Prolactin - Tren/Deca

[Sworder]

Has anybody personally gotten elevated prolactin to the point where the nipple was secreting a white liquid?
Or elevated prolactin as confirmed by labs?

If so, how much tren /deca were you running and was a SSRI used at the same time?

[Atomini]

The issue of elevated prolactin is an interesting one.

It can be kept in control by keeping estrogen levels from rising, and also from the use of a prolactin antagonist as you probably already know. What's also funny is that progestins are actually SUPPOSED to inhibit prolactin secretion, but for some reason, progestins such as Trenbolone and Nandrolone end up causing an increase in prolactin. We all know how things are SUPPOSED to be in theory, but in practice it can be very different, especially in a game like this where every individual reacts differently to different compounds compared to the next person.

As a precaution, I always run a prolactin antagonist when running Trenbolone regardless. I will take zero chances of this, thank you very much. Aside from that, I am sure you can find plenty of people who have had high prolactin levels in bloodwork with the resulting symptoms of lactation and/or anorgasmia, and so on and so forth.

[Atomini]

By the way, why would you ask if an SSRI was used simultaneously?

[Sworder]

The issue of elevated prolactin is an interesting one.

It can be kept in control by keeping estrogen levels from rising, and also from the use of a prolactin antagonist as you probably already know. What's also funny is that progestins are actually SUPPOSED to inhibit prolactin secretion, but for some reason, progestins such as Trenbolone and Nandrolone end up causing an increase in prolactin. We all know how things are SUPPOSED to be in theory, but in practice it can be very different, especially in a game like this where every individual reacts differently to different compounds compared to the next person.
As a precaution, I always run a prolactin antagonist when running Trenbolone regardless. I will take zero chances of this, thank you very much. Aside from that, I am sure you can find plenty of people who have had high prolactin levels in bloodwork with the resulting symptoms of lactation and/or anorgasmia, and so on and so forth.

Progestins such as tren and decagynecomastia but we need to question if tren/deca can cause an increase in prolactin!

I know that my brother doesn't run an AI nor does he run caber while doing 700mg Tren/week. Personally, I always have to run a strong dose of AI or I will have problems. You have to sometimes question where the rumors started from as it may be perpetuated by other motives rather than concerning your health. You can not deny the silence of people complaining of this phantom rumor if you would estimate the number of tren/deca users whom don't use an AI/DA.

By the way, why would you ask if an SSRI was used simultaneously?

Certain SSRIs have been shown to cause hyperprolactinaemia.

[jimmyinkedup]

I dont believe there is an increase in prolactin at all from progestins. In fact id be very surprised to see bloodwork that shows elevated prolactin without a corresponding elevation in estrogen. What progsterone , or progestins do however do, is cause an upregulation of the prolactin receptor. HOWEVER ironically enough that upregulation does not take place in breast tissue. Prolactin does NOT equal gyno. It does explain some of the sexual sides some may experience and the only real course of action is a dopamine agonist to lower proactin ..even though it may not even technically be elevated!! There are progesterone antagonists , female birth control , ie morning after pill etc., but their use is far from practical.
As Nandi pointd out years ago ..estrogen management really is the key man.

[Sworder]

Growth hormone, insulin, prolactin and total thyroxine in the plasma of sheep implanted with the anabolic steroid trenbolone acetate alone or with oestradiol.
http://www.ncbi.nlm.nih.gov/pubmed/7017853
Abstract:

The mode of action of the anabolic steroid trenbolone acetate (19-norandrost-4,9,11-trien-3-one-17-acetate) was studied through the endogenous hormonal response of castrated male sheep to subcutaneous implantation of 140 mg of trenbolone acetate and 20 mg of oestradiol both separately and in combination. Radioimmunoassay of delta-4,9,11-trienic steroids and oestradiol-17 beta in plasma confirmed that simultaneous administration of trenbolone acetate with oestradiol led to a significantly greater persistence of oestradiol-17 beta residues in plasma (P less than 0.05) than with implantation of oestradiol alone. Oestradiol treatment increased concentrations of growth hormone and insulin (P less than 0.05; P less than 0.001 respectively) in plasma samples collected weekly. Trenbolone acetate by itself had no significant effect and the oestrogenic response was blocked on the simultaneous implantation of trenbolone acetate and oestradiol (despite higher plasma levels of oestradiol-17 beta with this treatment). Plasma total thyroxine was markedly depressed to 45 per cent of its basal level by trenbolone acetate, alone or with oestradiol (P less than 0.001) and depressed to 80 per cent of basal by oestradiol treatment alone (P less than 0.001). Plasma prolactin was unaltered by the above treatments.



Can't seem to find all those studies on trenbolone in humans ;P

[Sworder]

I dont believe there is an increase in prolactin at all from progestins. In fact id be very surprised to see bloodwork that shows elevated prolactin without a corresponding elevation in estrogen. What progsterone , or progestins do however do, is cause an upregulation of the prolactin receptor. HOWEVER ironically enough that upregulation does not take place in breast tissue. Prolactin does NOT equal gyno. It does explain some of the sexual sides some may experience and the only real course of action is a dopamine agonist to lower proactin ..even though it may not even technically be elevated!! There are progesterone antagonists , female birth control , ie morning after pill etc., but their use is far from practical.
As Nandi pointd out years ago ..estrogen management really is the key man.

I agree 100%

[Metalject]

I dont believe there is an increase in prolactin at all from progestins. In fact id be very surprised to see bloodwork that shows elevated prolactin without a corresponding elevation in estrogen. What progsterone , or progestins do however do, is cause an upregulation of the prolactin receptor. HOWEVER ironically enough that upregulation does not take place in breast tissue. Prolactin does NOT equal gyno. It does explain some of the sexual sides some may experience and the only real course of action is a dopamine agonist to lower proactin ..even though it may not even technically be elevated!! There are progesterone antagonists , female birth control , ie morning after pill etc., but their use is far from practical.
As Nandi pointd out years ago ..estrogen management really is the key man.

Great Post!

[dec11]

never, i start with an AI from the get go on tren and never had probs.

as stated, control the estro from day one and all should be good.

[Swifto]

Progestins such as tren and decagynecomastia but we need to question if tren/deca can cause an increase in prolactin!


I know that my brother doesn't run an AI nor does he run caber while doing 700mg Tren/week. Personally, I always have to run a strong dose of AI or I will have problems. You have to sometimes question where the rumors started from as it may be perpetuated by other motives rather than concerning your health. You can not deny the silence of people complaining of this phantom rumor if you would estimate the number of tren/deca users whom don't use an AI/DA.



Certain SSRIs have been shown to cause hyperprolactinaemia.

Where have you read Nandrolone

[Sworder]

Competitive progesterone antagonists: receptor binding and biologic activity of testosterone and 19-nortestosterone derivatives.
http://www.ncbi.nlm.nih.gov/pubmed/446***

Abstract:
Testosterone and 19-nortestosterone derivatives were evaluated in a developmental scheme designed to identify competitive progesterone antagonists having abortifacient activity. Compounds that displayed significant binding to the rabbit uterine progesterone receptor were followed in biologic tests for progestational, antiprogestational, and abortifacient activities. Of the seven compounds tested for both progestational and antiprogestational activity, only one, 5 alpha-dihydronorethindrone, behaved exclusively as an antagonist. Five other 19-nortestosterones (19-nortestosterone, 17 beta-hydroxyestra-4, 9(10)-dien-3-one, norethindrone, norethindrone acetate, and R 2323) proved to be mixed agonists/antagonists. 5 alpha-Dihydronorethindrone, norethindrone, and 19-nortestosterone terminated pregnancy during the postnidatory period in rats; in addition, the latter two compounds inhibited progesterone-supported pregnancy in spayed rats and curtailed pregnancy during the postnidatory period in hamsters. These results demonstrate that several 19-nortestosterone derivatives bind to the uterine progesterone receptor and behave either as antagonists or mixed agonists/antagonists.

