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Thread: Letrozole~femara

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    Default Letrozole~femara

    Letrozole~femara

    Letrozole

    (femara)

    Letrozole (Femara) is the chemical name of Novartis´ selective third generationAromatase Inhibitor (AI). This drug was developed to fight breast cancer by inhibiting the aromatization. It is usually used as a part of an aggressive treatment in post-menopausal women, to fight and reverse the spread of breast cancer after other treatments (such as Tamoxifen therapy) has failed. It´s probably the most efficient product on the market for this purpose currently (5) It is very similar in structure and action to it´s predecessor Arimidex.

    Letrozole (Femara) also does quite a few things which would be of interest to both bodybuilders and athletes. Firstly, it has been shown to reduce estrogen levels by 98% or greater (1). In at least one documented incidence, Letrozole (Femara) reduced estrogen in the test subject to undetectable levels, and increased LH, FSH and SHBG (4). Clearly this is all of interest to bodybuilders, as less estrogen in the body means less chance of certain side effects such as water-retention, Gynocomastia, and acne. This makes Letrozole (Femara) an appropriate choice for even the heaviest bulking or cutting cycles including harsh androgens. Also, if you are a competitive bodybuilder, Letrozole (Femara) is a must have product for contest prep; no other Ancillary compound will produce a dry and tight look like Letro will.

    An effective dose of Letrozole (Femara) is .25-.5mg/day (I use .25mgs/day), but be forewarned, if you go over that amount, it can kill your sex drive. Also worth noting is that there´s a rebound effect on your estrogen when you come off Letrozol. Maximum inhibition of the aromatase enzyme has been found to happen at doses as low as 100mcg! (2)

    Letrozole (Femara)´s effects on serum lipids (cholesterol, both HDL and LDL) are, in the words of one researcher: "inconsistent. " Clearly, however, you´ll eventually suffer an impaired lipid profile and immune system if you keep your estrogen levels too low for too long. Your sex drive will also probably suffer from extraordinarily low levels of estrogen present.

    As previously mentioned, Letrozole (Femara) can be used to raise LH and FSH (which are hormones which signal your testes to produce more testosterone). It also, of course, will raise your testosterone levels (6) via this mechanism. Again, this is of interest to athletes and bodybuilders for obvious reasons. Letrozole (Femara), of course, can be used for post-cycle-therapy (PCT) to raise test levels, but for various reasons, Tamoxifen may be a better choice. Still, I have successfully used Letrozole (Femara) for this purpose.

    How good is this compared with Aromasin and Arimidex, it´s too other main rivals? Well, In non-cellular systems, Letrozole (Femara) is 2-5 times more potent than anastrozole and exemestane in its inhibition of the aromatase enzyme and activity, and in cellular systems it is 10-20x more potent! It also lasts quite a long time in your body,but takes awhile to get going& Letrozole (Femara) has a whopping 2-4 day (!) ½ life, and you need to take Letrozole (Femara) for 60 days to get a steady blood plasma level (8).

    Those are impressive numbers, but here´s one of the most interesting things about Letrozole (Femara):

    It may reduce/eliminate/reverse existing gynocomastia!
    In a study conducted on mice (*no, I know it´s not perfect), gyno-like-changes in the mammary gland were totally destroyed! Here´s a direct quote from that study:
    "Our results also indicate aromatase overexpression-induced changes in mammary glands can be abrogated [destroyed] with very low concentrations of the aromatase inhibitor, Letrozole (Femara)."(7)
    In addition, I´ve used Letro to get rid of my own gyno, as has a friend of mine, and we both used it at a dose of 2.5mgs/day, tapering down to .25mgs/day, and then finally off..the gyno never returned in both our cases.

    I´d say that this stuff is pretty great, considering its availability and cost (when you consider the fact that .25mgs/day is more than enough protection from estrogen-related sides on most cycles), not to mention it´s overall utility for a variety of functions (destroying gyno, preventing estrogenic sides, and for PCT).

