Pubmed is giving me zero hits on Mesterolone + gynecomastia.

I am about to pick up some proviron to help offset my pubertal gyno and I am sure that it is very effective(up there with andractim) regarding gyno treatment.

However,my memory fails me as to what dosage should be used and I've no studies to reference.

Any help?

Haven't you ridden the Proviron bus before?

Proviron won´t take your gyno out.

first you wanna lose you bf to single digits to see how much of the gyno is pseudo ( fat) or actual mamary tissue. after getting to single digits you go get a loan , pay on 24 - 36 months and go do surgery. i don´t no how much is a gyno surgery over there bu it can´t be so expensive.

Proviron @ 60mg ED isn't doing squat for my gyno, FWIW. I'd say the money.

Have you tried letro and/or extended ralox usage while cutting?

my thoughts exactly if pubertal gyno is the case. proviron is great to rverese AAS induced gyno though.

Worst advice ever. sorry. Have you seen gyno-reduction surgery pre and post pics? I would say 95% of the people I have seen look bad after the surgery. If you plan on wearing a shirt the rest of your life and never going without one then sure go for it.

I personally like Masteron. I have tried letro and didnt really notice a change.

Have you tried Havoc already? Given the cost and availability, it's worth a shot.

Liorrh -- Can you expound a little on the changes that occur over time with gyno? Why does AAS / recently onset gyno seem fairly easy to reverse, whereas long-term pubescent gyno is quite difficult?



AFAIK, nobody on this board has seen jack shit WRT gyno and havoc.

EDIT: AAMAOF, in my next anti-gyno cycle, I'm going to start with a little havoc just to hopefully shut down my HPTA a little before I start using a worthwhile androgen, so that my E will be in the basement from the get-go with the DHT.

Dash,can you please post the gyno related proviron (masteron maybe?) study you sent to me a whileback in this thread?

It may very well have been masteron which you cited earlier and not proviron,I can't recall,I deleted the email with the study.





I'm not Lior but his assertion that pubertal gyno is much more difficult to treat than newly acquired/induced drug (AAS,dutasteride ,whatever) gyno is spot on.

Something along the lines of a longer amount of time is needed for the cells to dry out before atoposis can occur as the pubertal gyno cells have a firm planting/grip opposed to the newly acqquired gyno which is relatively transient.This is a shit explanation though and I'd also like to hear Lior's reasoning.

I think that (provided dashforce posts the study to confirm my belief) that proviron or masteron may prove to be a decent kickstart in promoting gyno cell dealth.I'm not suggesting that a month of either one would show much if any visible results.Raloxifene would still be needed (and in my case,a Lipoderm/Napalm topical for the bulk of the fatty tissue) over the course of 9-12 months.

To clarify,my gyno was originally pubertal in nature and I successfully (temporarily) got rid of it by cutting to 10% several years ago,in conjunction with a jacked up Lipoderm-Y.I added a A DHT derivitive to the Lipo-Y,I think I used 5-MAA) for two months or so.

Shortly after obtaining that state of leanness I decided to bulk and that is when my gyno reappeaared in full,as my body fat level increased almost two fold.

I believe it was subsequently aggravated by finasteride,duatseride(both were dropped after no offect on MPB) and androgen usage over the past few years.In summation,I have no hard lumps nor pointy niples-just a vastly disproportionate amount of fat on both pecs.

At any rate,I plan on starting on 20mg Havoc tomorrow (after my liver test is done in the morning) in 2 divided dosages on an empty stomach.

So it will be,as of now:
Havoc-20mg for a month
proviron or masteron-4-6 weeks,dosage unknown,immediately after Havoc
25mg clomid ED with 1 tab of anastroloze every 3 days for optimal test levels(within high end of normal range)
Raloxifene at 60mg to start while on Havoc (IU have little ralox on hand ATM) and 120mg for 9-12 months.

All the while b/f would be low (10-12%,which is low for me),calories cycled to average out in a deficit with Napalm applied to pecs ED.


I intend on long term clomid/ana usage for TRT so that would not be dropped,the SERM usage may also help prevent rebound after the ralox is dropped a year down the line.