Yes, often Nandrolone is lumped together with Trenbolone and they are assumed to exhibit the same behavior. This is not true! But I have found data to support it in this case.

Also, from a discussion the other day I found out that Cabergoline is suppressive to growth hormone /IGF-1. I think that cabergoline/DA is a waste of money and do not provide a benefit for its purposed action. Could you add some more thoughts to the topic other than the a[nt]gonist activity of the compounds?

[Swifto]

There is conflicting data on this subject actually. Both with Trenbolone and Nanrdolone.

Be careful not to confuse binding affinity with intrinsic activity.

[Sworder]

/>
I didn't mention affinity nor interpret data based on affinity.

In the end there doesn't seem to be any data whatsoever showing that these two compounds increase prolactin. It may be one of the biggest myths in the steroid world, it would be good to reconsider the use for cabergoline in trenbolone cycles. Also, you notice that nobody recommends a DA for the nandrolone

[Sworder]

The effect of trenbolone on acetate growth, blood hormones and metabolites, and nitrogen balance of beef heifers
http://journals.cambridge.org/action...ne&aid=7365892

Abstract:

Four animals from a group of eight Hereford × Friesian heifers weighing approximately 365 kg were implanted with 300 mg trenbolone acetate at the beginning of a 60-day trial period. Treated heifers grew more quickly (P<0·05) and converted food to liveweight gain more efficiently (P < 0·01) than untreated cdntrols. They had lower overall concentrations for serum albumin and plasma urea (P<0·01), the differences being maintained throughout the diurnal periods studied. No significant differences were recorded in the mean values for serum total protein, plasma glucose or free fatty acids. Similarly, the absence of significant differences in the mean values for serum growth hormone, insulin and prolactin suggested that these hormones did not mediate the response to trenbolone acetate. Implanted heifers had a significantly greater retention of nitrogen (P<0·01) which was mainly due to a reduction in the excretory products associated with total urinary nitrogen.

[Swifto]

The effect of trenbolone on acetate growth, blood hormones and metabolites, and nitrogen balance of beef heifers
http://journals.cambridge.org/action...ne&aid=7365892

Abstract:

Four animals from a group of eight Hereford × Friesian heifers weighing approximately 365 kg were implanted with 300 mg trenbolone acetate at the beginning of a 60-day trial period. Treated heifers grew more quickly (P<0·05) and converted food to liveweight gain more efficiently (P < 0·01) than untreated cdntrols. They had lower overall concentrations for serum albumin and plasma urea (P<0·01), the differences being maintained throughout the diurnal periods studied. No significant differences were recorded in the mean values for serum total protein, plasma glucose or free fatty acids. Similarly, the absence of significant differences in the mean values for serum growth hormone, insulin and prolactin suggested that these hormones did not mediate the response to trenbolone acetate. Implanted heifers had a significantly greater retention of nitrogen (P<0·01) which was mainly due to a reduction in the excretory products associated with total urinary nitrogen.

Beef heifers...

I think you need to give google a rest.

[Sworder]

Beef heifers...

I think you need to give google a rest.

You aren't going to find a lot of studies on trenbolone in humans!! This is how science is done, experiment on animals and extrapolate information to humans. But no matter how much I Google I can't seem to find anything that supports trenbolone increases PROLACTIN. It is heiferpoop, broscience, a myth!!

Edit: Maybe that is too harsh. If I put it like this, it is not supported by science. Also, Progestins are NOT Progesterone!! They aren't the same compound and they won't signal the brain to start producing prolactin.

[Swifto]

You aren't going to find a lot of studies on trenbolone in humans!! This is how science is done, experiment on animals and extrapolate information to humans. But no matter how much I Google I can't seem to find anything that supports trenbolone increases PROLACTIN. It is heiferpoop, broscience, a myth!!

Edit: Maybe that is too harsh. If I put it like this, it is not supported by science. Also, Progestins are NOT Progesterone!! They aren't the same compound and they won't signal the brain to start producing prolactin.