    References:

    1. Clin Cancer Res. 2005 Apr 15;11(8):2809-21.
    2. J Clin Endocrinol Metab. 1995 Sep;80(9):2658-60.
    3. Eur J Obstet Gynecol Reprod Biol. 2002 Nov 15;105(2):161-5
    4. Epilepsy Behav. 2004 Apr;5(2):260-3
    5. Semin Oncol. 2004 Dec;31(6 Suppl 12):3-8.
    6. Diabetes Obes Metab. 2005 May;7(3):211-5.
    7. J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):27-34. Aromatase overexpression transgenic mice model: cell type specific expression and use of Letrozole (Femara) to abrogate mammary hyperplasia without affecting normal physiology.
    8. (Clin Cancer Res. 2003 Jan;9(1 Pt 2):468S-72S.).

    http://www.chemoneresearch.com/product.php?id=Mw
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    This may be a basis for using Letro to reduce mammery gland tissue (gyno).



    Aromatase overexpression transgenic mice model: cell type specific expression and use of letrozole to abrogate mammary hyperplasia without affecting normal physiology.

    Mandava U, Kirma N, Tekmal RR.
    Department of Gynecology and Obstetrics, Emory University, 4217 Woodruff Memorial Building, 1639 Pierce Drive, Atlanta, GA 30322-4710, USA.

    Our recent studies have shown that overexpression of aromatase results in increased tissue estrogenic activity and induction of hyperplastic and dysplastic lesions in female mammary glands and gynecomastia and testicular cancer in male aromatase transgenic mice. Both aromatase mRNA and protein are overexpressed in transgenic mammary glands and its expression is not limited to epithelial cells. However, it is more in epithelial than in stromal cells. Our results also indicate aromatase overexpression-induced changes in mammary glands can be abrogated with very low concentrations of the aromatase inhibitor, letrozole. Low concentration of letrozole had no effect on normal physiology as indicated by no significant change in the circulating levels of estradiol and follicle stimulating hormone as well as no change in estrogen responsive genes such as the progesterone receptor and lactoferrin in the uterine tissue. These observations indicate that the expression of aromatase in both epithelial and stromal cells can influence the complex interactions of biochemical pathways leading to mammary carcinogenesis and that the aromatase inhibitor, letrozole can be used as chemopreventive agents without affecting normal physiology.

    PMID: 11850204 [PubMed - indexed for MEDLINE]
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    Use of the aromatase inhibitor letrozole to treat male infertility.

    Patry G, Jarvi K, Grober ED, Lo KC.
    Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada. kochman@hadassah.org.il

    OBJECTIVE: Report the case of induction of spermatogenesis with the aromatase inhibitor letrozole. DESIGN: Case report. SETTING: University Infertility center. PATIENT(S): A 31-year-old man with primary infertility, normal volume azoospermia, normal follicle stimulating hormone (FSH) levels and pattern of nonobstructive azoospermia (NOA) on a testicular biopsy. INTERVENTION(S): The patient was given the aromatase inhibitor letrozole for 4 months and had repeated FSH, testosterone, LH levels, semen analyses, and finally a testicular biopsy. MAIN OUTCOME MEASURE(S): Results of a testis biopsy. RESULT(S): Testis biopsy showed normal spermatogenesis following 4 months of letrozole therapy. CONCLUSION(S): This is the first case report on the use of letrozole to treat male infertility and the first case report on the induction of spermatogenesis in a man with NOA using any aromatase inhibitor.

    PMID: 19524225 [PubMed - indexed for MEDLINE]
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    Letrozole powerfully lowers Estradiol in women.




    Use of ultrasensitive recombinant cell bioassay to measure estrogen levels in women with breast cancer receiving the aromatase inhibitor, letrozole.

    Klein KO, Demers LM, Santner SJ, Baron J, Cutler GB Jr, Santen RJ.
    Children's Hospital of Orange County, California 92668, USA.

