No such thing as "prolactin induced gyno" (prove me wrong)

[tilebreaker]

OK, first things first...the thread title is meant to provoke some discussion. I'm not sold on the idea of "prolactin induced gyno" but I'd like to hear people's explanations of this and find out where they are getting their info from. And I realize that this should probably be in the science section, but I think a lot of people don't look there and more people here will hopefully get something out of this.

Statements about "prolactin induced gyno" often appear in discussions about "progestins" and "progesterone gyno." I feel that there is a lot of confusion about these two hormones and how they relate to gyno formation. I'd like to try to give my perspective on this and why I feel these are incorrect, or at least too simplistic explanations for the potential of a given compound to cause gyno symptoms.

I'm going to start with a discussion of progesterone and "progestins" and then talk a bit about prolactin. Hopefully all this will stimulate a good discussion. Like I said above, I'd like to hear where people are getting their info on "progestin gyno" and "prolactin gyno."


What does progesterone do?

In women, progesterone has multiple roles during pregnancy It causes changes in uterine tissue necessary for implantation and aids in the development of the breast ductal system in preparation for lactation.

Progesterone is a key precursor and steroidogenic intermediate for all bioactive natural steroids and the progesterone receptors A and B are structurally and evolutionarily the closest members of the nuclear receptor superfamily to the androgen receptor. Yet, although progesterone has crucial gestational and lactational roles in female reproductive physiology, it has no well established role in male reproductive physiology apart from a possible role in sperm function (234), possibly via non-genomic rather than a classically genomic mechanism (235). Nevertheless functional nuclear progesterone receptors are expressed in male brain, smooth muscle and reproductive, but not most non-reproductive tissues (236). Synthetic progestins, steroidal structural agonistic analogs of progesterone, are potent inhibitors of pituitary gonadotropin secretion used widely for female contraception and hormonal treatment of disorders such as endometriosis, uterine myoma and mastalgia. Used alone, progestins suppress spermatogenesis but cause androgen deficiency including impotence (237, 238) so androgen replacement is necessary. Non-human primate studies indicate that this is mediated via a central hypothalamic-pituitary site of action rather than direct effects on the testis (239).
http://endotext.com/male/male15/maleframe15.htm

Other effects we are interested in:

1) Antagonism of 5alpha-reductase. One theory is that progesterone competes with testosterone for binding to 5a-R. This would reduce the conversion of T to DHT and thus lower DHT levels. In males, this can be considered a "feminizing effect."

2) Elevates SHBG levels. SHBG binds to testosterone much better than to estrogen. Therefore, increased SHBG levels will decrease free test levels faster than free estrogen. This will create a transient imbalance in the free (active) T/E ratio. (On a side note, this difference in affinity for SHBG also means that estrogen can be released from SHBG "more easily" than test by supplements that are meant to interfere with test-SHBG interactions).

3) Can be converted to androstenedione, which can then be converted to estradiol. Increased levels of progesterone could lead to increased circulating estrogen.

4) In men, excess progesterone can rapidly shut down the HPTA.

5) Down-regulate or up-regulate ER expression? (Haven't found a clear answer to this yet, but it is an important question)


What is a progestin?

From my experience, on this and other boards you can find lots of references to such and such steroid/prosteroid/prohormone being a "progestin" and thus a string of warnings for people to watch out for gyno (which isn't a bad warning under any circumstances, really). However, many of these compounds, at least from what I can tell, are not, in fact progestins, at least in a strictly chemical sense. Here's Patrick Arnold talking about progestins:

most of these componunds people are calling progestins are not really progestins. they share vague chemical similarity with known pharmaceutical progestins and maybe have slight progestational activity but in my expert opinion would NOT fall into the category of progestin. they would be considered in the androgen class.

case in point would be estra-4,9-dien-3,17-dione

[a] "progestin is something that has progestational activity. but the complicated thing is most androgens have a certain degree of progestational activity (albeit minor for most)

its really a subjective call. certainly something like norethindrone from birth control pills can be considered a progestin (even though it has substantial androgenic activity). and then norethandrolone would be considered an androgen (even though it is very close in structure to norethindrone and has substantial progestational activity)

then there is the chemical aspect of what is a progestin

there are two classes of progestins - the C20-keto progestins such as classic progesterone and its derivatives, and the 17alpha-ethynyl estren derivatives such as norethindrone and norgestrel

i would think anything that is not in these structural classes would not be considered a progestin by an authority in this field. the only supplement i am aware of that fit this definition was the stuff that was in the old methyl-1-p (which was a C20-keto derivative)"

So as you can see, one problem is that while most of these compounds cannot be chemically classified as progestins, it is, as PA said, possible that some of them (or some of their metabolites) may have some level of activity at the progesterone receptor. I, for one, would like to see such info for many of these compounds, but I doubt that I could scour PubMed for the next year and be able to compile a halfway decent chart of "compounds and their metabolites that may or may not have progestational activity (that may or may not lead to gyno)."

