Progesterone and Prolactin

sethroberts

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I wrote a quick article on progesterone and prolactin. This is all I could think of at the moment but feel free to question and hopefully we can get a discussion going that will flesh this out. No cliffs -- you actually have to read it -- it is not that long.

There is much confusion, conjecture and bro’lore surrounding prolactin and progesterone and how to control them to avoid gynecomastia, loss of libido and shutdown. A lot of confusion surrounds the misconception that these two hormones are one in the same. They are, in fact, two totally different hormones, with two totally different mechanisms of action and totally different effect profiles in the body.

Prolactin is a peptide hormone of 199 amino acids that is similar in structure to growth hormone. Prolactin is produced in the anterior pituitary in cells called lactotropes. Prolactin is secreted in an episodic fashion throughout the day. Its secretion is inhibited by dopamine and stimulated by estrogen, stress, TRH, and other factors such as suckling and nipple manipulation. Prolactin acts through prolactin receptors present on the surface of cells. In the human, these receptors are stimulated by GH and prolactin with equal potency. Prolactin initiates and maintains lactation in the estrogen primed breast. Prolactin is not a growth factor in breast tissue which is why it is necessary for breast tissue to be primed by the growth promoting action of estrogen in order for prolactin to exert its effects. Even so, lactation is prevented in the presence of high levels of estrogen and progesterone, such as those that exist in pregnancy, and lactation only proceeds with a drop in estrogen/progesterone levels post delivery. Prolactin inhibits gonadotropin secretion and therefore suppresses the hypothalamic pituitary gonadal axis and the production of testosterone.

Progesterone is a steroid hormone that binds to intracellular progesterone receptors that act in the nucleus of cells. Progesterone is produced in males by the adrenal glands and males have the same plasma level of progesterone as women d o during the follicular phase of the menstrual cycle. There are actually two progesterone receptors. A functional receptor and a nonfunctional receptor that acts to suppress the activity of the functional receptor. Progesterone antagonizes the effect of estrogen by reducing estrogen receptor levels. This is exemplified by the use of progestins to fight estrogen responsive breast cancer. Progesterone has a potent suppressive effect on gonadotropin secretion and has been used as a contraceptive agent in men.

There is no evidence that controlling prolactin will prevent or treat gynecomastia. Many of the issues that are being attributed to prolactin can be explained through other mechanisms. While reducing prolactin may help with reduced libido and shutdown due to AAS, the potential risks involved with using dopaminergics to reduce prolactin levels probably outweighs the benefits. If estrogen is controlled during a cycle, then prolactin is unlikely to be elevated and unlikely to cause a problem.
 

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A great read, that certainly helped clear things up! thanks seth :)
 
crazyfool405

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seth,

my blood work on pplex mdrol bridge showed E2 lowered from 28 to 21 and prolactin levels raised,

what woulda caused this?
 
sethroberts

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seth,

my blood work on pplex mdrol bridge showed E2 lowered from 28 to 21 and prolactin levels raised,

what woulda caused this?

What else were you using (including supps) and how high were they elevated?
 
crazyfool405

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Nothing else was being used maybe some cissus that's it. Ill have to check the number it elevated to tho.
 
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Good info.

So high estrogen levels induces prolactin secretion ?

What is progestin ?

Do both PH and progesterone play a role in the development of gyno, or is it only prolactin levels?

Thank you sir.
 
crazyfool405

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prolactin went from 5.8 to 7 .3,

TSH ultra sensitive went from 5.92 to 4.77
T3 total went from .99 to .72
igf1 from 449 to 111
FSH from 2.8 to 1.3
LH from 2.8 to 2.6
Test from 501 to 36
E2 from 25 to 21

this is pre then on cycle results.
 
sethroberts

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prolactin went from 5.8 to 7 .3,

TSH ultra sensitive went from 5.92 to 4.77
T3 total went from .99 to .72
igf1 from 449 to 111
FSH from 2.8 to 1.3
LH from 2.8 to 2.6
Test from 501 to 36
E2 from 25 to 21

this is pre then on cycle results.
You didn't include units of measurement but I am ssuming that your range for prolactin was <25 is normal. An "increase" from 5.8 to 7.3 would not be considered clinically relevent since it is not outside the normal range and since the magnitude of change was within the range of diurnal variation. The change in IGF-1 levels is interesting but as I have stated elsewhere, plasma IGF-1 levels are generally not relevent towards building muscle. I am guessing that your SHBG levels were down and therefore your free estradiol was probably significantly elevated even though there was only a slight drop in total levels -- which could account for the slight increase in prolactin levels thoguh again, it could just be diurnal variation.

