Progesterone and Prolactin

[chudds]

wow guys a whole host of info here!

right now i am 4 weeks after a course of superdrol and it has cause some gyno, now i have been all over the boards and came to the conclusion that i need to do get hold of cabaser (carbogoline) to supress my prolactin levels... i have done this but with no effect!

i currently have cabaser and nolva on hand and i was scared to use the nolva as it was considered bad for this type of gyno.

now from what i have read it would be best for me to run a low dose of nolva for an extended period of time so that my SHBG levels would be up after a while... my question is if i took cabaser at the same time would this have me coverd or surpress my SHGB

i want to bring up letro as a hot potato here and what role that would play as iv not seen it mentioned yet....

from all the boards i have read it seems this is the most knowledgeable and i woud greatly respect your opinion on this matter thanks lee

 

[sethroberts]

If you are referring to Big Cat, you're not alone. He's a smart guy, but sometimes seems to either not think out of the box or have some agenda against certain steroids (particularly 2nd-Gen. OTC ones). I've watched other "gurus" (Patrick Arnold, Dr. D, etc.) rip apart his "theories" on BB.com over the years. I have not considered him a guru or "the final word" on endocrine physiology for years. He loves to quote Vida text (which is a very valuable resource), but doesn't seem to venture too far for other sources.

Elevated E2 causes the prolactin receptors to become more sensitive, therefor possibly not requiring a rise in serum prolactin to cause a "prolactin effect." Is that enough to cause lactation in a human male? I don't know, but I don't discount it either.

Nobody, not even myself, should be considered the final word on anything. I am not perfect and I do not know everything. There are too many people on these boards who refuse to admit that they are ever wrong because they are afraid that if they are ever wrong that they somehow lose credibility. if noone ever questions the status quo, our knowledge will never grow.

Now, I will say that a qualified opinion always carries more weight than an unqualified one (that is why they have experts testify in court) but good ideas can come from anywhere. It is easy from me. I can stay here and state my theories and answer questions or I can not. My expertise is recognized outside of these boards. The difficult part is for the guys looking for answers because they have to weed through the bullsh-t and make a determination as to who is believable and what is a good idea.

 

[sethroberts]

Im still standing by my recommendation of vitex and possibly an AI for the control of progestin based gyno. (perhaps even in cases of non-progestin based gyno)

I think it’s obvious that prolactin is a contributing growth factor, although it may not be the “root” of the cause. But who cares.

Rather than administering a toxic SERM, or an AI that may push HDL down to unfavorable levels, it seems most logical (to me) to simply suppress prolactin for period and thus handicap gyno growth through this mechanism.

BTW, Ive worked with AAS/GH using athletes who have had gyno issues. In this case, where further estrogen suppression is undesirable, I simply recommend they reduce their hGH therapy. Guess what, the gyno stops.

By simply by reducing a co-factor (eg, GH, prolactin, IGF-1, ect) you can manage gyno issues. That’s my approach.

-Eric

The only issue I have with that is that you might be overlooking the potential dangers of dopaminergic modulation while you malign "toxic" nolva. GH is known to be mitogenic in the breast so your conlcusion about reducing dose in those cases is spot on.

 

[thebigt]

I was, and I agree. Although did not witness the bb.com shredding as I avoid that board usually. Only reason I referenced him was b/c that quote on the Tren compounds is parroted on the boards as gospel truth with no one contradiciting it, so much so that I more or less believed it, as much for a lack of contradictory evidence as anything else.



I'll buy that, E and PRO have a converse relationship - but what's causing elevated E2? Just regular suppression + SHBG offset? Wouldn't think this would be enough. Or... if the compound is not binding the progesterone receptor (or not very strongly), are we looking at simple aromatization issues here? Everything could be avoided by simply adding an AI? Sounds too easy, although I don't think I've seen anyone run a Tren designer with an AI (although I admit I haven't searched).

look at cel's xtren/formestane log in the review section, no sides related to estrogen/prolactin so far.

 

[Heracles25]

People started invoking "new" mechanisms for the induction of gyno in the late 1990's -- As far as I know, I was one of the first people proposing progesterone receptor activation as a potential cause of gyno back then. I have changed my mind since then as I have accumulated knowledge over the years. There is no evidence that progesterone or prolactin intitiate gynecomastia but plenty of evidence that estrogen does. All of this stemmed fro mthe fact that people were complaining of gyno from anadrol but also fron tren and nandrolone none of which were supposed to convert to estrogen. What I realized a while ago is that there is no need to invoke exotic mechanisms. Pher and superdrol do not convert to estrogen (nor does tren or anadrol) but they do suppress SHBG. SHBG is actually protective against breast tissue growth beyond just sequestering estrogens (you can read more about this in my book ). The removal of this protective effect as weel as the increase in "free" estrogen from the reduction in SHBG can explain some of the propensity for forming gyno with these compounds. With nandrolone, trenbolone, and other 19-norsteroids, there is also the added production of 5-alpha reduced metabolites that are weak androgens (there is some evidence that tren is metabolized in this fashion) which upstes the androgen to estrogen rati and further contributes to the ability to produce gyno.