I feel that for discussion's sake, when talking about compounds we should try to know whether they are progestins or androgens with some progestational activity. For example, nandrolone supposedly is able to activate the PR (progest. receptor) about 1/5th as well as progesterone itself, whereas trenbolone is closer equal activation. Neither of these compounds can be chemically classified as progestins, yet have substantial progestational activity.

(continued below)

[tilebreaker]

Gynecomastia?

Almost 25% of all cases of gynaecomastia are currently classified as idiopathic. In this group of patients, circulating sex hormones, SHBG and gonadotrophins are within reference limits. The development of gynaecomastia is attributed to an altered tissue response which may be due to reduction in androgen receptors (75) and/or a local increase in aromatase activity in the breast.(46) Reduction in androgen receptors may be congenital or induced by drugs.

Ann Clin Biochem 2001; 38: 596-607

The effects of progesterone listed above, namely reduced levels of DHT and elevated SHBG may be integral to any role in gyno formation.

Here's another quote that I think is relevant (but I don't know the original source) talks about the contribution of DHT levels:

"In addition to elevated IGF-1, lowered DHT levels resulting from endogenous testosterone suppression may contribute to gyno from non aromatizing steroids. Gyno is a reported side effect from finasteride use. Some have attributed this to elevated estrogen levels due to the fact that there is more testosterone to be aromatized, since less test is being converted to DHT. Other researches think that DHT has a direct antiestrogenic effect on breast tissue.

Studies have shown that DHT can actually block estrogen from binding to the estrogen receptor in mammary tissue (1). DHT also is an aromatase inhibitor (2). Even more interesting is the fact that transdermal DHT cream has been used successfully to treat gyno (3).

It may be that the estrogen/DHT ratio is more important to the development of gyno than the estrogen/testosterone ratio."

So what may be happening is:

1) Progestin/progesterone ---> increased progesterone receptor signaling (which leads to) --> increased IGF-1 expression ----> stimulation of alveolar hyperplasia (not sure exactly how much this contributes to gyno)

2) Progestin/progesterone ---> increased progesterone receptor signaling--> lowered DHT levels ---> decreased antiestrogenic DHT activity in breast tissue = decreased DHT block of estrogen receptors in breast AND decreased DHT anti-aromatase activity in breast

The question that must be asked for each individual androgen is how much relative progestational activity does it have.

For example if nandrolone blocks DHT formation more so than trenbolone, but trenbolone elevates SHBG more than nandrolone, the relative importance of these effects will determine which compound is more likely to lead to gyno. By most accounts, nandrolone is more effective at this (especially when combined with test, which likely results in elevated estrogen at the same time), suggesting that the effects on DHT are more critical.


Prolactin

Where does prolactin come into this? Prolactin is a pituitary hormone that causes lactation. During pregnancy, it is the combined rise in estrogen and progesterone that contributes to prolactin production, i.e. progesterone causes development of the gland, and estrogen causes accumulation of prolactin that will eventually cause secretions (both of which probably depend on GH and IGF-1 signaling). In women, the drop in estrogen and progesterone after birth basically releases a hold on prolactin induced milk secretion. Here, estrogen and progesterone suppress lactation until after the baby is born; then levels of E and P drop off and prolactin takes over.


Is there a similar thing happening in men taking progestational androgens? In this case it might be that increased E and progestational signaling (if you're on a suppressive compound that also acts on the progesterone receptor) causes gyno formation (and increased prolactin levels), and then when you stop the compound and go into PCT (loss of E and progestational signaling), lactation is possible.

In men,

In general, an increase in effective oestrogen/androgen ratio, irrespective of the cause, may actually stimulate prolactin release and increase circulating concentrations.

Ann Clin Biochem 2001; 38: 596-607

and

http://www.endotext.org/male/male14/male14.htm

Prolactin stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobulo-alveolar differentiation only with concomitant progesterone.

and with regard to gyno:

Although prolactin receptors have been demonstrated in breast tissue, including gynecomastia [19], hyperprolactinemia probably plays an indirect role in gynecomastia by causing central hypogonadism. Most men with gynecomastia do not have elevated serum prolactin levels, and not all men with hyperprolactinemia develop gynecomastia. Nevertheless, it has been shown in cultured breast cancer cells that prolactin and sex steroid receptors (especially the progesterone receptor [PgR]) may be coexpressed and may cross-regulate each other?s expression [20,21]; acute prolactin treatment produced an increase in PgR and a decrease in AR content. If this were to occur in the breast tissue of hyperprolactinemic men, the resulting increase in PgR expression and decrease in AR expression could promote breast tissue growth and result in gynecomastia.

[19] Gill S, Peston D, Vonderhaar BK, et al. Expression of prolactin receptors in normal, benign, and malignant breast tissue: an immunohistological study. J Clin Pathol 2001;54:956?60.

[20] Ormandy CJ, Hall RE, Manning DL, et al. Coexpression and cross-regulation of the prolactin and sex steroid hormone receptors in breast cancer. J Clin Endocrinol Metab 1997;82(11): 3692?9.