Your T3 decreased likely due to an increase in T3 uptake secondary to a decrease in TBG levels -- it is not known if phera and mdrol do this but it doeas occur with several other orals so based on your blood tests it seems likely that one or both of them does.
 
sethroberts

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Good info.

So high estrogen levels induces prolactin secretion ?

What is progestin ?

Do both PH and progesterone play a role in the development of gyno, or is it only prolactin levels?

Thank you sir.
Progestin is to progesterone as androgen is to testosterone. Progestin is the class, progesterone is the prototypical example.

In my opinion, neither progesterone nor prolactin play a significant role in most cases of gynecomastia -- just estrogen. (I assume the PH you are referring to somehow means progesterone?)
 
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Great summary of these Seth. I learned a lot, but now i just have more questions. I'm assuming this thread came about due to everyone and their brother taking "tren" orals? I have seen a lot of gyno questions with people mixing these up lately.

Could you please clarify that last post on progestin? Progesterone and prolactin are subcategories to it?

When gyno is accompanied by leaky nips it is most important still to control the estrogen buildup, because that is the main factor? Everyone seems to recommend caber in these cases.
 

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So the 'Trenadrol' and 1-t tren, or infact real treneblone which are 'progestins' which hormone do these actually increase?
 
Eric Potratz

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Great summary of these Seth. I learned a lot, but now i just have more questions. I'm assuming this thread came about due to everyone and their brother taking "tren" orals? I have seen a lot of gyno questions with people mixing these up lately.

Could you please clarify that last post on progestin? Progesterone and prolactin are subcategories to it?

When gyno is accompanied by leaky nips it is most important still to control the estrogen buildup, because that is the main factor? Everyone seems to recommend caber in these cases.
Progesterone
Nandrolone
Trenbolone

…. All “progestins” because of the chemical structure on the 17 position.

I want to comment on this thread real quick...

I see a clear reduction in gyno related symptoms when using an anti-prolactin based sups (vitex) during the use of progestin based anabolics. Although there may not be a published trial on bros preventing gyno with anti-prolactins from progestins… there is a clear connection.

I say be cautious and use Vitex during a progestin based cycle anyway, it will reduce the total mammary stimulation and help avoid the whole gyno problem.

-Eric
 
Eric Potratz

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So the 'Trenadrol' and 1-t tren, or infact real treneblone which are 'progestins' which hormone do these actually increase?
Im not sure on Trenadrol… (it might be the same 19-nor molecule we refer to as TREN, but Im not sure)

our "TREN" will convert to dienalone, which is very similar to Trenbolone. (its actually a chemical intermediate used in the manufacturing process)

Both of them are “progestins”…. But also very strong androgens.

-Eric
 
Mass_69

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I wrote a quick article on progesterone and prolactin. This is all I could think of at the moment but feel free to question and hopefully we can get a discussion going that will flesh this out. No cliffs -- you actually have to read it -- it is not that long.

There is much confusion, conjecture and bro’lore surrounding prolactin and progesterone and how to control them to avoid gynecomastia, loss of libido and shutdown. A lot of confusion surrounds the misconception that these two hormones are one in the same. They are, in fact, two totally different hormones, with two totally different mechanisms of action and totally different effect profiles in the body...

...Many of the issues that are being attributed to prolactin can be explained through other mechanisms. While reducing prolactin may help with reduced libido and shutdown due to AAS, the potential risks involved with using dopaminergics to reduce prolactin levels probably outweighs the benefits. If estrogen is controlled during a cycle, then prolactin is unlikely to be elevated and unlikely to cause a problem.
THANK YOU!! I have tried explaining the differences between these 2 hormones in the past and it drives me crazy how many threads there are that either use these 2 names interchangibly or assume that using a "progestin" steroids causes "prolactin sides." I've always preached that if you want to control "prolactin side-effects" to be sure and control estrogens.
 
