Possible gyno need help

jbryand101b said:
I've been very clear on what I was referring to regarding shut down.

I've never experienced limp dick with letro because I've always ran cialis and inhibit p with it.

Too much or too little estrogen will have a negative impact on libido. All aromatase inhibitors have this potential side effect.
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None like letro my brother.
 
jbryand101b said:
I didn't. I never went to medical school so I was unaware of the scientific term "dick shut down"

Though, nothing is wrong with the dick or its workings, just your libido.
Lots of ways to fix this.
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Yup. Take an anti-prolactin with a 19-nor to prevent prl gyno. Also, adex can leave the door wide open for rebound if a dose is missed.... Which is possible with our current OP.
 
Fzisn1 said:
Yup. Take an anti-prolactin with a 19-nor to prevent prl gyno. Also, adex can leave the door wide open for rebound if a dose is missed.... Which is possible with our current OP.
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I knew I had discussed this with Patrick Arnold a while ago, here is some info

bryan101b said:
someone posted a link to post written , no references or sources given, but thought i'd paste it to get pa's opinion.
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With use of 19-nor-testosterone compounds, such as trenbolone and nandrolone esters, there is a considerably high percentage of individuals who suffer from gynecomastia with galactorrhea (lactation from the nipple) and often times prolonged erectile dysfunction (ED). These are probably the most disturbing acute side effects experienced by the AAS user and bodybuilding enthusiast. The ED often lasts for over a year with little relief for the uniformed, although there are some drugs to combat these problems. There is still some mystery surrounding the exact cause of these side effects noted by users of the 19-nor compounds. In this article I will discuss what I think are the most likely mechanisms that lead to the above problems associated with these compounds and the best remedies for the side effects as well as strategies to avoid, minimize or mitigate them with use of these compounds.


19-nor compound Effects
Trenbolone and nandrolone, while classified as androgens, closely resemble the progestins as they have in common the absence of the 19 methyl present on the common precursor cholestane, which is the precursor of all steroid molecules in humans. Progestins are a group of synthetic compounds related to progesterone and are used therapeutically and in scientific research in the areas of fertility and cancer research. In estrogen primed tissue progestins are known to mediate breast development. Progesterone levels are known to correlate with prolactin secretion and progesterone receptor signaling is tied in with a signal transduction loop leading to the production of prolactin, an important protein hormone involved in gestational development of the breast as well as sexual function in both men and women. Due to the interaction of progesterone and prolactin with the tissues of the body the gestating woman takes on some necessary characteristics. Her breasts enlarge but do not secrete milk. The ovaries are altered and no longer secrete as much estrogen and switch primarily to progesterone secretion. Upon birth progesterone levels decline as the endometrium and sustaining tissues of the uterus are no longer needed. Once progesterone levels diminish lactation ensues under the direction of prolactin. Through the mechanoreceptors of the breast prolactin secretion is maintained and mother reaches a level of sexual satiation from prolactin's effects on sexual functions. A series of sex hormones including progesterone are maintained at a level that reduces FSH and LH resulting in continued suppression of ovulation.

Interestingly, there is a neuroendorcine link between dopamine secretion, progestins and prolactin secretion in the brain. In the arcuate nucleus of the hypothalamus there is a group of dopaminonergic neurons that are responsive to progesterones. Progenstins bind to neurons in this region and reduces dopamine secretion locally leading to increased prolactin secretion and decreased secretion of GnRH (and thus LH and FSH) into the hypophysial portal blood. This series of physiologic responses may explain the loss of sexual function in nandrolone and trenbolone users.

Bodybuilding and the Progesterone - Prolactin link

As stated above, progesterone signaling is correlated with increased levels of prolactin secretion from the anterior pituitary gland. Progesterone and progestins are strong suppressors of GnRH and therefore LH and FSH. Therefore, the presence of progestins like nandrolone or trenbolone could be expected to be strong HPTA suppressors in the male user. Prolactin is negatively regulated by dopamine and positively regulated by thyrotropin-releasing factor and other neuropeptides. The first compound and drugs that mimic it are important for mitigating the undesired side effects seen with use of the 19-nor androgens and these will be discussed later.

In some sense the male bodybuilder who uses 19-nor androgens has feminized his body to a similar state as that of a gestating or breast feeding woman. Much like the gestating woman his breasts begin to enlarge and may secrete a small amount of fliud. His gonads are atrophied and his LH and FSH are greatly diminished. Sexual activity is blunted as erections are far less frequent and he feels strangely satisfied as if he has achieved an orgasm recently but has not. These are the effects potentiated by the progestin like qualities of the 19-nor compound(s). How can this state be treated and, better yet, can this state be avoided while using 19-nor testosterone derivatives?