[21] Gutzman JH, Miller KK, Schuler LA. Endogenous human prolactin and not exogenous human prolactin induces estrogen receptor a and prolactin receptor expression and increases estrogen responsiveness in breast cancer cells. J Steroid Biochem Mol Biol 2004;88:69?77.

from: Endocrinol Metab Clin N Am (2007) 36: 497?519

While prolactin and progestins on their own don't seem to cause gyno, is it possible that something similar to the post-pregnancy lactation in women could happen in men taking progestational androgens? In this case it might be that increased E and progestational signaling (if you're on a suppressive compound that also acts on the progesterone receptor) causes gyno formation (and increased prolactin levels), and then when you stop the compound and go into PCT (loss of E and progestational signaling), lactation is possible.

(continued below)

[tilebreaker]

This is an important excerpt from an article by Karl Hoffman that I believe sums up a lot of the issues here:

PROGESTERONE AND PROLACTIN INDUCED GYNECOMASTIA

Before delving into this subject, I'd like to say first and foremost, that in users of anabolic/androgenic steroids (AAS) the first step in combating the development of gynecomastia, or male breast enlargement, is to eliminate the causative agent: the anabolic steroid. Drug-induced gynecomastia almost invariably resolves on its own when a person quits taking the drugs responsible for it, if caught before permanent fibrosis develops. Unfortunately, most AAS users don't want to employ this simple approach, for obvious reasons, so the foregoing will all be under the assumption that a person wants to prevent or treat gyno and still continue steroid use.

In the belief that certain anabolic steroids increase prolactin levels as well as act as agonists at the progesterone receptor, some have advocated the use of antiprolactin agents, like bromocriptine, or progesterone receptor blockers like RU-486 to treat AAS related gynecomastia, in lieu of more traditional drugs like tamoxifen.

In truth, the etiology of gynecomastia is unknown and a number of agents including estrogens, progestins, GH, IGF-1, and prolactin may be involved. However, most authorities believe that a decreased (T+DHT)/E ratio is central to the development of gyno, and that blocking the effects of estrogen, or increasing T + DHT levels, is central to ameliorating the problem.

Regarding prolactin, androgens decrease prolactin levels whereas estrogens increase prolactin. Non-aromatizing androgens have never been shown to elevate prolactin levels in humans, but testosterone has, due to its aromatization to estradiol (19). Prolactin secreting tumors, or prolactinomas, are often associated with gyno. But in these cases the prolactin is believed to induce gyno by suppressing testosterone production: "Prolactinomas that are sufficiently large to cause gynecomastia do so as a result of impairment of gonadotropin secretion and secondary hypogonadism" (20). However, this is a moot issue in AAS users whose gonadotropin secretion is already blunted.

According to research cited in (20), prolactin may have a direct stimulatory effect on mammary tissue development, but only in the presence of high estrogen levels.

The presence of mild hyperprolactinaemia is therefore not uncommon in patients with estrogen excess. Significant primary hyperprolactinaemia, on the other hand, may directly stimulate epithelial cell proliferation in an estrogen-primed breast, causing epithelial cell proliferation and gynaecomastia.

So rather than focusing solely on lowering prolactin levels which may be elevated in users of aromatizing androgens, attacking estrogen should be the first line of action.

GH and IGF-1 are considered critical to the proliferation of mammary tissue. An excellent review of the role played by these hormones, as well as a general overview of gynecomastia can be found here: https://web.archive.org/web/20070314...e14/male14.htm

Since elevated GH and IGF-1 are considered important to the anabolic effect of AAS, it would be impractical and counterproductive to attempt to prevent gynecomastia by blocking GH/IGF.

Progesterone acts in concert with estrogen to promote breast development, and at least part of any role played by synthetic progestins may be to stimulate IGF-1 production in the breast. But again, blocking the action of progesterone or synthetic progestins is not practical. Specific progesterone receptor antagonists like RU-486 block not only the progesterone receptor, but the androgen receptor as well, and have actually been associated with the development of gynecomastia (21). In any case, progesterone is thought to act on the breast to enhance the effects of estrogen (22) so once again, attacking estrogen is the easiest and most logical approach.

DHT gel (Andractim) or a generic knockoff might help as well. DHT is thought to act as an aromatase inhibitor (23) and perhaps compete directly with estrogen for binding at the estrogen receptor (24). DHT has been used in several case reports and controlled trials to successfully treat gynecomastia. So perhaps a viable strategy would be to combine DHT gel with tamoxifen. I would recommend tamoxifen rather than an aromatase inhibitor due to the simple fact that tamoxifen has been widely used in numerous controlled studies to successfully treat gynecomastia, whereas the evidence to support the efficacy of aromatase inhibitors is scanty at best.

