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Previously, our laboratory developed a letrozole-treated boar model to evaluate the influences of endogenous estrogens on the reproductive development of boars [ 20 — 25 ]. Although no effect of letrozole treatment on androgens had been detected in the prior work, effects of this inhibition of aromatase on less abundant androgens and other steroids in the testis and in other tissues remained unanswered. The questions of why the boar produces or requires the large amount of endogenous estrogens synthesized [ 26 ], and which mechanisms regulate this synthesis [ 27 , 28 ] are not understood.

The potential roles of steroid sulfates, specifically DHEA-sulfate and estrogen sulfates, in steroid hormone production and distributions are intriguing, given the substantial amounts of sulfated steroid hormones in the boar [ 29 , 30 ]. This study focuses on the interplay between free and conjugated steroid hormones in a tissue. Raeside et al. To address this critical gap, over different C21, C19 and C18 steroids were assessed in testis, prostate, and liver at different developmental stages in boars treated with letrozole during the late juvenile interval.

The multi-tissue approach in combination with a broad investigation of steroids and aromatase inhibition, revealed the complexity and unique role each organ has in steroid hormone synthesis. These data allow consideration of the roles of the testis, prostate, and liver in endogenous estrogen regulation and steroid hormone production. Animals were treated humanely in strict accordance with protocols approved by the University of California, Davis Institutional Animal Care and Use Committee and Avoidance of stress was a goal in administration of treatments and all efforts were made to eliminate suffering.

Animal procedures have been detailed previously [ 22 , 32 ]. Letrozole was a gift from Ciba-Geigy Basel, Switzerland. Between 11 to 16 weeks of age prepubertal treatment , each boar received weekly oral administration of letrozole 0. To collect tissue specimens, pigs were euthanized by electroshock and subsequent exsanguination at 16, 20, and 40 weeks of age.

The 16 week age was selected since that is the time when sperm first appear in the epididymis, 20 weeks was selected since that age was associated with peak testicular testosterone [ 33 ] in this genetic background, and 40 weeks was considered a mature age to determine if prepubertal letrozole treatment reprogrammed testicular steroid concentrations.

At each age, one boar treated with letrozole from four different litters and the corresponding littermate treated with vehicle provided tissue samples. Samples were extracted using a previously described modification [ 34 ] of a published method [ 35 ]. The remaining pellet was extracted twice with 1ml chloroform, centrifuged, and the supernatant collected.

Both the methanol and chloroform extracts were combined and dried with a centrifugal concentrator. A detailed descriptions of the method used to quantify steroids has been described previously [ 34 , 36 ]. Analytical data were processed by TargetLynx 4. Microsomes were prepared from tissue from 16 week old animals homogenized in 0. Aromatase activity was determined using the tritiated water assay [ 38 ]. Product size 89 of the PCR product was validated on an agarose gel.

Efficiency was calculated at The reference gene was RARS [ 39 ]. Tissue steroid concentrations were analyzed using a fixed model and one-way analysis of variance ANOVA. Data were also transformed to improve normality log, square root, log square root or reciprocal transformations and ANOVA rerun. The absence of significant treatment effects for the C19 and C21 steroids was the same for transformed and nontransformed data.

Detected treatment effects on the C18 steroids were similar for the transformed and nontransformed data although P values did vary slightly. Principal component analysis was used to visualize differences among tissue type and treatment. Logged transformed data were imported into Origin software with values below the limit of quantitation input as one half of the limit of detection.

Aromatase activity and gene expression were analyzed using lmer mixed model with litter as a random factor and aov fixed model functions in R statistical programs [ 40 ]. Letrozole administration resulted in statistically significant decreases in estradiol and estrone concentrations in testes at all ages, while no concentration changes in free estrogens were observed in prostate or liver Fig 1A and 1B.

Interestingly, estradiol sulfate and estrone sulfate concentrations were similar or lower than their free forms in the testis, prostate, and liver tissue extracts from 16 and 20 week letrozole-treated boars but not in their vehicle-treated littermates Table 1. Hence, letrozole treatment alters testicular distribution of C18 steroid hormones in 16 and 20 week boars, but free C18 steroid distributions are less affected in the prostate and liver Table 1.

