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Dbol causing prolactin related gyno???

Showy0023

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I feel like such a noob asking this but anyway:

I am using a test blend 400 mg/ml (250 mg long estered / 150 mg short) E5D. I am also taking 30 mg of dbol daily. I have been taking Exemestane (12.5mg ED) since I started. Over the weekend I started getting some painful lumps back under the nipples. I immediately bumped the exemestane to 25 mg/day and added parmi @ 0.25 mg/day. Does this sound like the right thing to do? The only other time this has happened was on a long test/deca cycle and the parmi worked wonders!!!! I find it very interesting that one can run a cycle (whatever it may be) and have no sides......then run the same cycle again and get sides!!!!

Thanks,

Showy
 
Had the same thing happen with Dbol. Still don't understand it, but I will avoid the Dbol for a while.
 
Yeah its weird..I am on a good anti-e. I have no oily skin / acne....no mood swings.....water retention is very mild. So I think I can rule out an estro surge. I am going to give the parmi a week to start working.
 
Great link Macro, never knew that.
Thank you.
 
I know that drol can cause prolactin related gyno. However, dbol from what I know does not. To the OP, try squeezing your nips and see if anything discharges. If so then it is prolactin related gyno, if not then it's probably estrogen related gyno which I'm willing to bet it is just from the compounds you mentioned.
 
I know that drol can cause prolactin related gyno. However, dbol from what I know does not. To the OP, try squeezing your nips and see if anything discharges. If so then it is prolactin related gyno, if not then it's probably estrogen related gyno which I'm willing to bet it is just from the compounds you mentioned.

I don't know about the op, but I experienced 'spontaneous lactation' from dbol. Felt a weird coolness, looked down, and noticed I had 'leaked' into my shirt. Yuck.
Surprised the heck out of me. It can happen...
:(
 
I appreciate the responses. It is definitely prolactin related. Woke up this morning after 2 days of treatment (parmi) and the tenderness / pain is almost gone!!!! Love this stuff.........just wish I knew that dbol could have caused this before hand!!!!
 
I was reading an article by big cat that said that estrogen related gyno can sometimes lactate so they get confused sometimes. But obviously don't take a chance.

Also, I got gyno from using dbol, even though I was running it w/ 1mg adex. I'm about to run some letro to get rid of it, but I've never had any issues with any other steroids giving me gyno, even without an AI.
 
I was reading an article by big cat that said that estrogen related gyno can sometimes lactate so they get confused sometimes. But obviously don't take a chance.

Also, I got gyno from using dbol, even though I was running it w/ 1mg adex. I'm about to run some letro to get rid of it, but I've never had any issues with any other steroids giving me gyno, even without an AI.

Do you have link to the article?

Thanks,

Showy
 
big cat fails to see the forest because of the trees. he is young, but that really is no excuse for someone that claims to be a scientist. (credentials are rather irrellevant within this sphere anyways, in all truth, since only recently have steroid receptor actions become vogue in research again. he makes child like errors in reasoning, like assuming that the increases in dopaminergic activity from androgens and progestins mean that they cannot cause prolactin issues. Sadly this is exactly the opposite excess dopamine is a common cause of prolactin issues.

he rants on an on about estrogen. yippee.... estrogen is everywhere, we all have had high level exposure at some point... we all have some extent of tissue development either from postnatal exposure or puberty (well all, is strong... most). he also makes erroneous conclusions about plasma hormone levels. just because plasma hormones are not elevated (and will have to disagree with his rather mistaken impressions on what is "elevated) does not mean that autocrine or local levels are not sky high or that the receptors are not upregulated or promoted yielding inordinate activity to plasma or local levels.

also have to take issue with the idea that, and not sure how this nonsense became accepted, male breast tissue acts and is essentially the same as female tissue (the idea that receptor expression and subtype are the same as with women--- just not at all the case). its similar and it can be relatively the same, but it certainly does not have to be.
 