(19) Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F
Acta Endocrinol (Copenh) 1984 Feb;105(2):167-72

(20) Ismail AA, Barth JH.Ann Clin Biochem 2001 Nov;38(Pt 6):596-607

(21) Grunberg SM, Weiss MH, Spitz IM, Ahmadi J, Sadun A, Russell CA, Lucci L, Stevenson LL J Neurosurg 1991 Jun;74(6):861-6

(22) Nomura K, Suzuki H, Saji M, Horiba N, Ujihara M, Tsushima T, Demura H, Shizume K
J Clin Endocrinol Metab 1988 Jan;66(1):230-2

(23) Perel E, Stolee KH, Kharlip L, Blackstein ME, Killinger DW
J Clin Endocrinol Metab 1984 Mar;58(3):467-72

(24) Casey RW, Wilson JD.
J Clin Invest 1984 Dec;74(6):2272-8

http://www.mindandmuscle.net/article..._hoffman/myths

Conclusions:

It seems that all the problems that come with increased progestational activity may require high estrogen to become really noticable...so if you can stop the estrogen (on cycle or during the "rebound"), you should have a good chance of avoiding the progestational sides...that's my theory from my reading, anyway.

And finally, prolactin does NOT cause gyno (well, only in extremely rare cases) in most PH/DS/AAS users. It can cause lactation if gyno (generally caused by low T/E ratio, i.e. low T, high E; increased progestational activity is also involved) has progressed to the point where the ductal systems are more developed and prolactin levels have risen enough to trigger lactation. Increased prolactin and subsequent lactation is a side effect of gyno, not a cause.


More info on general male and female endocrinology:

http://endotext.com/male/index.htm

http://endotext.com/female/index.htm

[tilebreaker]

Hopefully, I haven't made any gross informational errors in putting this together, but if so, please let me know...

[tilebreaker]

chirp...chirp...(crickets)


Jeez...guess I should have written about creatine or something.

I was hoping to help with some of the misinformation floating around here, but maybe it's too little (or too much for some), too late...

Maybe I'll get a mod to put this in the science section...

[Madevilz]

might have more chances for a reply in the supplement science forum

[XCriticalBenchX]

I can't prove you wrong, nor can i read all of that lol, but I go for personal experiences over literature. When I used a compound that raises prolactin levels very high, I for sure did not have estrogen rebound causing my sensitive nips. Tamox, Adex, and Letro did nothing to help. Caber, Vitex, and B6 which all reduce prolactin solved my problem.

Mike

[iForce Dave]

I can't prove you wrong, nor can i read all of that lol, but I go for personal experiences over literature. When I used a compound that raises prolactin levels very high, I for sure did not have estrogen rebound causing my sensitive nips. Tamox, Adex, and Letro did nothing to help. Caber, Vitex, and B6 which all reduce prolactin solved my problem.

Mike

Agree here, same thing. I trust my own experiences over books, and everything xCBx said I have seen before.

[tilebreaker]

I can't prove you wrong, nor can i read all of that lol, but I go for personal experiences over literature. When I used a compound that raises prolactin levels very high, I for sure did not have estrogen rebound causing my sensitive nips. Tamox, Adex, and Letro did nothing to help. Caber, Vitex, and B6 which all reduce prolactin solved my problem.

Mike

Yeah, I'm not saying those things won't work if you end up with high prolactin levels.

Can I ask which compounds you felt were really bad for this? And do you know prolactin levels were high from blood tests or b/c those worked for you?

[tilebreaker]

Anyway, I was just trying to say that generally prolactin levels don't go up unless estrogen and/or progesterone levels go up (or more precisely, relative ratios get skewed), and that it could be a problem with androgens that can aromatize, but less likely with those that don't.

[neuron]

Certain isomers can decrease plasma availability of neurotransmitter precursors (specifically phenylalanine and tyrosine) which can induce hyperprolactinemia and gynecomastia via hypogonadism.

[Big Cat]

Nice work. Sorry for the necrobump, but found this information more interesting now than ever. Interesting tidbits you may want to add is that androgens overall decrease prolactin. another is that gyno has always and still is treated solely with anti-estrogen therapy (barring surgery once it gets too big and androgen therapy if the cause is hypogonadism) with no research being done into newer or better ways of treatment. This lends further credence that neither progestins nor prolactin plays any role in gyno in the absence of estrogen, and that standard anti-estrogen therapy (preferably at the receptor to avoid direct drug/ER interactions) should cause gyno to regress in any and all cases.

Its also crucial to remember that nandrolone is in fact estrogenic, estimated at about 60 percent as estrogenic as estradiol itself, because it can activate Estrogen receptor elements through the AR. Neither PR blockers, aromatase inhibitors or estrogen receptor blockers had any significant effect on the estrogenic action of nandrolone. (for references do a search for my post "profiles for the book" in the AAS section) and that this and not some illustrious unproven effect is the reason that it can cause gyno.

50+ years of research and countless blood tests have always shown androgens to decrease prolactin levels, with no account ever of androgens having a positive effect on prolactin of prolactin signalling in healthy tissue in the absence of estrogen.

Weidenbach et al (1980) performed a study in castrated and adrenalectomized rats. These rats showed a severe drop in prolactin levels. Treatment with testosterone did not affect prolactin, but treatment with estradiol drastically increased prolactin. The reason for the drop in prolactin in these rats was therefore likely due to the removal of estrogen-producing organs, clearly demonstrating the estrogen-dependency of prolactin release.