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Progestin is to progesterone as androgen is to testosterone. Progestin is the class, progesterone is the prototypical example.

In my opinion, neither progesterone nor prolactin play a significant role in most cases of gynecomastia -- just estrogen. (I assume the PH you are referring to somehow means progesterone?)
Sorry, typo, i meant prolactin releasin hormone PRH not PH.

So if tren nor pplex aromatize, why in your opinion "some" users experience lactation with tren clones or pheraplex ?
It's confusing, no one really has a clear answer, i hope you do.
 
crazyfool405

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If progesterone antagonizes estrogen then why do we see kactation with deca and tren which are known progestins. Shouldn't if they are prigestins prevent lactaion and gyno?
 

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so seth,

in general, for those who are using progestins like tren, prodienelone, nandrolone, etc... what is the best ancilliary / support you could use to control estrogen? maybe a moderate AI like anastrozole? you stress controlling estrogen, but to what degree (and with what)?
 
crazyfool405

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I've even heard lactation with epi and superdrol as well. A lot of the 5a reduced steroids seem to cause that
 
Eric Potratz

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If progesterone antagonizes estrogen then why do we see kactation with deca and tren which are known progestins. Shouldn't if they are prigestins prevent lactaion and gyno?
Steroids or progestins may be doing a lot of things…

They may be increasing prolactin release from the lactotropes, they may be offsetting E2/E1 from the binding proteins, they may be down-regulating DHT to the point where estrogen and progesterone have no antagonism, ect…

Progestins can and do cause gyno whatever the reason may be… reducing prolactin helps reduce this occurrence, as well as reducing estrogen.

-Eric
 
Frank Reynolds

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Steroids or progestins may be doing a lot of things…

They may be increasing prolactin release from the lactotropes, they may be offsetting E2/E1 from the binding proteins, they may be down-regulating DHT to the point where estrogen and progesterone have no antagonism, ect…

Progestins can and do cause gyno whatever the reason may be… reducing prolactin helps reduce this occurrence, as well as reducing estrogen.

-Eric
But what is your feelings on using drugs like caber/Pramipexole for this?

Are you in agreement with Seth, that reducing estrogen will be enough to keep gyno away, while on these compounds?
 
crazyfool405

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i was on epi as well as npp, and test, i stopped the epi and im still on npp and test and within 24 hours, my gyno came back
 

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yea epi really does eat at estrogen... i'm one week on and can feel a reduction in my gyno, just about as small as its ever been.
 
sethroberts

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Great summary of these Seth. I learned a lot, but now i just have more questions. I'm assuming this thread came about due to everyone and their brother taking "tren" orals? I have seen a lot of gyno questions with people mixing these up lately.

Could you please clarify that last post on progestin? Progesterone and prolactin are subcategories to it?

When gyno is accompanied by leaky nips it is most important still to control the estrogen buildup, because that is the main factor? Everyone seems to recommend caber in these cases.
No, Progestin is a class of hormone of which progesterone belongs. Prolactin is not related in the least and actually belongs to a "class" of peptide hormones that includes GH.

When gyno is accompanied by leaky nips a clinically elevated prolactin level it would then be appropiate to control prolactin but we need to clarify what "leaky nip" are. Galactorrhea is pretty rare in men and even in those with hyperprolactinemia (high prolactin levels) it is still only present in about 50% of cases. Squeezing your nipples is not a good practice to get into. Nipple manipulation itself can cause discharge (1: J Adolesc Health Care. 1984 Jul;5(3):210-2. Benign galactorrhea/breast discharge in adolescent males probably due to breast self-manipulation.Rohn RD.). Truly leaky nips or lactation is unlikely (though not impossible) to occur in the absence of gynecomastia.

Profilactively treating with cabergoline or another drug for this purpose is a bad idea and may actually initiate the problem you are trying to solve by reducing dopamine sensitivity in galactotropes.
 
crazyfool405

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No, Progestin is a class of hormone of which progesterone belongs. Prolactin is not related in the least and actually belongs to a "class" of peptide hormones that includes GH.