I'm pretty sure I know what "science is" Sworder.

I've backed every dam claim I have ever made with a reference or multiple references.

If you don't believe that, please go through my threads/articles/posts and tell me where I haven't.

You wont find much on 19-Nor's and Prolactin, its a question thats been raised for years and years with no proof that progestins raise PRL directly.

[ironbeck]

good thread

[Sworder]

I am sorry if I offended you, but you seemed to disregard the study just because it is not conducted on humans. I think this is a interesting subject to discuss, and I feel comfortable stating that there isn't enough scientific evidence to suggest that Trenbolone increases prolactin. Do you disagree? I honestly don't know where or how this rumor came to be. All I do know is that:
1. There is no scientific evidence to support it.
2. I have never lactated from trenbolone use even at 600mg+/week
3. I have never heard of anybody lactating or having elevated prolactin levels with trenbolone being the cause. I have asked a lot of people personally about this through PMs.

You wont find much on 19-Nor's and Prolactin, its a question thats been raised for years and years with no proof that progestins raise PRL directly.

Exactly!!! So why take cabergoline or other DA? It's a waste of money.

[Atomini]

Sworder,

Progestins, in vitro (and in theory) are actually INHIBITORS of prolactin secretion. However... Trenbolone in varying degrees between users DOES increase prolactin secretion and the only evidence we have unfortunately is anecdotal, but its there with bloodwork and all. I agree: Trenbolone SHOULDN'T cause prolactin secretion and should actually suppress it due to its Progestogenic nature, but the fact is that in some people for unknown reasons it does increase prolactin secretion. And the reason why I support using a prolactin antagonist while running any Progestogenic 19-nor is to keep those levels down in the first place - prolactin has an intense inhibitory effect on libido, sex drive, and the ability to achieve orgasms. We see constant reports of people having sex drive and libido issues when using compounds like trenbolone and deca , and when a prolactin antagonist is inserted into the mix, it solves their libido issues.

I ran Trenbolone once (with 400mg/week of Testosterone ) and waited until week 3 to begin using my standard 1mg/week of Cabergoline - no AI used. At the end of week 2 I had bloodwork done, and prolactin was in the 300s. Taking 1mg of caber took me down to 4. What's strange is that bloodwork in an identical Trenbolone cycle later on with 400mg/week of Testosterone and no AI showed no increase in Prolactin. For unknown reasons in humans, the issue of Prolactin secretion is a dodgy one and different people respond differently at different times, even. As an overall precaution, I always run Cabergoline regardless on any Trenbolone cycle.

I wish there were studies done on humans with Trenbolone that we could look at and finally know the truth behind this, but unfortunately there aren't any and likely won't be any in the near future.

[Swifto]

Sworder,

Progestins, in vitro (and in theory) are actually INHIBITORS of prolactin secretion. However... Trenbolone in varying degrees between users DOES increase prolactin secretion and the only evidence we have unfortunately is anecdotal, but its there with bloodwork and all. I agree: Trenbolone SHOULDN'T cause prolactin secretion and should actually suppress it due to its Progestogenic nature, but the fact is that in some people for unknown reasons it does increase prolactin secretion. And the reason why I support using a prolactin antagonist while running any Progestogenic 19-nor is to keep those levels down in the first place - prolactin has an intense inhibitory effect on libido, sex drive, and the ability to achieve orgasms. We see constant reports of people having sex drive and libido issues when using compounds like trenbolone and deca , and when a prolactin antagonist is inserted into the mix, it solves their libido issues.

I ran Trenbolone once (with 400mg/week of Testosterone ) and waited until week 3 to begin using my standard 1mg/week of Cabergoline - no AI used. At the end of week 2 I had bloodwork done, and prolactin was in the 300s. Taking 1mg of caber took me down to 4. What's strange is that bloodwork in an identical Trenbolone cycle later on with 400mg/week of Testosterone and no AI showed no increase in Prolactin. For unknown reasons in humans, the issue of Prolactin secretion is a dodgy one and different people respond differently at different times, even. As an overall precaution, I always run Cabergoline regardless on any Trenbolone cycle.