[WIULifter]

nice compilation of information

[Big Cat]

One thing that has been shown to cause an increase in prolactin however :

1: Curr Opin Clin Nutr Metab Care. 2007 Jan;10(1):46-51. Links
Effects of L-arginine supplementation on exercise metabolism.McConell GK.
Department of Physiology, The University of Melbourne, Parkville, Victoria, Australia. mcconell@unimelb.edu.au

PURPOSE OF REVIEW: To describe the influence of acute and chronic administration of L-arginine on metabolism at rest and during exercise. RECENT FINDINGS: There has been substantial examination of the effect of infusion and ingestion of L-arginine at rest. It has been clearly demonstrated that L-arginine administration improves endothelial function in various disease states. In addition, L-arginine infusion at rest increases plasma insulin, growth hormone, glucagon, catecholamines and prolactin. Such hormonal changes affect metabolism. There has, however, been very little examination of the effect of increases in L-arginine availability during exercise. This is important to study as there is preliminary evidence that L-arginine infusion, probably via increases in nitric oxide (NO), alters skeletal-muscle metabolism during exercise. There is a need for further research, especially to understand the mechanisms of how L-arginine affects exercise metabolism and also to determine whether the hormonal responses that occur in response to L-arginine at rest are also present to some extent during exercise. SUMMARY: This line of research may have important therapeutic implications as there are indications that L-arginine augments the effects of exercise training on insulin sensitivity and capillary growth in muscles.

Maybe all those guru's out there claiming there is such a thing as prolactin gyno should start advising people to stop taking NO supplements. Just a thought ...

[__AM__]

Interesting read indeed,repped!

[Jimus Maximus]

Interesting read indeed,repped!

This has been a very interesting read for me too, and thanks for all the info

Yep I have gyno. Gyno from messing around with Methoxy TRN (which is a 19nor compound) and not following PCT protocol 100% correctly by which I mean I ran Tamox as you might think would work 40/40/30/20/10 but gyno developed and didn't go. Right nip has a lump an it's getting bigger. Pretty painful, sometimes very. I actually plucked up the courage to go to the docs and she told me to 'let it settle' - basically do nothing. Not the best advice IMO. They refused to prescribe Letro, so I've gone down the internet route of self med with Letro as this IS getting bigger and still painful. Had this since Mid January I just hope I'm not too late

Got 2.5mg tabs. I've read a LOT about this, sadly not before all this **** gonna start with 1/2 a tab e/d and gradually ramp up to a max of 2.5mg e/d. I'm gutted that itkicked off. I'm will kill my sex drive and the Mrs will not be happy. I aint' got the heart to tell her the mess I'm in she would only worry.

I hope the Letro kills it, or at least shrinks it a lot. I will be running a course of nolva to combat the e-rebound

There's still a lot I don't know. I've learned my lesson tho I can't live with this any more. The purpose of this post is to let people know what has happened, and to gain any information, help or advice from anyone who wants to contribute

Waiting 14 days for delivery now.great.

EDIT> also meant to ask. In order to get b/f down (currently around 15%) I'm running EC stack - is this likely to conflict / should I stop it when I run in the Letro or would it even be complimentary? I personall don't see why it would be a bad thing but what do I know?

[Big Cat]

This has been a very interesting read for me too, and thanks for all the info

Yep I have gyno. Gyno from messing around with Methoxy TRN (which is a 19nor compound) and not following PCT protocol 100% correctly by which I mean I ran Tamox as you might think would work 40/40/30/20/10 but gyno developed and didn't go. Right nip has a lump an it's getting bigger. Pretty painful, sometimes very. I actually plucked up the courage to go to the docs and she told me to 'let it settle' - basically do nothing. Not the best advice IMO. They refused to prescribe Letro, so I've gone down the internet route of self med with Letro as this IS getting bigger and still painful. Had this since Mid January I just hope I'm not too late

Got 2.5mg tabs. I've read a LOT about this, sadly not before all this **** gonna start with 1/2 a tab e/d and gradually ramp up to a max of 2.5mg e/d. I'm gutted that itkicked off. I'm will kill my sex drive and the Mrs will not be happy. I aint' got the heart to tell her the mess I'm in she would only worry.

I hope the Letro kills it, or at least shrinks it a lot. I will be running a course of nolva to combat the e-rebound

There's still a lot I don't know. I've learned my lesson tho I can't live with this any more. The purpose of this post is to let people know what has happened, and to gain any information, help or advice from anyone who wants to contribute

Waiting 14 days for delivery now.great.

EDIT> also meant to ask. In order to get b/f down (currently around 15%) I'm running EC stack - is this likely to conflict / should I stop it when I run in the Letro or would it even be complimentary? I personall don't see why it would be a bad thing but what do I know?

If nolva didn't help, letro isn't likely to help either. You should probably have stuck with the nolva and discontinued the drug. Having said that, cutting aids, or cutting plain and simple will not interfere, in fact its likely to help. Adipose tissue is a prime tissue that produces aromatase.