    The development of well tolerated, potent, specific, and nontoxic aromatase inhibitors for the treatment of postmenopausal women with estrogen-dependent breast cancer has been a major goal of recent studies. The third generation inhibitors now under investigation are nearly 10,000-fold more potent than first generation compounds. Currently available RIAs for plasma estradiol lack sufficient sensitivity to measure levels during aromatase inhibition and, thus, to assess drug potency precisely. The availability of an ultrasensitive bioassay for estradiol provided the opportunity to accurately assess the potency of a new third generation triazole aromatase inhibitor, letrozole (CGS 20267). We used this assay to measure estradiol levels in 14 women with metastatic breast cancer given letrozole at doses of 100 micrograms to 5.0 mg/day over a 12-week period. The lack of differences between doses and sampling times allowed pooling of data. Basal estradiol levels of 7.2 +/- 1.9 pmol/L (mean +/- SEM, 1.95 +/- 0.52 pg/mL) fell to 0.26 +/- 0.11 pmol/L (0.07 +/- 0.03 pg/mL) during the first 6 weeks of therapy and to 0.48 +/- 0.18 pmol/L (0.13 +/- 0.05 pg/mL) during the second 6 weeks of therapy. Although plasma estradiol levels measured by RIA were significantly correlated with levels measured by bioassay (r = 0.79; P < 0.01), the degree of suppression assessed by the bioassay (95 +/- 2% after 6 weeks) was greater than that determined by the RIA (81 +/- 4%), presumably due to improved ability to measure very low estradiol levels. We conclude that plasma estradiol is suppressed by letrozole to lower levels than previously observed, with equivalent suppression at all doses studied. A slight, although not statistically significant, rebound in estradiol levels occurs during the second 6 weeks of therapy compared to the first 6 weeks. Maximum inhibition of aromatase is achieved at letrozole doses as low as 100 micrograms.

    PMID: 7673408 [PubMed - indexed for MEDLINE]
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    Letrozole takes a very long time for steady state plasma levels compared to other Aromatase Inhibitors.




    Pharmacology and pharmacokinetics of the newer generation aromatase inhibitors.

    Buzdar AU.
    Department of Breast Medical Oncology, The University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA. abuzdar@mdanderson.org

    The newer generation aromatase inhibitors (AIs) as a class show efficacy and tolerability benefits over previously established treatments in postmenopausal women with advanced breast cancer. At clinically administered doses, the plasma half-lives of anastrozole (1 mg once daily), letrozole (2.5 mg once daily), and exemestane (25 mg once daily) are 41-48 h, 2-4 days, and 27 h, respectively. Time to steady-state plasma levels is 7 days for both anastrozole and exemestane and 60 days for letrozole. Androgenic side effects have only been reported with exemestane. Anastrozole treatment has no impact on plasma lipid levels, whereas both letrozole and exemestane have an unfavorable effect. From indirect comparisons, anastrozole shows the highest degree of selectivity compared with letrozole and exemestane, in terms of a lack of effect on adrenosteroidogenesis. To date, there are no data suggesting any major differences in clinical efficacy between the newer generation AIs anastrozole and letrozole. Based on the observed pharmacological profiles, however, it cannot be assumed that the AIs will display the same tolerability and safety profiles when given for extended periods of time in the adjuvant setting. The effects of anastrozole, letrozole, and exemestane are being investigated in the adjuvant setting, and these data will elucidate the possible long-term consequences of the pharmacological effects reported after short-term exposure.

    PMID: 12538502 [PubMed - indexed for MEDLINE]
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    Letrozole once a week normalizes serum testosterone
    in obesity-related male hypogonadism

    Sandra Loves1, Janneke Ruinemans-Koerts2 and Hans de Boer1
    Departments of 1Internal Medicine and 2Clinical Chemistry, Ziekenhuis Rijnstate, Wagnerlaan 55, 6800 TA Arnhem, The Netherlands
    (Correspondence should be addressed to H de Boer; Email: hdeboer@alysis.nl)

    Abstract

    Objective: Isolated hypogonadotropic hypogonadism (IHH) is frequently observed in severely obese men,
    probably as a result of increased estradiol (E2) production and E2-mediated negative feedback on
    pituitary LH secretion. Aromatase inhibitors can reverse this process. This study evaluates whether
    letrozole once a week can normalize serum testosterone in severely obese men and maintain its long
    term effect.

    Design: Open, uncontrolled 6-month pilot study in 12 severely obese men (body mass indexO
    35.0 kg/m2) with obesity-related IHH and free testosterone levels !225 pmol/l, treated with 2.5 mg
    letrozole once a week for 6 months.

    Results: Six weeks of treatment reduced total E2 from 123G11 to 58G7 pmol/l (P!0.001, meanG
    S.E.M.), and increased serum LH from 4.4G0.6 to 11.1G1.5 U/l (P!0.001). Total testosterone rose
    from 5.9G0.5 to 19.6G1.4 nmol/l (P!0.001), and free testosterone from 163G13 to 604G
    50 pmol/l (P!0.001). Total testosterone rose to within the normal range in all subjects, whereas free
    testosterone rose to supraphysiological levels in 7 out of 12 men. The testosterone and E2 levels were
    stable throughout the week and during the 6-month treatment period.