I wish there were studies done on humans with Trenbolone that we could look at and finally know the truth behind this, but unfortunately there aren't any and likely won't be any in the near future.

Although there isnt solid data on prolactin LEVELS raising from 19-Nors, I'm pretty sure the estrogen receptor is a co-binding factor in prolactin receptor expression (PRLR). This can make us far more sensitive to PRL even if its not increased or wildly out of range. This theory also fits well with the ER being the causitive factor in PRL issues.

[Capebuffalo]

Wow guys please continue. I am learning and thinking all at the same time

And I'm close to running test and 2 nor 19's together and this is very helpful for me

[Swifto]

J Steroid Biochem Mol Biol. 2002 Oct;82(2-3):263-8.

Estradiol stimulates expression of two human prolactin receptor isoforms with alternative exons-1 in T47D breast cancer cells.

Leondires MP, Hu ZZ, Dong J, Tsai-Morris CH, Dufau ML.
Source

National Institute of Child Health and Human Development, Section Molecular Endocrinology, Endocrinology and Reproduction Research Branch, National Institutes of Health, Bethesda, MD 20892-4510, USA.
Abstract

Human prolactin receptor (hPRLR) expression is regulated by estradiol-17beta (E(2)) in vivo in animal tissues, and in vitro in normal human endometrial cells and in MCF7 human breast cancer cells. The objective of this study was to determine the effect of E(2) on the expression of two recently described hPRLR isoforms with distinct exons-1, hE1(3) and hE1(N1) that are transcribed from the generic hPIII promoter, also present in the rat and mouse, and the human-specific promoter hP(N1), respectively. Also, to determine the effect of estradiol on the hPIII promoter activity in cancer cells. T47D breast cancer cells were examined using quantitative competitive RT-PCR for the level of expression of two alternative non-coding exon-1 transcripts, hE1(3) and hE1(N1) following incubation with E(2) in presence or absence of the E(2) receptor antagonist ICI 182,***. The effects of estradiol were also evaluated in cells transiently transfected with constructs of hPIII promoter luciferase reporter gene. E(2) significantly increased the expression of both hPRLR mRNA transcripts, hE1(3) and hE1(N1). In transfection studies E(2) activated the hPIII promoter. This effect of estradiol was markedly inhibited by coincubation with the E(2) receptor antagonist. Our results demonstrate a stimulatory effect of estradiol on the expression of hPRLR mRNA species with alternative exons-1, hE1(3) and hE1(N1) possibly through activation of their corresponding promoters. The lack of a formal ERE in these promoters suggested that the effect of estradiol is mediated through association of the activated ER with relevant DNA binding transfactor(s). These findings support the role of E(2) in the regulation of hPRLR expression in human breast cancer cell lines.

PMID:
12477494
[PubMed - indexed for MEDLINE]

Not ideal as we also know that normal brest tissue can sometimes respnd differently than cancer cell tissue (PgR expression).

[Atomini]

Although there isnt solid data on prolactin LEVELS raising from 19-Nors, I'm pretty sure the estrogen receptor is a co-binding factor in prolactin receptor expression (PRLR). This can make us far more sensitive to PRL even if its not increased or wildly out of range. This theory also fits well with the ER being the causitive factor in PRL issues.

Yes, agreed, which is also why for the most part, controlling E2 levels should control Prolactin.

Wow guys please continue. I am learning and thinking all at the same time

And I'm close to running test and 2 nor 19's together and this is very helpful for me

Getting any bloodwork done while on that? Would be interesting to see what the readings are for a cycle with two 19-nors.

[Capebuffalo]

Yes, agreed, which is also why for the most part, controlling E2 levels should control Prolactin.



Getting any bloodwork done while on that? Would be interesting to see what the readings are for a cycle with two 19-nors.