I'd rather not have surgery done.

its been long time since I researched that. ancedotally in my hamster AAS induced gyno went away. I belive its the differnence between prolifferation and differntiation.

With Masteron I did 50mg ED. I did not expect gyno reduction, thats not the reason I took mast. My gyno WAS from pubertal growth. (and general fat-assness) I noticed incredible gyno reduction.

Surprising result and surprising dosage as well.Dashforce dropped me a little knowledge via PM,which does not jive with such a high dosage of masteron,50mg injectible masteron per week is what is researched to work on gyno.

Let me get this straight,you injected 50mg masteron every day(and for how long)?

Can you expound on the gyno reduction i.e.was it estrogen mediated (soft)fat or more mammory(hard lumps,pointy nips) gland tissue?

It looks like proviron would be better suited to those with my pseudo and Dasforce apparently agrees:



"Hey man, I really think you're mistaking my recommendation of "Masteron" for "Mesterolone." The compounds are similar (but NOT the same) and are reported to have similar effects, but masteron is injectable DHT, the one in the study I sent you (used at 50 mg / wk), aka drostanolone propionate / dromostanolone propionate. That's the one with the research that I know of.


A quick pubmed search of mesterolone yields a few results, but I don't see anything to do with gyno/mammary cell function. However, it should still work well as a hardening agent / antiestrogen, and your pseudo-gyno fat should be most responsive to this type of therapy, I would think. It's my guess that your gyno has more to do with estrogen-mediated fat deposition patterns than actually mammary tissue, and Anabolics 2006 seems to praise mesterolone for its benefits in this area (recommends it strongly for women looking to firm up the areas that estrogen fucks up their fat deposition).

Llewellyn recommends 25-100 mg daily for men. As I said, the masteron (DHT) injectable was 50 mg/wk, but who really knows how that translates to mesterolone/proviron (DHT-like), which is oral. My best guess would be to start in the middle and see how that does -- 25 mg morning, 25 mg night. Just a guess, though. Don't mistake me trying to help you out here for me actually knowing WTF I'm talking about, as I know little about proviron."

Yeah sorry for being short on the info. Yes, I had Masteron Prop. I ran a EQ, Test Prop, and Masteron cycle. I ran 50mg Mast ED (or 75 EOD if i got busy) this was an 8 week cycle. Like I said I was not running Mast for its gyno reduction. I believe some was estrogen mediated from insufficient PCT earlier in life. The majority I would say was mammory. I used to have to wear two shirts, one tight fitting undershirt and one normal. Now I can wear one shirt and not look like I need a bra!

I strongly disagree. They most likely had bad surgeons.

Sorry for the redundancy but just to confirm:

Your gyno mostly fell into the category of hard tissue /lump/pointy nipple and not fat in an overly abundant/disproportionate estrogenic appearance on your chest?

Are you saying that you injected the masteron on a daily basis and did not take it orally ED?

LOL, I was a fat kid all my life... I ALSO screwed up on an AAS cycle, I had not PCT. So, I am sure it was both. But i had pointy nipples and and abundance of tissue.

Yes I injected 50mg daily or 75 every other day depending on if i worked a 24hr or longer shift.

I'm in a similiar situation/background as yourself but lack any hard tissue (discernable to my touch anyway) or pointy nipples.

Injectible epi + ralox would be ideal as that is easier as far as MPB acceleration is concerned.

Failing that,my stack outline as above with proviron as the sole AAS (havoc as a lead in) is what I will go with.

I would also recommend masteron over proviron.

Agreed...



Why? Longer half-life?



Looks like JBarna might have a point -- as a propionate ester, Masteron should have a half life of only a few days. Maybe multiple injections weekly would be ideal, as once/week (as in the attached study) would probably bring plasma levels down very far (close to zero) between injections.

EDIT: attached study shows results for epitiostanol (the injectable mother of havistane, pretty much unsourceable, as far as I'm concerned) 10 and 20 mg/week, and masteron 50 mg/week on gyno, over 10 weeks IIRC).

Someone finally agreed with me? Hell ya. 2 points for me! I have been waiting on this moment all my life...

Epi powder is available from Chinese suppliers/web sites but not to private individuals apparently so it may as well be unsourceable.

