Gyno on TREN

Rebound is bro science in general. Can be that you just dropped the dbol and you reached your highest e2 just when you stopped it. Are you following me?


Would not use dopamine antagonist in anyway unless I really have too. Go read what happens when you start playing with dopamine in your body. It's a trio of dopamine and two other hormones. They balance themselves out all together. You screw with one you screw with all of them and getting it back it's a fucking nightmare. Would not use.


I believe is not that progesterone gyno doesn't exist but what happens is that most ppl let the e2 slip out of control and then says they got gyno from Tren or deca when in fact they got gyno from e2.

Go see if 99-% of th ppl that claim they have gyno from Tren or deca have blood test to prove it. They don't... If they had they would see that e2 were out of whack
 
This subject always frustrates me because I want to dip back into Tren or deca one day. I'm intimidated by Tren from when I brewed finaplix h and got puffy nips & some lactation many yrs ago. Back then I'd only use nolva and was very successful to nvr get gyno. Ran several test cycles alone and some with dbol, test w/winstrol, test w/Eq, then got brave and used test/fina 75mg ED(6weeks). Got minor puffy nips and mini marble left nip. I quit the Tren and upped the nolva and the marble reduced to bb size ball thank God!

I'm not trying to argue or discredit you @Docd187123 , hell I've asked help from you several times through pm. I would just like to know how to avoid gyno with Tren. I understand the vets say control E2 but there's some guys that swear caber worked to rid of the lump like a member here @lucabratzi Their are others I've heard and researched but hardly any concrete evidence like you have mentioned.

Monitor bloods and make sure you're controlling your estrogen properly. If gyno develops add in nolvadex or raloxifene.

I'm sure theres science that says caber doesn't work for gyno from deca. But for me it worked. For tren gyno it didn't. Don't ask me why.

Unfortunately I go by trial and error w myself and figure out what works. Nolva for tren worked quickly.

Next npp run maybe I'll run a little more Adex and see if that prevents it.

I've also heard someone here say there's a "withdrawal effect" of some sort coming off caber. But from what I've read that's for patients that take high doses for years. Not the steroid user that uses it on certain occasion. @Docd187123 did u tell me that or was it someone else? Also do U any insight on that?

I know I've mentioned DAWS before. Not sure if I did with you particularly or not. As with withdrawals from anything, yes, it depends on dose and duration. I've not hit that stage myself but the couple times I did try DA's I did not feel myself the next few days. I wasn't aware of DAWS at that time so I'm not sure it was a placebo effect.

Can anyone explain why you'd get gyno after coming off of dbol, none of the injectables changed in dose when I came off... Yet I still got gyno only after dropping the Dbol. This happened to another person in this thread as well.

You could have had the gyno beforehand and had it exacerbated from the dbol or the dbol just started it. Gyno doesn't simply manifest overnight. The environment that started the process could have been done an over (your dbol use) and you only noticed it after coming off.

Rebound
25mg aromasing daily
20mg Novaldex daily
For four weeks minimum

There is no such thing as estrogen rebound.
 
Bigfella

Estrogen rebound for want of a better term can happen due to a number of reasons. Either estrogen levels are still too high once protection measures are ceased, Test levels havn't been sufficiently recovered leaving E levels too high in the T/E ratio, or your recovery has resulted in a spiked T, which will convert to excess E and give a gyno favourable environment once again.
 
Bigfella

Estrogen rebound for want of a better term can happen due to a number of reasons. Either estrogen levels are still too high once protection measures are ceased

Estrogen levels will not rise above pretreatment values once "protection measures" are ceased. They'll teturn to homeostasis.

Test levels havn't been sufficiently recovered leaving E levels too high in the T/E ratio

That's not a rebound effect at all. Either way, if test levels haven't recovered, and test is low, than estrogen would be low as well not high unless there was another factor involved.

or your recovery has resulted in a spiked T, which will convert to excess E and give a gyno favourable environment once again.

A rise in T can provide a concomitant rise in E. Again, this is not a rebound effect at all.
 
I was taking pharma adex the entire time, and only when I finished the dbol was when a lump started to form and they hurt. I've had gyno in the past, and I had surgery to remove it, but the surgeon didn't remove enough. It flares up periodically on cycle, but this case has me dumbfounded as after I stopped the most likely compound to cause a flare up is when it actually flared up... Makes no sense.
 
High prolactin
Caber will sort it out

Not true bc you are taking other AAS that elevate E-2 which can certainly influence the development of GCM.

I can't begin to tell you how many times I've attempted to confirm this bro science Prolactin/19Nor association, and NOT ONCE was an elevated prolactin level detected.

It's ashame misinformation of this nature continues to permeate AAS forms bc it often leads to inappropriate and ineffective therapy.