When gyno is accompanied by leaky nips a clinically elevated prolactin level it would then be appropiate to control prolactin but we need to clarify what "leaky nip" are. Galactorrhea is pretty rare in men and even in those with hyperprolactinemia (high prolactin levels) it is still only present in about 50% of cases. Squeezing your nipples is not a good practice to get into. Nipple manipulation itself can cause discharge (1: J Adolesc Health Care. 1984 Jul;5(3):210-2. Benign galactorrhea/breast discharge in adolescent males probably due to breast self-manipulation.Rohn RD.). Truly leaky nips or lactation is unlikely (though not impossible) to occur in the absence of gynecomastia.

Profilactively treating with cabergoline or another drug for this purpose is a bad idea and may actually initiate the problem you are trying to solve by reducing dopamine sensitivity in galactotropes.
even dostinex 1 time a week just to keep the LH levels raised and possible prolactin controled?

i just take .5mg 1x per week in the middle of the week
 
sethroberts

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Progesterone
Nandrolone
Trenbolone

…. All “progestins” because of the chemical structure on the 17 position.

I want to comment on this thread real quick...

I see a clear reduction in gyno related symptoms when using an anti-prolactin based sups (vitex) during the use of progestin based anabolics. Although there may not be a published trial on bros preventing gyno with anti-prolactins from progestins… there is a clear connection.

I say be cautious and use Vitex during a progestin based cycle anyway, it will reduce the total mammary stimulation and help avoid the whole gyno problem.

-Eric
Actually, they are considered progestins because of the lack of a carbon at the C-19 position.

Vites has been shown to have estrogenic and progestational effects in addition to its prolactin lowering potential. With this mix of activities, it is difficutl to say what effect it is having and if it may be causing more harm than good.
 
sethroberts

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Im not sure on Trenadrol… (it might be the same 19-nor molecule we refer to as TREN, but Im not sure)

our "TREN" will convert to dienalone, which is very similar to Trenbolone. (its actually a chemical intermediate used in the manufacturing process)

Both of them are “progestins”…. But also very strong androgens.

-Eric
Dienolone is actually more similar to nandrolone than to trenbolone in terms of binding affinity (trenbolone = 134AR, 74PR, dienolone 134AR, 17PR, nandrolone 154AR, 20PR) especially towards the progesterone receptor. Additionally, whereas trenbolone does not convert to estrogen, nandrolone does and it is possible that dienolone does as well. They are all strong androgens. Being a chemical intermediate is irrelevent.
 
sethroberts

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Sorry, typo, i meant prolactin releasin hormone PRH not PH.

So if tren nor pplex aromatize, why in your opinion "some" users experience lactation with tren clones or pheraplex ?
It's confusing, no one really has a clear answer, i hope you do.
I am somewhat doubtful that these are true caes of lactation. If they do occur, then it is likely due to concurrent use of AI's which may suppress estrogen to the level where prolactin that is not clinically elevated may be able to stimulate lactation.
 
sethroberts

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If progesterone antagonizes estrogen then why do we see kactation with deca and tren which are known progestins. Shouldn't if they are prigestins prevent lactaion and gyno?
It depends, deca is not a strong PR binder and likely is a partial agonist. Partial agonists can have results that appear to be antagonistic depending on the environment in which they are acting. I also think the use of AIs may be contributing -- see above post. With Tren, you need to distinguish between trenbolone and the "tren" designers. The tren designers I have already explained above that thye are more similar to nandrolone. As I stated, I am somewhat skeptical of lactation claims but that doesn't mean that it isn't possible. As I stated above, the use of caber and others as well as the use of AI's may actually be instigiating these reports.
 
sethroberts

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But what is your feelings on using drugs like caber/Pramipexole for this?

Are you in agreement with Seth, that reducing estrogen will be enough to keep gyno away, while on these compounds?
I would caution against "reducing" estrogen as I do think that AIs may be partially to blame. "Controlling" estrogen is preferable and I am partial to SERMS for this purpose. Especially for non-aromatizing or low aromatizing compounds because the reduction in SHBG and the increased "free" estrogens will not be helped by AI's.
 
sethroberts

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i was on epi as well as npp, and test, i stopped the epi and im still on npp and test and within 24 hours, my gyno came back
Is this what you were on before the bridge with phera/mdrol?