My thought ( and I have spoken to others ) is if I run 800 mgs of tren a
Is there a difference in running 400 mgs NPP and 400 mgs tren a
It is still 800 mgs of a nor 19. Not trying to hijack but interested if extra
precautions need to be taken fro prolactin
I'm on 8 reload 2 deload so blood work not accurate for a start point.

[jimmyinkedup]

J Steroid Biochem Mol Biol. 2002 Oct;82(2-3):263-8.

Estradiol stimulates expression of two human prolactin receptor isoforms with alternative exons-1 in T47D breast cancer cells.

Leondires MP, Hu ZZ, Dong J, Tsai-Morris CH, Dufau ML.
Source

National Institute of Child Health and Human Development, Section Molecular Endocrinology, Endocrinology and Reproduction Research Branch, National Institutes of Health, Bethesda, MD 20892-4510, USA.
Abstract

Human prolactin receptor (hPRLR) expression is regulated by estradiol-17beta (E(2)) in vivo in animal tissues, and in vitro in normal human endometrial cells and in MCF7 human breast cancer cells. The objective of this study was to determine the effect of E(2) on the expression of two recently described hPRLR isoforms with distinct exons-1, hE1(3) and hE1(N1) that are transcribed from the generic hPIII promoter, also present in the rat and mouse, and the human-specific promoter hP(N1), respectively. Also, to determine the effect of estradiol on the hPIII promoter activity in cancer cells. T47D breast cancer cells were examined using quantitative competitive RT-PCR for the level of expression of two alternative non-coding exon-1 transcripts, hE1(3) and hE1(N1) following incubation with E(2) in presence or absence of the E(2) receptor antagonist ICI 182,***. The effects of estradiol were also evaluated in cells transiently transfected with constructs of hPIII promoter luciferase reporter gene. E(2) significantly increased the expression of both hPRLR mRNA transcripts, hE1(3) and hE1(N1). In transfection studies E(2) activated the hPIII promoter. This effect of estradiol was markedly inhibited by coincubation with the E(2) receptor antagonist. Our results demonstrate a stimulatory effect of estradiol on the expression of hPRLR mRNA species with alternative exons-1, hE1(3) and hE1(N1) possibly through activation of their corresponding promoters. The lack of a formal ERE in these promoters suggested that the effect of estradiol is mediated through association of the activated ER with relevant DNA binding transfactor(s). These findings support the role of E(2) in the regulation of hPRLR expression in human breast cancer cell lines.

PMID:
12477494
[PubMed - indexed for MEDLINE]

Not ideal as we also know that normal brest tissue can sometimes respnd differently than cancer cell tissue (PgR expression).

Its tricky because i definitively recall reading that e2 did not effect PRLR expression in the pituitary at all. I will look to see if i can find it. Ive also read that testosterone has an inhibitory effect and estrogen a stimulatory one. This one is all over.
I will say this ...show me one set of bloodwork where e2 is manged properly where a progestin increased prolactin. I dont think you can do it (not you Swifto - commenting on the general thread topic)..because i dont think it does.

[jimmyinkedup]

Check this out : http://onlinelibrary.wiley.com/doi/1...9.00439.x/full
Shows quite an increase in mRNA expression re prolactin based on dosage of nandrolone ....
See this one is all over ....

[BUTTERYGOODNESS]

Wow!!! All this makes me wanna be an endocrinologist. So much info

[BUTTERYGOODNESS]

What are some good books on the endo system

[jimmyinkedup]

Heres one that shows progestins have anti PRL activity ! http://www.ncbi.nlm.nih.gov/pubmed/3919048

[Sworder]

Although there isnt solid data on prolactin LEVELS raising from 19-Nors, I'm pretty sure the estrogen receptor is a co-binding factor in prolactin receptor expression (PRLR). This can make us far more sensitive to PRL even if its not increased or wildly out of range. This theory also fits well with the ER being the causitive factor in PRL issues.