Subcutaneous injections would probably allow one to get away with 2 shots per week whilst maintaining peak plasma levels,in theory anyway.

http://www.avantlabs.com/forum/index.php?showtopic=23794

Any thoughts on using both 50mg masteron per week and 50mg mesterolone ED for 8 weeks?

The former split into 2 injections per week and the latter being split between an AM and PM dose.

Along with ralox on cycle and post for months afterward while running havoc at 20mg ED for 3 weeks beforehand?

I'd much rather go all out and deal with worsesides (aggravation of my MPB being my chief concern) once as opposed to having to do another cycle,of either one of them alone with ralox.

Liver values would be tasted halfway in other than that I see no plausible reason not to use both,hedging my bets.

It may seem redundant but as my gyno is of questionable nature and origin(pubertal to begin with but aggravated by test e and dutasteride usage in the past) and both masteron and proviron have distinct advantages towards the two different categories of gyno I have to wonder why not.

I would do strong androgenics topically, it really doesn't matter which ones IMO. if this doesn't get your gyno down only surgery can.

Son of a bitch.. can't find where dashforce posted a study conccluding that if your can eliminate estrogen in the mammaries cell apoptosis occurs.. Anyhow, I suggested a suicide inhibitor plus a topical AE. But it looks like attacking IL-6 might help in the fight against estrogen in the tata's.

Experimental Therapeutics



British Journal of Cancer (2003) 88, 630-635.
doi:10.1038/sj.bjc.6600785

Inhibition of IL-6+IL-6 soluble receptor-stimulated aromatase activity by the IL-6 antagonist, Sant 7, in breast tissue-derived fibroblasts

A Purohit1, A Singh1, M W Ghilchik2, O Serlupi-Crescenzi3 and M J Reed1

1Endocrinology and Metabolic Medicine, Faculty of Medicine, Imperial College, St Mary's Hospital, London W2 1NY, UK

2The Breast Clinic, Central Middlesex Hospital, Acton Lane, Park Royal, London NW10 7NS, UK

3Department of Immunology (LABIO), Sigma-Tau S.p.A., Via Pontina Km 30,400, 00040 Pomezia (RM), Italy



Correspondence to: Professor MJ Reed, E-mail: m.reed@ic.ac.uk

Received 15 August 2002; revised 25 November 2002; accepted 28 November 2002



Interleukin 6 (IL-6) and its soluble receptor (IL-6sR) can markedly stimulate aromatase activity in cultured fibroblasts derived from normal or malignant breast tissues. IL-6 acts by binding to a low-affinity membrane-spanning receptor (IL-6R), which must associate with a high-affinity receptor (gp130) for signal transduction to occur. Sant 7 is a mutated form of IL-6 that can bind to the IL-6R, but inhibits its ability to interact with the gp130 signal transducing protein. In this study, we have used Sant 7 to examine its ability to inhibit IL-6+IL-6 soluble receptor (IL-6sR)-stimulated aromatase activity in breast tissue-derived fibroblasts. As previously observed, IL-6+IL-6sR markedly stimulated aromatase activity (7.7-20.8-fold) in fibroblasts derived from reduction mammoplasty tissue, tissue proximal to tumours and breast tumours. Sant 7 inhibited basal aromatase activity in some fibroblasts by 25-30% that had a high basal activity, but almost completely blocked the ability of IL-6+IL-6sR to stimulate aromatase activity. The IC50 for the inhibition of IL-6+IL-6sR-stimulated aromatase activity by Sant 7 was 60 ng ml-1. A comparison of the effects of prostaglandin E2 (PGE2), which can also regulate aromatase activity, and IL-6+IL-6sR revealed a greater degree of aromatase stimulation by IL-6+IL-6sR. Sant 7, however, inhibited PGE2-stimulated aromatase activity by 70% suggesting that PGE2 acts, in part, by stimulating IL-6 production. Much of the IL-6 and IL-6sR available to stimulate breast tumour aromatase activity may originate from infiltrating macrophages and lymphocytes. The ability to block aromatase stimulation by these factors may offer a novel therapeutic strategy for reducing oestrogen synthesis in breast tumours.


add androgenic compunds and we have no moobs. I'd like that very much.