Have taken OT many time with great size and strenth gains without as much water reten as dbol. No Sidessss!!! whatsoever

So OT can't convert to estrogen.....is there any chance it can cause prolactin related problems as talked about in this thread?

Thanks,

Showy
 
I was reading an article by big cat that said that estrogen related gyno can sometimes lactate so they get confused sometimes.

I don't understand the basis of such a claim. How could he know that some cases of male lactation are due exclusively to estrogen? To susbtantiate such a claim you would have to biopsy a gynecomastic breast and show that it does not express any prolactin receptors. Did "big cat" perform such a study or reference one that did?

Even as a conjecture this is highly questionable because all of the evidence suggests otherwise. Studies using knockout mice[1] indicate that lactation barely occurs (in females) in the absence of prolactin.

Histological studies show that estrogen receptor (ER) is expressed in the same breast tissue as prolactin receptor (PRLR)[2], namely in the epithelial cells that line the ducts and acini of mammary gland tissues. More relevantly, Gill et al (2001) found that gynecomastic breast tissue expressed PRLR and ER with expression of PRLR also in the epithelial cells' cytoplasm as opposed to just the lumina.

The sum of evidence [2] suggests that ER and PRLR are co-expressed and crossregulated and that decoupling occurs only in certain breast cancers. This suggests that lactation due exclusively to estrogen is highly unlikely.

The crossregulated nature of PRLR and ER may explain why using an AI or SERM will arrest some cases of male breast lactation (I know of at least one case where this has been the case) but this doesn't entail that prolactin was not implicated and that an equal or better response would not have been gained by using a dopamine agonist.
 
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those and a hundred other reasons. Yet people pick a position, as BC and others have, and defend it unto death.

have tried explaining how dopamine increases from AAS are prolactin suppressing at first, but thats only at first (time to shift varies, and there are lots of factors other than neurotransmitters at play). Since dopamine excess (and the norepinephrine excess that stims and AAS generally induce) will lead to greater toxic metabolite formation and over time damage tuberofundular dopamine neurons as well as other within the substantia nigra, leading to either poor prolactin suppression by dopamine or even prolactin release (since dopamine action in one area with out cocommitant action in another acts inductively).

do find it odd that these simple concepts as well as the extremely simple notion that suppression of progesterone and subsequent increased binding of progestins and androgens in general will produce effects that are quite unprogesterone like, and problematic when PgR inducers like tamoxifen are used (or that they might affect the promoters which can change tamoxifens action from antagonistic to agonistic or somewhere in between.

also a bit surprised at the deathlike grip with which they hold onto the "estrogen" theory of gynecomastia, or the fact that they fail to grasp that there are numerous non aromatase produced metabolites and xenoestrogen that can be present and also can affect promoters. of course then there is also the stubborn clinging to the idea (a rather ludicrous one) that expression of receptors and promoters within male breast tissue (induced often by a wide mixture of androgens, estrogens and progestins as well as numerous growth factors-- quite different than found in women) will produce tissue and receptor expression that is identical to females.


or perhaps most importantly that estrogen and tissue development have been present or occured for most people at one time or another during development (usually high level exposure to E as well as PRL--actually quite often more PRL) in the post natal and pubertal periods. SO even if sticking to the E must be present, well it was and if you have such tissue, it does attempt to sustain itself and can (because it produces locally higher levels of things like aromatase as well as growth factors, prostaglandins and PRL). So even if the must stick to E theory, realizing that local levels can be high even when plasma are not.


end of rant....
 
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Damn seems like a lot can increase prolactin. I think very high test doses will do it as well. As well as anadrol. I had no clue about eq though, I didnt think that converted to anything.
 
Damn seems like a lot can increase prolactin. I think very high test doses will do it as well. As well as anadrol. I had no clue about eq though, I didnt think that converted to anything.

Eq is subject to aromatization
 
Macro,
How long until Prami reaches a therapeutic level and begins to bring down Prolactin levels?
 

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