before and after treatment. Each subject was given the Spector Sexual Desire Inventory and the Depression/Anxiety Stress Scale before and immediately after treatment. Subjects were also asked to estimate the number of actual sexual acts before and after treatment. Results. Inventory data showed a rise in dyadic desire in both treatment arms. Mean actual sexual acts rose from 0.33 to 1.5 in the testosterone group and from 0.43 to 1.29 for the letrozole group. Luteinizing hormone increased in seven of seven men on letrozole. Serum testosterone increased in seven of seven men on letrozole. There were no adverse events from either medication.
CONCLUSION: Letrozole may be useful in the management of men on HAART who have low sexual desire.

Short-term aromatase inhibition: effects on glucose metabolism and serum leptin levels in young and elderly men

Abstract
Objective To assess and compare the effects of short-term aromatase inhibition on glucose metabolism, lipid profile, and adipocytokine levels in young and elderly men.
Design and methods Ten elderly and nine young healthy men were randomized to receive letrozole 2.5 mg daily or placebo for 28 days in a crossover design.
Results Both in young and elderly men, active treatment significantly increased serum testosterone (+128 and +99%, respectively) and decreased estradiol levels (−41 and −62%, respectively). Fasting glucose and insulin levels decreased in young men after active intervention (−7 and −37%, respectively) compared with placebo. Leptin levels fell markedly in both age groups (−24 and −25%, respectively), while adiponectin levels were not affected by the intervention. Lipid profile was slightly impaired in both groups, with increasing low density lipoprotein-cholesterol levels (+14%) in the younger age group and 10% lower levels of APOA1 in the elderly. A decline in IGF1 levels (−15%) was observed in the younger age group. No changes in weight or body mass index were observed in either young or old men.
Conclusions Short-term aromatase inhibition appears to affect glucose metabolism in young men, and lipid metabolism, including leptin secretion, in young and elderly men. Furthermore, the short period of exposure suggests that these changes might be mediated by direct effects of sex steroids rather than by changes in body composition.

Aromatase inhibitors (AI) have been used in males in idiopathic short stature, constitutional delay of puberty, precocious puberty, gynecomastia, oligospermia, hypogonadism related to obesity and ageing.

Introduction
Aromatase inhibitors (AI) have been used in the treatment of idiopathic short stature (ISS), constitutional delay of puberty (CDP) and precocious puberty in boys to increase adult height. Moreover, it has been used in the management of gynecomastia, oligospermia and male hypogonadism related to obesity and ageing.[1,2,3] This retrospective study was carried out to assess the efficacy of letrozole, an AI, in varied conditions in Indian males.
Go to:
Case Reports
Case A
A 15-year-old male presented with macromastia. He had delayed puberty.
Wt - 62.7 kg; Ht - 155 cm; Sexual Maturation Rate (SMR) - G1P1, testes - 3 ml, stretched penile length (SPL) - 5 cm.
LH - 6.3 IU/L, follicle-stimulating hormone (FSH) - 2.9 IU/L, prolactin (PRL) - 5.1 ng/ml, normal thyroid-stimulating hormone (TSH) and T4.
Testosterone (T) - 43.8 ng/dl and estradiol (E2) - 9.79 pg/ml. T/E2 = 4.4:1. He was prescribed letrozole 2.5 mg - 3 times/week.
After 6 months of AI therapy:
Wt - 68.8 kg; Ht - 158.5 cm; SMR - G3P3, testes 10 ml, SPL - 6 cm. There was insignificant change in breast enlargement.
T - 331.62 ng/dl; E2-8.05 pg/ml. T/E2 = 41.2.
There was 650% increase in T and 17.9% decrease in E2.
Case B
A 14-year-old male was referred for obesity. He had delayed puberty.
Wt - 66.6 kg; Ht - 158 cm; SMR - G1P1, SPL - 4 cm.
LH - 3.59 IU/L; FSH - 2.48 IU/L; PRL - 13.8 ng/ml, normal TSH and T4.
T - 25.81 ng/dl; E2 - 141.3 pg/ml; T/E2 = 0.18:1.
He was prescribed injection T - 100 mg monthly and letrozole 2.5 mg - 3 times/week for 4 months. After 3 weeks of last dose of injection T and 3 days of last dose of letrozlole: Wt - 68.9 kg; Ht - 159.5 cm; SMR-G2P2, SPL ~5 cm.
T - 310.6 ng/dl; E2 - 13.15 pg/ml; T/E2 = 23.6:1.
There was ~1100% increase in T and 90% decrease in E2.
Case C
A 23-year-old male was referred for management of hypogonadism.
Wt - 55.9 kg; Ht - 161 cm; body mass index - 21.6; no anosmia; SMR - G1P1, SPL - 4 cm. LH <0.07 IU/L, FSH - 0.032 IU/L, PRL - 4.93 ng/ml, T - 13 ng/dl.
He was prescribed injection T - 100 mg every 3 weeks along with letrozole 2.5 mg - 2 times/week. After 3 weeks of last (4th) injection T and 3 days of last letrozole dose: T - 74 ng/dl.
There was 469% increase in T.
Case D
A 27-year-old male was referred for poor semen quality. His total functional sperm fraction (TFSF), denoted by sperm count (×106) by normal morphology (%) by normal motility (%), was 70 × 106/ml × 30% × 30% =6.3.
T - 257.9 ng/dl; E2 - 35.8 pg/ml; T/E2 = 7.2:1.
He was prescribed letrozole - 2.5 mg - 2 times/week.
After 1 month of therapy: T - 754.9 ng/dl; E2 - 28.5 pg/ml; T/E2 = 26.5:1.
There was 200% increase in T and 20% decrease in E2.
TFSF - 80 × 106 × 70% × 30% =16.8.
Go to:
Discussion
AI have been used in boys with ISS and CDP to increase adult height.[1,4,5] Boys with ISS with a mean age of 11 years were treated with letrozole 2.5 mg once daily or placebo for 2 years. There was a gain of 5.9 cm in predicted adult height in the letrozole treated group.[4] A significant increase in predicted adult height has also been observed in boys with CDP who were treated with a combination of T and letrozole.[5] AI slow down epiphyseal maturation by lowering E2 levels. This approach proved successful in other conditions, too, viz. aromatase excess syndrome, sertoli cell tumors and testotoxicosis (along with antiandrogen).[1] AI have limited efficacy in the treatment of gynecomastia; hence, they are not recommended as a first line treatment for gynecomastia.[1] Significant improvement in SMR was observed in CDP cases (Case A and B). There was marked improvement in SMR in case A with “sole” therapy with letrozole, but insignificant response in gynecomastia. Case B was treated with a “combination” of T and letrozole.
AI therapy is associated with a sustained increase in FSH and a positive effect on sperm concentration and motility.[1] Case D (T <300 ng/dl; T/E <10:1) showed improvement in semen quantity and quality with letrozole even though sperm count was normal. Some men with severe oligospermia (<5 × 106/ml), low T levels (<300 ng/dl), T (ng/dl) to E2 (pg/ml) ratio <10 and normal gonadotropins concentration may have a treatable endocrinopathy. AI have been successfully used in this subset of patients.[1,3,6] 2.5 mg/d letrozole for 6 months has been shown to improve seminal parameters (denoted by TFSF).[3]
AI have been used in the treatment of hypogonadism related with obesity and ageing. Letrozole 2.5 mg once a week produced sustained normalization of serum total T in males with obesity related hypogonadism; however, free T rose to supraphysiological levels emphasizing the need for estimation of free T during AI treatment.[2]
It has been suggested that aromatase is less suppressed in the testis compared with adipocytes and muscle tissue. It is questionable whether AI are able to stimulate T production sufficiently in men with truly low T levels.[1] There was a marked increase in T with combination treatment with T and letrozole in CDP (Case B) as compared with Idiopathic Hypogonadotropic Hypogonadism (IHH) (Case C) where there was lesser response with the same combination therapy. The marked increased in T with letrozole in CDP as compared to lesser response in IHH can aid in distinguishing the two conditions with the use of AI.
Most of the recent studies with AI in boys and adult men do not show a major detrimental effects (including bone).[1] The harmful effects are unlikely if the dose is carefully adjusted (even weekly) based on T and E2 levels.[3]
This retrospective study in Indian males showed insignificant effect of AI in gynecomastia and IHH, significant effect in CDP and some benefit in improving seminal parameters. Moreover, this study highlights the importance of estimating E2 (along with T and gonadotropins) in various endocrinopathies, which can be benefitted by reducing E2 by AI.
Further prospective, randomized, blinded, placebo-controlled, long-term studies are needed to clarify the role of AI in the management of growth impairment, male infertility and hypogonadism.