Many 19-nor androstane compounds, especially nandrolone, and their active metabolites are long lived and can go on causing problems far beyond the period of their use. So the effects of these progestin-like compounds can go on for many months. Although it is suspected that for instance nandrolone could bind to the progesterone receptor like its progestin cousins this is not known for sure. In fact it may induce progestogenic and estrogenic effects through interaction with the androgen receptor, although this mechanism is not understood. However, the overwhelming evidence as far as clinical presentation and response to therapy would indicate that prolactin is the end culprit in at least the sexual dysfunction side effects. As discussed previously, dopamine negatively regulates prolactin secretion. There are two effective medications that can mimic dopamine that have been used successfully and safely to control 19-nor associated side effects. These are bromocriptine and cabergoline. Both of these are ergot derivatives and potent D2 dopamine receptor agonists. These compounds will significantly reduce prolactin secretion. A dose of 2.5 mg/day for the former and 0.5 mg 2-3 times a week for the later seems to be effective doses. Another important observation is that breast tissue must be estrogen sensitized for progesterone / prolactin induced development and lactation to occur. Therefore it may be useful to include a mild dose of aromatase inhibitor when using these compounds.

Post Cycle Therapy for 19-nor Compounds

The bottom line is that after a drug regimen that includes these compounds the user will likely be severely HPTA suppressed. Unlike other compounds the 19-nor compounds have the added nuisance of long lived metabolites that appear to be active toward GnRH suppression and prolactin secretion. Therefore, the goal in a 19-nor androstane PCT will be aggressive in starting the HPTA with the added problem of suppression of prolactin secretion. The HPTA should be attacked on two fronts to include the testes and the hypothalamus. HCG will be used to mimic LH and FSH and a SERM such as tamoxifen and or clomiphene will be used. In addition, to control prolactin secretion, either bromocriptine or cabergoline will be added. A PCT to treat 19-nor compound use might look like the strategy outlined below.


Week

Minus 2-0 HCG 500 U EOD
0-6 Clomid 50 mg
3-8 Nolvadex 20 mg
Throughout Cabergoline 0.5 mg EOD


Other comments

Cabergoliner should be used throughout the cycle at 2 x per week at 0.5 mg to mitigate prolactin effects during 19-nor compound use. HCG can also be used at 250-500 U 2x a week intermittently throughout the cycle as well.
An aromatase inhibitor should also be used during 19-nor use and dose adjusted to the androgens used.
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For the op ill share my discussions with pa, have to dig back to 2011 though.:

Patrick Arnold said:
nandrolone itself actually is quickly metabolized and eliminated

when it is injected in the form of the decanoate however it is very fat soluble so that ester can deposit in fatty tissues and stick around for a long time - slowly releasing nandrolone over weeks and months
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bryan101b said:
figured i'd start a thread hoping for some data based info, or as much as we can find.

here is what i got to start with:

Hyperprolactinaemia, or excess serum prolactin, is associated with hypoestrogenism (and it looks like also could be low testosterone as well?)

Hyperprolactinemia can result from: (a list of things, this stuck out from pa's recent write up on thyroid hormones and steroids in md)

Excess thyrotropin-releasing hormone (TRH), usually in primary hypothyroidism

so im not sure, i can speculate all day, but thought this may be a good place for me, and others to begin researching for what they can.

thoughts, or opinions on this subject?
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Patrick Arnold said:
hyperprolactinemia will cause HPTA suppression which will then lower production of sex steroids (estrogen, testosterone, etc)

its important to remember the cause and effect here, or we can easily reach false conclusions
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More data courtesy of pa:
Patrick Arnold said:
how about this

1) Peripheral (hormonal) actions
The peripheral actions of oxytocin mainly reflect secretion from the pituitary gland. (See Invalid Link Removed for more detail on its action.)
  • Invalid Link Removed - in Invalid Link Removed (Invalid Link Removed) mothers, oxytocin acts at the Invalid Link Removed, causing milk to be 'let down' into Invalid Link Removed Invalid Link Removed, from where it can be excreted via the Invalid Link Removed
2)

De Jager N, Hudson NJ, Reverter A, et al. Chronic exposure to anabolic steroids induces the muscle expression of oxytocin and a more than fifty fold increase in circulating oxytocin in cattle. Physiol Genomics. Invalid Link Removed