    Conclusion: Letrozole 2.5 mg once a week produced a sustained normalization of serum total
    testosterone in obese men with IHH. However, free testosterone frequently rose to supraphysiological
    levels. Therefore, a starting dose <2.5 mg once a week is recommended.

    European Journal of Endocrinology 158 741–747

    http://www.eje-online.org/cgi/reprint/158/5/741.pdf
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    Comparative Assessment in Young and Elderly Men of the Gonadotropin Response to Aromatase Inhibition

    Guy G. T’Sjoen, Vito A. Giagulli, Hans Delva, Patricia Crabbe, Dirk De Bacquer and Jean-Marc Kaufman


    Department of Endocrinology (G.G.T., H.D., P.C., J.-M.K.), Ghent University Hospital, 9000 Ghent, Belgium; Department of Public Health (D.D.B.), Ghent University, 9000 Ghent, Belgium; and Department of Internal Medicine Subdivision Endocrinology (V.A.G.), Ospedale Putignano-Noci, 70017 Bari, Italy
    Address all correspondence and requests for reprints to: G. T’Sjoen, M.D., Department of Endocrinology, Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium. E-mail: guy.tsjoen@ugent.be .

    Context: Aging in men is associated with a decline in serum testosterone (T) levels.
    Objective: Our objective was to assess whether decreased T in aging might result from increased estradiol (E2) negative feedback on gonadotropin secretion.
    Design and Setting: We conducted a comparative intervention study (2004) in the Outpatient Endocrinology Clinic, Ghent University Hospital.
    Participants: Participants included healthy young and elderly men (n = 10 vs. 10).
    Interventions: We used placebo and letrozole (2.5 mg/d) for 28 d, separated by 2 wk washout.
    Main Outcome Measures: We assessed changes in serum levels of free E2, LH, and FSH, free T, SHBG, and gonadotropins response to an iv 2.5-µg GnRH bolus.
    Results: As assessed after 28 d of treatment, letrozole lowered E2 by 46% in the young men (P = 0.002) and 62% in the elderly men (P < 0.001). In both age groups, letrozole, but not placebo, significantly increased LH levels (339 and 323% in the young and the elderly, respectively) and T (146 and 99%, respectively) (P value of young vs. elderly was not significant). Under letrozole, peak LH response to GnRH was 152 and 52% increase from baseline in young and older men, respectively (P = 0.01). Conclusions: Aromatase inhibition markedly increased basal LH and T levels and the LH response to GnRH in both young and elderly men. The observation of similar to greater LH responses in the young compared with the elderly does not support the hypothesis that increased restraining of LH secretion by endogenous estrogens is instrumental in age-related decline of Leydig cell function.

    http://jcem.endojournals.org/cgi/reprint/90/10/5717
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    good read. on another thread mike arnold goes into info about a recent study about the effects of letro on estrogen. it says that previous studies were mistaken and that 2.5 mgs a day only reduce estrogen by60-70%(cant remeber) how did it work for you on.25mgs a day,also did you need to preload it for a few weeks for it to take full effect?

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    Super Moderator heavyiron's Avatar
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    Quote Originally Posted by weightslayer View Post
    good read. on another thread mike arnold goes into info about a recent study about the effects of letro on estrogen. it says that previous studies were mistaken and that 2.5 mgs a day only reduce estrogen by60-70%(cant remeber) how did it work for you on.25mgs a day,also did you need to preload it for a few weeks for it to take full effect?
    Yes, I taught Mike the info on AI use in men. 2.5mg daily reduces E2 about 46-62% in men. The higher your T levels the LESS the E2 supression. See the post above yours.
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    Quote Originally Posted by heavyiron View Post
    Yes, I taught Mike the info on AI use in men. 2.5mg daily reduces E2 about 46-62% in men. The higher your T levels the LESS the E2 supression. See the post above yours.
    so can we pre load the letro
    IF THE BAR ISNT BENDING ITS NOT HEAVY ENOUGH GO WORKOUT WITH THE YOGA CROWD CHICKEN SHIT

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    Quote Originally Posted by wildjojo1 View Post
    so can we pre load the letro
    There is some evidence that Letro may take longer to reach steady state plasma levels so preloading it makes sense.
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    You said "In addition, I´ve used Letro to get rid of my own gyno, as has a friend of mine, and we both used it at a dose of 2.5mgs/day, tapering down to .25mgs/day, and then finally off..the gyno never returned in both our cases."