Testosterone boost from letrozole
·0.02 mg of Letrozole increased testosterone by 45% after 2 days
·0.1 mg of Letrozole increased testosterone by 49% after 2 days
·0.5 mg of Letrozole increased testosterone by 48% after 2 days
·1 mg of Letrozole increased testosterone by 41% after 2 days
·2.5 mg of Letrozole increased testosterone by 74% after 3 days
·10 mg of Letrozole increased testosterone by 97% after 2 days
·30 mg of Letrozole increased testosterone by 113% after 3 days


At the end of the day, I feel letro (like many compounds) has its place BUT it needs to be used within the proper cycle with the correct dosage and length. I am personally not a fan of taking ANYTHING extremely long term without any breaks.

Favorite post so far

 

[BamBam0319]

Invalid Link Removed
There is my tren advice thread if anyone has any input, so that we can keep it out of this thread. Anyone else that has questions about tren and dosing can jump in and get some answers too

 

[BeastFitness]

Favorite post so far

AWESOME! Any specific research you'd wanna see?

Invalid Link Removed
There is my tren advice thread if anyone has any input, so that we can keep it out of this thread. Anyone else that has questions about tren and dosing can jump in and get some answers too

RIGHT ON man!! Thanks for posting it up in here so we can send people in the right direction!

 

[Joedoubledose]

AWESOME! Any specific research you'd wanna see?



RIGHT ON man!! Thanks for posting it up in here so we can send people in the right direction!

Hmmm info on deca and its effects on ligaments/joints specifically

 

[BeastFitness]

Hmmm info on deca and its effects on ligaments/joints specifically

There are two that I feel are decent reads if you can get access to the full text.


[Effects of nandrolone decanoate on bone mineral content and intestinal absorption of calcium].

Abstract
To evaluate the effects of a long-term treatment with nandrolone decanoate on metabolism of the skeleton, a double-blind randomized study was carried out in women with joint diseases without metabolic bone derangement. Ten patients were treated with 50 mg of nandrolone decanoate every three weeks for two years; in six subjects a treatment with placebo was performed. As it concerns plasma calcium and phosphate, serum alkaline phosphatase, urinary excretion of calcium, phosphate, hydroxyproline and cAMP, as parathyroid index, it was not observed significant differences in the two examined groups. While in placebo group at the end of the study the intestinal radiocalcium remained unchanged and bone mineral content showed a slight decrease, on the contrary nandrolone decanoate treatment promoted a significant improvement in intestinal calcium absorption and an increase in bone mineral content.

Collagen synthesis in postmenopausal women during therapy with anabolic steroid or female sex hormones.