I did not know this. Very interesting.

 

[sethroberts]

I did not know this. Very interesting.

It is very interesting and is unknown in the message board (and dare i say) the steroid using community.

 

[Heracles25]

It is very interesting and is unknown in the message board (and dare i say) the steroid using community.

I always knew that most steroids suppressed SHBG to some extinct, others like DHT, Winny and so on did a better job but never knew about the other effectst that you listed.

Great thread and thanks for taking the time to do this. Maybe post this at bb.com. I post there the most, but there are ALOT of questions in regards to prolactin, progesterone, gyno and so forth.

 

[Frank Reynolds]

The only issue I have with that is that you might be overlooking the potential dangers of dopaminergic modulation while you malign "toxic" nolva. GH is known to be mitogenic in the breast so your conlcusion about reducing dose in those cases is spot on.

I was under the impression Caber had was "toxic" to the liver as well, no?

 

[sethroberts]

I was under the impression Caber had was "toxic" to the liver as well, no?

Hepatic Impairment: Since Cabergoline is extensively metabolized by the liver, caution should be used, and careful monitoring exercised, when administering Cabergoline to patients with hepatic impairment.

There is also some potential for cardiac valvulopathy but that is generally with longer term use.

The larger concern is not even listed as a potential side effect. In the lab we used dopamine agonists to desensitize dopamine receptors. We did it to mimic parkinson's and though i doubt that is a concern here, the desensitization is a concern because the loss of dopaminergic suppression of lactotropes could actually result in prolactin excess.

 

[Eric Potratz]

Eric, question for you: the Tren designers, of which 1-T Tren is one, all obviously market as being very similar to trenbolone. Yet the chemical structure of the end hormone after enzymatic conversion may (from what I understand) actually be closer to nandrolone. Any insight on this?

If you look at the molecule structure of dienolone you can see it's somewhere between nandrolone and Trenbolone, but since it doesn’t aromatize (and considering its overall effects) I’d say it much closer to trenbolone.

-Eric

 

[sethroberts]

If you look at the molecule structure of dienolone you can see it's somewhere between nandrolone and Trenbolone, but since it doesn’t aromatize (and considering its overall effects) I’d say it much closer to trenbolone.

-Eric

Their is no proof one way or the other as to whether it aromatizes and the binding affinities say that it is closer to nandrolone.

Nandrolone Dienolone Trenbolone
AR 154 134 197
PR 20 17 74

 

[Dragon13]

Their is no proof one way or the other as to whether it aromatizes and the binding affinities say that it is closer to nandrolone.

Nandrolone Dienolone Trenbolone
AR 154 134 197
PR 20 17 74

Yeah, based on info in this thread - I'm kinda leaning towards maybe it does. That would explain a whole heck of a lot, and make running an AI with the Trens the simple solution.

 

[crazyfool405]

Hepatic Impairment: Since Cabergoline is extensively metabolized by the liver, caution should be used, and careful monitoring exercised, when administering Cabergoline to patients with hepatic impairment.

There is also some potential for cardiac valvulopathy but that is generally with longer term use.

The larger concern is not even listed as a potential side effect. In the lab we used dopamine agonists to desensitize dopamine receptors. We did it to mimic parkinson's and though i doubt that is a concern here, the desensitization is a concern because the loss of dopaminergic suppression of lactotropes could actually result in prolactin excess.

do you feel .5 mg of Caber will do more harm then good at 1 dose per week? will it be ok to use it especially on npp and test, and soon to be test and Tren?

 

[Random181]

seth, eric: what are your views on Bromocriptine in the event of prolactin problems? will it be effective against 1-t tren gyno? (if any occurs) im also confused about its long term effects, will there be any effects of a short 1.25mg ED sort of course if I needed it to cure issues on/after 1-t tren? Do either of you also have views on running it on cycle, or is it just overkill?

 

[gelin]

Seth,

I’d appreciate it if you could touch on the anadrol-winstrol relationship. It’s got me a little confused.

Anadrol doesn’t aromatize obviously… Historically its sides have been attributed to progestins, as it binds PR but not AR. Now, you’ve stated that the release of bound estrogens due to lowered SHBG levels, as well as the loss of the general protective effects of SHBG can explain gyno with certain compounds such as SD, phera, anadrol and tren. That makes sense to me so far.