To that end I challenge you to investigate the number of times forum members, from Meso and elsewhere, have posted their "own" 19Nor/prolactin experiences, never making efforts toward confirmation thru lab testing.

In fact I believe it's prophetic to know EVERY time I've challenged a prolactin induced GCM post, by suggesting confirmatory lab testing, no one has returned
to cite an elevated prolactin level, IF they return at all!
 
I was taking pharma adex the entire time, and only when I finished the dbol was when a lump started to form and they hurt. I've had gyno in the past, and I had surgery to remove it, but the surgeon didn't remove enough. It flares up periodically on cycle, but this case has me dumbfounded as after I stopped the most likely compound to cause a flare up is when it actually flared up... Makes no sense.

Why does this not make any sense? Of course it does bc you are cycling Dbol and TT both are well established to raise E-2 levels.

Another fact many overlook is the PRIMARY site of TT-E-2 aromatization is fatty tissue and the chest wall region is fat laden in many respects.

If you ever get a chance to observe a BB on AAS undergoing liposuction for GCM do so, bc the difference is truly remarkable IME.

It should be OBVIOUS the water content of that which is being sucked out is considerably higher than those not using AAS.

It seems those who are predisposed to GCM are also more apt to develop "bloat" within the adipose cells about the anterior chest wall region.

This may explain why some BB note an improvement in their GCM with isolated AI therapy.

(Some actually complain the use of AI only TX makes their GCM look worse, perhaps bc shrinkage of the SURROUNDING fatty tissue, makes the more centrally positioned E-2 dependent breast tissue appear more prominent)
 
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Why does this not make any sense? Of course it does bc you are cycling Dbol and TT both are well established to raise E-2 levels.

Another fact many overlook is the PRIMARY site of TT-E-2 aromatization is fatty tissue and the chest wall region is fat laden in many respects.

If you ever get a chance to observe a BB on AAS undergoing liposuction for GCM do so, bc the difference is truly remarkable IME.

It should be OBVIOUS the water content of that which is being sucked out is considerably higher than those not using AAS.

It seems those who are predisposed to GCM are also more apt to develop "bloat" within the adipose cells about the anterior chest wall region.

This may explain why some BB note an improvement in their GCM with isolated AI therapy.

(Some actually complain the use of AI only TX makes their GCM look worse, perhaps bc shrinkage of the SURROUNDING fatty tissue, makes the more centrally positioned E-2 dependent breast tissue appear more prominent)

I believe the part that doesn't make sense to him is why didn't the gyno begin while he was on dbol. He says it only started after cessation of dbol but he still was on test. Gyno isn't formed overnight and it's my guess that he only noticed it after stopping the dbol but by then it had already begun growing.
 
I believe the part that doesn't make sense to him is why didn't the gyno begin while he was on dbol. He says it only started after cessation of dbol but he still was on test. Gyno isn't formed overnight and it's my guess that he only noticed it after stopping the dbol but by then it had already begun growing.

Perhaps and one thing I know based on years of dealing with those who have developed GCM is; the devil is in the details.

Like oh doc you think the following may also have contributed?

- I'm running HCG
- I started and the stopped SERM PCT
- I just finished an Adrol cycle
- Does Deca effect E-2 levels for more than a few days

I'm NOT suggesting these apply to the SHM per say but considering the limited fund of knowledge regarding GCM in many Meso noobs, failure to mention important factors is the rule rather than the exception IME.
 
Is AI pharma grade is another one. So many ppl running fake AI or underdosed stuff.

But yeah as I said before... No one has ever blood to prove this Tren/deca gyno. I'm on deca cycle at the moment and in few weeks I'll draw blood for the monthly checkup I usually do. I have baseline of progesterone and prolactin before starting :) so we can compare and see if it really gets elevated :)
 
Is AI pharma grade is another one. So many ppl running fake AI or underdosed stuff.

But yeah as I said before... No one has ever blood to prove this Tren/deca gyno. I'm on deca cycle at the moment and in few weeks I'll draw blood for the monthly checkup I usually do. I have baseline of progesterone and prolactin before starting :) so we can compare and see if it really gets elevated :)

PLEASE post the results bc I've grown so weary of hearing the same old lame "everyone is different" excuse! :)
 
Oh and just in case some don't know how to correlate an "elevated" serum prolactin level to that which is consistent with the development of GCM,, a brief review of the Risperidine literature provides some guidance.

In summary one author uses the following:

Normal MALE Prolacin level
- is LESS THAN 20ng/ml

MILD HYPERPROLACTINEMIA
- less than 100ng/ml

MODERATE HP
- between 100-200ng/ml

SEVERE HP
- greater than 200ng/DL

So what Jim, lol

We need something to use as a BASELINE comparison.