    How long did you run 2.5 mgs before tapering down and would this have a very negative effect on blood lipids and cholesterol levels. Just curious because i would like to try this but poor cholesterol runs in my family so if the legnth is not very long im going to give it a go

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    So if your running letro as ai on cycle how many mgs would I need a day??? Can you give me the exact break down

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    i have read that letro can also lower progesterone and prolactin as well as estrogen. is this true? i have not been able to find info to back up this claim. here is where i read it though, the part in BOLD UNDERLINE


    Trenbolone is also a noted progestin: it binds to the receptor of the female sex hormone progesterone (with about 60% of the actual strength progesterone) (17). In sensitive people this can lead to bloat and breast growth worse still, Trenbolone's active metabolite 17beta-trenbolone has a binding affinity to the progesterone receptor (PgR) that is actually greater than progesterone itself (18). No need to panic though, the anti-estrogens letrzole or fulvestrant can lower progesterone levels, and combat any progestenic sides.




    FROM STEROID.COM


    Trenbolone (Trenbolone Acetate)

    The drug Trenbolone is, without a doubt, the most powerful injectable anabolic steroid used by Steroid.com members to gain muscle. However the full properties of the drug are not always fully understood. This profile will separate fact from fiction and help steroid.com members decide if Trenbolone is right for them.

    Trenbolone is similar to the highly popular steroid Nandrolone, in that they are both 19-nor steroids, meaning that a testosterone molecule has been altered at the 19th position to give us a new compound. Unlike Nandrolone however Trenbolone is an excellent mass and hardening drug with the majority of gains being muscle fiber, with minimal water retention (1) It has an unbelievable anabolic (muscle building) score of 500. When you compare that to Testosterone, which itself is a powerful mass builder, and has an anabolic score of 100 you can begin to fathom the muscle building potential of Trenbolone. What makes Trenbolone so anabolic? Numerous factors come into play. Trenbolone greatly increases the level of the extremely anabolic hormone IGF-1 within muscle tissue (2). And, its worth noting that not only does it increase the levels of IGF-1 in muscle over two fold, it also causes muscle satellite cells (cells that repair damaged muscle) to be more sensitive to IGF-1 and other growth factors(3). The amount of DNA per muscle cell may also be significantly increased (3).

    Trenbolone also has a very strong binding affinity to the androgen receptor (A.R), binding much more strongly than testosterone (4). This is important, because the stronger a steroid binds to the androgen receptor the better that steroid works at activating A.R dependent mechanisms of muscle growth. There is also strong supporting evidence that compounds which bind very tightly to the androgen receptor also aid in fat loss. Think as the receptors as locks and androgen's as different keys, with some keys (androgen's) opening (binding) the locks (receptors) much better than others. This is not to say that AR-binding is the final word on a steroids effectiveness. Anadrol doesnt have any measurable binding to the AR& and we all know how potent Anadrol is for mass-building.

    Trenbolone increases nitrogen retention in muscle tissue (5). This is of note because nitrogen retention is a strong indicator of how anabolic a substance is. However, it's incredible mass building effects do not end there. Trenbolone has the ability to bind with the receptors of the anti-anabolic (muscle destroying) glucocorticoid hormones (6). This may also has the effect of inhibiting the catabolic (muscle destroying) hormone cortisol (7).

    Yet another amazing trait that must be noted is its ability to improve feed efficiency and mineral absorption in animals given the drug (8). To help you understand what this means for you, feed efficiency is a measurement of how much of an animals diet is converted into meat, and the more food it takes to produce this meat, the lower the efficiency. Conversely, the less food it takes to produce meat the, higher the efficiency& well you get the idea. Animals given Trenbolone gained high quality weight without having their diet adjusted, thus improving feed efficiency. Finding new compounds which can improve feed efficiency is a billion dollar industry, and has spawned many nutritional advances in the bodybuilding world over the last few decades (CLA, Whey Protein, and HMB are compounds which spring to mind as having first been introduced by the livestock industry). What does this translate to for the hard training athlete? The food you eat will be better utilized for building lean muscle, and vitamins and minerals are also better absorbed which may keep you healthier during cycle.