Running winny alongside anadrol seems to cut down on sides. Yet winny supposedly knocks down SHBG levels greatly. It’s also been said that winny has “anti-progestagenic” effects. I don’t know what that really entails. If anadrol’s sides are indeed due to freed estrogen and a lowered SHBG environment, can you explain what happens when winny is added to the model? Why aren't anadrol's sides more pronounced? TIA.

 

[sethroberts]

do you feel .5 mg of Caber will do more harm then good at 1 dose per week? will it be ok to use it especially on npp and test, and soon to be test and Tren?

The only appropriate use of bromocriptine is in the presence of clinically elevated prolactin levels (and of course as prescribed and under the supervision of a physician) -- imo there is no reason to use it otherwise.

 

[sethroberts]

Seth,

I’d appreciate it if you could touch on the anadrol-winstrol relationship. It’s got me a little confused.

Anadrol doesn’t aromatize obviously… Historically its sides have been attributed to progestins, as it binds PR but not AR. Now, you’ve stated that the release of bound estrogens due to lowered SHBG levels, as well as the loss of the general protective effects of SHBG can explain gyno with certain compounds such as SD, phera, anadrol and tren. That makes sense to me so far.

Running winny alongside anadrol seems to cut down on sides. Yet winny supposedly knocks down SHBG levels greatly. It’s also been said that winny has “anti-progestagenic” effects. I don’t know what that really entails. If anadrol’s sides are indeed due to freed estrogen and a lowered SHBG environment, can you explain what happens when winny is added to the model? Why aren't anadrol's sides more pronounced? TIA.

There is no evidence that oxymetholone binds to the PR and though its AR binding is low, its has been shown that its effects are mediated through the AR. Running winny may seem to cut down on the sides but this is not in controlled tests -- only through anecdotal reports. I suggested its use as such back in 1997 or 1998. Winstrol is a strange molecule -- it binds receptors for which there is no known function (or whose function is still being elucidated). I also talk a lot in my book about how different steroids alter adrenal function and how this may have a role in producing gynecomastia.

 

[crazyfool405]

The only appropriate use of bromocriptine is in the presence of clinically elevated prolactin levels (and of course as prescribed and under the supervision of a physician) -- imo there is no reason to use it otherwise.

libido purposes, seems to help me a little in that area when i take it. just wondered if it would be more more harm then good while on test and progestins, im using adex EOD though

 

[sethroberts]

libido purposes, seems to help me a little in that area when i take it. just wondered if it would be more more harm then good while on test and progestins, im using adex EOD though

If prolactin is elevated and is causing decreased libido then it would be valid to use it for that purpose. Do you have any evidence that prolactin is elevated?

 

[crazyfool405]

If prolactin is elevated and is causing decreased libido then it would be valid to use it for that purpose. Do you have any evidence that prolactin is elevated?

im using it 1x a week for protective measure, because i need to pick up my labs from my last blood test.

but i still have a little gyno so i know my e2 is a tad high or higher then it should be as well as my growth factors which may lead to that prolactin increase.

 

[sethroberts]

im using it 1x a week for protective measure, because i need to pick up my labs from my last blood test.

but i still have a little gyno so i know my e2 is a tad high or higher then it should be as well as my growth factors which may lead to that prolactin increase.

The only question then is, if prolactin is not elevated, would there be any point to using caber?
but, since you are already taking it, it may confound the test results (if you were taking it before the blood test)

 

[crazyfool405]

The only question then is, if prolactin is not elevated, would there be any point to using caber?
but, since you are already taking it, it may confound the test results (if you were taking it before the blood test)

i cant remember, i dont think soo i think i started the next day

 

[sethroberts]

i cant remember, i dont think soo i think i started the next day

Well then it may be enlightneing to see your prolactin level when it comes back. Please share. I just wonder how many people are treating "elevated" prolactin when there is, in fact, no real elevation.

 

[Trauma1]

Damn - It looks like a missed quite a bit in the week i was gone. I have some catching up to do with reading.

I have some good endocrine/pathophysiology info to add to this discussion.

 

[crazyfool405]

Well then it may be enlightneing to see your prolactin level when it comes back. Please share. I just wonder how many people are treating "elevated" prolactin when there is, in fact, no real elevation.

i can call and try having them fax my labs over, its a 40min drive to go there just tp pick them up.;

 

[crazyfool405]

Damn - It looks like a missed quite a bit in the week i was gone. I have some catching up to do with reading.

I have some good endocrine/pathophysiology info to add to this discussion.

id love to hear

 

[fueledpassion]

Firstly, only trenbolone is a strong PR binder, dienolone and nandrolone are not -- they bind but are actually quite weak. The rest of what you wrote (I can address more fully in a little while -- I am heading out at the moment) is more or less correct (there are some things that I will take issue with later) but the whole ball of wax can be summed up by saying that in the absence of elevated estrogen, prolactin and progesterone will not cause gynecomastia so I go back to my original statement that if you control estrogen, then you will limit gyno. If prolactin and or gyno cannot cause gyno in the absence of elevated estrogen then they are not the root cause.