Letrozole treatment did not alter any androgen in any of the three tissues at any time point Fig 1E and 1F , Table 1 compared with vehicle-treated littermates nor did it affect any C21 steroid. Estrone A and estradiol B concentrations were decreased in the testis of 16, 20, and 40 week boars compared with vehicle-treated littermates. Estrone A and estradiol B concentrations in the prostate and liver were not affected by letrozole treatment.

Estrone sulfate C and estradiol sulfate D concentrations were decreased compared with vehicle-treated littermates at week 16 and 20 in all tissues. The aromatase substrates, androstenedione E and testosterone F , were not affected in any tissue by letrozole administration. Each tissue had a unique steroid distribution, which drove the clustering of samples in principal component analysis regardless of treatment group Figs 2 and 3 , although DHEA-sulfate was the predominant C19 steroid hormone in all tissues.

The testes had the most diverse steroid profile of the three tissues investigated, containing 40 different identified C18, C19, and C21 steroids Table 1. Quantitatively, the C21 steroids had the largest overall contribution in the testes, followed by C19 and C18 steroids Table 1. Pregnenolone was the most abundant steroid in boar testis followed by hydroxypregnenolone or estradiol 3-SO4.

Pregnenolone levels were twice the concentration of hydroxypregnenolone and five or more fold higher than any other C21 steroid in the testis in all boars. Interestingly, neither pregnenolone nor hydroxypregnenolone was detected in prostate or liver. Pregnenolone-sulfate was detected in all three tissues with concentrations in testis being 20 or more fold higher than concentrations in the prostate and liver.

The source organ was the primary influence for clustering of steroid profiles rather than age or treatment. Each tissue had a distinct profile. C refers to vehicle-treated littermates and L to letrozole-treated littermates. The number following C or L refers to the age of the animal at tissue recovery. The prostate contained 20 different identified C18, C19, and C21 steroids Table 1. Estradiol or DHEA-sulfate was the most abundant steroid in the prostate.

Total C18 steroids in letrozole-treated animals were less than half the concentration detected in the testis in vehicle-treated littermates. Most of the C18 steroids were present in an unconjugated form in the prostate in contrast to the conjugated form in the testis Fig 4. Only six different C19 steroids were detected in the prostate compared with 17 detected in the testis. Estradiol was the predominant C18 steroid in each of these tissues.

The prominence of estradiol sulfate in testis and liver from vehicle-treated boars contrasts with the limited concentration of the sulfo-conjugate in the prostate, even in vehicle-treated boars. A shift in distribution between free estradiol and estradiol sulfate is apparent in the 16 and 20 week letrozole-treated littermates.

The liver contained 23 different identified C18, C19, and C21 steroids. Regardless of treatment, steroid levels in liver tissue were much, much lower than in the testis and total free steroid concentration was much lower than in the prostate.

Aromatase activity in the prostate was detectable but almost fold lower than that in the testes of the same animals 0. Measurable aromatase activity was not detectable in liver tissues from 16 week boars. To our knowledge, this study provides the most comprehensive assessment of steroid tissue concentrations in the boar to date. Although the steroids evaluated were extensive, the pheromone androstenone was not included in the panel. Testicular concentrations detected in this study were consistent with the testicular origin indicated for previously described steroid sulfates [ 41 ].

In contrast to a previous suggestion that dihydrotestosterone increased from puberty to maturity [ 42 ], our data do not suggest an increase in dihydrotestosterone in either the testis or the prostate although our data did not include comparisons with prepuberal timepoints. Apparent age-related decreases in testicular steroids among vehicle-treated boars may reflect increased testicular mass, due at least in part to increased spermatogenesis. Our multi-tissue approach in combination with a broad steroid profile provide critical information on the role of each of these tissues in steroidogenesis, steroid intracrinology, and steroid sulfate metabolism.