Abstract
The effect of anabolic steroid therapy and estrogen-progestogen substitution therapy on serum concentration of procollagen type III aminoterminal peptide (PIIINP), a measure of collagen synthesis, in postmenopausal women was studied in two double-blind studies: (1) 39 women allocated to treatment with either 50 mg nandrolone decanoate as an intramuscular depot or placebo injections every third week for 1 year, and (2) 40 women allocated to receive either 2 mg 17 beta-estradiol plus 1 mg norethisterone acetate daily or placebo tablets for 1 year. Serum PIIINP was measured every 3 months during the study. Anabolic steroid therapy resulted in a more than 50% increase (P less than .001) in serum PIIINP at 3 months, which thereafter decayed but remained significantly increased throughout the study period. Serum PIIINP showed the same pattern during estrogen-progestogen therapy, but to a lesser degree. We conclude that anabolic steroids stimulate type III collagen synthesis in postmenopausal women, while estrogen-progestogen therapy may have such an effect, but only to a lesser degree.




You can see deca improved collagen synthesis and bone mineral content. These studies used a low dosage and if you dosages at a minimum of 100mgs per week you should see joint pain alleviate (100mgs is higher than the dosages used in the studies above.) Overall the research and anecdotal evidence point to deca being tremendous for overall joint and ligament pain relief and growth/repair.

 

[Joedoubledose]

There are two that I feel are decent reads if you can get access to the full text.


[Effects of nandrolone decanoate on bone mineral content and intestinal absorption of calcium].

Abstract
To evaluate the effects of a long-term treatment with nandrolone decanoate on metabolism of the skeleton, a double-blind randomized study was carried out in women with joint diseases without metabolic bone derangement. Ten patients were treated with 50 mg of nandrolone decanoate every three weeks for two years; in six subjects a treatment with placebo was performed. As it concerns plasma calcium and phosphate, serum alkaline phosphatase, urinary excretion of calcium, phosphate, hydroxyproline and cAMP, as parathyroid index, it was not observed significant differences in the two examined groups. While in placebo group at the end of the study the intestinal radiocalcium remained unchanged and bone mineral content showed a slight decrease, on the contrary nandrolone decanoate treatment promoted a significant improvement in intestinal calcium absorption and an increase in bone mineral content.

Collagen synthesis in postmenopausal women during therapy with anabolic steroid or female sex hormones.

Abstract
The effect of anabolic steroid therapy and estrogen-progestogen substitution therapy on serum concentration of procollagen type III aminoterminal peptide (PIIINP), a measure of collagen synthesis, in postmenopausal women was studied in two double-blind studies: (1) 39 women allocated to treatment with either 50 mg nandrolone decanoate as an intramuscular depot or placebo injections every third week for 1 year, and (2) 40 women allocated to receive either 2 mg 17 beta-estradiol plus 1 mg norethisterone acetate daily or placebo tablets for 1 year. Serum PIIINP was measured every 3 months during the study. Anabolic steroid therapy resulted in a more than 50% increase (P less than .001) in serum PIIINP at 3 months, which thereafter decayed but remained significantly increased throughout the study period. Serum PIIINP showed the same pattern during estrogen-progestogen therapy, but to a lesser degree. We conclude that anabolic steroids stimulate type III collagen synthesis in postmenopausal women, while estrogen-progestogen therapy may have such an effect, but only to a lesser degree.




You can see deca improved collagen synthesis and bone mineral content. These studies used a low dosage and if you dosages at a minimum of 100mgs per week you should see joint pain alleviate (100mgs is higher than the dosages used in the studies above.) Overall the research and anecdotal evidence point to deca being tremendous for overall joint and ligament pain relief and growth/repair.

Nice , do you use peer reviewed journals btw?

 

[BeastFitness]

Nice , do you use peer reviewed journals btw?

I do! I try and post the most relevant QUALITY pieces of literature that pertain to the subject. Sadly, with AAS, theres A LOT of research that still needs to be done in a peer reviewed setting.

 

[Joedoubledose]

I do! I try and post the most relevant QUALITY pieces of literature that pertain to the subject. Sadly, with AAS, theres A LOT of research that still needs to be done in a peer reviewed setting.

That's great to hear ! Some people think just because it's a study the results are automatically valid . Sad part about research is we rarely see as much of the negative findings because we all know positive results is what gets funding :/

 

[Rodja]

That's great to hear ! Some people think just because it's a study the results are automatically valid . Sad part about research is we rarely see as much of the negative findings because we all know positive results is what gets funding :/

AAS is a different beast because of the ethical portion of designing a study and the legal issues of a scheduled substance. There's data on many AAS out there, but the applicability of most of it is, at best, shaky. AIs and SERMs will have far more data because of the larger portion of potential subjects due to both HRT and cancer applications.

 

[BeastFitness]

That's great to hear ! Some people think just because it's a study the results are automatically valid . Sad part about research is we rarely see as much of the negative findings because we all know positive results is what gets funding :/

AAS is a different beast because of the ethical portion of designing a study and the legal issues of a scheduled substance. There's data on many AAS out there, but the applicability of most of it is, at best, shaky. AIs and SERMs will have far more data because of the larger portion of potential subjects due to both HRT and cancer applications.

Plus with research in general, THERE WILL ALWAYS BE FLAWS! There is no such thing as a perfect study and for every 10 studies that support a claim you can find 10 to negate it. Thats why I'm such a huge fan of using research AND anecdotal evidence to formulate proper decisions.

Plus…finding research and then experimenting if half the fun! With training, nutrition, and supplementation!

 

[Whacked]

I'd love to hear some real world feedback related to the post regarding 100mg Deca/week as a long term treatment dose for joints (and soft tissue issues).

Specifically, if it has any adverse sexual (or other) sides at that dose and time needed to experience said benefit(s).

I read some info awhile back about Deca and NPP being very toxic to the kidneys. I had never heard that before about these 2 agents and it spooked me a bit due to the lack of resiliency of the kidneys.