Molecular mechanisms in skeletal muscle associated with anabolic steroid treatment of cattle are unclear and we aimed to characterise transcriptional changes. Cattle were chronically exposed (68 ± 20 days) to a steroid hormone implant containing mg Invalid Link Removed acetate and 20mg estradiol (Revalor-H). Biopsy samples from 48 cattle (half treated) from Longissimus dorsi muscle (LD) under local anaesthesia were collected and gene expression levels were profiled by microarray, covering 44 unique bovine genes. One hundred and twenty one genes were differentially expressed (DE) due to the implant (99.99% posterior probability of not being false positives). Among DE genes, a decrease in expression of a number of fat metabolism associated genes, likely reflecting the lipid storage activity of intramuscular adipocytes, was observed. The expression of IGF1 and genes related to the extra-cellular matrix, slow twitch fibres and cell cycle (including SOX8, a satellite cell marker) was increased in the treated muscle. Unexpectedly, a very large 21- (microarray) to 97- (real time quantitative PCR) fold higher expression of the mRNA encoding the neuropeptide hormone oxytocin was observed in treated muscle, We also observed an ~50-fold higher level of circulating oxytocin in the plasma of treated animals at the time of biopsy. Using a co-expression network strategy OXTR was identified as more likely than IGF1R to be a major mediator of the muscle response to Revalor-H. A re-investigation of in vivo cattle LD muscle samples during early to mid-fetal development identified a > fold increased expression of OXT, coincident with myofibre differentiation and fusion. We propose that oxytocin may be involved in mediating the anabolic effects of Revalor-H treatment.
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Great article. I'm in the minority that can get away with prami i suppose, so I am curious why it wasn't mentioned. Another reasonI don't personally run caber, one in which I forgot about, was the fact that it's an ergot derivative and whether it holds true or not, I'm not running that when I get occasionally 5-paneled.

But I took that stuff serious (prami). I seriously started very low.... Like a 20th (1/20) of an iu in a 200 mcg/mL dosage. That's 10 micrograms. I don't recommend it because i know first hand of people who've been hospitalized bc of it but it works better for me.

I'll never use deca again, personally bc I find deca sides to be significantly greater than tren but that's just me.
 
RH2012 said:
i've read that bf contains aromatase. i've noticed that the skinny guys dont get gyno like the people with higher bf levels. bill phillips, aka butt plug lol, said that in MM2K magazine years ago. just mention it cause alot of peple who get gyno easy should seriously consider shedding some bodyfat.
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I mostly agree. I must be the proud owner of many receptors in my chest area though. At around 8% I was developing gyno. And my nipples have always been small and I never had any pubertal gyno or any sign of the possibility till I cycled the right stuff.
 
RH2012 said:
i've read that bf contains aromatase. i've noticed that the skinny guys dont get gyno like the people with higher bf levels. bill phillips, aka butt plug lol, said that in MM2K magazine years ago. just mention it cause alot of people who get gyno easily should seriously consider shedding some bodyfat.
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Aromatase lingers in fat for sure. I was single digits though.
 
its pretty hard to know what to properly do when you all write diffrent things
but yet you all say i shouldnt start with tren before the lumps are gone. so i will not.
instead i could continue my sustanon and add rexobol or oxymetholone 50mg ed for a few weeks extra?
how should my progress then look like?
letro or caber
armidex + nolva?
 
This is why I don't post research to back up things I say anymore.
People ask for the proof and when I post it, NO ONE ACTUALLY READS IT.

I dont keep a file with all the data I've read ( well, I do have some files on methylated steroids Henryv sent me) so I have to go and do the exact same research as that person could do.
But really searching for data based info isn't as easy as going to roidxxx.com/w/e
 
jbryand101b said:
This is why I don't post research to back up things I say anymore.
People ask for the proof and when I post it, NO ONE ACTUALLY READS IT.

I dont keep a file with all the data I've read ( well, I do have some files on methylated steroids Henryv sent me) so I have to go and do the exact same research as that person could do.
But really searching for data based info isn't as easy as going to roidxxx.com/w/e
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^+1
 
ok would this work?
1-4 1,25mg femera EOD
600mg b6 ed
5-6 40 mg nolva ed
7-8 if needed 20mg ed nolva
would this work?
i can not get my hands on prami or dostinex sadly:/

or is it a must that i do 2,50 mg ed of femera?
 
jbryand101b said:
Don't listen to him, he doesn't know what he's talking about.
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-If all you have are erect nipples and a small lump underneath, will Nolva and formeron suffice in pct to remove the gyno?
-I ask this as pct for me starts tonight, and it will take 2 weeks to receive the Lectro...should I order it and add it in in 2 or so weeks?
-what would the protocol be?
 
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