    Trenbolone is also a highly androgenic hormone, when compared with Testosterone, which has an androgenic ratio of 100; Trenbolone's androgenic ratio is an astonishing 500. Highly androgenic steroids are appreciated for the effects they have on strength as well as changing the estrogen/androgen ratio, thus reducing water and under the skin. As if the report on Trenbolone was not good enough, it gets better; Trenbolone is extraordinarily good as a fat loss agent. One reason for this is its powerful effect on nutrient partitioning (9). It is a little known fact is that androgen receptors are found in fat cells as well as muscle cells(10), androgens act directly on the A.R in fat cells to affect fat burning.(11) the stronger the androgen binds to the A.R, the higher the lipolytic (fat burning) effect on adipose tissue (fat)(11). Since some steroids even increase the numbers of A.R in muscle and fat (11, 12) this fat loss effect would be amplified with the concurrent use of other compounds, such as Testosterone.
    Trenbolone promotes red blood cell production and increases the rate of glycogen replenishment, significantly improving recovery (13). Like almost all steroids, it's effects are dose dependant with higher dosages having the greatest effects on body composition and strength. Mental changes are a notorious side effect of Trenbolone use (15), androgens increase chemicals in the brain that promote aggressive behavior(16), which can be beneficial for some athletes wanting to improve speed and power.

    Trenbolone's chemical structure makes it resistant to the aromatize enzyme (conversion to estrogen) thus absolutely no percentage of Trenbolone will convert to estrogen. Trenbolone administration would not promote estrogenic side effects such as breast tissue growth in men (gynecomastia, bitch tits) accelerated fat gain, decline in fat break down and water retention. Trenbolone is also resistant to the 5- alpha-reductase enzyme, this enzyme reduces some steroid hormones into a more androgenic form, in this case however this does not matter. Trenbolone boasts an androgenic ratio of 500. It can easily cause adverse androgenic side effects in people who are prone to hair loss, prostate enlargement, oily skin and acne. Unfortunately Trenbolone's potential negative side effects do not end there. Trenbolone is also a noted progestin: it binds to the receptor of the female sex hormone progesterone (with about 60% of the actual strength progesterone) (17). In sensitive people this can lead to bloat and breast growth worse still, Trenbolone's active metabolite 17beta-trenbolone has a binding affinity to the progesterone receptor (PgR) that is actually greater than progesterone itself (18). No need to panic though, the anti-estrogens letrzole or fulvestrant can lower progesterone levels, and combat any progestenic sides. The use of a 19-nor compound like trenbolone also increases prolactin & . bromocriptine or cabergoline are often recommended to lower prolatin levels (20). Testicular atrophy (shrunken balls) may also occur; HCG used intermittently throughout a cycle can prevent this. (21) It is also wise for Tren users to closely monitor their cholesterol levels, as well as kidney function and liver enzymes, as Tren has the potential to negatively affect all of those functions. Finaplix, being a powerful progestin, will also shut down natural testosterone production which even a relatively small dose and keep the testosterone level suppressed for an extended period of time, this can lower libido and cause erectile dysfunction (fina dick). It is essential that you always stack Finaplix with testosterone.

    The acetate ester is a very short-chain ester attached to the Finaplix molecule. It has an active life of 2-3 days but to keep blood levels of trenbolone elevated and steady, daily injections are often recommended. The acetate ester provides a rapid and high concentration of the hormone which is beneficial to those seeking quick gains, coupled with a rapid clearing time the acetate ester can be discontinued on the onset of adverse side effects.

    Now that the properties of Trenbolone Acetate have been explained we can better understand how to use it in order to maximize its advantages. Evidence suggests that Finaplix when stacked with estrogen promotes more weight gain that Trenbolone alone(22), now Im not telling you to go pop some birth control with your Tren but the addition of aromatizing orals such as Dianabol and a long estered testosterone such as Cypionate or Enanthate would produce great gains in a bulking cycle. For a cutting cycle Finaplix is the best choice you have; Trenbolone's powerful effect on nutrient shuttling allows a user to restrict calories and remain in a state of positive nitrogen balance (remember what that means?). The cortisol reducing effect and binding to the glucocorticoid receptor will greatly reduce the catabolic effects of harsh dieting and excessive amounts of cardio and not to mention that Finaplix itself may burn fat (due to its strong AR-binding). A good choice to stack with Tren in a cutting cycle is Winstrol. Winstrol has a low binding affinity to the AR and thus will act in your body in vastly different ways than the Tren (i.e. in non-receptor mediated action). In addition, Winstrol is a DHT-based drug and Tren is a 19-nor& throw in some Testosterone (prop), and you'll have a cutting cycle which takes advantage of all 3 major families of Anabolic Steroids (Testosterone, 19-nor, and DHT), as well as vastly different AR-binding affinities and mechanisms of action.