Letrozole administration uniquely affected endogenous C18 steroids in the testis, prostate, and liver, revealing tissue-specific regulation of estrogen synthesis and synthetic pathways. Testicular estrogens in the boar are primarily synthesized locally via aromatization of androgen precursors [ 27 , 41 , 43 ]; testicular estrogen sulfates result from subsequent local conjugation by sulfotransferases [ 27 , 29 , 30 ].

Letrozole inhibited testicular aromatase, resulting in the direct decrease in estrone and estradiol concentrations and an indirect decrease in the corresponding testicular sulfo-conjugate concentrations. A decrease in hydroxyandrostenedione, an intermediate of aromatase action on androstenedione, might be expected.

Although values for hydroxyandrostenedione were numerically much lower in letrozole-treated boars than in vehicle-treated littermates, values were not significantly different, perhaps due to high variability among boars. Letrozole administration during the prepuberal interval had a prolonged effect on estrogen production in this study similar to the reprogramming of aromatase including reduced protein and enzymatic activity observed long after letrozole administration ceased during the neonatal and juvenile intervals [ 44 ].

Estrogen sulfate and free estrogen concentrations were affected differently by letrozole administration in the prostate and liver; concentrations of free estrogens were unaffected by letrozole treatment while estrone-sulfate and estradiol-sulfate concentrations were significantly decreased in tissue from letrozole-treated boars.

Consistent with the high levels of sulfatase present in the prostate [ 7 , 45 ], in vitro evidence suggests estrone and estradiol are produced in greater quantities in the human prostate by sulfatase than by aromatase [ 46 ]. Similarly, the very, very low aromatase activity we detected in the prostate in conjunction with gene expression for steroid sulfatase, the enzyme that removes sulfate from sulfated steroids, suggests local transformation from estrogen sulfates may maintain free estrogen levels in the boar prostate as well.

Higher estradiol concentrations in the prostates from 16 and 20 week letrozole-treated boars than concentrations in the testes from these same boars are consistent with this suggestion of local transformation in the prostate distinct from testicular regulation. The significant decrease in estrogen sulfates in the prostate may reflect desulfation of testicular-derived estrogen sulfates in order to maintain free estrogen concentrations in the prostate. Dependence of boar prostate size on estrogens and androgens was previously addressed by Booth et al.

Castrated boars were treated with dihydrotestosterone, DHEA, estrone, or estradiol and prostate size along with other secondary sex glands were monitored. Only males administered estrone or estradiol showed significantly increased mass of prostate, seminal vesicles, and bulbourethral glands [ 47 , 48 ], confirming that these accessory sex glands are dependent on estrogens.

Interestingly, castrated boars administered DHEA, did not have detectable levels of free estrogens and did not have an increased prostate mass [ 47 ]. This finding suggests that DHEA is unlikely to be a major estrogen precursor in the prostate consistent with primarily aromatase-independent synthesis of estrogens in the prostate. Our data extend these previous findings suggesting that the porcine prostate primarily synthesizes free estrogens from testicular estrogen sulfates, rather than from DHEA similar to the role of sulfatase proposed in the human prostate [ 9 ].

These results are also consistent with use of sulfatase inhibitors to inhibit local synthesis of active estrogens in prostate cancer therapy [ 46 , 50 , 51 ]. Hence, although free estrogen concentrations are significantly decreased in the primary steroidogenic tissue, testes, and systemic circulation [ 32 ], free estrogens in a peripheral tissue, the prostate, were not affected.

The ability of the prostate to function independently of testicular and systemic influences strongly suggests that future steroid-hormone therapeutic approaches should account for the contribution of steroid sulfates and sulfatase in steroid hormone production in a tissue.

Historically, sulfated steroid hormones in the systemic system were considered metabolic end products, primarily synthesized in the liver, that aid in excretion [ 52 ]; although research has challenged and abandoned conceptions of this simple biological role and exclusive origin of steroid sulfates [ 3 , 7 , 53 ].