 

[hairygrandpa]

^^^^ me too!

 

[BeastFitness]

I'd love to hear some real world feedback related to the post regarding 100mg Deca/week as a long term treatment dose for joints (and soft tissue issues).

Specifically, if it has any adverse sexual (or other) sides at that dose and time needed to experience said benefit(s).

I read some info awhile back about Deca and NPP being very toxic to the kidneys. I had never heard that before about these 2 agents and it spooked me a bit due to the lack of resiliency of the kidneys.

^^^^ me too!

I definitely can provide some results from 3 various clients I worked with that had previous joint and soft tissue issues/damage. For confidentially sake, I will call them client 1, 2, and 3.

First off, to address the hepatoxicity levels, no matter what, ANY AAS WILL HAVE SOME EFFECT/STRAIN SYSTEMICALLY. However, when looking at injectables like deca, NPP, test, eq, or primo, they are not considered very toxic to organs where as orals like anavar, dbol, and winny are very hepatoxic. Another thing you need to remember is the DOSAGE is more likely to correlate to organ damage than the duration (in many cases using an example like 100mgs deca for 10 weeks VS 600mgs deca for 5 weeks.) The dosage on a week to week basis seems to correlate to higher side effects VS the actual duration of usage.

So onto the real world feedback from 3 of my clients (ranged over the past 6 months to 2 years so its a fairly decent timeline to get a good idea.) Keep in mind I won't be talking about their entire cycle or training but merely emphasizing the effects of deca.


Client 1
Issue: Severe elbow tendinitis
Main Compound Used: Deca
Dosage: 100 mgs per week
Duration: 6 weeks
Results: Tendinitis completely went away between weeks 3/4 and we lowered the RPE on compounds movements as the cycle ended to allow his joints to adapt and to keep the tendinitis from flaring up again

Client 2
Issue: Severe Patellar tendinitis
Main Compound Used: Deca/NPP (as he used this in the past and it helped keep sides down)
Dosage: 100-200 mgs per week (varied)
Duration: 4 weeks
Results: Tendinitis resolved itself within 2 weeks where we introduced cissus and mega-dosed fish oil as we pulled the deca/npp out

Client 3
Issue: Broken arm
Main Compound Used: Deca
Dosage: 75-100 mgs per week (this client was a hyper responder)
Duration: 12 weeks
Results: After this client had his cast removed he had lingering pain emphasized around his elbow. He was a hyper responder to deca so rather than mega dosing it for a shorter duration, we only used the bare minimum to see joint/soft tissue benefits longer term. If i remember correctly it took a good 8-9 weeks before the joint itself felt 100% at which time we pulled back on the compounds of his entire cycle and focused on an acclimation phase of training.

All in all, I'm a huge fan of deca for overall joint repair and collagen synthesis. As you can see, the dosage and duration truly depends on the person's severity of pain, the issue itself, and how they respond to these compounds. It really does vary from case to case and it something that should be monitored and adjusted accordingly.

(Forgive me if I made any mistakes in this post as I was going through old notes and trying to keep it all straight.)

 

[Whacked]

Nice. Thank you

RE: 100mg Deca/week

1) Did these subjects just inject once/week?

2) Any bloat/discernible water weight/edema experienced from these low doses?

3) How long does it take for the relief to be observed?

4) What is the propensity for kidney toxicity from long term Deca/NPP use?

***I concur that orals are more toxic "acutely" but IMHO, I would rather tax the liver than the kidneys so this topic is not so black and white.

 

[BeastFitness]

Today's Research is Focused on Primo (as requested by a friend off these boards.)

We know primo is well known for pretty fairly mild in terms of estrogenic side effects as well as a very week androgenic compound.

Estrogenic Side Effects
-DHT-derivative anabolic steroid (it does not exhibit any interaction with aromatase)
-side effects are completely void of any estrogenic side effects which means no water retention, high blood pressure, or gyno

Androgenic Side Effects
-Low androgenic strength rating (compared to test)
-Androgenic side effects include increased sebum secretion (you'll get oily skin), increased acne, bodily and facial hair growth, and the increased risk of Male Pattern Baldness
-One big advantage to primo is the that it doesn't interact with the 5-Alpha Reductase enzyme

HPTA, Endogenous Testosterone Production
-Considered mild in its test suppression side effect (if doses are kept low)

Hepatotoxic Side Effects
-Void of the typical C17-alpha alkylation (AKA no measurable hepatotoxic effects on the body.)
-Oral forms haven't demonstrated any changes in liver enzyme values


Cardiovascular Side Effects
-Cardiovascular strain and negative cholesterol changes (reduction of HDL and increases of LDL)


Some research on primo


Side effect of metenolone enanthate on rats heart in puberty: morphometrical study.

Abstract
The aim of this study was the investigation of effects of the metenolone enanthate (ME) that is used among athletes as doping and muscle amplifier, on hearts of male and female rats that are in puberty using morphometrical methods. A total of 36 rats which were divided into three separate groups (Experiment, ME; vehicle, PO; control, C) each consisting of 6 male and 6 female rats were used. 0.5 mg/kg metenolone enanthate was applied intraperitoneally into experiment subjects 5 times a week over a period of 4 weeks. At the end of experiment, rats were euthanized and their hearts were cut at the level of musculus papillaris after the fixation in formalin. Hearts were taken out and embedded in paraffin wax. Photos were taken at cut surfaces, and thickness, diameters and surface area levels were measured. Left ventriculus mass (LVM) and left ventriculus mass index (LVMI) were calculated. In the study LVM (p<0.005) and LVMI (p<0.05) were found to be significantly higher in the ME group in females whereas left ventricular lumen diameter (LVLD) were found to be significantly lower (p<0.05). Thus left ventricular hypertrophy development was observed. LVM and LVMI were found to be similar in ME and C groups among male rats and the highest level of these data were found in the group. LVM and LVMI were higher among females (p<0.006). In conclusion, it has been shown that the adverse effects of ME on heart were developing starting from puberty and resulting with the enlargement of the heart and left ventricular hypertrophy and especially among females this condition was more evident. It has also been discussed that the continuous use of drugs may further enhance this condition.