I just came back from work and addressed almost all the posts since then so go back to the first page to catch up :)
 
Frank Reynolds

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I would caution against "reducing" estrogen as I do think that AIs may be partially to blame. "Controlling" estrogen is preferable and I am partial to SERMS for this purpose. Especially for non-aromatizing or low aromatizing compounds because the reduction in SHBG and the increased "free" estrogens will not be helped by AI's.
Got ya..

This is interesting as i have probably read "don't use nolva with tren(progestins) as it will cause gyno/make gyno worse" a thousand times..
 
sethroberts

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Got ya..

This is interesting as i have probably read "don't use nolva with tren(progestins) as it will cause gyno/make gyno worse" a thousand times..
I would love to see the argument behind that.
 
sethroberts

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I posted a comment in that thread. That is a classic case of misinterpretation of the literature. Nolvadex may increase progesterone receptors in the uterus but not likely in the breast. Just because something happens in one tissue type does not mean it will happen in all types -- that is what makes different tissues and organs different! Also, most papers I see show tamoxifen downregulating estrogen receptors in the breast so a slight increase in progesterone receptors would likely not be a problem.
 
mooch2321

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so seth...if lactation is occuring, its not neccesarily high levels of prolactin but the difference in the levels of estrogen and prolactin....how should this be treated at this point....let estrogen levels raise or take a prolactin antagonist? Couldnt we be causing other problems by letting estrogen rebound?
 
sethroberts

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so seth...if lactation is occuring, its not neccesarily high levels of prolactin but the difference in the levels of estrogen and prolactin....how should this be treated at this point....let estrogen levels raise or take a prolactin antagonist? Couldnt we be causing other problems by letting estrogen rebound?
If lactation is truly occuring then at that point I would get a blood test to confirm elevated prolactin or severly suppressed estrogen and then I would take caber. I cannot stress how bad it is to supress estrogen to very low levels.

Obviously the idea would be to not get to the point of either getting gyno or lactating but I think sometimes people get too overzealous in the other direction and wind up causing themselves harm through polypharmacy.
 
mooch2321

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can you define truly occuring....if a nipple is squeezed and beads of liquid are excreted would you consider this true lactation or are we looking for more discharge?
 
sethroberts

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can you define truly occuring....if a nipple is squeezed and beads of liquid are excreted would you consider this true lactation or are we looking for more discharge?
I would likely classify that under "stop squeezing your nipples". It would need to be more of a discharge. Did you see the reference above to self-manipulation and lactation?
 
sethroberts

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sorry i missed that post....
for the scrolling-impaired :)

Benign galactorrhea/breast discharge in adolescent males probably due to breast self-manipulation.Rohn RD.
Three adolescent males presented with nipple discharge. In two boys, the expressed secretion was clinically consistent with galactorrhea. Galactorrhea/breast discharge is a rare complaint in males of any age. Although galactorrhea is commonly associated with a neuroendocrine disorder or drug ingestion, the work-up in each, including basal prolactin level, was normal. Reluctantly, each by admitted to breast self-manipulation to reduce gynecomastia. When the behavior was discontinued, the galactorrhea/breast secretion ceased. Clinicians should be aware of this heretofore undescribed and apparently benign phenomenon. If basal hyperprolactinemia is absent in a male with a breast discharge and a history of breast manipulation, then an extensive work-up is not usually indicated.

PMID: 6429109 [PubMed - indexed for MEDLINE
 
Eric Potratz

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Actually, they are considered progestins because of the lack of a carbon at the C-19 position.

Vites has been shown to have estrogenic and progestational effects in addition to its prolactin lowering potential. With this mix of activities, it is difficutl to say what effect it is having and if it may be causing more harm than good.
Correct, it is the lack of carbon in the 19 position, my typo.

Im not sure what your implying by saying Vitex has “estrogenic” or “progestational” effects. Im not aware of any research that shows any constituent of Vitex having agonistic action at the PR or ER.

If you are referring to a stimulus effect at the female hypothalamus/pituitary of estrogen or progesterone, I hope you’re not assuming this stimulatory effect applies to males.

-Eric
 
Eric Potratz

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Vites has been shown to have estrogenic and progestational effects in addition to its prolactin lowering potential. With this mix of activities, it is difficutl to say what effect it is having and if it may be causing more harm than good.
There is a 1-to-1 relationship with gyno and tren in some individuals, however with the introduction of something like vitex, these gyno symptoms go away. There is a connection with “sore, sensitive and puffy” nipples in males and the reduction with subsequent vitex supplementation.