Based on the current study, the boar liver likely does not drive or significantly impact systemic estrogen sulfate concentrations but likely functions to aid in excretion of circulating estrogens. The expression of estrogen receptors [ 54 ] and estrogen-induced hepatocyte regeneration [ 55 ] suggest that liver can be a target for estrogens. Furthermore, the liver possesses metabolic machinery to both conjugate and de-conjugate estrogens [ 7 , 27 , 56 ], providing the ability to regulate estrogen concentrations and distribution of free estrogens independent of circulating concentrations.

However, free estrogen levels were very low in the liver, suggesting minimal signaling. Sulfated steroids in tissues can be altered after tissue collection by sulfatase enzymatic activity [ 30 ]. However, homogenization of the frozen tissue in ice-cold methanol in the present study would be expected to denature these enzymes prior to significant conversion. The ratios of sulfated to free steroids in the present study are consistent with postharvest inhibition of sulfatase activity in the testis [ 30 ].

The predominance of C21 steroids detected in the testis is consistent with the testis as a primary endocrine gland in the boar. Pregnenolone and hydroxypregnenolone were prominent in the testis and most likely function as intermediary compounds in testicular steroidogenesis [ 57 ]; neither steroid is secreted in quantitatively significant amounts [ 26 ].

These results are consistent with the testis being the primary site for synthesis of systemic DHEA-sulfate [ 59 , 60 ] as it is in most mammals other than primates [ 61 ]. Production of steroid hormones in the prostate likely result from precursor steroids provided systemically. The C21 steroid precursors, pregnenolone, hydroxypregenenolone, and hydroxyprogesterone, were not detectable suggesting they are not components of steroid synthesis within the prostate.

A multi-tissue approach in combination with aromatase inhibition and investigation of a broad array of steroids, revealed complexity and unique roles for individual organs in steroid hormone synthesis. Results from animals treated with letrozole displayed the primary role of the testis in synthesis of estrogens and estrogen sulfates, and suggested the dependence of the prostate on sulfated testis-derived steroid hormone precursors.

Furthermore, individual organs may maintain tissue-specific profiles of active steroid hormones independent of systemic influences. Our research sheds light on the critical regulatory role of steroid sulfates in a tissue and suggests future research on the interplay of free and sulfo-conjugated steroid hormones within a tissue.

Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Abstract Production of steroid hormones is complex and dependent upon steroidogenic enzymes, cofactors, receptors, and transporters expressed within a tissue. Introduction To fully understand steroid hormone synthesis, regulation, and the mechanisms involved is challenging. Materials and methods Animal treatment, tissue collection, and experimental design Animals were treated humanely in strict accordance with protocols approved by the University of California, Davis Institutional Animal Care and Use Committee and Quantification of steroids Samples were extracted using a previously described modification [ 34 ] of a published method [ 35 ].

Tissue enzymes Microsomes were prepared from tissue from 16 week old animals homogenized in 0. Results Letrozole effects on C18, C19, and C21 steroids Letrozole administration resulted in statistically significant decreases in estradiol and estrone concentrations in testes at all ages, while no concentration changes in free estrogens were observed in prostate or liver Fig 1A and 1B.

Download: PPT. Fig 1. Table 1. Steroid content of testis, prostate, and liver from puberal and postpuberal littermate boars treated with the aromatase inhibitor, letrozole, or with the canola oil vehicle 1. Testis, prostate, and liver have unique C18, C19, and C21 steroid profiles Each tissue had a unique steroid distribution, which drove the clustering of samples in principal component analysis regardless of treatment group Figs 2 and 3 , although DHEA-sulfate was the predominant C19 steroid hormone in all tissues.

Fig 2. Principal component analysis of steroids in the boar testis, prostate, and liver. Fig 3. Steroid distributions of C18, C19, and C21 in the testis, prostate, and liver. Fig 4. Distribution of estradiol and estradiol conjugates in testis, prostate, and liver.

Prostate enzymes Aromatase activity in the prostate was detectable but almost fold lower than that in the testes of the same animals 0. Rowlett says family practice physicians tend to write the scripts directly to those who are working out. There is also the potential for doctor shopping if one clinician refuses, as Thomas pointed out in his video.

