Gyno or Lower Chest Fat

[dr jim]

Any drug can harm you! Taking them as directed certainly diminishes the chances of adverse effects.
These are the known complications from AAS EVEN if used appropriately;
1) Erythrocytosis
2) HTN
3) Dyslipidemia
4) suppressed HTPA functioning
5) gonadal atrophy
6) hypogonadism
7) infertility
8) gynecomastia
9) erectile dysfunction
10) and LAST but not LEAST, irrational thought on behalf of long term users,

Regs


Jim

Oh FYI, these side effects are UNEQUIVOCALLY PROVEN to occur even if AAS are "taken properly", albeit in most instances the complications are directly proportional to the patients age, the potency, dose used, and some cases such as gynecomastia, highly idiosyncratic.

Regs
Jim

 

[dr jim]

The following is a quote from Dr. Scally



Not to make an appeal to authority but are you saying he's wrong?

---------------------------------------------
Your comparing apples to oranges fella. To suggest TT or E-2 has the same effect on peripheral or pituitary prolactin receptors or production in "normal" patients without deranged prolactin/dopamine physiology because of a Macro-Prolactinima, is being naive.

And I know Dr S is NOT making that suggestion either.

Fact is I've never heard S proclaim any CLINICALLY relevant connection exists between TT and Prolactin such that in otherwise normal males the use of AAS causes breast changes because of PROLACTIN.

The etiology which has been proven for those with AAS associated gynecomastia, galactorrhea etc is mediated via E-2.

Why don't you investigate Dr S therapy for gynecomastia for patients using ANY AAS? I promise he or I don't believe prolactin is the issue, which is why SERMs rather than D-2 agonists are considered the DOC.

Finally I'm still awaiting the first patient who has gynecomastia and a causative elevation in serum Prolactin.

Why is that important? Because after more than FIFTY YEARS of AAS use not even a single case report exists which supports this notion or belief.

So indeed if found I've got something which is bound for a JOURNAL PUBLICATION, no BS!

Best
Jim

 

[Get Some]

You can take AAS properly yet still develop complications. You can also take AAS and not get any. I always go by the scientific method and supplement that info, which is sometimes lacking, with anecdotal evidence. Personally I refuse to rely solely on anecdotal evidence.

YOU can live a "healthy" life and still die of cancer or some other bullshit disease like Leukemia (terrible ****ing disease that I lost a family member to). It's impossible to weigh the risk of doing "something" when you are taking a risk just by being alive.

 

[Get Some]

Just to throw in my $0.02 from my PERSONAL EXPERIENCE.... Gyno from 19-nors was very different from gyno that I experienced with test, dbol, etc. Test and dbol gave me a lump in the breast... tren (different cycle) turned my nipple into a giant puffball with no lump. How can this be explained? I thought for sure I had read somewhere that elevated e2 from aromatizable aas can have a negative effect on prolactin levels when also using a 19-nor product. I believe this to be true, but I don't necessarily think that caber/prami will have a positive effect in reducing these issues.

This is why I have argued that if you are running a cutting cycle, you should run the test far lower than the tren to avoid the amount of aromatization that will occur, thereby minimizing the prolactin issues. Also, you don't need as much test when you are cutting IMO as it is only there as the "base" hormone so just run enough to feel "right" and go from there.

I could post article after article on this subject and this thread could go on for 20 more pages... but honestly I'm sick of this kind of stuff. As you get older you realize that things do not work out by chance, there's a reason for everything. I learned that running lower test on a tren run and supplementing aromasin or letro will keep my gyon in check. I do that because it's what works for me and I would urge the rest of you to find out if that or something else works for you. Instead of turning people off from actually reading this thread because it's longer than Great Expectations, I prefer to give real world suggestions based on personal experience. I'm all for a separate thread debating this issue but clearly this thread stemmed from a question on how to correct a situation that may or may not exist. So let's be civil and either answer the original question or at least give some words of advice like IM did.

OP - I would urge you to do as IM says and go see a doctor. I am thinking about doing the same myself and I'm sure dr jim would agree that the ONLY way to completely eradicate gyno is to have the glands surgically removed. If insurance covers it, great!

To everyone else - you stay classy ID

 

[Docd187123]

---------------------------------------------
Your comparing apples to oranges fella. To suggest TT or E-2 has the same effect on peripheral or pituitary prolactin receptors or production in "normal" patients without deranged prolactin/dopamine physiology because of a Macro-Prolactinima, is being naive.

And I know Dr S is NOT making that suggestion either.

Fact is I've never heard S proclaim any CLINICALLY relevant connection exists between TT and Prolactin such that in otherwise normal males the use of AAS causes breast changes because of PROLACTIN.

The etiology which has been proven for those with AAS associated gynecomastia, galactorrhea etc is mediated via E-2.

Why don't you investigate Dr S therapy for gynecomastia for patients using ANY AAS? I promise he or I don't believe prolactin is the issue, which is why SERMs rather than D-2 agonists are considered the DOC.