I like all the info you've given and the responses and questions, although some of it is exhaustive to say the least. So with that statement, I want to get to brass tax on this subject.

What to do on cycle and PCT for Tren? I can firmly agree with you on the matter of controlling estrogen to avoid gyno of any type, but you don't recommend the use of AI's, even the weaker ones, while on cycle. Why? I thought AI's did just that -- control estrogen levels. And yes, I heard about the whole idea of Tren shutting you down and making the body "vulnerable" to "free" estrogen, which is suspect to cause all this gyno in the first place. AI's don't have any affect on free estro?

I would almost think a reasonable dose of AI while on cycle would work just fine. That is what I'm currently doing, and so far no problems have arised. Of course, I'm using Formex, which is formestane. The me and thebigT are the current people using Tren and formestane, although he is using the transdermal form, I am not.

But the real question for myself is how to come off the AI once the cycle is over. Cold turkey sounds like a recipe for estrogen spikes to me. What would you recommend?

 

[Eric Potratz]

I like all the info you've given and the responses and questions, although some of it is exhaustive to say the least. So with that statement, I want to get to brass tax on this subject.

What to do on cycle and PCT for Tren? I can firmly agree with you on the matter of controlling estrogen to avoid gyno of any type, but you don't recommend the use of AI's, even the weaker ones, while on cycle. Why? I thought AI's did just that -- control estrogen levels. And yes, I heard about the whole idea of Tren shutting you down and making the body "vulnerable" to "free" estrogen, which is suspect to cause all this gyno in the first place. AI's don't have any affect on free estro?

I would almost think a reasonable dose of AI while on cycle would work just fine. That is what I'm currently doing, and so far no problems have arised. Of course, I'm using Formex, which is formestane. The me and thebigT are the current people using Tren and formestane, although he is using the transdermal form, I am not.

But the real question for myself is how to come off the AI once the cycle is over. Cold turkey sounds like a recipe for estrogen spikes to me. What would you recommend?

If these steroids are causing gyno by releasing E2 through SHBG down-regulation or competitive binding then an AI won’t do anything to prevent gyno from the circulating E2. (or the low levels of antagonistic DHT) Therefore, Seth suggests a SERM to block the action of estrogen.

The theory makes sense, but I would still caution against the SERM administration and instead opt for prolactin control. (Being a potent co-factor in breast growth, perhaps keeping it in the sub-physiological range will partly cripple estrogens ability to induce mammary growth)

-Eric

 

[Eric Potratz]

seth, eric: what are your views on Bromocriptine in the event of prolactin problems? will it be effective against 1-t tren gyno? (if any occurs) im also confused about its long term effects, will there be any effects of a short 1.25mg ED sort of course if I needed it to cure issues on/after 1-t tren? Do either of you also have views on running it on cycle, or is it just overkill?

Yeah, no reason for the bromo… I would just stick with the Vitex.

-Eric

 

[fueledpassion]

If these steroids are causing gyno by releasing E2 through SHBG down-regulation or competitive binding then an AI won’t do anything to prevent gyno from the circulating E2. (or the low levels of antagonistic DHT) Therefore, Seth suggests a SERM to block the action of estrogen.

The theory makes sense, but I would still caution against the SERM administration and instead opt for prolactin control. (Being a potent co-factor in breast growth, perhaps keeping it in the sub-physiological range will partly cripple estrogens ability to induce mammary growth)

-Eric

The only problem is, I still have this feeling of "iffiness". I dont really see a conclusion or a general agreement in theory. I see one very educated man in this thread in the matters of hormones and everyone else either 1) sharing results, or 2) asking questions like myself. Heck, I'm gonna get all of these products and keeping searching for a perfect way to combine the dosages in PCT. So far, I have this:

Formex
Nolva
ZMA

and I might consider buying the Vitrix stuff, since I've heard good results in libido enhancements, or I might opt for Hydrotest. So if anyone on here has experience with the same or similar PCT please chime in on how to use them together in regards to Tren or Trenlike PH's. Thanks.

 

[samadhismiles]

Hepatic Impairment: Since Cabergoline is extensively metabolized by the liver, caution should be used, and careful monitoring exercised, when administering Cabergoline to patients with hepatic impairment.

There is also some potential for cardiac valvulopathy but that is generally with longer term use.

The larger concern is not even listed as a potential side effect. In the lab we used dopamine agonists to desensitize dopamine receptors. We did it to mimic parkinson's and though i doubt that is a concern here, the desensitization is a concern because the loss of dopaminergic suppression of lactotropes could actually result in prolactin excess.

so are you saying that you could get a prolactin 'rebound' effect after stopping cabergoline treatment?