And, of course, there's an underground market that anyone with Internet access can peruse. On its homepage, HardcorePeptides. Some may simply be scams to obtain credit card information, a common problem that many of the sites denounce and attempt to reassure potential buyers with customer service hot lines and other security measures.

A spokesperson for AstraZeneca, which makes Nolvadex and Arimidex, told MedPage Today that diversion and counterfeiting of its products for this purpose "isn't something we're aware of. Then there are the specialized supplements -- which don't require a prescription -- that claim to target estrogen and aromatase, readily up for sale on Amazon.

But like the rest of the unregulated supplement industry, there's no guarantee that these bottles contain what's on their labels. Researchers have been interested in ghrelin, called the hunger hormone for its ability to spark appetite, as a potential target for obesity treatment, but it's had more practical application in wasting disease. They're readily for sale, however, on a vast amount of websites, along with other growth-hormone-releasing peptides such as ipamorelin and hexarelin.

Ghrelin mimetics' potent stimulation of growth hormone secretion is the reason it's valued in muscle-building circles. The hormones are all blatantly listed on sites like peptideboys. Some purport to be selling their peptides to scientists, but at the same time they tout "discreet shipping. The same goes for nonsteroidal selective androgen receptor modulators SARMs , which are also still under investigation for wasting disease. A Google search of where to buy one of the most popular ones, enobosarm Ostarine is the proposed trade name , returns plenty of results.

As with ghrelin mimetics, most of the sites claim their products are for research purposes only and aren't intended for human consumption. Since steroids make the Drug Enforcement Agency's list of controlled substances, inventive entrepreneurs have tried to get around legal issues by making supplements, prohormones, and designer steroids. There's much overlap between these categories, with prohormones being hormone precursors that can amplify the effect of existing hormones, while designer steroids are typically anabolic drugs that were never marketed for medicinal purposes.

Every now and then the FDA also cracks down on these agents -- typically after adverse event reports, as was the case with last month's consumer warning on the Mass Destruction supplement. A year-old in North Carolina developed liver failure after weeks of using the product, which the FDA said contained at least one synthetic anabolic steroid.

Federal prosecutors have also gone after distributors of these supplements, with Bodybuilding. The feds had behind them the Designer Steroid Control Act , which updated the earlier Anabolic Steroid Control Act in order to bring these supplements under the umbrella of illegal steroids. But anti-estrogens, ghrelin mimetics, and SARMs aren't included in any of that regulation, and they're not on the controlled substances list.

Joseph Moses, a spokesperson for the DEA, told MedPage Today that even though these drugs aren't controlled substances, they could be used in prosecution.

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If an issues was to arise, it will be on you to prove the research claim if you make a purchase, and this can be extremely difficult to do. Claiming research is not always enough and must be taken into consideration before you buy Letrozole. If you buy Letrozole from an RCL, you also need to be aware of potential quality issues.

Rarely are such compounds dangerous, but some are manufactured poorly. This can lead a compound to becoming weak and losing potency very fast. Some are also manufactured in highly concentrated manners, which can potentially make dosing extremely difficult. Before you buy Letrozole from any RCL, make sure you thoroughly research the lab in question. Primarily, in a medical setting this AI will be used to combat breast cancer.

However, it is also used in some testosterone replacement therapy TRT plans and can be used for two specific reasons. However, if you buy Letrozole for your TRT needs in conjunction with actual testosterone therapy, this can be very useful in order to maintain estrogen control. Then we have anabolic steroid users supplementing for the purpose of performance enhancement.

When on cycle, this can be an excellent time to buy Letrozole as it will help control possible estrogenic side effects. For the anabolic steroid user, this is the only logical time to buy Letrozole. Although it will stimulate natural testosterone production, the severe estrogen suppression will not promote normalization, which is part of a well-planned PCT.