Finally I'm still awaiting the first patient who has gynecomastia and a causative elevation in serum Prolactin.

Why is that important? Because after more than FIFTY YEARS of AAS use not even a single case report exists which supports this notion or belief.

So indeed if found I've got something which is bound for a JOURNAL PUBLICATION, no BS!

Best
Jim

I never stated PRL causes gynecomastia. I know it doesn't and that prolactin induced gyno doesn't exist. I know SERMs are the standard treatment for gyno outside of surgery bc I've read the literature and have quite a few doctors and a pharmacist in my family who I query on these matters regularly. I think you misunderstood what I was trying to say.

The he poster I quoted in that reply said he wouldn't put anything in his body that could cause lactation. I stated testosterone could indirectly cause lactation through elevated E2 and PRL.

 

[dallas]

Well I have my answers and thank you all.

 

[dr jim]

I never stated PRL causes gynecomastia. I know it doesn't and that prolactin induced gyno doesn't exist. I know SERMs are the standard treatment for gyno outside of surgery bc I've read the literature and have quite a few doctors and a pharmacist in my family who I query on these matters regularly. I think you misunderstood what I was trying to say.

The he poster I quoted in that reply said he wouldn't put anything in his body that could cause lactation. I stated testosterone could indirectly cause lactation through elevated E2 and PRL.

=======================================================

Yea great point mate, because your last comment imparts another important factor!. However any AAS which aromatizes may and usually does increase E-2, yet the degree of that change AND the physiologic response is highly individualistic.

Nonetheless although there is no doubt some mates will develop Gynecomastia changes with minimal perturbations of their E-2 level, others seemingly never manifest ANY breast alterations.

There is no doubt ALL mates would develop some degree of Gyneco IF E-2 was driven high enough or if a TT:E-2 reversal transpired (E-2 > TT), because the latter is the therapeutic goal for TRANSSEXUALS who "want breasts".

Indeed it shouldn't be to surprising, the absolute amount of E-2 required is also quite variable and appears to be dependent upon the quantity of E-2 dependent breast tissue from the outset. (I've no doubt the "non-respnders" to traditional E-2 dosing would also be resistant to cycling standard AAS dosages.)

Ok so what about lactation in these he/she's?

Lactation is a very complex process that involves the timely interaction of THREE primary hormones. Included are E-2 Progesterone and Prolactin.

A brief review may aid some of the naysayers whom cling the their antiquated bro lore.

First E-2 must be elevated VERY ELEVATED to ensure mammary gland and duct devel

 

[dr jim]

=======================================================

Yea great point mate, because your last comment imparts another important factor!. However any AAS which aromatizes may and usually does increase E-2, yet the degree of that change AND the physiologic response is highly individualistic.

Nonetheless although there is no doubt some mates will develop Gynecomastia changes with minimal perturbations of their E-2 level, others seemingly never manifest ANY breast alterations.

There is no doubt ALL mates would develop some degree of Gyneco IF E-2 was driven high enough or if a TT:E-2 reversal transpired (E-2 > TT), because the latter is the therapeutic goal for TRANSSEXUALS who "want breasts".

Indeed it shouldn't be to surprising, the absolute amount of E-2 required is also quite variable and appears to be dependent upon the quantity of E-2 dependent breast tissue from the outset. (I've no doubt the "non-respnders" to traditional E-2 dosing would also be resistant to cycling standard AAS dosages.)

Ok so what about lactation in these he/she's?

Lactation is a very complex process that involves the timely interaction of THREE primary hormones. Included are E-2 Progesterone and Prolactin.

A brief review may aid some of the naysayers whom cling the their antiquated bro lore.

First E-2 must be elevated VERY ELEVATED to ensure mammary gland and duct devel

Suffice it to say at close to TEN "hormones" are involved in pregnancy induced lactation. And although "lactation" is achievable in the majority of male/female transsexuals the quantity (a daily BCP or conjugated estrogens such as Premarin) and duration (1-2 YEARS).

Obviously the dosage required FAR exceeds any cycle period. Moreover many patients are placed on androgen suppressive therapy to further ensure an TT:E-2 reversal and or a E-2 level ranging between 100-200 ng/ml.

While studies in transexuals have supported the notion markedly elevated E-2 can in fact increase SERUM Prolactin, the prerequisites are in no way achievable thru AAS cycling, unless perhaps that UGL has pulled the dirty deed and substituted estrogens for androgens, lol!

Another point worth emphasizing, galactorrhea will not occur even if the Prolactin level is increased CONSIDERABLY unless the breast tissue has been "primed by E-2" with an abrupt decline of the latter, shortly thereafter. This rapid fall of E-2 is responsible for the surge of prolactin in pregnant females, and classically follows "suckling" on behalf of the newborn.

This negative feedback loop is important, no critical, for the development of galactorrhea/lactation!

THE POINT?