The study you're referring to was originally posted by Darius in his Gynecomastia: your days are numbered thread, 1st page. I've reposted it in a few other threads.

Immunology has some powerful implications in.... well everything. It's just way too complicated for my dumb ass.

Andractim seems to be the topical of choice for this purpose.

Super cool shit

I'll have a log with pictures up sometime in the next couple months.

Strong androgens (andractim being king of these) would be good if I did in fact have AAS induced gyno or more accurately worded,puffy nipples and/or hard mass present.

My gyno is pubertal in nature but compounded by AAS usage as well as Dutasteride usage (at an earlier time from the AAS).

In short,I have both varieties of "gyno"-estrogen mediated adipose and (possibly) mammory gland tissue.I have no hard mass present.

Proviron would deal with the soft tissue and masteron would deal with the hard tissue,I cannot see them failing to live up to the efffect of Andractim.If anything,the two together would offer me better results,in my specific case.

A guy like Dashforce would probably do better than I with Andractim than either masteron and certainly better than Proviron(Proviron being likely useless in his case).He has no disproportionate fat tissue on his chest as I do.

Also,if I'm going to deal with side effects (hair loss) that is unavoidable from any DHT related compound I'd rather use something that will increase nutrient partitioning (masteron+proviron stacked) than Andractim,which will have no effect whatsoever in that regard.




Basically,how would liver toxicity be effected (assuming my liver is in relatively good condition now) by using proviron (50mgED) +masteron (50mg weekly)for 10 weeks with Havoc at 20mg for 3 weeks beforehand?

you mean toxicicty to the liver right? not toxicity of liver. standatd protection regimen of NAC, Milk Thistle, fish oil, maybe Sam-E, Lecitin/PPC would suffice.
Why not use topical? stop pounding on partiotioning agents.

considering this is all brotelligence and theories I think you should go with which ever is more readily available and log it as you go. Who knows... maybe my hampster will be interested as well.

FUCK ME RUN'N!

Effect of conjugated linoleic acid on bovine mammary cell growth, apoptosis and stearoyl Co-A desaturase gene expression.Keating AF, Zhao FQ, Finucane KA, Glimm DR, Kennelly JJ.
Department of Agricultural, Food and Nutritional Sciences, University of Alberta, Edmonton, Alberta, Canada T6G 2E1; Department of Animal Science, University of Vermont, Burlington, VT 05401, USA.

The effects of the primary biologically active conjugated linoleic acid (CLA) isomers (cis-9, trans-11 and trans-10, cis-12; 15-150muM) on growth and survival of the bovine mammary cell-line, Mac-T, were evaluated using cell enumeration and TUNEL assay. Previous studies have shown that high concentrations of CLA induced severe milk fat depression and have had negative effects on milk yield and composition whereas the impact of lower doses has been a modest depression in milk fat percent. In this study, we show that increasing concentrations of both CLA isomers had negative impacts on cell growth, including reduced cell number at concentrations of 35muM and above (P<0.05) and a two-fold increase in induction of apoptosis in the mammary cells. Changes in cell morphology occurred with large vacuole-like structures in the cytoplasm, nuclear shrinkage and changes of nuclear shape to kidney shape. Insulin did not significantly affect apoptosis in CLA-treated cells. In addition, the effect of increased doses of CLA and the interaction of CLA and insulin on the bovine stearoyl Co-A desaturase (Scd) gene promoter was also analyzed. While a significant difference in the Scd promoter transcriptional activity was not observed in cells treated with different concentrations of CLA, insulin significantly enhanced Scd promoter activity in CLA-treated cells. Our in vitro data support the hypothesis that high levels of CLA may induce in vivo apoptosis in the mammary gland.

PMID: 17959332 [PubMed - as supplied by publisher]

liorrh - how close are our mammaries to cows?

Mice as well:

Conjugated linoleic acid induces mast cell recruitment during mouse mammary gland stromal remodeling.Russell JS, McGee SO, Ip MM, Kuhlmann D, Masso-Welch PA.
Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.