Which DRUG/s have been shown to increase serum Prolactin levels, above statistical chance?

Does such an elevation result in clinical signs of hyperprolactinemia such as; impotence, GCM, galactorrhea?

What serum Prolactin level is required to establish causation?

The answer to the above is Risperidone and the level REQUIRED based on that data ranges between 50-100ng/ml.

Fact is the LOWEST prolactin level I could locate was 121ng/DL in a patient who developed GCM while on Risperidone, any lower level posts are greatly appreciated.

I lowered the "required" prolactin level to 50ng/DL bc one's E-2 level could have a marked effect on the development of GCM

To that end understand how difficult it will be to confirm or refute the prolactin/19Nor/ GCM association in the presence of elevated E-2 !



Hope that helps guys.
 
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Next up, what clinical feature is most SPECIFIC for hyperprolactemia!

(Meaning, if you have this particular sign/symptom hyperprolactinemia becomes the PRIMARY CONSIDERATION)
 
And the answer is:

GALACTORRHEA

I only mention this bc of the confusion many have about its significance.

Pathologic Galactorrhea is the SPONTANEOUS secretion of a "milk like" liquid from the CENTRAL AEROLA breast area.

It does NOT require MANUAL EXPRESSION such as "squeezing my nips", or does the fluid have a semi-solid "cottage cheese" like consistency.

Finally bc the responsible mechanisms are almost always manifested via ductile breast tissue, the expression should occur at the nipple or aerola region.
 
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Well it's a myth that's etched in stone within the BB community. So much so, it's become factual myth :)

The way I see it is that there are two separate myths that tend to overlap one another.

On one hand you have the people who claim 19-nor AAS raise prolactin. And on the other hand you have the people who claim prolactin can cause gyno.

Then to completely throw a wrench into the equation, you have the people who think any sort of itchiness or soreness at the nipple means gyno so when they get a sore nipple while running tren the issue becomes "OMG I got prolactin induced gyno from a 19-nor" and they are led to believe that tren raises prolactin and prolactin causes gyno.

It's a big clusterfuck no matter which way you look at it.
 
Indeed and if one follows the historical rationale used by many of the 19Nor/Prolactin proponents, it should become obvious such grossly flawed logic is used as the basis for "bro science".

To that end, the mindless parroting of anecdotal experiences as being factual equivalents continues to plague AAS forums with no end in sight.

I mean heck some of this misinformation is so FULL OF HOLES it compels one to suspect the respondents gave no thought to the "theories" whatsoever.

For example;

The bro science 19Nor/Prolactin
"connection" is as follows (at least this how I've heard it explained by some "experienced" forum members.

1- 19Nor AAS bind to the PROGESTERONE receptor

2- binding the PG receptor increases the production of PG?

3- heightened levels of PG increase either E-2 and/or Prolactin

4- elevated PRL results in GCM.

Now that's a fascinating theory but it's also absolutely and completely BOGUS, bc about the only association proven factual, esp in non-pregnant females is number ONE!

Imagine the theories one could concoct if similar logic was applied to the ANDROGEN RECEPTOR?

Like ah bc androgens bind the androgen receptor they result in increased TT levels, when the antithesis is known to occur in most cell types!
 
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On one hand you have the people who claim 19-nor AAS raise prolactin. And on the other hand you have the people who claim prolactin can cause gyno.

Bc the predisposition to GCM is for all intents and purposes, defined at or around puberty, hormonal changes per say will NOT effect the responsiveness of E-2 dependent breast tissue.

Stated another way, the influence of hormones on breast tissue are analogous to the those changes observed from AAS on SKM.... HYPERTROPHY.

To that end although PRL can accelerate ductile hypertrophy its influence on breast acinar/alveoli tissue is paltry compared to that of either progesterone and estrogen in particular.

The is further evidenced by the observation galactorrhea is by far the most common complaint in those with an isolated PR elevation, while GCM is minimal and often not noted on behalf of the patient.

These associations are reasonably well established and perhaps should received greater emphasis on my earlier posts.
 
I believe the part that doesn't make sense to him is why didn't the gyno begin while he was on dbol. He says it only started after cessation of dbol but he still was on test. Gyno isn't formed overnight and it's my guess that he only noticed it after stopping the dbol but by then it had already begun growing.

This is exactly why it doesn't make sense. I was running .5m pharma adex, but I believe it wasn't effective due to an error in manufacturing. Like I said, I got surgery a few years ago and not enough was taken out so I'm not overly worried, I plan on going back under the knife within the next year to get it taken care of once and for all.

Thanks for the replies. Dbol is a no-go for me.
 
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