 

[sethroberts]

If these steroids are causing gyno by releasing E2 through SHBG down-regulation or competitive binding then an AI won’t do anything to prevent gyno from the circulating E2. (or the low levels of antagonistic DHT) Therefore, Seth suggests a SERM to block the action of estrogen.

The theory makes sense, but I would still caution against the SERM administration and instead opt for prolactin control. (Being a potent co-factor in breast growth, perhaps keeping it in the sub-physiological range will partly cripple estrogens ability to induce mammary growth)

-Eric

The only problem is that prolactin control wil ldo nothing for the elevated estrogen and with a reduction in prolactin, estrogen is likely to go higher.

 

[sethroberts]

so are you saying that you could get a prolactin 'rebound' effect after stopping cabergoline treatment?

Absolutely. Possibly long term depending on how severe the desensitization in dopaminergic neurons.

 

[sethroberts]

The only problem is, I still have this feeling of "iffiness". I dont really see a conclusion or a general agreement in theory. I see one very educated man in this thread in the matters of hormones and everyone else either 1) sharing results, or 2) asking questions like myself. Heck, I'm gonna get all of these products and keeping searching for a perfect way to combine the dosages in PCT. So far, I have this:

Formex
Nolva
ZMA

and I might consider buying the Vitrix stuff, since I've heard good results in libido enhancements, or I might opt for Hydrotest. So if anyone on here has experience with the same or similar PCT please chime in on how to use them together in regards to Tren or Trenlike PH's. Thanks.

When there is a perfect consensus, that is when you should be very skeptical.

 

[Eric Potratz]

The only problem is, I still have this feeling of "iffiness". I dont really see a conclusion or a general agreement in theory. I see one very educated man in this thread in the matters of hormones and everyone else either 1) sharing results, or 2) asking questions like myself. Heck, I'm gonna get all of these products and keeping searching for a perfect way to combine the dosages in PCT. So far, I have this:

Formex
Nolva
ZMA

and I might consider buying the Vitrix stuff, since I've heard good results in libido enhancements, or I might opt for Hydrotest. So if anyone on here has experience with the same or similar PCT please chime in on how to use them together in regards to Tren or Trenlike PH's. Thanks.

Just FYI, Im just talking about 460mg/day of the generic vitex... not all the fancy stuff on the market.

-Eric

 

[Eric Potratz]

with a reduction in prolactin, estrogen is likely to go higher.

How do you propose?

 

[Brenn]

Excellent thread everyone, absolutely riveting!

I have a complicated question about PRE-Cycle therapy, based on my limited knowledge. i.e. Setting up a good environment for avoiding gyno. Ideally, I'd rather avoid it than deal with it.

From the reading of this thread, I gleaned this: Tren, Tren desigers and possible Anadrol etc. cause a lowering of SHBG, which releases bound Estrone Sulfate, which in the presence of raised PG or PG sensitivity = possible gyno. Or maybe the Estrone Sulfate alone causes it.

The question is thus:
Would a low-dosed AI for a month or so before a cycle help avoid the arising of Gyno symptoms once on a cycle of Tren or the "Tren" designers?

My thinking (however dimly lit) is like this: By suicidal inhibition of Aromatase for a month, most aromatase is inhibited. During this time, SHBG bound Estrone Sulfate clears the body by regular enzymatic process. New SHBG is produced, but is not bound to Estrone Sulfate as there would be little to bind to due to the AI. So when the Tren Designer is introduced, there is no Estrone Sulfate to be released, so less gyno risk. Follow up by taking Nolva on cycle to avoid whatever problems may arise from the DS/AAS

I ask about a month period as I've heard that it is roughly the enzymatic turnover time for aromatase. (Journal of Broscience et. al 2009).

Or by doing the above, would we just be setting up a major estro-rebound in PCT?

Is there any way to set up the body for a cycle of Tren/Designers?

Thanks again for the excellent read!

 

[fueledpassion]

Excellent thread everyone, absolutely riveting!

I have a complicated question about PRE-Cycle therapy, based on my limited knowledge. i.e. Setting up a good environment for avoiding gyno. Ideally, I'd rather avoid it than deal with it.

From the reading of this thread, I gleaned this: Tren, Tren desigers and possible Anadrol etc. cause a lowering of SHBG, which releases bound Estrone Sulfate, which in the presence of raised PG or PG sensitivity = possible gyno. Or maybe the Estrone Sulfate alone causes it.

The question is thus:
Would a low-dosed AI for a month or so before a cycle help avoid the arising of Gyno symptoms once on a cycle of Tren or the "Tren" designers?