-Eric
 
Eric Potratz

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Dienolone is actually more similar to nandrolone than to trenbolone in terms of binding affinity (trenbolone = 134AR, 74PR, dienolone 134AR, 17PR, nandrolone 154AR, 20PR) especially towards the progesterone receptor. Additionally, whereas trenbolone does not convert to estrogen, nandrolone does and it is possible that dienolone does as well. They are all strong androgens. Being a chemical intermediate is irrelevent.
Actually, it’s the double bond the 9th position that prevents the aromatization of dienolone. It simply cannot bind with aromatase.

I have plenty of experience with Trenbolone, nandrolone and dienolone base and I can say without a doubt that dienolone has characteristics closer related to Trenbolone than nandrolone. The dry gains, hot flashes, potent CNS activation, insomnia, ect… (Even the compounds characteristics are similar - yellowish hue, burns the mucous membranes, ect)
 
Eric Potratz

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I posted a comment in that thread. That is a classic case of misinterpretation of the literature. Nolvadex may increase progesterone receptors in the uterus but not likely in the breast. Just because something happens in one tissue type does not mean it will happen in all types -- that is what makes different tissues and organs different! Also, most papers I see show tamoxifen downregulating estrogen receptors in the breast so a slight increase in progesterone receptors would likely not be a problem.

I can also tell you from personal experience that Nolva is a very poor choice for combating progestin related gyno. It simply doesn’t work.

I wouldn’t call it misinterpretation of the literature either. Nolva up regulates progesterone receptor. If it does it in the endometrium, this is enough reason for me to suspect it also does it in breast tissue. (but of course, I can’t force anyone to adopt my logic)

I also suspect (although have no references) that other SERM’s may up-regulate the progesterone receptor similar to nolvadex. I simply have fallen out of favor of using SERMs for the treatment of gyno, especially progestin based gyno.

As I have said already, I have most success with suppressing prolactin or estrogen, and reducing the total stimulatory action on mammary gland via these mechanisms.

You have some interesting theory’s and I can agree with most of what you are saying, but I have to make it clear to the members that there other point of views on this subject… simply because I have a vested interest that my customer don’t have gyno symptoms when using our products.

I say use Vitex if you are using 19-nor, and an possibly an AI if an aromatizable steroid is used.

-Eric



Effects of tamoxifen on steroid hormone receptors and hormone concentration and the results of DNA analysis by flow cytometry in endometrial carcinoma.
M Nola, et al
Gynecol Oncol, Mar 1999; 72(3): 331-6.

Tamoxifen increases the plasma estrogen-binding equivalents and has an estradiol agonistic effect on histologically normal premenopausal and postmenopausal
Gorodeski, G.I., et al.
endometrium. Fertil. Steril, 57, 320-327. (1992)

Estrogen and progesterone receptor expressors o£ decidual endometrium in a postmenopausal woman treated with tamoxifen and megestrol acetate.
Cohen, I., Shulman, A., Altaras, M., Tepper, R., Cordoba, M. and Beyth, Y.
Gynecol. Obstet. Invest., 38, 127-129. (1994)
 
sethroberts

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Correct, it is the lack of carbon in the 19 position, my typo.

Im not sure what your implying by saying Vitex has “estrogenic” or “progestational” effects. Im not aware of any research that shows any constituent of Vitex having agonistic action at the PR or ER.

If you are referring to a stimulus effect at the female hypothalamus/pituitary of estrogen or progesterone, I hope you’re not assuming this stimulatory effect applies to males.

-Eric
1: J Agric Food Chem. 2001 May;49(5):2472-9. Links
Evaluation of estrogenic activity of plant extracts for the potential treatment of menopausal symptoms.Liu J, Burdette JE, Xu H, Gu C, van Breemen RB, Bhat KP, Booth N, Constantinou AI, Pezzuto JM, Fong HH, Farnsworth NR, Bolton JL.
Department of Medicinal Chemistry and Pharmacognosy, UIC/NIH Center for Botanical Dietary Supplements Research, College of Pharmacy, M/C 781, University of Illinois at Chicago, 833 South Wood Street, Chicago, Illinois 60612, USA.