Conjugated linoleic acid (CLA) is a dietary chemopreventive agent that induces apoptosis in the mammary adipose vascular endothelium and decreases mammary brown adipose tissue (BAT) and white adipose tissue (WAT). To determine onset and extent of stromal remodeling, we fed CD2F1/Cr mice diets supplemented with 1 or 2 g/100 g mixed CLA isomers for 1-7 wk. BAT loss, collagen deposition, and leukocyte recruitment occurred in the mouse mammary fat pad, coincident with an increase in parenchymal-associated mast cells in mice fed both levels of CLA. Feeding experiments with purified isomers (0.5 g/100 g diet) demonstrated that these changes were induced by trans-10, cis-12 CLA (10,12-CLA), but not by cis-9, trans-11 CLA (9,11-CLA). This stromal remodeling did not require tumor necrosis factor (TNF)-alpha, a major cytokine in mast cells, as TNF-alpha null mice demonstrated collagen deposition, increased leukocytes, and BAT loss in the mammary fat pad in response to 10,12-CLA. To test the hypothesis that mast cells recruited in response to 10,12-CLA were required for stromal remodeling, Steel mice (WBB6F1/J-kit(W)/kit(W-V)), which lack functional mast cells, were examined for their stromal response to 10,12-CLA. Both wild-type and Steel mice showed a significantly increased leukocytic adipose infiltrate, collagen deposition, and decreased adipocyte size, although BAT was maintained in Steel mice. These results demonstrate that 10,12-CLA induces an inflammatory and fibrotic phenotype in the mouse mammary gland stroma that is independent of TNF-alpha or mast cells and suggest caution in the use of 10,12-CLA for breast cancer chemoprevention.

PMID: 17449582 [PubMed - indexed for MEDLINE]

obviously this is suggesting the old theory that we need the right isomers to prevent mast accution, BUT I think I'd risk acrewing a mast (low risk mind you) in lue of killing my tit cells.

here we have a case of human cancer cells (MCF-7)

[Effect of apoptosis in human mammary cancer (MCF-7) cells induced by cis9, t11-conjugated linoleic acid][Article in Chinese]


Liu J, Chen B, Yang Y, Wang X.
Public Health College, Harbin Medical University, Harbin 150001, China.

OBJECTIVE: To determine the effect of cell apoptosis induced by c9, t11-conjugated linoleic acid was investigated in human mammary cancer cells (MCF-7), which were treated with various c9, t11-CLA concentrations (25, 50, 100 and 200 mumol/L), with a negative control. METHODS: In this study, the methods of the curve of cell growth, cell apoptosis detecting in fluorescent and electronic microscope and flow cytometry, and expression of p53 protein were employed. RESULTS: The cell growth of MCF-7 cells was inhibited by c9, t11-CLA. Eight day after treatment with various concentrations of c9, t11-CLA, as mentioned above, the inhibition rates were -6.0%, 45.2%, 99.0% and 99.4%, respectively. Apoptotic cells of morphology from MCF-7 cells treated by different concentrations of c9, t11-CLA were observed by fluorescent and electronic microscope and the frequency of apoptosis in MCF-7 cells by flow cytometry showed increasingly with concentrations of c9, t11-CLA increased. While the expression of p53 protein in MCF-7 cells was decreased with the doses of c9, t11-CLA increased. CONCLUSION: c9, t11-CLA can induce the effect of apoptosis in MCF-7 cells and its may be one of mechanisms for the inhibitory effect of c9, t11-CLA in human cancer cells.

PMID: 15098480 [PubMed - indexed for MEDLINE]





ok guys, forgive me if this has already been dicussed as I know CLA has been POUNDED into the wall and I don't want to resurrect that whole fiasco once again BUT I just got into research gyno and I'm learning a shit ton each day. I'd rather make myself look like a dickweed than NOT post this shit up as it's a good find.

the abolishment of ignorance is always an enlightening experience.

again, sorry to prattle on blind here but... I'm getting a woody. I'll be including CLA in my anti gyno struggle from now on...