My thinking (however dimly lit) is like this: By suicidal inhibition of Aromatase for a month, most aromatase is inhibited. During this time, SHBG bound Estrone Sulfate clears the body by regular enzymatic process. New SHBG is produced, but is not bound to Estrone Sulfate as there would be little to bind to due to the AI. So when the Tren Designer is introduced, there is no Estrone Sulfate to be released, so less gyno risk. Follow up by taking Nolva on cycle to avoid whatever problems may arise from the DS/AAS

I ask about a month period as I've heard that it is roughly the enzymatic turnover time for aromatase. (Journal of Broscience et. al 2009).

Or by doing the above, would we just be setting up a major estro-rebound in PCT?

Is there any way to set up the body for a cycle of Tren/Designers?

Thanks again for the excellent read!

Thats a really good question and I too would like to hear some educated opinions on the matter.

 

[Dragon13]

The only problem is that prolactin control wil ldo nothing for the elevated estrogen and with a reduction in prolactin, estrogen is likely to go higher.

Which makes an even more compelling case for an on-cycle AI or SERM.

 

[Mass_69]

From the reading of this thread, I gleaned this: Tren, Tren desigers and possible Anadrol etc. cause a lowering of SHBG, which releases bound Estrone Sulfate, which in the presence of raised PG or PG sensitivity = possible gyno. Or maybe the Estrone Sulfate alone causes it.

FYI - Elevated androgens in general cause a lowering of SHBG (as do elevated insulin, cortisol, among other things). Estrogens & thyroid hormones, among other things, raise SHBG. I'm not sure if there are specific androgens that do not lower SHBG, but my guess would be the less androgenic (the androgen) is, the less of a lowering effect it has on SHBG.

 

[Dragon13]

Very interesting thread on another site. See:

http://www.t-nation.com/free_online_forum/sports_training_performance_bodybuilding_gear/help_my_late_pct_superdrol_has_ruined_me_?id=2985069&pageNo=0

Read through the whole thing, but about 25% down on page 2 you'll see the tie-in with the this topic.

 

[Brenn]

Hey Mass69, Roger that, very true. I mentioned those Trens and Anadrol as they seem to lower SHBG AND result in problems for many folks. (AD50 I really enjoyed when I was younger BTW). For some reason, other SHBG lowering AAS don't seem to have the same nasty reputation. I wish I knew why.

I'm really curious to find the differences between AAS's that affect SHBG the same way, as Tren and Anadrol (Superdrol), but don't cause nearly the same amount of Gyno hassle.

For example: Winni and Proviron are so great at lowering SHBG, and are often taken to enhance the effectiveness of a Test cycle, raise free test etc. But I've never heard of Winnie or Proviron causing this problem, as we know they are taken to offset gyno risk! Tendons that snap like dry twigs, yes! But not the Gyno so much. Something else is going on there that doesn't seem to depend solely on SHBG being down. So it must be in combination with PG being up? But then what about Anadrol, wheres the PG? I'd love to know.

With 19-nors and Tren, we can say they are progesterones and, that the action on PG and PG sensitivity is to blame, in combo with the SHBG lowering. But Interestingly, in another thread on this here board, there was a discussion about SD and Gyno.

One member interviewed many users and the ones that reported Gyno after SD almost always included and AI in their PCT. The ones who used SERM only, far less Gyno.

They theorized that it was because of supressed E for too long (on cycle, then into PCT) then came off the AI after PCT, the AI cycles out of the system, then WHAM! Estrogen sensitivity + raised E2 = "delayed gyno"...seemed convincing.

However, if the info in this thread is on target, perhaps it works like this: With a Clomid protocol for example, in basic terms Test rises, but so does E2 to a lesser degree. With a rise in E2 from the Clomid therapy, SHBG rises with it, giving (as Seth said) protective effects in the breast tisue = no gyno.

Alternatively:
Post cycle CLOMID + AI would suppress this E2 rise from the clomid and also the SHBG rise with it, also further enhance E2 sensitivity, then a few weeks/months later...delayed gyno. So when PCT is finished: Low SHBG, rising E2, E2 sensitivity...gyno

Much like IKEA furniture however, after making this (cough) "theory" there is still an extra part left out...Progesterone. Where does it fit with the Lowered SHBG + E2 sensitivity/rise? Dunno. As hormones normalise, is there a rise in PG also?

Ok guys, (taking of my Broscientist Lab coat and hat with the mirror thing), off to work.

Fun thread...I got a bottle SD that I'm keen to use, but I gotta work this out beforehand!

 

[Dragon13]

Hey Mass69, Roger that, very true. I mentioned those Trens and Anadrol as they seem to lower SHBG AND result in problems for many folks. (AD50 I really enjoyed when I was younger BTW). For some reason, other SHBG lowering AAS don't seem to have the same nasty reputation. I wish I knew why.