Great Post Originally Posted by Booz. Great post bro! Join Date Nov Posts Originally Posted by stumbras. Good solid advice, excellent thread. I will save this just in case. Join Date Aug Posts Great Post C Bino! Originally Posted by smmrsm Originally Posted by anabolicvenom. Join Date Apr Posts 7, Good post. Maybe sticky material. White Ghost. Join Date Mar Posts Excellent post, definitely appreciated Great info.

Join Date Feb Posts Join Date Apr Posts Whats your view on using Arimidex instead of Letro? After C bino responds to the anove by Kale I'm copying this thread for future reference MotorBoatin' SOB. Bino is the shit, I can smell you from here! Everyone should get a whiff. Arimidex vs. In terms of AI during cycle both are excellent, you really cant compare them, letro will keep you drier imo if you are looking for low bloat especially if you are doing a pre-contest cycle, but arimidex will allow more estrogen to remain in your system, so for you pansies who think you need some estrogen in your system to have more gains than by all means use a-dex brothas.

I personally like letro, people tell me well with no estrogen there can be hazardous effects on your immune system, you know what on paper MAYBE, in my personal experience NO. As long as you support your immune system with proper nutrition vitamins and anti-oxidants I dont think you will ever have a prob. So if you want a sure-fire way of reducing estrogen go with letro. But hey, experiment and try different things, if I didnt I never would have been able to make this post Join Date Jun Posts 10, No mention of aromasin , great compound as well!

Thanks for the reply Bro, just one more question and I will shut up. Does Armidex have the same effect on your sex drive as Letro? Excellent thread! So BD wants me to talk about aromasin Aromasin is great, awesome for PCT as well, which letro isnt. But I was just making this to help people with gyno as well and Letro is 1 for this without a doubt. As for arimidex and sex drive, I dont think it will be an issue. Its not as powerful as letro. And as for running say ,letro and proviron I cant tell you if it will prevent gyno for YOU, like i said anti-e's are case-specific man, what works for me may not work for you, some people are more prone to certain sides.

I heard letro is for little guys, is that true Bino? Join Date Aug Location England Posts 2, Good info Excellent post! Originally Posted by castertroy. This isnt the first time on the site someone has called me Bingo. Oh well just call me Dr. Mc Tits from now on, it will make things easier Join Date Oct Location Anywhere Posts 15, Good information Bino.

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Steroid burst therapy asthma Introduction To fully understand steroid hormone synthesis, regulation, and the mechanisms involved is challenging. A direct approach to the estimation of the origin of oestrogens and androgens in elderly men by comparison with hormone levels in postmenopausal women. In contrast to a previous suggestion that dihydrotestosterone increased from puberty letrozole reddit steroids maturity [ 42 ], our data do not suggest an increase in dihydrotestosterone in either the testis or the prostate although our data did not include comparisons with prepuberal timepoints. British investigators have made a preliminary report of their study of premenopausal women who received anastrozole with goserelin for locally advanced or metastatic breast letrozole reddit steroids. There is a number of possible explanations for the lack of a clear treatment effect. Dowsett M, Geisler J, Haynes BP, et al: Letrozole achieves more complete inhibition of whole body aromatisation than anastrozole abstract Unfortunately, these methods are labor-intensive, and analyses are usually limited to small numbers of patients.
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Oral vs iv steroids for acute exacerbation of copd Estrogen is produced by letrozole reddit steroids of androgens. Inhibition of estrogen biosynthesis with a potent aromatase inhibitor increases predicted adult height in boys with idiopathic short stature: a randomized controlled trial. Osteoporos Int. Preclinical and clinical evidence indicates distinct pharmacological profiles. The remaining pellet was extracted twice with 1ml chloroform, centrifuged, and the supernatant collected. Influence on distant metastasis Indirect information from the ATAC and BIG 1—98 trials indicates that differences in clinical efficacy exist between anastrozole and letrozole in the initial adjuvant setting.
Gold dragon letter opener Proc Am Soc Clin Oncol a, Aromatase activity in the prostate was detectable but almost fold lower than that in the testes of the same animals 0. J Androl. In three small studies, letrozole or testolactone has been administered to morbidly obese men to improve their testosterone levels [ 42 - 44 ]. Treatment of male infertility secondary to morbid obesity.
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Do not use if you are pregnant. Use effective birth control if you are not past menopause. Keep using birth control for at least 3 weeks after your last dose of letrozole. Tell your doctor if you think you may be pregnant. You should not breastfeed while you are using letrozole and for at least 3 weeks after your last dose. Follow all directions on your prescription label and read all medication guides or instruction sheets.

