Androgens, AI's, SERMs, and gyno

[gimmewings]

I posted a thread a few weeks ago regarding the use of AI/SERM's for treatment of gyno. Now I suspected that attempting to do so while on cycle (running test) may give better results as opposed to running them off cycle.

I received feedback that stated it would not change the outcome; however, after reading up I decided that it would. This is because adrogens (test) inhibit glandular development. Also, androgens themselves have been used with mixed results as a clinical treatment for gyno (as have tamox and AI's).

Given this evidence I feel that running test has a better chance of reducing/reversing gyno in conjunction with AI's and/or SERM's than compared to just AI's and/or SERM's.

[mickdiesel]

thank you sir for that

[gimmewings]

Does anyone agree, disagree, or not really give a shit?

[james21]

do you have anything to back this up? Putting extrogenous test in your system will make your body produce more estro .... and elevated levels of prolactin

[gimmewings]

I have heard a few accounts of this being effective; though I have no empirical support.

Does the male body "produce" estrogen?

[pimpdawgin]

I have heard a few accounts of this being effective; though I have no empirical support.

Does the male body "produce" estrogen?

Indirectly, yes. Aromatase, an enzyme, can convert testosterone into estrogen (estradiol, I believe). And the more test you take, the more conversion will occur.

[Kratos]

You know I agree as I posted so in one of your threads, the only thing I would add is instead of testosterone use something more androgenic. A DHT like masteron or mdht would be ideal + hrt dose of test + letro.

[gimmewings]

You know I agree as I posted so in one of your threads, the only thing I would add is instead of testosterone use something more androgenic. A DHT like masteron or mdht would be ideal + hrt dose of test + letro.

What does "hrt" mean?

What is "mdht?"

[chuckt12345]

i had gyno since i was 19
when i ran test e at 500mg/wk i actually lost about 1/3 or it,, im not sure if it was from the loss of fat or what but it did go down instead of up

[kfrost06]

What does "hrt" mean?

What is "mdht?"

hrt is hormone replacement therapy sometimes called trt for testosterone replacement therapy. That's when you take a weekly dose of testosterone of about 100-250mg/wk.

[J*U*icEd]

i can't see how this would work... i would think the exact opposite and gyno would get worse... but im real interested... is there some sort of information, an experiment, or a source that i can take a look at and get some insight on this... id really like somebody to explain how this would mechanically work other then "it just does"... im not tryin to be an ass i just want more info on the subject and im really interested

[Kratos]

A physiologic role for testosterone in limiting estrogenic stimulation of the breast.Dimitrakakis C, Zhou J, Wang J, Belanger A, LaBrie F, Cheng C, Powell D, Bondy C.
Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA.

OBJECTIVE: The normal ovary produces abundant testosterone in addition to estradiol (E(2)) and progesterone, but usually only the latter two hormones are "replaced" in the treatment of ovarian failure and menopause. Some clinical and genetic evidence suggests, however, that endogenous androgens normally inhibit estrogen-induced mammary epithelial proliferation (MEP) and thereby may protect against breast cancer. DESIGN: To investigate the role of endogenous androgen in regulating mammary epithelial proliferation, normal-cycling rhesus monkeys were treated with flutamide, an androgen receptor antagonist. To evaluate the effect of physiological testosterone (T) supplementation of estrogen replacement therapy, ovariectomized monkeys were treated with E(2), E(2) plus progesterone, E(2) plus T, or vehicle. RESULTS: We show that androgen receptor blockade in normal female monkeys results in a more than twofold increase in MEP, indicating that endogenous androgens normally inhibit MEP. Moreover, we show that addition of a small, physiological dose of T to standard estrogen therapy almost completely attenuates estrogen-induced increases in MEP in the ovariectomized monkey, suggesting that the increased breast cancer risk associated with estrogen treatment could be reduced by T supplementation. Testosterone reduces mammary epithelial estrogen receptor (ER) alpha and increases ERbeta expression, resulting in a marked reversal of the ERalpha/beta ratio found in the estrogen-treated monkey. Moreover, T treatment is associated with a significant reduction in mammary epithelial MYC expression, suggesting that T's antiestrogenic effects at the mammary gland involve alterations in ER signaling to MYC. CONCLUSIONS: These findings suggest that treatment with a balanced formulation including all ovarian hormones may prevent or reduce estrogenic cancer risk in the treatment of girls and women with ovarian failure.