It matters NOT what the prolactin level is because in the absence of an INCREASED E-2 clinically relevant breast alterations simply DO NOT OCCUR. So once again, treat the cause of that "increased Prolactin level", as rare as it is IN CYCLISTS, by either lowering E-2 with an AI, or by "blocking" the receptors responsible for it's physiologic effects using a SERM.

This study emphasizes a few salient points IMO

Best
jim

 

[graniteman]

Say what you want, I'm reading a shit ton of info. Good stuff gents carry on !

 

[Docd187123]

=======================================================

Yea great point mate, because your last comment imparts another important factor!. However any AAS which aromatizes may and usually does increase E-2, yet the degree of that change AND the physiologic response is highly individualistic.

Nonetheless although there is no doubt some mates will develop Gynecomastia changes with minimal perturbations of their E-2 level, others seemingly never manifest ANY breast alterations.

There is no doubt ALL mates would develop some degree of Gyneco IF E-2 was driven high enough or if a TT:E-2 reversal transpired (E-2 > TT), because the latter is the therapeutic goal for TRANSSEXUALS who "want breasts".

Indeed it shouldn't be to surprising, the absolute amount of E-2 required is also quite variable and appears to be dependent upon the quantity of E-2 dependent breast tissue from the outset. (I've no doubt the "non-respnders" to traditional E-2 dosing would also be resistant to cycling standard AAS dosages.)

Ok so what about lactation in these he/she's?

Lactation is a very complex process that involves the timely interaction of THREE primary hormones. Included are E-2 Progesterone and Prolactin.

A brief review may aid some of the naysayers whom cling the their antiquated bro lore.

First E-2 must be elevated VERY ELEVATED to ensure mammary gland and duct devel

I agree with this and it backs my personal experience. The level of E2 elevation to develop gyno is highly variable. A friend got gyno with E2 around 110pg/ml if memory serves me while I had E2 levels of 379pg/ml using bunk adex. I didn't develop gyno but I was holding about 9lbs of water bc of it.

Also agree with the comment about TT:E2 ratios as a ratio in favor of E2 could cause gyno while not necessarily having to be elevated by much.

 

[Docd187123]

Suffice it to say at close to TEN "hormones" are involved in pregnancy induced lactation. And although "lactation" is achievable in the majority of male/female transsexuals the quantity (a daily BCP or conjugated estrogens such as Premarin) and duration (1-2 YEARS).

Obviously the dosage required FAR exceeds any cycle period. Moreover many patients are placed on androgen suppressive therapy to further ensure an TT:E-2 reversal and or a E-2 level ranging between 100-200 ng/ml.

While studies in transexuals have supported the notion markedly elevated E-2 can in fact increase SERUM Prolactin, the prerequisites are in no way achievable thru AAS cycling, unless perhaps that UGL has pulled the dirty deed and substituted estrogens for androgens, lol!

Another point worth emphasizing, galactorrhea will not occur even if the Prolactin level is increased CONSIDERABLY unless the breast tissue has been "primed by E-2" AND there is an abrupt decline of the latter.

This negative feedback loop is important for the development of galactorrhea!

THE POINT?

It matters NOT what the prolactin level is because in the absence of an INCREASED E-2 clinically relevant breast alterations simply DO NOT OCCUR. So once again, treat the cause of that "increased Prolactin level", as rare as it is IN CYCLISTS, by either lowering E-2 with an AI or by blocking it's physiologic effects using a SERM.

I thought this study emphasizes a few salient points IMO

Best
jim

to my knowledge, and correct me if wrong here, but E2 is what causes ductal cell hyperplasia and progesterone causes alveolar hyperplasia which is what the milk actually flows through? Elevated PRL or PGR can also cause increased sensitivity to PRL?

Mi always mention E2 management as the primary defense against rising PRL levels. I'm in complete agreement there as the vast majority can get by without dopamine agonists simply by controlling E2. I have never read anything supporting SERM use in this case though. Would you happen to have any literature on the topic?

 

[dr jim]

to my knowledge, and correct me if wrong here, but E2 is what causes ductal cell hyperplasia and progesterone causes alveolar hyperplasia which is what the milk actually flows through? Elevated PRL or PGR can also cause increased sensitivity to PRL?

Mi always mention E2 management as the primary defense against rising PRL levels. I'm in complete agreement there as the vast majority can get by without dopamine agonists simply by controlling E2. I have never read anything supporting SERM use in this case though. Would you happen to have any literature on the topic?

I am only referencing the OPTIMAL treatment of gynecomastia using SERMS and there are several studies which support that opinion.

The use of AI's are best reserved as adjunctive Gynecomastia therapy, OR for reducing the peripheral effects of E-2 such as "bloat" or for generalized fluid retention.

So yep IMO these dopamine agonists are the wrong treatment for the wrong diagnosis, for the wrong reasons and simply should NOT be used by those cycling AAS, unless of course they are PREGNANT TRANSEXUALS with a MACRO-PROLACTINOMA,

Respects
jim