Conjugated linoleic acid inhibits proliferation and induces apoptosis of normal rat mammary epithelial cells in primary culture.Ip MM, Masso-Welch PA, Shoemaker SF, Shea-Eaton WK, Ip C.
Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, New York, 14263, USA. mip@sc3101.med.buffalo.edu

The trace fatty acid conjugated linoleic acid (CLA) inhibits rat mammary carcinogenesis when fed prior to carcinogen during pubertal mammary gland development or during the promotion phase of carcinogenesis. The following studies were done to investigate possible mechanisms of these effects. Using a physiological model for growth and differentiation of normal rat mammary epithelial cell organoids (MEO) in primary culture, we found that CLA, but not linoleic acid (LA), inhibited growth of MEO and that this growth inhibition was mediated both by a reduction in DNA synthesis and a stimulation of apoptosis. The effects of CLA did not appear to be mediated by changes in epithelial protein kinase C (PKC) since neither total activity nor expression nor localization of PKC isoenzymes alpha, beta II, delta, epsilon, eta, or zeta were altered in the epithelium of CLA-fed rats. In contrast, PKCs delta, epsilon, and eta were specifically upregulated and associated with a lipid-like, but acetone-insoluble, fibrillar material found exclusively in adipocytes from CLA-fed rats. Taken together, these observations demonstrate that CLA can act directly to inhibit growth and induce apoptosis of normal MEO and may thus prevent breast cancer by its ability to reduce mammary epithelial density and to inhibit the outgrowth of initiated MEO. Moreover, the changes in mammary adipocyte PKC expression and lipid composition suggest that the adipose stroma may play an important in vivo role in mediating the ability of CLA to inhibit mammary carcinogenesis. Copyright 1999 Academic Press.

PMID: 10388518 [PubMed - indexed for MEDLINE]

Nice,I'll start on CLA as of today.I've got a bottle left over from 3 years ago which I chucked in my freezer after losing interest in CLA for fat loss.


As far as the prolactin angle is concerned,here's something I came across:




Prolactin
Int Clin Psychopharmacol 1987 Apr;2(2):97-102

The influence of S-adenosylmethionine (SAM) on prolactin in depressed patients.

Thomas CS, Bottiglieri T, Edeh J, Carney MW, Reynolds EH, Toone BK

Twenty subjects entered a double-blind placebo-controlled trial of SAM in
depression. Prolactin concentrations were measured before and after 14 days'
treatment. There was a highly significant fall in prolactin concentrations in
the SAM-treated group.

OR/AND

J Psychiatr Res 1990;24(2):177-84

Neuroendocrine effects of S-adenosyl-L-methionine, a novel putative
antidepressant.

Fava M, Rosenbaum JF, MacLaughlin R, Falk WE, Pollack MH, Cohen LS, Jones L,
Pill L

Clinical Psychopharmacology Unit, Massachusetts General Hospital, Harvard
Medical School, Boston 02114.

S-adenosyl-L-methionine (SAMe), a putative antidepressant, is a naturally
occurring substance whose mechanism of action is still a matter of speculation.
It has been recently postulated that SAMe may increase the dopaminergic tone in
depressed patients. Since dopamine inhibits both thyrotropin (TSH) and
prolactin secretion, we investigated the effects of treatment with SAMe on the
TSH and prolactin response to thyrotropin-releasing-hormone (TRH) stimulation
in 7 depressed outpatient women (mean age: 46.1 +/- 7.2 years) and 10 depressed
outpatient men (mean age: 38.0 +/- 10.0 years) participating in a six-week open
study of oral SAMe in the treatment of major depression. At the end of the
study, there was a significant reduction after treatment with SAMe in the
response of both prolactin and TSH to TRH stimulation in the group of depressed
men compared to pre-treatment values. On the other hand, in the group of
depressed women, the posttreatment prolactin response to TRH did not appear to
change when compared to pre-treatment and the TSH response to TRH challenge
tended even to augment slightly after treatment with SAMe. Our results, at
least in depressed men, seem to support the hypothesis of a stimulating effect
of SAMe on the dopaminergic system.

what's the easiest/strongest way to increase dopamine levels? I don't have to time research it now, but I'll be back. We're fuck this gyno up.

Bromocriptine is a potent dopamine agonist but I'm unsure as to where it fits into gyno.