Eight botanical preparations that are commonly used for the treatment of menopausal symptoms were tested for estrogenic activity. Methanol extracts of red clover (Trifolium pratense L.), chasteberry (Vitex agnus-castus L.), and hops (Humulus lupulus L.) showed significant competitive binding to estrogen receptors alpha (ER alpha) and beta (ER beta). With cultured Ishikawa (endometrial) cells, red clover and hops exhibited estrogenic activity as indicated by induction of alkaline phosphatase (AP) activity and up-regulation of progesterone receptor (PR) mRNA. Chasteberry also stimulated PR expression, but no induction of AP activity was observed. In S30 breast cancer cells, pS2 (presenelin-2), another estrogen-inducible gene, was up-regulated in the presence of red clover, hops, and chasteberry. Interestingly, extracts of Asian ginseng (Panax ginseng C.A. Meyer) and North American ginseng (Panax quinquefolius L.) induced pS2 mRNA expression in S30 cells, but no significant ER binding affinity, AP induction, or PR expression was noted in Ishikawa cells. Dong quai [Angelica sinensis (Oliv.) Diels] and licorice (Glycyrrhiza glabra L.) showed only weak ER binding and PR and pS2 mRNA induction. Black cohosh [Cimicifuga racemosa (L.) Nutt.] showed no activity in any of the above in vitro assays. Bioassay-guided isolation utilizing ER competitive binding as a monitor and screening using ultrafiltration LC-MS revealed that genistein was the most active component of red clover. Consistent with this observation, genistein was found to be the most effective of four red clover isoflavones tested in the above in vitro assays. Therefore, estrogenic components of plant extracts can be identified using assays for estrogenic activity along with screening and identification of the active components using ultrafiltration LC-MS. These data suggest a potential use for some dietary supplements, ingested by human beings, in the treatment of menopausal symptoms.

1: Pak J Biol Sci. 2007 Jul 15;10(14):2300-7.Links
The effects of Vitex agnus castus extract and its interaction with dopaminergic system on LH and testosterone in male mice.Nasri S, Oryan S, Rohani AH, Amin GR.
Department of Biology, Parand Branch, Azad University, Tehran, Iran.

The purpose of this study was to evaluate the probable effects of Vitex agnus castus (Vac.) on the male reproductive physiology. It is a well known fact that LH secretion from the anterior pituitary of mammals is controlled by many neurotransmiters such as dopamine. In this experiment, we have studied the effect of Vac. extract on the LH and testosterone hormones and its interaction with the dopaminergic system on male mice. In order to evaluate these effects, we used the hydroalcoholic Vac. extract (for extraction we used percolation technique) injection with the following doses: 65, 165, 265, 365 and 465 mg kg-', bromocriptine as a dopamine receptor agonist (5, 10, 20 mg kg(-1)) and haloperidol as a dopamine receptor antagonist (1, 1.5, 2, 2.5, 3 mg kg(-1)). To study the interaction between Vac. extract and dopaminergic system, we injected the optimum doses of Vac. with bromocriptine or haloperidol at the same time. Intraperitoneal injections were applied in all experiments, once a day for 30 days. The control group remained intact and the sham group received vehicle. After the last injection, we collected the animal blood serums for hormonal assays. LH and testosterone were measured by Radio Immuno Assay (RIA). LH and testosterone, showed significant decrease in bromocriptine group and haloperidol increased these hormones. Vac. extract decreased significantly the LH and testosterone levels. The coadministration of Vac. extract and bromocriptine decreased LH and testosterone. Coadministration of Vac. extract and haloperidol decreased LH and testosterone levels. These results suggest: dopamine regulates the gonadotroph-leydig cells axis. It appears that Vac. exertes effects through dopaminergic system and other pathways. The findings of this study show we can use Vac. extract for pathological cases of increasing LH and testosterone.
 
sethroberts

sethroberts

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There is a 1-to-1 relationship with gyno and tren in some individuals, however with the introduction of something like vitex, these gyno symptoms go away. There is a connection with “sore, sensitive and puffy” nipples in males and the reduction with subsequent vitex supplementation.

-Eric
So if there is a 1:1 ratio then everyone who takes tren gets gyno?
 
crazyfool405

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Is this what you were on before the bridge with phera/mdrol?