I'm really curious to find the differences between AAS's that affect SHBG the same way, as Tren and Anadrol (Superdrol), but don't cause nearly the same amount of Gyno hassle.

For example: Winni and Proviron are so great at lowering SHBG, and are often taken to enhance the effectiveness of a Test cycle, raise free test etc. But I've never heard of Winnie or Proviron causing this problem, as we know they are taken to offset gyno risk! Tendons that snap like dry twigs, yes! But not the Gyno so much. Something else is going on there that doesn't seem to depend solely on SHBG being down. So it must be in combination with PG being up? But then what about Anadrol, wheres the PG? I'd love to know.

With 19-nors and Tren, we can say they are progesterones and, that the action on PG and PG sensitivity is to blame, in combo with the SHBG lowering. But Interestingly, in another thread on this here board, there was a discussion about SD and Gyno.

One member interviewed many users and the ones that reported Gyno after SD almost always included and AI in their PCT. The ones who used SERM only, far less Gyno.

They theorized that it was because of supressed E for too long (on cycle, then into PCT) then came off the AI after PCT, the AI cycles out of the system, then WHAM! Estrogen sensitivity + raised E2 = "delayed gyno"...seemed convincing.

Bingo. Exactly what I think causes the "delayed gyno" phenomenon. This is especially true with all the OTC PCT users out there. You can't get a true SERM OTC. All the products guys get OTC- Reversitol, Novedex, etc etc - are AIs. You run 4 weeks at a steady dose, estrogen has been killed, test has recovered somewhat, you have a heightened sensitivity to E... That's why if you use an AI in PCT, you absolutle MUST taper down.

However, if the info in this thread is on target, perhaps it works like this: With a Clomid protocol for example, in basic terms Test rises, but so does E2 to a lesser degree. With a rise in E2 from the Clomid therapy, SHBG rises with it, giving (as Seth said) protective effects in the breast tisue = no gyno.

Hmmm, I'll buy that.

Alternatively:
Post cycle CLOMID + AI would suppress this E2 rise from the clomid and also the SHBG rise with it, also further enhance E2 sensitivity, then a few weeks/months later...delayed gyno. So when PCT is finished: Low SHBG, rising E2, E2 sensitivity...gyno

Exactly.

Much like IKEA furniture however, after making this (cough) "theory" there is still an extra part left out...Progesterone. Where does it fit with the Lowered SHBG + E2 sensitivity/rise? Dunno. As hormones normalise, is there a rise in PG also?

Ok guys, (taking of my Broscientist Lab coat and hat with the mirror thing), off to work.

Fun thread...I got a bottle SD that I'm keen to use, but I gotta work this out beforehand!

Progesterone can only cause gyno in the presence of E, so it's a player but only secondarily. However, part of my thinking is that perhaps compounds with strong affinity for the PR receptor can cause gyno in the presence of normal E levels simply because the PR receptor is being activated so strongly - although based on Seth's direct refutation of the Big Cat Tren Theory, maybe Tren compunds don't have this issue. Some others may, however.

Finally, don't forget about prolactin! I still believe it can be a growth factor, similar to PR above. High prolactin can cause lactation/breast growth even in the presence of "normal" levels of E. Check out the link I posted above. Obviously anecdotal, but interesting nontheless.

Great post, BTW.

 

[crazyfool405]

some articles just to read...

 

[Brenn]

Hey Dragon,
Good stuff there. Especially the bit about the Prolactin. I read the post you linked to as well, interesting reading. Here's a question: Is prolactin always estrogen induced, or is it (as the T-nation article mentions) possibly a separate action of a mal-functioning pituitary? I hope by addressing E2 we are addressing MOST of the problem.

All this leaves me wondering about alternative methods of controlling this gyno problem. Perhaps including low-dosed AAS like Winstrol in a Tren or Tren-like stack would impart some of it's "moob"-protective benefits on-cycle? Or will this drive SHBG into a deep and dangerous hole, that results in Double-D's. Wish I knew!

I've always been old-school with this stuff: I use the lowest dose necessarry to get the result I want. Stop when the weight I want is achieved or continue a bit longer if it is not. I'd love to try these Tren designers, but need more answers. Nothing is worth wrecked pecs, IMO. It takes away from the look I'm going for

 

[spiderduncan]

Subscribed for more information.

 

[sethroberts]

Progesterone can only cause gyno in the presence of E, so it's a player but only secondarily. However, part of my thinking is that perhaps compounds with strong affinity for the PR receptor can cause gyno in the presence of normal E levels simply because the PR receptor is being activated so strongly - although based on Seth's direct refutation of the Big Cat Tren Theory, maybe Tren compunds don't have this issue. Some others may, however.

Finally, don't forget about prolactin! I still believe it can be a growth factor, similar to PR above. High prolactin can cause lactation/breast growth even in the presence of "normal" levels of E. Check out the link I posted above. Obviously anecdotal, but interesting nontheless.