    Ironically, even though Trenbolone ( Tren ) is an excellent contest prep drug, it lowers your thyroid level(23), and this raises prolactin. I recommend taking T3 (25mcgs/day) along with your Tren to avoid elevating your prolactin too high via this route.
    Also, this drug is a poor choice for athletes who rely on cardiovascular fitness to play a sport. Trenbolone ( Tren ), anecdotally at least, reduces many athletes ability to sustain high levels of endurance. Unfortunately, this makes Tren a poor choice for many.

    As of now the main source of Trenbolone is from implants for cattle being converted into an injectable or transdermal compound, from powder, and of course Underground Labs. "Home brewing" powder or cattle implants seems to be the preferred method of obtaining injectable Trenbolone Acetate, because the user would have much more control over the potency and sterility of the drug. Trenbolone is much more expensive than other anabolic steroids ranging from 15 U.S dollars per gram of powder or 150 U.S for a single 10 ml bottle. The cost of Trenbolone should not matter, it is worth every penny.
    Trenbolone Acetate Profile


    • (17beta-Hydroxyestra-4,9,11-trien-3-one)
    • (Trenbolone Base + Acetate Ester)
    • Formula: C20 H24 O3
    • Molecular Weight: 312.4078
    • Molecular Weight (base): 270.3706
    • Molecular Weight (ester):60.0524
    • Formula (base): C18 H22 O2
    • Formula (ester): C2 H4 O2
    • Melting Point (base): 183-186C
    • Melting Point (ester):16.6C
    • Manufacturer: Cattle implants, British Dragon, Various
    • Effective Dose (Men):50-150mg ED
    • Effective Dose (Women): Not recommended
    • Active life: 2-3 days
    • Detection Time: 5 months
    • Anabolic/Androgenic ratio: 500/500

    References:


    1. Br J Nutr. 1978 Nov;40(3):563-72.
    2. J Cell Physiol. 2004 Nov;201(2):181-9.
    3. Endocrinology. 1989 May;124(5):2110-7.
    4. Toxicol Sci. 2002 Dec;70(2):202-11.15
    5. J Anim Sci. 1994 Feb;72(2):515-22.
    6. APMIS. 2001 Jan;109(1):1-8.
    7. J Anim Sci. 1990 Sep;68(9):2682-9.
    8. APMIS. 2001 Jan;109(1):1-8.
    9. J Anim Sci. 1992 Nov;70(11):3381-90.
    10. Am J Physiol. 1998 Jun;274(6 Pt 1):C1645-52.
    11. Biochim Biophys Acta. 1995 May 11;1244(1):117-20.
    12. J Appl. Physiol.94 1153-61 2003
    13. J Vet Med A Physiol Pathol Clin Med. 2001 Aug; 48(6):343-52
    14. Toxicol Sci. 2002 Dec;70(2):202-11.15
    15. Steroid.com forums.
    16. Med Sci Sports Exerc. 2003 Jan; 35(1):32-8
    17. Cancer Res 1978 Nov; 38(11 Pt 2):4186-98
    18. APMIS. 2000 Dec;108(12):838-46.
    19. Curr Med Res Opin. 2001;16(4):276-84
    20. 2003 drug handbook.
    21. Pharmacol Biochem Behav. 1988 Mar; 29(3):489-93.
    22. J Anim Sci. 1997 May;75(5):1256-65.
    23. Res Vet Sci. 1981 Jan;30(1):7-13

  15. #15

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    I have letro never used it maybe when i get back on my TRT and a few other goodies i want to try lol i will get on the letro a bit to reduce bloating. Heavy when during a cycle would you suggest taking it.
    I back eees normal https://www.youtube.com/watch?v=I6Zb92IfHkI

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