[Kratos]

Effects of an oral contraceptive combination with or without androgen on mammary tissues: a study in rats.Jayo MJ, Register TC, Hughes CL, Blas-Machado U, Sulistiawati E, Borgerink H, Johnson CS.
Pathology Associates International, Advance, NC 27006, USA. [email protected]

OBJECTIVES: Oral contraceptive (OC) therapy has long been known to produce hypoandrogenemia. However, androgens are not part of any OC therapy available to women. This project was designed to evaluate the effects of low-estradiol containing OC, with or without methyltestosterone (MT), on cell proliferation and progesterone receptor (PgR) expression in mammary gland epithelia of virgin female rats. METHODS:Sixty rats were divided into four groups. One group received OCs, whereas a second group received OC plus MT. A third group of rats was treated with an antiandrogen to mimic the hypoandrogenemic effects caused by OC therapy. All treated groups were compared with age-matched untreated controls. RESULTS: After 15 weeks of treatment, no inflammatory, precancerous, or cancerous lesions were observed in any treatment group. OC plus MT therapy caused significant suppression of epithelial proliferation, a reduction in the number of proliferating cell nuclear antigen-labeled cells, and an increase in the number of PgR-labeled cells. CONCLUSIONS: Our results suggest that a medication containing an estrogen-progestin-androgen combination has antiproliferative effects in mammary glands of experimental animals that could prove to have breast-protective potential in women.

PMID: 10964026 [PubMed - indexed for MEDLINE]

[kfrost06]

Both those studies are for females. Males produce the hormones differently then females.

[Kratos]

Biological actions of androgens.Mooradian AD, Morley JE, Korenman SG.
Though unnecessary for life itself, androgens are essential for the propagation of the species and for establishment and maintenance of the quality of life of males through their support of sexual behavior and function, muscle strength, and sense of well-being. In carrying out its many functions, T acts both as hormone and prohormone. It is an outstanding example of the diverse evolutionary utilization of a primitive informational molecule both among and within species. Not only does T act through the androgen receptor both unchanged and via 5 alpha-reduction, but it acts in tissues with a high aromatase level as an estrogen via the estrogen receptor. Furthermore, DHT, binding to the estrogen receptor, can act as an inhibitor of estrogen action. The products of androgen metabolism may also play active regulatory roles in hematopoiesis and in the regulation of certain hepatic enzymes. Table 3 summarizes the actions of secreted T in males indicating the probable effector hormone. While gross hypogonadism is uncommon, mild androgen insufficiency may be much more frequent, especially in older men, and in those receiving treatment for chronic medical conditions. It is quite possible that such individuals would benefit from appropriate androgen therapy were it available, but the current forms of replacement therapy are not very satisfactory. Better approaches are required. With the exception of a small number of secreted proteins, the products of transcription induced by androgens are not, as yet, known. When the androgen receptor gene is cloned it will be possible to identify androgen-regulated genes and their products. It will then be possible to design agents selectively producing specific desired androgenic effects.

PMID: 3549275 [PubMed - indexed for MEDLINE]

[Kratos]

Effects of long-term androgen administration on breast tissue of female-to-male transsexuals.Slagter MH, Gooren LJ, Scorilas A, Petraki CD, Diamandis EP.
Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, 600 University Avenue, Toronto, ON, M5G 1X5, Canada.