Fatal outcome of a patient with severe aplastic anemia after treatment with metenolone acetate.

Abstract
A 75-year-old man suffering from severe aplastic anemia was treated first with cyclosporin A, then with steroid pulse therapy, and subsequently with metenolone acetate. Marked elevation of transaminases was detected following initiation of treatment with metenolone acetate. This was followed by hepatic failure and death. Histopathological findings in autopsy specimens were compatible with the diagnosis of drug-induced liver impairment, for which metenolone acetate was considered the most likely causative agent. Liver impairment as a side effect of the use of this drug has been thought to be mild, reversible and rather infrequent. However, as demonstrated in the case described here, it is apparent that extreme caution should be exercised when using this drug in debilitated patients.

The effects of testosterone propionate and methenolone enanthate on the healing of humeral osteotomies in the Wistar rat.

Abstract
A randomized blind prospective study was carried out to determine if an anabolic androgenic steroid with a high anabolic/androgenic ratio, Group A, (1/0.05) methenolone enanthate (me), compared to an anabolic/androgenic agent with a low anabolic/androgenic ratio, Group B, (1.0/1.0) testosterone propionate (tp), compared to a control, Group C, cottonseed oil (co), affected midhumeral osteotomy healing in 100 two-month-old female Wistar rats. The rats received 4 mg/kg me, 4 mg/kg te, and equal volumes of co weekly. The rats were sacrificed at 2, 4, and 6 weeks. The entire humerus with the healing osteotomy was carefully dissected until all soft tissue attachments were stripped. The healing callus was then subjected to (1) biochemical analysis (hexosamine, hydroxyproline, and calcium), (2) biomechanical testing (progressive distraction of the callus at 1 mm/min on an electrohydraulic materials test system, model 1331, Instron Corp, Canton, MA, and (3) histology. Results of the biochemical testing demonstrated that the percentage of calcium in the healing callus at 2 weeks in group B (tp) was 7.3 +/- 1.0, and this value was greater than that in group C (co), 4.8 +/- 1.6 (p greater than .01), and greater than that in group A (me), 5.6 +/- 0.6 (p greater than .01). At 4 weeks, the percentage of calcium in the callus in group B (tp) was 6.8 +/- 1.9, in group A (me) 7.3 +/- 3.7, and these values were both greater than that in group C (co), 3.9 +/- 2.2 (p greater than .02 and .01, respectively). At 6 weeks the percentage of calcium in the callus in group B (tp) was 11.7 +/- 3.9 and in group A (me) 12.7 +/- 3.9, and again these values were both greater than that in group C (co), 6.7 +/- 2.6 (p greater than .02 and .01, respectively). The remainder of the biochemical analysis, hexosamine and hydroxyproline content, did not show a statistical difference in groups A, B, and C at 2, 4, and 6 weeks. The biomechanical studies and histology also failed to show statistical differences between the three groups at 2, 4, and 6 weeks. The conclusion of this study is that an agent with a low androgenic activity does not increase calcium callus concentrations early in the course of fracture healing compared to an agent with higher androgenic activity. As healing progresses, both agents increase the concentration of calcium in osteotomy healing. The clinical significance of this study is that agents with low androgenic activities favorably influence osteotomy healing and may be clinically useful because they lack unwanted virilizing activity.

A clinical and experimental study of the effects of some anabolic steroids on hepatic structure and function.

Abstract
An attempt to discover by functional and histologic methods the role of anabolic steroids in the regeneration of diseased human livers and in livers of rats that had been experimentally damaged by poison is reported. 25 patients with liver cirrhosis were treated for 12 weeks with 100 mg methenolone enanthate im twice a week. Functional and histologic studies were made before and after treatment. Methenolone treatment significantly reduced serum bilirubinemia and alkaline phosphatases and increased total proteins, albumin, kalemia, and total cholesterolemia. Histologically there was persistence of previous cellular infiltration, a greater tendency to steatosis with oil drops in the cytoplasm, and increase in mitosis with binucleation. Cirrhosis patients were considered to have shown improvement in some parameters due to the enzymatic-induction effect of the methenolone. A parallel experiment was carried out on 40 male Wistar rats. Some of the rats were castrated surgically 20 days before the experiments. Rat livers were damaged by either carbon tetrachloride inhalation; castration plus carbon tetrachloride inhalation; castration, carbon tetrachloride inhalation, and administration of testosterone; or castration, carbontetrachloride inhalation plus methenolone injection. Carbon tetrachloride was given by spray for 40 consecutive days. Testosterone was given in doses of 10 mg/kg daily and methenolone in doses of 50 mg/kg daily during the last 20 days of carbon tetrachloride inhalation. Each rate received a total dose of 200 mg/kg testosterone and 1000 mg/kg methenolone. Rats were killed 40 days after completion of therapy and livers were studied histologically. In rats poisoned with carbon tetrachloride, whether castrated or not, necrosis, alteration of the lobular structure, and distortion of centro-lobular veins was found. In those rats also given testosterone or methenolone, histologic changes we re similar to those found in the human cases given methenolone. In spite of results obtained in these studies the indiscriminate clinical use of methenolone enanthate is considered to be controversial.