[Bring_The_Pain]

1: Curr Opin Clin Nutr Metab Care. 2007 Jan;10(1):46-51. Links
Effects of L-arginine supplementation on exercise metabolism.McConell GK.
Department of Physiology, The University of Melbourne, Parkville, Victoria, Australia. mcconell@unimelb.edu.au

PURPOSE OF REVIEW: To describe the influence of acute and chronic administration of L-arginine on metabolism at rest and during exercise. RECENT FINDINGS: There has been substantial examination of the effect of infusion and ingestion of L-arginine at rest. It has been clearly demonstrated that L-arginine administration improves endothelial function in various disease states. In addition, L-arginine infusion at rest increases plasma insulin, growth hormone, glucagon, catecholamines and prolactin. Such hormonal changes affect metabolism. There has, however, been very little examination of the effect of increases in L-arginine availability during exercise. This is important to study as there is preliminary evidence that L-arginine infusion, probably via increases in nitric oxide (NO), alters skeletal-muscle metabolism during exercise. There is a need for further research, especially to understand the mechanisms of how L-arginine affects exercise metabolism and also to determine whether the hormonal responses that occur in response to L-arginine at rest are also present to some extent during exercise. SUMMARY: This line of research may have important therapeutic implications as there are indications that L-arginine augments the effects of exercise training on insulin sensitivity and capillary growth in muscles.



Maybe all those guru's out there claiming there is such a thing as prolactin gyno should start advising people to stop taking NO supplements. Just a thought ...

So what exactly did they mean by an acute and chronic dosage? Do you have the dosages tested on in your full text?

[Jimus Maximus]

If nolva didn't help, letro isn't likely to help either. You should probably have stuck with the nolva and discontinued the drug. Having said that, cutting aids, or cutting plain and simple will not interfere, in fact its likely to help. Adipose tissue is a prime tissue that produces aromatase.

**** coming from Big Cat I'm inclined to believe what you're sayin. That ain't good. I did complete 5 weeks 40/40/30/20/10 tapering down on Nolva - are you saying I should have kept on with it? When I was on the final 10mg e.d the lump wasn't too bad

I gotta try the Letro before I go down the surgery route. It seems that here in the UK the docs don't recognise this condition so I feel it's gonna take a while to sort out, so in the meantime I gotta try and reduce it at least. I've read a few gyno reduction threads and I am hoping it's gonna reduce the size and pain at least, although I know it wont totally get rid of it

Recognising that diet is also key, is there anything else I can be doing to help rid myself of this or make it more bearable?

[Big Cat]

**** coming from Big Cat I'm inclined to believe what you're sayin. That ain't good. I did complete 5 weeks 40/40/30/20/10 tapering down on Nolva - are you saying I should have kept on with it? When I was on the final 10mg e.d the lump wasn't too bad

I gotta try the Letro before I go down the surgery route. It seems that here in the UK the docs don't recognise this condition so I feel it's gonna take a while to sort out, so in the meantime I gotta try and reduce it at least. I've read a few gyno reduction threads and I am hoping it's gonna reduce the size and pain at least, although I know it wont totally get rid of it

Recognising that diet is also key, is there anything else I can be doing to help rid myself of this or make it more bearable?

Its fatty tissue for the most part, so dieting will surely help. Some people have also had great success using andractim gel applied directly to the gyno. I take it you aren't taking the supplement anymore ? That would be step one. Sticking with nolva would have been best indeed. An Ai won't do anything for you that the nolva wasn't unless you are diagnosed with high estrogen levels, in which longer term treatment is necessary and an AI would do you well.

If your gyno has progressed past a certain size, an endo will surely recommend surgery, and he would be right. But as long as you fall under the type 1 gyno category, it should still be treatable by restoring your A:E ratio. Some of this may still happen naturally, as you recover further from your product use. Such product can be extremely harsh on the HPTA and significantly lengthen recovery.

[Big Cat]

So what exactly did they mean by an acute and chronic dosage? Do you have the dosages tested on in your full text?

I've no idea, haven't read the full study yet. Its likely completely irrelevant as well, i've never know arginine to cause gyno in a person. I posted it mostly as a jab at the idiots who believe in prolactin gyno. They clearly don't understand prolactin too well.

[Jimus Maximus]

Its fatty tissue for the most part, so dieting will surely help. Some people have also had great success using andractim gel applied directly to the gyno. I take it you aren't taking the supplement anymore ? That would be step one. Sticking with nolva would have been best indeed. An Ai won't do anything for you that the nolva wasn't unless you are diagnosed with high estrogen levels, in which longer term treatment is necessary and an AI would do you well.

If your gyno has progressed past a certain size, an endo will surely recommend surgery, and he would be right. But as long as you fall under the type 1 gyno category, it should still be treatable by restoring your A:E ratio. Some of this may still happen naturally, as you recover further from your product use. Such product can be extremely harsh on the HPTA and significantly lengthen recovery.

Sorry to hijack this thread. Big Cat - I'm not on anything other than EC right now. I'm gonna look into andractim gel. I'm also gonna keep the diet clean. Tonight I'm doing cardio for 1hr and will keep that up.