Our aim was to examine the effects of androgen administration on breast tissue histology of female-to-male transsexuals and to study the immunohistochemical expression of three human tissue kallikreins, hK3 (PSA), hK6, and hK10. We studied 23 female-to-male transsexuals who were treated with injectable testosterone for 18-24 months. We also used 10 control female breast tissues. All tissues were fixed in buffered formalin, embedded in paraffin, and examined by hematoxylin-eosin staining and immunohistochemical staining for PSA, hK6, and hK10. Females treated with androgens exhibited similar involutionary changes as those seen in breast of menopausal women, such as marked reduction of glandular tissue, involution of the lobuloalveolar structures, and prominence of fibrous connective tissue, but presence of only small amounts of fat tissue. Fibrocystic lesions were generally not observed. In immunohistochemistry, in control breast tissues, we found moderate to strong cytoplasmic immunoexpression of hK6 and hK10 in the epithelial ductal and lobuloalveolar structures, but myoepithelial cells were negative. Luminal secretions were also positive. In menopausal breast, the immunoexpression of hK6 and hK10 was weaker and focal. No control case showed immunoexpression for PSA. In female-to-male transsexuals, one case showed focal PSA cytoplasmic immunoexpression in the epithelium of moderately involuting lobules. Long-term administration of androgens in female-to-male transsexuals causes marked reduction of glandular tissue and prominence of fibrous connective tissue. These changes are similar to those observed at the end-stage of menopausal mammary involution.

PMID: 16618941 [PubMed - indexed for MEDLINE]

[Kratos]

Complications of androgen-deprivation therapy in men with prostate cancer.Chen AC, Petrylak DP.
Department of Medicine, College of Physicians and Surgeons, Columbia University, 177 Fort Washington Avenue, MHB 6-435, New York, NY 10032, USA. [email protected]

Androgen-deprivation therapy (ADT) is indicated for the treatment of metastatic prostate cancer and locally advanced disease. In addition to sexual side effects, long-term ADT results in several other changes, including hot flashes; gynecomastia; changes in body composition, metabolism, and the cardiovascular system; osteoporosis; anemia; psychiatric and cognitive problems; and fatigue and diminished quality of life. This review discusses these complications of ADT and treatments aimed at reducing them. It is important for clinicians to anticipate these effects and to initiate measures to prevent or minimize them in order to maintain quality of life in prostate cancer survivors.

PMID: 15869725 [PubMed - indexed for MEDLINE]

[kfrost06]

Complications of androgen-deprivation therapy in men with prostate cancer.Chen AC, Petrylak DP.
Department of Medicine, College of Physicians and Surgeons, Columbia University, 177 Fort Washington Avenue, MHB 6-435, New York, NY 10032, USA. [email protected]

Androgen-deprivation therapy (ADT) is indicated for the treatment of metastatic prostate cancer and locally advanced disease. In addition to sexual side effects, long-term ADT results in several other changes, including hot flashes; gynecomastia; changes in body composition, metabolism, and the cardiovascular system; osteoporosis; anemia; psychiatric and cognitive problems; and fatigue and diminished quality of life. This review discusses these complications of ADT and treatments aimed at reducing them. It is important for clinicians to anticipate these effects and to initiate measures to prevent or minimize them in order to maintain quality of life in prostate cancer survivors.

PMID: 15869725 [PubMed - indexed for MEDLINE]

^^^I like this one. I often find that I get my gyno symptoms after a cycle and this could be why. very low test/estrogen ratio. Very interesting find, to think test can lead to AND hinder gyno. I be willing to quess having steady levels play a factor.

Good work AGAIN Kratos!

[Kratos]

In my mind androgens supresss breast tissue growth and estrogen induces breast tissue growth. How can it hurt to supress tissue growth at the same time you are taking away stimuation for growth? Who knows if it works or not?

[RA]

I posted a thread a few weeks ago regarding the use of AI/SERM's for treatment of gyno. Now I suspected that attempting to do so while on cycle (running test) may give better results as opposed to running them off cycle.

I received feedback that stated it would not change the outcome; however, after reading up I decided that it would. This is because adrogens (test) inhibit glandular development. Also, androgens themselves have been used with mixed results as a clinical treatment for gyno (as have tamox and AI's).

Given this evidence I feel that running test has a better chance of reducing/reversing gyno in conjunction with AI's and/or SERM's than compared to just AI's and/or SERM's.

I dont see where you have enough evidence to draw a conclusion.

[bigpapabuff]

Great info on this thread. Thanks Guys