I am pretty sure the estrogen RECEPTOR and the prolactin RECEPTOR don't interact. Those ligands don't go together. They are both receivers, estradiol may be a co-activator or something like that but receptor interaction, no. But I think you just mistakenly wrote receptor in there, either way! It is actually well-established that estrogen and progesterone play a prominent role in the production of prolactin. Controlling estrogen is always going to be an issue while on cycle and even more so with Trenbolone

Do we need to even need to go into "prolactin gyno" or is that a dead horse already?

Atomini makes a comment on the loss of libido from deca /fina being a result of prolactin.. Prolactin has an effect on libido yes, but honestly I will not even go into the libido issue as that is one of the biggest mysteries in science. Brain chemistry, sex hormones, sex hormones effect on brain chem, toxicity issues on libido specific tissue, anxiety, stress, the list goes on... If it was established that trenbolone even increased prolactin then this may be looked at. Have you ever contemplated that some people think about deca/fina d1ck so much that it becomes the causation. It is possible then the administration of a DA causes a placebo effect. It's comical and feasible.

[Sworder]

Wow guys please continue. I am learning and thinking all at the same time

And I'm close to running test and 2 nor 19's together and this is very helpful for me

I have ran Test 600/Tren 600/ Deca 300 before without any problems related to prolactin or anything to that sort, libido was sky high as well! Nandrolone is subject to aromatase which you have to additionally account for when you dose your AI. Running cabergoline won't hurt but it isn't need... But then again you are altering dopamine/serotonin balance as well as reducing hGH and IGF-1, okay so it may have some down-sides! But then again you aren't taking any chances of the infamous prolactin sides that nobody seems to get when properly managing e2. Which you should be doing anyway.

[Sworder]

I've backed every dam claim I have ever made with a reference or multiple references.
If you don't believe that, please go through my threads/articles/posts and tell me where I haven't.

The key here is to keep it in normal ranges when "on cycle", not high off the charts and not too low. To low and we can experience a host of other side effects, from loss of labido, energy, joint problems, CNS function, anxiety and erectile dysfunction.

http://forums.steroid.com/showthread...o#.UHPFYFFZZX8

If you call me out like that I am gonna have to respond, not going to scour your threads but I remember reading that one. If you would please show me a study showing the correlation between low e2 and libido(with testosterone levels being in the 50th percentile) I would stand corrected. I have searched far and wide for that correlation but have only found one and that one was lacking in some data. I am not stating I don't believe it, just asking for a reference to the data as you claim to always have one or two. I usually try to refrain from absolute terms such as never or always.

Edit: If you do please send a link in a PM and I will update this post showing the relation. Would like to refrain from soiling the thread with too much off-topic discussions.

[Capebuffalo]

I have ran Test 600/Tren 600/ Deca 300 before without any problems related to prolactin or anything to that sort, libido was sky high as well! Nandrolone is subject to aromatase which you have to additionally account for when you dose your AI. Running cabergoline won't hurt but it isn't need... But then again you are altering dopamine/serotonin balance as well as reducing hGH and IGF-1, okay so it may have some down-sides! But then again you aren't taking any chances of the infamous prolactin sides that nobody seems to get when properly managing e2. Which you should be doing anyway.

Thanks for the response. Caber will be on hand and e2 will be under control as always.

[Swifto]

http://forums.steroid.com/showthread...o#.UHPFYFFZZX8

If you call me out like that I am gonna have to respond, not going to scour your threads but I remember reading that one. If you would please show me a study showing the correlation between low e2 and libido(with testosterone levels being in the 50th percentile) I would stand corrected. I have searched far and wide for that correlation but have only found one and that one was lacking in some data. I am not stating I don't believe it, just asking for a reference to the data as you claim to always have one or two. I usually try to refrain from absolute terms such as never or always.

Edit: If you do please send a link in a PM and I will update this post showing the relation. Would like to refrain from soiling the thread with too much off-topic discussions.

Sure.

Run Letrozole and 5mg/ED and tell me what happens to your labido clever clogs.