I have some libido edge testosterone cream which I got on hand for when I run the Letro, to try and keep libido up but looks like andractim gel will help there as well

Regarding size - it's larger in area than the size of my nip, you can't actually SEE it but sure can feel it, almost 'grab' it

Thanks for your help man hope I can get back in the game soon

[Psylence]

Sorry to hijack this thread. Big Cat - I'm not on anything other than EC right now. I'm gonna look into andractim gel. I'm also gonna keep the diet clean. Tonight I'm doing cardio for 1hr and will keep that up.

I have some libido edge testosterone cream which I got on hand for when I run the Letro, to try and keep libido up but looks like andractim gel will help there as well

Regarding size - it's larger in area than the size of my nip, you can't actually SEE it but sure can feel it, almost 'grab' it

Thanks for your help man hope I can get back in the game soon

I know your going to run letro but if you still have nolva you might want to consider trying a couple more weeks of that. Research if you can run both at the same time? not sure. Obviously usually you would avoid this but considering its best to jump on this early. Your doctor obviously doesn't have experience treating cases such as yours and if you want professional help get a referral for an endocrinologist.

The use of tamoxifen for gynaecomastia has been studied previously in several centres. The table shows
the various published studies on the use and efficacy of tamoxifen for physiological gynaecomastia in the English literature.6?9 Only two of these studies6 9 have more than 10 patients and both showed resolution of lump
and pain in 80% of cases. A recent study from our own unit in 36 cases confirms this figure (83% resolution of
lump).10 Ting et al also found tamoxifen to be more efficacious than danazol.6 Importantly only minor and
reversible side effects were reported. This confirms findings that tamoxifen used in male breast cancer
appears to have no serious side effects.11 Tamoxifen appears to be successful, safe, and avoids operation and
on present evidence should be regarded as the first line treatment of gynecomastia.

Endocrine treatment of physiological gynaecomastia: Tamoxifen seems to be effective
Hamed N Khan and RW Blamey
BMJ. 2003 August 9; 327(7410): 301–302. doi: 10.1136/bmj.327.7410.301.
PMCID: PMC1126712

[igive]

I think I understand about 80% of this. In PH/DS buyer terms, is there any compounds one should avoid? Can there be any problems with 19nor products, which I believe = progestine. For example, would it be wise to avoid tren products.

Thanks

[Big Cat]

I think I understand about 80% of this. In PH/DS buyer terms, is there any compounds one should avoid? Can there be any problems with 19nor products, which I believe = progestine. For example, would it be wise to avoid tren products.

Thanks

Most of them should be avoided. there's a good reason none of these things were ever considered suitable for medical use. The tren compounds especially seem to be moderate androgens with high progestagenic activity. With the poor state and access to PCT for most OTC users these drugs are the worst. Recovery is harsh and not worth the gains. Conditions of hypogonadism can ensue, for prolonged periods of time (this is already often seen with actual trenbolone) which can reduce quality of life (libido, gyno, gains, you name it).

[Big Cat]

Sorry to hijack this thread. Big Cat - I'm not on anything other than EC right now. I'm gonna look into andractim gel. I'm also gonna keep the diet clean. Tonight I'm doing cardio for 1hr and will keep that up.

I have some libido edge testosterone cream which I got on hand for when I run the Letro, to try and keep libido up but looks like andractim gel will help there as well

Regarding size - it's larger in area than the size of my nip, you can't actually SEE it but sure can feel it, almost 'grab' it

Thanks for your help man hope I can get back in the game soon

Not my thread and it was dead for 3 years, so you didn't hijack anything I just bumped it and added some info because I believe this is an important topic today. Too many people tricked into believing things that aren't true because some pseudo-scientific guru can't explain whats going on.

[thauncle]

bump for others to read pretty good info here

[Al Swearengen]

good thread is good

[legalgear]

Lowering Prolactin can potentially lead to among others: reduced testosterone, reduced sperm counts and reduced immunity. Quit messing with your endocrine system for no reason. Keep your prolactin at NORMAL levels and stop using things like Bromocriptine and L-Dopa just "because"

Clin Pharmacol Ther. 1995 Sep;58(3):354-9.
Restoration of normal sperm characteristics in hypoprolactinemic infertile men treated with metoclopramide and exogenous human prolactin.

Ufearo CS, Orisakwe OE.

Department of Physiology, Faculty of Medicine, Nnamdi Azikiwe University, Nigeria.