Effect of methenolone enanthate (NSC-64967) in advanced cancer of the breast

Abstract
Methenolone enanthate, a synthetic long-acting anabolic steroid, was evaluated by a randomized study in the treatment of advanced carcinoma of the breast in postmenopausal women following the protocol established by the Cooperative Breast Cancer Group. Of 27 patients receiving methenolone enanthate, (48%) had objective improvement. There were no improvements in 13 patients receiving testosterone propionate. The median duration of therapy and the median period of survival from the onset of hormone therapy to death or present living time was greater for the responders to methenolone enanthate than the nonresponders. The unusual high incidence of regression from methenolone enanthate therapy may be due to the massive dose employed, a defect in the method of study being employed in clinical trials, a difference that could occur by chance alone or a difference in the biological nature of the disease in the two groups. Since the difference may indicate that methenolene enanthate is an effective hormone, further studies are warranted.



Many people compare a high dose of primo to tren for its ability to increase lean mass, vascularity, density, and overall hardness/conditioning (reduces subq water retention. Overall it stacks well with many aromatizing drugs and although some studies bring up health being a major concern, those specific pieces of research seem to have many flaws which we cannot take as applicable information to the general population.

 

[NoAddedHmones]

Today's Research is Focused on Primo (as requested by a friend off these boards.)

We know primo is well known for pretty fairly mild in terms of estrogenic side effects as well as a very week androgenic compound.

Estrogenic Side Effects
-DHT-derivative anabolic steroid (it does not exhibit any interaction with aromatase)
-side effects are completely void of any estrogenic side effects which means no water retention, high blood pressure, or gyno

Androgenic Side Effects
-Low androgenic strength rating (compared to test)
-Androgenic side effects include increased sebum secretion (you'll get oily skin), increased acne, bodily and facial hair growth, and the increased risk of Male Pattern Baldness
-One big advantage to primo is the that it doesn't interact with the 5-Alpha Reductase enzyme

HPTA, Endogenous Testosterone Production
-Considered mild in its test suppression side effect (if doses are kept low)

Hepatotoxic Side Effects
-Void of the typical C17-alpha alkylation (AKA no measurable hepatotoxic effects on the body.)
-Oral forms haven't demonstrated any changes in liver enzyme values


Cardiovascular Side Effects
-Cardiovascular strain and negative cholesterol changes (reduction of HDL and increases of LDL)


Some research on primo


Side effect of metenolone enanthate on rats heart in puberty: morphometrical study.

Abstract
The aim of this study was the investigation of effects of the metenolone enanthate (ME) that is used among athletes as doping and muscle amplifier, on hearts of male and female rats that are in puberty using morphometrical methods. A total of 36 rats which were divided into three separate groups (Experiment, ME; vehicle, PO; control, C) each consisting of 6 male and 6 female rats were used. 0.5 mg/kg metenolone enanthate was applied intraperitoneally into experiment subjects 5 times a week over a period of 4 weeks. At the end of experiment, rats were euthanized and their hearts were cut at the level of musculus papillaris after the fixation in formalin. Hearts were taken out and embedded in paraffin wax. Photos were taken at cut surfaces, and thickness, diameters and surface area levels were measured. Left ventriculus mass (LVM) and left ventriculus mass index (LVMI) were calculated. In the study LVM (p<0.005) and LVMI (p<0.05) were found to be significantly higher in the ME group in females whereas left ventricular lumen diameter (LVLD) were found to be significantly lower (p<0.05). Thus left ventricular hypertrophy development was observed. LVM and LVMI were found to be similar in ME and C groups among male rats and the highest level of these data were found in the group. LVM and LVMI were higher among females (p<0.006). In conclusion, it has been shown that the adverse effects of ME on heart were developing starting from puberty and resulting with the enlargement of the heart and left ventricular hypertrophy and especially among females this condition was more evident. It has also been discussed that the continuous use of drugs may further enhance this condition.

Fatal outcome of a patient with severe aplastic anemia after treatment with metenolone acetate.

Abstract
A 75-year-old man suffering from severe aplastic anemia was treated first with cyclosporin A, then with steroid pulse therapy, and subsequently with metenolone acetate. Marked elevation of transaminases was detected following initiation of treatment with metenolone acetate. This was followed by hepatic failure and death. Histopathological findings in autopsy specimens were compatible with the diagnosis of drug-induced liver impairment, for which metenolone acetate was considered the most likely causative agent. Liver impairment as a side effect of the use of this drug has been thought to be mild, reversible and rather infrequent. However, as demonstrated in the case described here, it is apparent that extreme caution should be exercised when using this drug in debilitated patients.

The effects of testosterone propionate and methenolone enanthate on the healing of humeral osteotomies in the Wistar rat.