I remember Viator posting that he spoke with two endocronologists and both said that prolactin was the cause of pubertal induced gyno though.

Pubertal gyno responds to androgens.

Of course,I wasn't suggesting otherwise.

I'm just saying that prolactin may play a signifigant role that we are unaware of yet.

Bromo is used to treat hyperprolactinemia.

Quote Lyle in Bromocriptine:

A final, and less polite possibility is that hardcore male bodybuilders are just a
bunch of pansies. Considering the role of prolactin in promoting maternal behavior in
females (74) along with the increases in estrogen and progesterone (the
stereotypically ’female’ hormones) following a steroid cycle, this third conclusion may
not be too far off. High levels of ’female’ hormones after a cycle, along with depressed
testosterone levels, may be turning hardcore male bodybuilders into a bunch of
wimps. Perhaps bromocriptine, in conjunction with other post-cycle drugs, can help
them find their testicles again.
I should mention that there is an increasing belief on these same boards that
prolactin is the root cause of gyno (i.e. bitch-tits, an overdevelopment of breast tissue
in males). Like so many elements of bodybuilding lore, this is incorrect even if it
sounds sciency and cutting edge. Prolactin’s primary role is to promote fat storage
and milk production in already existing breast fat (41). Prolactin is especially potent in
this regard, stimulating fat storage in breast fat cells which have been ’primed’ by
estrogen first.
But the fat cells have to be there in the first place and most lean men don’t have
a lot of fat cells in the chest area. Development of fatty tissue in the breast (i.e. an
increase in the number of fat cells, called adipogenesis or fat-cell hyperplasia) in men
is under the control of estrogen and progesterone, just as in women. This is why
gyno is a common occurrence during puberty (where estrogen/progesterone levels in
men can become abnormally high) and in pot smokers (smoking pot raises estrogen
levels).
While high levels of prolactin may promote fat storage in the fat cells which
develop, estrogen and progesterone are still the primary culprits in initiating the
process of developing gyno. As such, the typical cocktail of anti-estrogens and/or
progesterone blockers are still the best approach to avoid developing gyno from
steroid use. Blocking prolactin with bromocriptine is missing the point of what s really
causing the gyno.

prevention and apoptosis of what's already there are two different things entirely, that said I think that's a very useful post and I thank you for it. Bromo as Colin said is a dopa agonist which is what i was looking for. If lyle is sporting it as an anti gyno suggestion while on cycle we've gotta be barking up the right tree here folks.

Proviron and/or masteron
ralox or letro (apparently preferable ralox from what i understand)
CLA
bromo
andrictim

anti gyno stack of aphrodite, Goddess of nipples.

Why include andractim when masteron and proviron are both in use?

That would work out to introducing a hell of a lot of DHT into the body,two compounds should suffice.Maybe a lower dose of Andractim once per day alternated with Napalm all other application (12 hour interval) times would be helpful but I'm not sold nor overly fond of using 3 DHT based compounds at once.



Nightop has posted that GTE should be included in a gyno reduction cycle,I can't remember why but the study below indicates that GTE's effect is enhanced when NAC is added.This is a study involving cancer and not mammory glands but even so:



Free Radic Biol Med. 2007 Dec 23 [Epub ahead of print]

N-Acetylcysteine enhances the lung cancer inhibitory effect of epigallocatechin-3-gallate and forms a new adduct.

Lambert JD, Sang S, Yang CS.

Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA.The major tea polyphenol, (-)-epigallocatechin-3-gallate (EGCG), inhibits carcinogenesis in many in vivo models. Many potential mechanisms of action have been proposed based on cell line studies, including prooxidant activity. In the present study, we studied the effect of N-acetylcysteine (NAC) on the inhibitory effects of EGCG on lung cancer cell growth. We found that NAC (0-2 mM) dose dependently enhanced the growth inhibitory activity of EGCG against murine and human lung cancer cells. The combination of NAC and EGCG caused an 8.8-fold increase in apoptosis in CL13 mouse and H1299 human lung cancer cells compared to treatment with either agent alone. Addition of 2 mM NAC increased the stability of EGCG in the presence of CL13 cells (t(1/2)=8.5 h vs 22.7 h). Intracellular levels of EGCG were increased 5.5-fold by the addition of 2 mM NAC. HPLC and LC-MS analyses of cell culture medium from CL13 cells treated with EGCG and NAC for 24 h revealed that EGCG-2'-NAC was time dependently formed. This adduct was not formed in the absence of NAC. The present results show that under cell culture conditions, EGCG and NAC interact to form a previously unreported adduct, EGCG-2'-NAC, which may contribute to enhancement of EGCG-mediated cell killing.