We investigated the effects of induced increase in prolactin levels on spermatogenesis in 20 infertile men with hypoprolactinemia using exogenous human prolactin (hPRL) and metoclopramide. The subjects were selected from a population of 175 infertile men in whom the prevalence of hypoprolactinemia was 33.14%. Mean basal plasma prolactin was 2.79 +/- 0.62 ng.ml-1 in the infertile men and 9.57 +/- 2.14 ng.ml-1 in the normal control subjects. At the sixteenth week, mean plasma prolactin was 9.41 +/- 1.3 ng.ml-1 in subjects treated with exogenous hPRL and 5.2 +/- 0.7 ng.ml-1 in subjects treated with metoclopramide. Mean basal sperm concentration was approximately 8.8 million per milliliter in the infertile men and 41.5 million per milliliter in the normal control subjects. Mean sperm concentration was approximately 37 million per milliliter in subjects treated with exogenous hPRL, whereas the peak mean value was 23 million per milliliter in subjects treated with metoclopramide for 16 weeks. At basal conditions, the mean percentages of abnormal sperm were 66.75% +/- 14.93% and 21.36% +/- 4.78% in infertile and normal subjects, respectively. In subjects treated with exogenous hPRL and metoclopramide, the mean percentage of abnormal sperm were 24.7% and 31%, respectively, at week 16. Mean plasma prolactin, mean sperm concentration and the mean percentage of abnormal sperm were 3.3 +/- 1.4 ng.ml-1, 7 million per milliliter, and 60.5, respectively, in the infertile subjects after drug withdrawal at week 14. In normal control subjects, there was no significant difference (p = 0.01) in the plecebo effect. We therefore conclude that the low prolactin levels in this group of infertile men may be one of the primary causes of their infertility.

J Androl. 1985 Jan-Feb;6(1):10-4.
Induced hypoprolactinemia and testicular steroidogenesis in man.

Suescun MO, Scorticati C, Chiauzzi VA, Chemes HE, Rivarola MA, Calandra RS.

The effects of short-term hypoprolactinemia on the pituitary-gonadal axis were evaluated in a group of patients with untreated prostatic carcinoma. Each patient was studied prior to and during 7-day oral administrations of bromocriptine (2.5 mg q.i.d.). Serum LH, prolactin (PRL), androst-4-ene-3,17 dione (androstenedione), testosterone, and 5 alpha-androstane-3 alpha, 17 beta-diol (5 alpha-Diol) levels, as well as intra-testicular testosterone, dihydrotestosterone (DHT), 5 alpha-Diol and zinc (Zn) concentrations, were determined. Daily administration of bromocriptine caused a marked suppression of serum PRL (mean +/- SEM, 23.8 +/- 2.5 vs. 6.4 +/- 1.0 ng/ml) without concomitant changes in serum LH levels (mean +/- SEM, 8.3 +/- 1.6 vs. 8.9 +/- 2.1 ng/ml). Hypoprolactinemia induced a significant decrease (P less than 0.05) in the mean peripheral testosterone levels; but 5 alpha-Diol and androstenedione remained unchanged. However, in testicular tissues, bromocriptine treatment resulted in significant increases in mean concentrations of total androgens (P less than 0.001), testosterone (P less than 0.001) and DHT (P less than 0.02). Testicular levels of 5 alpha-Diol were not significantly altered. There was no change in Zn levels in basal conditions and during bromocriptine administration. These results indicate that short-term suppression of serum PRL levels in man affects basal testicular function without altering serum LH. However, a direct action of bromocriptine on the human gonad cannot be excluded.

Andrologia. 1985 Mar-Apr;17(2):172-7.
Bromocriptine, a dopamine agonist, directly inhibits testosterone production by rat Leydig cells.

Chambon M, Grizard G, Boucher D.

We investigated the direct effects of bromocriptine (BR) on both basal and hCG-stimulated testosterone production by rat collagenase-dispersed Leydig cells. In a final volume of 2.2 ml, 2.10(6) Leydig cells were incubated at 33 degrees C for 3 h either alone or with various amounts of hCG (1. 10. 10(2). 10(3). 10(4) mUI/vial) and BR (1.5 10(-9), 1.5 10(-7), 1.5 10(-5) M); BR was dissolved in 20 microliters of ethanol. BR (1.5 10(-5) M) decreased significantly both basal and hCG-stimulated testosterone production whereas at lower doses, BR had no effect. These results suggest that the dopamine itself may regulate rat Leydig cell function and that there is room for criticism of BR-induced hypoprolactinemia as an experimental model to study the effect of prolactin on the androgenic function.

Fertil Steril. 1991 Feb;55(2):355-7.
Effects of chronic bromocriptine-induced hypoprolactinemia on plasma testosterone responses to human chorionic gonadotropin stimulation in normal men.

Oseko F, Nakano A, Morikawa K, Endo J, Taniguchi A, Usui T.

Department of Medicine, Shimane Medical University, Japan.

To study the role played by normal levels of plasma prolactin (PRL) in the secretion of testosterone (T) in the testes, we induced hypoprolactinemia with a daily dose of 5 mg bromocriptine administered orally in five normal men 20 to 35 years of age for 8 weeks. The basal PRL, T, luteinizing hormone, follicle-stimulating hormone, and maximum responses of plasma T to human chorionic gonadotropin (hCG) stimulation were measured every 2 weeks. Basal levels of plasma T were reduced in the 1st 2-week-long period of hypoprolactinemia. In the 4-week-long period of hypoprolactinemia, the maximal response of plasma T to hCG stimulation was significantly reduced. The findings suggest that normal levels of plasma PRL may play an important role in the secretion of T in the human testes in vivo.

[jessemccoll]

Please be kind and help me find a solution. Picture on my profile