Abstract
A randomized blind prospective study was carried out to determine if an anabolic androgenic steroid with a high anabolic/androgenic ratio, Group A, (1/0.05) methenolone enanthate (me), compared to an anabolic/androgenic agent with a low anabolic/androgenic ratio, Group B, (1.0/1.0) testosterone propionate (tp), compared to a control, Group C, cottonseed oil (co), affected midhumeral osteotomy healing in 100 two-month-old female Wistar rats. The rats received 4 mg/kg me, 4 mg/kg te, and equal volumes of co weekly. The rats were sacrificed at 2, 4, and 6 weeks. The entire humerus with the healing osteotomy was carefully dissected until all soft tissue attachments were stripped. The healing callus was then subjected to (1) biochemical analysis (hexosamine, hydroxyproline, and calcium), (2) biomechanical testing (progressive distraction of the callus at 1 mm/min on an electrohydraulic materials test system, model 1331, Instron Corp, Canton, MA, and (3) histology. Results of the biochemical testing demonstrated that the percentage of calcium in the healing callus at 2 weeks in group B (tp) was 7.3 +/- 1.0, and this value was greater than that in group C (co), 4.8 +/- 1.6 (p greater than .01), and greater than that in group A (me), 5.6 +/- 0.6 (p greater than .01). At 4 weeks, the percentage of calcium in the callus in group B (tp) was 6.8 +/- 1.9, in group A (me) 7.3 +/- 3.7, and these values were both greater than that in group C (co), 3.9 +/- 2.2 (p greater than .02 and .01, respectively). At 6 weeks the percentage of calcium in the callus in group B (tp) was 11.7 +/- 3.9 and in group A (me) 12.7 +/- 3.9, and again these values were both greater than that in group C (co), 6.7 +/- 2.6 (p greater than .02 and .01, respectively). The remainder of the biochemical analysis, hexosamine and hydroxyproline content, did not show a statistical difference in groups A, B, and C at 2, 4, and 6 weeks. The biomechanical studies and histology also failed to show statistical differences between the three groups at 2, 4, and 6 weeks. The conclusion of this study is that an agent with a low androgenic activity does not increase calcium callus concentrations early in the course of fracture healing compared to an agent with higher androgenic activity. As healing progresses, both agents increase the concentration of calcium in osteotomy healing. The clinical significance of this study is that agents with low androgenic activities favorably influence osteotomy healing and may be clinically useful because they lack unwanted virilizing activity.

A clinical and experimental study of the effects of some anabolic steroids on hepatic structure and function.

Abstract
An attempt to discover by functional and histologic methods the role of anabolic steroids in the regeneration of diseased human livers and in livers of rats that had been experimentally damaged by poison is reported. 25 patients with liver cirrhosis were treated for 12 weeks with 100 mg methenolone enanthate im twice a week. Functional and histologic studies were made before and after treatment. Methenolone treatment significantly reduced serum bilirubinemia and alkaline phosphatases and increased total proteins, albumin, kalemia, and total cholesterolemia. Histologically there was persistence of previous cellular infiltration, a greater tendency to steatosis with oil drops in the cytoplasm, and increase in mitosis with binucleation. Cirrhosis patients were considered to have shown improvement in some parameters due to the enzymatic-induction effect of the methenolone. A parallel experiment was carried out on 40 male Wistar rats. Some of the rats were castrated surgically 20 days before the experiments. Rat livers were damaged by either carbon tetrachloride inhalation; castration plus carbon tetrachloride inhalation; castration, carbon tetrachloride inhalation, and administration of testosterone; or castration, carbontetrachloride inhalation plus methenolone injection. Carbon tetrachloride was given by spray for 40 consecutive days. Testosterone was given in doses of 10 mg/kg daily and methenolone in doses of 50 mg/kg daily during the last 20 days of carbon tetrachloride inhalation. Each rate received a total dose of 200 mg/kg testosterone and 1000 mg/kg methenolone. Rats were killed 40 days after completion of therapy and livers were studied histologically. In rats poisoned with carbon tetrachloride, whether castrated or not, necrosis, alteration of the lobular structure, and distortion of centro-lobular veins was found. In those rats also given testosterone or methenolone, histologic changes we re similar to those found in the human cases given methenolone. In spite of results obtained in these studies the indiscriminate clinical use of methenolone enanthate is considered to be controversial.

Effect of methenolone enanthate (NSC-64967) in advanced cancer of the breast

Abstract
Methenolone enanthate, a synthetic long-acting anabolic steroid, was evaluated by a randomized study in the treatment of advanced carcinoma of the breast in postmenopausal women following the protocol established by the Cooperative Breast Cancer Group. Of 27 patients receiving methenolone enanthate, (48%) had objective improvement. There were no improvements in 13 patients receiving testosterone propionate. The median duration of therapy and the median period of survival from the onset of hormone therapy to death or present living time was greater for the responders to methenolone enanthate than the nonresponders. The unusual high incidence of regression from methenolone enanthate therapy may be due to the massive dose employed, a defect in the method of study being employed in clinical trials, a difference that could occur by chance alone or a difference in the biological nature of the disease in the two groups. Since the difference may indicate that methenolene enanthate is an effective hormone, further studies are warranted.



Many people compare a high dose of primo to tren for its ability to increase lean mass, vascularity, density, and overall hardness/conditioning (reduces subq water retention. Overall it stacks well with many aromatizing drugs and although some studies bring up health being a major concern, those specific pieces of research seem to have many flaws which we cannot take as applicable information to the general population.

Curious as to how this is a very weak androgenic compound? it is a DHT derivative after all.

 

[BeastFitness]

Curious as to how this is a very weak androgenic compound? it is a DHT derivative after all.