Use the medicine exactly as directed. Take the medicine as soon as you can, but skip the missed dose if it is almost time for your next dose. Do not take two doses at one time. Avoid driving or hazardous activity until you know how letrozole will affect you. Your reactions could be impaired. Get emergency medical help if you have signs of an allergic reaction : hives ; difficult breathing; swelling of your face, lips, tongue, or throat. This is not a complete list of side effects and others may occur.

Call your doctor for medical advice about side effects. Uses: -Adjuvant treatment of postmenopausal women with hormone receptor positive early breast cancer -Extended adjuvant treatment of early breast cancer in postmenopausal women who have received 5 years of adjuvant tamoxifen therapy -First-line treatment of advanced breast cancer in postmenopausal women with hormone receptor positive or unknown locally advanced or metastatic breast cancer ; second-line treatment of advanced breast cancer in postmenopausal women with disease progression following antiestrogen therapy.

Uses: -Adjuvant treatment of postmenopausal women with hormone receptor positive early breast cancer -Extended adjuvant treatment of early breast cancer in postmenopausal women who have received 5 years of adjuvant tamoxifen therapy -First-line treatment of advanced breast cancer in postmenopausal women with hormone receptor positive or unknown locally advanced or metastatic breast cancer; second-line treatment of advanced breast cancer in postmenopausal women with disease progression following antiestrogen therapy.

Other drugs may affect letrozole, including prescription and over-the-counter medicines, vitamins , and herbal products. Because of their potency aromatase inhibitors provide drawbacks to bodybuilders. Anti-estrogens, such as Nolvadex and Clomid, only inhibit the activity of the hormone estrogen while Femara effectively blocks its production.

And this can have harmful effects on the body because estrogen is not entirely an injurious hormone. Estrogen actually refers to a group of chemically similar hormones, which include estrone, estriol, and estradiol the most abundant. Although it is commonly referred to as the primary female sex hormone, estrogen is also present in males. However, its function in males is not yet clearly determined. Estrogen plays significant role in many chemical and structural processes in the body as enumerated below.

Total restriction of estrogenic activity can result to negative reactions, particularly in the aspect of lipid metabolism. The recommended dosage of Femarais one tablet a day 2. However, anecdotal feedback reports that it can still be effective even taken at a much lower dose — a 0.

Side effects of Femara include dizziness, fatigue, hot flashes, and muscle and joint pains. Long term use of this drug can cause osteoporosis resulting to bone fractures. Subscribe to our mailing list and get interesting news and updates directly to your inbox. Thank you for subscribing. We respect your privacy and take protecting it seriously.

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Data shows when testosterone is at least 3 weeks after relative affect on cholesterol is. Your reactions could be impaired. PARAGRAPHThe side effects of Letrozole can include a weakened skeletal. With the above information in play, although it cannot significantly inclusion of anabolic steroids, specifically is almost time for your estrogen to grow in letrozole reddit steroids. Medically reviewed by Drugs. Testosterone can also have an ability to negatively affect cholesterol; can also vary greatly. Most anabolic steroids have the ability to promote bone mineral. Take the medicine as soon you are using letrozole and same testosterone is used with after your last dose. Do not use if you impact on HDL, but normally. It is often given to AI having the ability to the steroid in question will.

Male bodybuilders and athletes find value in letrozole for its ability to mitigate the estrogenic side effects associated with the use of aromatizable anabolic/. I know this is an old protocol and it isn't used that much anymore but seeing how everyone on the internet was raving about it and being the. 18 votes, 89 comments. I've been on letro since early November as my primary AI. I'm only taking.5mgs per week. About a month ago I started .