I just came back from work and addressed almost all the posts since then so go back to the first page to catch up :)
nope i got gyno about 3 months after that cycle then started my other one (that im still on and will be for a lil while), long history,
 
sethroberts

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Actually, it’s the double bond the 9th position that prevents the aromatization of dienolone. It simply cannot bind with aromatase.

I have plenty of experience with Trenbolone, nandrolone and dienolone base and I can say without a doubt that dienolone has characteristics closer related to Trenbolone than nandrolone. The dry gains, hot flashes, potent CNS activation, insomnia, ect… (Even the compounds characteristics are similar - yellowish hue, burns the mucous membranes, ect)
Do you have any data to back up your assertion that the double bond in the 9th position prevents aromatization of dienolone? The 4,9,11 conjugated system makes it impossible for trenbolone to convert to estrogen but the lack of the 11 double bond in dienolone could allow the electron density of the double bond at the 9-position to actually aid in the formation of the conjugated a-ring system -- i.e. the formatin of estrogen.

Your personal experience of the end effects means nothing in the face of binding data to the contrary. Anecdotal information is useful but does not trump controlled scientific data. Oh, so it has a yellowish hue and burns the musuc membranes -- you just described probably >10,000 unrelated compounds.
 
sethroberts

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I can also tell you from personal experience that Nolva is a very poor choice for combating progestin related gyno. It simply doesn’t work.

I wouldn’t call it misinterpretation of the literature either. Nolva up regulates progesterone receptor. If it does it in the endometrium, this is enough reason for me to suspect it also does it in breast tissue. (but of course, I can’t force anyone to adopt my logic)

I also suspect (although have no references) that other SERM’s may up-regulate the progesterone receptor similar to nolvadex. I simply have fallen out of favor of using SERMs for the treatment of gyno, especially progestin based gyno.

As I have said already, I have most success with suppressing prolactin or estrogen, and reducing the total stimulatory action on mammary gland via these mechanisms.

You have some interesting theory’s and I can agree with most of what you are saying, but I have to make it clear to the members that there other point of views on this subject… simply because I have a vested interest that my customer don’t have gyno symptoms when using our products.

I say use Vitex if you are using 19-nor, and an possibly an AI if an aromatizable steroid is used.

-Eric



Effects of tamoxifen on steroid hormone receptors and hormone concentration and the results of DNA analysis by flow cytometry in endometrial carcinoma.
M Nola, et al
Gynecol Oncol, Mar 1999; 72(3): 331-6.

Tamoxifen increases the plasma estrogen-binding equivalents and has an estradiol agonistic effect on histologically normal premenopausal and postmenopausal
Gorodeski, G.I., et al.
endometrium. Fertil. Steril, 57, 320-327. (1992)

Estrogen and progesterone receptor expressors o£ decidual endometrium in a postmenopausal woman treated with tamoxifen and megestrol acetate.
Cohen, I., Shulman, A., Altaras, M., Tepper, R., Cordoba, M. and Beyth, Y.
Gynecol. Obstet. Invest., 38, 127-129. (1994)
You speak as if noone else has anecdotal information -- what you are also lacking is the education and experience in interpretting pharmacological data to formulate a hypothesis that is based on anything but conjecture. You company owners crack me up when you think that somehow you are qualified to make these determinations. If you knew anything about physiology and the action of estrogen you would know that endometrium and breast are very different tissues with very different responses to estrogens and SERMS. When those science type fellows talk about selective estrogen receptor modulators do you realize that they are talking about tissue selectivity and that while tamoxifen is used to fight breast cancer because it acts as an antagonist (with slight partial agonist activity) in the breast that those patients are at an increased risk of endometrial cancer because tamoxifen acts as an agonist in that tissue? You are certainly entitled to your opinion but just realize that it is an unqualified opinion of someone who is trying to defend a product that noone was bashing.
 
sethroberts

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nope i got gyno about 3 months after that cycle then started my other one (that im still on and will be for a lil while), long history,
your previous quote:
i was on epi as well as npp, and test, i stopped the epi and im still on npp and test and within 24 hours, my gyno came back

Ok, you said you were on epi, mpp and test you stopped epi and within 24 hours gyno came back, so this was three months after what?
 

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