Are you aware that estrogen is probably the hormone that keeps sex drive up in castrated men? Estrogen receptors are present in tissues involved in sexual behavior including several brain centers and pelvic floor muscles as well.

[Sworder]

Sure.
Run Letrozole and 5mg/ED and tell me what happens to your labido clever clogs.
Are you aware that estrogen is probably the hormone that keeps sex drive up in castrated men? Estrogen receptors are present in tissues involved in sexual behavior including several brain centers and pelvic floor muscles as well.

I apologize for the confusion I was asking for a reference not a proposal on how to conduct a "broscience" experiment. Controlled studies, not personal anecdotes is what counts. I am aware of estrogen's importance and have my own theories on the subject. I will update my first post if you can send me a reference otherwise I do not wish to further the discussion with personal theories. I would appreciate if you could comment on the prolactin posts so we stay on-topic

[Swifto]

I apologize for the confusion I was asking for a reference not a proposal on how to conduct a "broscience" experiment. Controlled studies, not personal anecdotes is what counts. I am aware of estrogen's importance and have my own theories on the subject. I will update my first post if you can send me a reference otherwise I do not wish to further the discussion with personal theories. I would appreciate if you could comment on the prolactin posts so we stay on-topic

What spcifically are you asking for? I stated estrogen has an importance in labdio, crush it and you'll lose your labido. Its not rocket science.

Your asking for a "study" on why having a too low estrogen level means loss of labido? Like I've said, run Letro at 5mg/ED and see what happens to your sex drive. I dont give a f*ck if you think thats "bro science". Just because a double blind controlled peer reviewed study may not exist on healthy males given large doses of AI's so their estrogen is zero or greatly impaired, you're telling me its not relivent. Give me a f*cking break. Dont get too caught up in "studies", sometimes personal experience is also relivant - isnt that whats using steroids is about? Do you know how often studies contradict one another?

Your beginning to anoy me with your nonsense. Go play with fire you moron. And, before you come back with some bullshit on whether or not that comment is needed, it is, it was, otherwise I wouldn't have said it.

[Sworder]

Your beginning to anoy me with your nonsense. Go play with fire you moron. And, before you come back with some bullshit on whether or not that comment is needed, it is, it was, otherwise I wouldn't have said it.

The topic about low e2 has existed for a long time in TRT and low estradiol has not been shown to correlate to low libido or sexual desire as the scientists term it. It hasn't been proven to relate. You stated that if you have low estrogen you will have low libido, you can re-read the quote. Specifically what I am asking for is evidence that this relation exists as I have exhausted a lot of energy on the topic. I would accept low-normal or below range as constituting low estrogen. You seem to try to make it seem like you were saying 0 estrogen, you said low estrogen, below normal range.

Yes, I do not accept personal experiences to hold much value if it is not backed by something proveable. This is why there is so much misinformation out there. Maybe this whole prolactin thing came from a person who was taking other medication which actually cause an increase in PRL? Tren cough now what genius came up with that? Yes, through personal experience and the misinformed conclusions drawn from that.

You said that you always have a reference or two about statements you made. I inquired about a reference to the low e2/low libido issue and you are failing to provide one. I don't know why you are trying to argue further when simply you could kill it with "I don't have a reference it is based on personal experience." How is it nonsense when I am asking you for a source? Don't worry, I don't care much if you call me a moron or use adult language. I can handle it

Edit: Can we get back on-topic instead of pointless arguing?

[jimmyinkedup]

http://onlinelibrary.wiley.com/doi/1...nticated=false

[Sworder]

http://onlinelibrary.wiley.com/doi/1...nticated=false

Their estrogen was 88.1 and 55.1 pmol/l during the stages where their libido improved. Kinda confusing as you don't see levels written in pmol/l or nmol/l but 20pg/ml would roughly correspond to 184pmol/l. So their estrogen was low when their libido improved..

Don't get me wrong, I definitely believe that estrogen has a role in libido. I am just arguing the statement that low estrogen = low libido because this isn't always the case as this study shows.