Compound:---------------------------------Androgenic------Anabolic
1-Testosterone------------------------------------100------200
Anabolicum Vister(Quinbolone)(oral Boldenone)--------50------100
Anadrol 50(Oxymetholone)---------------------------45------320
Anadur(Nandrolone Hexyloxyphenylpropionate)---------37-----125
Anatrofin(Stenbolone Acetate)------------------107-144-----267-332
Anavar(Oxandrolone)--------------------------------24------322-630
Andractim(Dihydrotestosteron)-------------------30-260-----60-220
Andriol(Testosterone Undecanoate)-----------------100------100
Androderm(Testosterone)---------------------------100------100
Androgel(Testosterone)-----------------------------100------100
Boldabol(Boldenone Acetate)-------------------------50------100
Cheque Drops(Mibolerone)-------------------------1,800------4,100
Danocrine(Danazol)----------------------------------37------125
Deca-Durabolin(Nandrolone Decanoate)---------------37------125
Deposterona(Testosterone Blend)-------------------100------100
Dianabol(Methandrostenolone)--------------------40-60------90-210
Dimethyltrienolone------------------------------10,000+-----10,000+
Dinandrol(Nandrolone Blend)--------------------------37------125
Durabolin(NPP)--------------------------------------37------125
Dynabol(Nandrolone Cypionate)----------------------37------125
Equipoise(Boldenone Undecylenate)------------------50------100
Esiclene(Formebolone)----------------------------No Data Available
Genabol(Norbolethone)------------------------------17------350
Halotestin(Fluoxymesterone)-----------------------850------1,900
Hydroxytestosterone--------------------------------25------65
Laurabolin(Nandrolone Laurate)----------------------37------125
Madol(Desoxymethyltestosterone)------------------187------1,200
Masteron(Drostanolone Propionate)---------------25-40------62-130
Megagrisevit-Mono(Clostebol Acetate)---------------25------46
MENT(Methylnortestosterone Acetate)--------------650------2,300
Mestanolone-----------------------------------78-254------107
Methandriol(Mythelandrostenediol)----------------30-60------20-60
Methyl-1-Testosterone------------------------100-220------910-1,600
Methyldienolone-------------------------------200-300------1,000
Methylhydroxynandrolone(MHN)---------------------281------1304
Methyltestosterone-----------------------------94-130------115-150
Metribolone(Methyltrienolone)---------------6,000-7,000------12,000-30,000
Miotolan(Furazabol)------------------------------73-94------270-330
Myagen(Bolasterone)-------------------------------300------575
Nilevar(Norethandrolone)-------------------------22-55------100-200
Omnadren(Testosterone Blend)---------------------100------100
Orabolin(Ethylestrenol)--------------------------20-400------200-400
Oral Turinabol------------------------------------None------100+
Oranabol(Oxymesterone)----------------------------50------330
Orgasteron(Normethandrolone)-----------------325-580------110-125
Parabolan(Tren Hexahydrobenzycarbonate)----------500------500
Primobolan(Methenolone Acetate)-----------------44-57------88
Primobolan Depot(Methenolone Enanthate)--------44-57------88
Prostanozol----------------------------------------n/a------n/a
Protabol(Thiomesterone)----------------------------61------456
Proviron(Mesterolone)---------------------------30-40------100-150
Sanabolicum(Nandrolone Cyclohexylpropionate)------37------125
Steranabol Ritardo(Oxabolone Cypionate)---------20-60------50-90
Superdrol(Methyldrostanolone)---------------------400------20
Sustanon 100 & 250-------------------------------100------100
Synovex(Testosterone Propionate & Estradiol)-------100------100
Test 400------------------------------------------100------100
Test Enanthate/Cypionate/Propionate/Susp & Blends-100------100
THG(Tetrahydrogestrinone)-----------------------No Data Available
Tren Acetate/Enanthate & Blends-------------------500------500
Winstrol(Stanozolol)---------------------------------30------320




you can see primo has high anabolic low androgenic ratio

 

[Rodja]

Curious as to how this is a very weak androgenic compound? it is a DHT derivative after all.

Same with anavar. The A:A rating needs to be taken with a massive grain of salt as they don't always pan out like they should on paper (methyldienelone, for example).

 

[BeastFitness]

Same with anavar. The A:A rating needs to be taken with a massive grain of salt as they don't always pan out like they should on paper (methyldienelone, for example).

EXACTLY!!!

In general, all AAS have basic chemical traits that cannot be changed BUT with everyone's individual genetic differences, no all compounds will react the same with everyone so having pure blanket statements with AAS is a horrible idea….research+anecdotal evidence

 

[Blergs]

Trenbolone seems to be the drug most talked about today (or at least, 75% of emails I receive are asking about it and its safety.) Obviously every drug is going to have positive and negative side effects and you cannot use only one research paper to justify or demonize using any kind of compound.

Invalid Link Removed

it also says its a SARM which is a joke... its a STEROID. there is sex hormones (test) then man made inventions out of it (steroids) then there are compounds NOT of the same structure and activate the androgen receptor and THOSE are SARMS....

also you cant ask the mouse how his mood is. i would not want to be on tren hrt and think the idea is a bit of a joke.... low dose or not. test it used up in many ways and thats what ill use for me hrt.

 

[BeastFitness]

also you cant as the mouse how his mood is. i would not want to be on tren hrt and think the idea is a bit of a joke.... low dose or not. test it used up in many ways and thats what ill use for me hrt.

^^^LMFAO!!! That bolded seriously made me laugh haha I love it!!!

So your not a fan of tren+test? Care to elaborate?

 

[NoAddedHmones]

Same with anavar. The A:A rating needs to be taken with a massive grain of salt as they don't always pan out like they should on paper (methyldienelone, for example).

Right, kind of what I'm alluding to, despite the ratio showing a low androgenic number, real life effects are a very different story for some.

 

[BeastFitness]

Right, kind of what I'm alluding to, despite the ratio showing a low androgenic number, real life effects are a very different story for some.

Yep agreed! I was talking specific about the rating as its "seen" as a lower androgenic compound compared to others. At the end of the day its all relative to the individual. Its no different with training, nutrition, supplementation, or compounds…it depends on the person.

 

[hairygrandpa]

Whacked , I'm currently on NPP (healing kick-starter) and Deca (long ester) with Test-E for knee problems. Look up my log if interested.

 

[Whacked]

Nice. Thank you

RE: 100mg Deca/week

1) Did these subjects just inject once/week?

2) Any bloat/discernible water weight/edema experienced from these low doses?

3) How long does it take for the relief to be observed?

4) What is the propensity for kidney toxicity from long term Deca/NPP use?

***I concur that orals are more toxic "acutely" but IMHO, I would rather tax the liver than the kidneys so this topic is not so black and white.

BUMP

 

[Whacked]

Whacked , I'm currently on NPP (healing kick-starter) and Deca (long ester) with Test-E for knee problems. Look up my log if interested.

Couldn't find it. Will you please share a link? Thanks HG !