Great post, BTW.

There is no evidence that progesterone causes gyno, even in the presence of estrogen. That is not to say that it is not possible. High prolactin levels will cause problems -- possibly even in the presence of "normal" levels of estrogen but unless you have a blood test showing elevated prolactin levels, I would assume estrogen first, prolactin last. At this point we have a ton of people blindly using caber and bromo (and even profilactively in some cases) with no evidence of prolactin elevation which has the possibility of seriously screwing up your pituitary.

 

[sethroberts]

Hey Mass69, Roger that, very true. I mentioned those Trens and Anadrol as they seem to lower SHBG AND result in problems for many folks. (AD50 I really enjoyed when I was younger BTW). For some reason, other SHBG lowering AAS don't seem to have the same nasty reputation. I wish I knew why.

I'm really curious to find the differences between AAS's that affect SHBG the same way, as Tren and Anadrol (Superdrol), but don't cause nearly the same amount of Gyno hassle.

For example: Winni and Proviron are so great at lowering SHBG, and are often taken to enhance the effectiveness of a Test cycle, raise free test etc. But I've never heard of Winnie or Proviron causing this problem, as we know they are taken to offset gyno risk! Tendons that snap like dry twigs, yes! But not the Gyno so much. Something else is going on there that doesn't seem to depend solely on SHBG being down. So it must be in combination with PG being up? But then what about Anadrol, wheres the PG? I'd love to know.

With 19-nors and Tren, we can say they are progesterones and, that the action on PG and PG sensitivity is to blame, in combo with the SHBG lowering. But Interestingly, in another thread on this here board, there was a discussion about SD and Gyno.

One member interviewed many users and the ones that reported Gyno after SD almost always included and AI in their PCT. The ones who used SERM only, far less Gyno.

They theorized that it was because of supressed E for too long (on cycle, then into PCT) then came off the AI after PCT, the AI cycles out of the system, then WHAM! Estrogen sensitivity + raised E2 = "delayed gyno"...seemed convincing.

However, if the info in this thread is on target, perhaps it works like this: With a Clomid protocol for example, in basic terms Test rises, but so does E2 to a lesser degree. With a rise in E2 from the Clomid therapy, SHBG rises with it, giving (as Seth said) protective effects in the breast tisue = no gyno.

Alternatively:
Post cycle CLOMID + AI would suppress this E2 rise from the clomid and also the SHBG rise with it, also further enhance E2 sensitivity, then a few weeks/months later...delayed gyno. So when PCT is finished: Low SHBG, rising E2, E2 sensitivity...gyno

Much like IKEA furniture however, after making this (cough) "theory" there is still an extra part left out...Progesterone. Where does it fit with the Lowered SHBG + E2 sensitivity/rise? Dunno. As hormones normalise, is there a rise in PG also?

Ok guys, (taking of my Broscientist Lab coat and hat with the mirror thing), off to work.

Fun thread...I got a bottle SD that I'm keen to use, but I gotta work this out beforehand!

You should pick up a copy of my book. I think it does a pretty good job of laying all of this out and gives several reasons for the difference in activity of different AAS.

Commercials aside Proviron is a really strong binder of SHBG but I have never seen any evidence that proviron decreases SHBG levels. But then again, people tend to stack mesterolone with aromatizing steroids. Winstrol reduces SHBG and we see that in the literature, but the reduction is not that severe -- only about 50%. Stronger androgens can decreases SHBG levels to only about 10% of control values - In one study, Anadrol reduced SHBG levels by 55 nmol/L which is a major decrease.

 

[Brenn]

Hi Seth,
I'm already on it! Looking into getting a copy now.

Ah, correct sir, I mis-spoke!...Proviron binds SHBG, not lowers it. Winnie lowers it, but not like Anadrol. Check.

Does bound SHBG have any protective benefit in the breast or otherwise?

Until this thread, I wasn't aware that SHBG had any role at all in gyno. I always thought SHBG was a biological verison of pure-evil, put on us by an angry God.

Thanks for taking the time, Seth. Looking forward to your book.

 

[sethroberts]

Hi Seth,
I'm already on it! Looking into getting a copy now.

Ah, correct sir, I mis-spoke!...Proviron binds SHBG, not lowers it. Winnie lowers it, but not like Anadrol. Check.

Does bound SHBG have any protective benefit in the breast or otherwise?

Until this thread, I wasn't aware that SHBG had any role at all in gyno. I always thought SHBG was a biological verison of pure-evil, put on us by an angry God.

Thanks for taking the time, Seth. Looking forward to your book.

Until recently, that is pretty much what I thought too. You have to realize that SHBG is not "bound" per se. It is in flux between being bound and unbound in an equilibrium state.