PMID: 18206665 [PubMed - as supplied by publisher]

overkill? Absolutely. I was simply stating the mother of all antigyno stacks that we've compiled thus far.

I'd imagine GTE + NAC would only enhance any results seen from CLA to induce apoptosis.

Amphetamine baby.

Amphetamine would be a bad idea,stimulants in general should be avoided while undertaking a gyno reduction cycle and that is one of the harshest choices available.

D-Termine has stated he has had excellent results with transdermal application of various AAS powders and as I hate needles I'm interested in using masteron transdermally.

I would guess that Nutraplanet's Penetrate to be the carrier,any thoughts as to wether Masteron would be just as efficient transdermally as if injected?

I was looking at twice weekly injections of masteron and would probably be applying a transdermal mast solution twice per day instead.If there is any likelihood of diminished effect via transdermal application I'll deal with pinning myself but...ugh.

I was only joking as far as amphetamine goes mate!

OK, I don't know anything about transdermals but - why use an esterified hormone for transdermal delivery? Masteron-no-ester would probably be more soluble in Penetrate anyway.

I wonder if the lipderm ultra carrier (minus the carbomer) might be better for an esterified hormone, unless Penetrate's octyl salicylate turns the trick.

Solubility?:

2a-methyl-dihydro-testosterone propionate
Molecular Weight: 360.5356
solubility ethanol: 10 mg/mL
45% (w/v) aq 2-hydroxypropyl-β-cyclodextrin: 4.4 mg/mL
H2O: insoluble

It is practically insoluble in water, soluble 1 in 6 of ethanol, 1 in 4 of acetone, 1 in 20 of ethyl oleate, and 1 in 30 of propylene glycol.

Penetrate Ingredients: Isopropyl alcohol, propylene glycol, ocytl salicylate, triglyceride complex, water, d-limonene

Lipoderm ultra: Benzyl Alcohol, Water,Isopropyl Alcohol. Triglyceride Complex,n-Methyl-2-Pyrrolidinone, Laurocapram,l-Methanol,and Carbomer.

lipoderm-Y: Isopropyl Alcohol.Benzyl Alcohol, Water,Triglyceride Complex,n-Methyl-2-Pyrrolidinone, Laurocapram,l-Methanol,and Carbomer

An enzyme breakdown inhibitor is always the strongest way.

this is pushing the limit is it not?

Anything with an MW of 700 or lower can be used transdermally (the smaller the better, obviously), but solubility is also a factor.

Thinking some more about this, prop ester (vs. the base hormone) might be a best of both worlds in terms of solubility in the carrier and "solubility" in the skin. Localized activity may still suffer though.

from meso:


Substance name
Mesterolone [USAN]
Chemical name Androstan-3-one, 17-hydroxy-1-methyl-, (1alpha,5alpha,17beta)-
Systematic name IUPAC: (1S,5S,8R,9S,10R,13S,14S,17S)-17-hydroxy-1,10,13-trimethyl-1,2,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydrocyclopenta[a]phenanthren-3-one
CAS number 1424-00-6
Merck Index Number Merck 11, 5817
Chemical formula C20-H32-O2
Molecular weight [b]304.467 g/mol
Bioavailability
Metabolism Hepatic
Elimination half-life ?
Excretion Urinary: 90%; Fecal: 6%
Pregnancy category X
Legal status Illegal (US); DEA Schedule III (US)
Routes of administration Oral [/b]


hmmm... looks like it's even better likeyhood as far as molecular weight goes than test p. but... we already know it isn't soluable in alcohol. See D-termine's suspension thread. I think Jeff bumped it recently.