Prolactin - Tren/Deca

[Sworder]

The effect of a combination of trenbolone acetate and oestradiol-17β on growth performance and blood, carcass and body characteristics of wether lambs
http://journals.cambridge.org/action...ne&aid=7359764
Abstract:
Nine Cheviot × Shetland castrated male lambs from a group of 24 of 28 kg initial live weight, were subcutaneously implanted with a combination of 60 mg trenbolone acetate and 12 mg oestradiol-17β at 105 days and again at 45 days before slaughter. Of the remaining lambs, nine were untreated and six were slaughtered at the start of the experiment as part of a comparative slaughter procedure. The lambs treated with the anabolic preparation grew significantly faster (P < 0·05), converted food to live weight and estimated carcass gain more efficiently, had heavier carcasses which were larger, and had greater estimated gains for protein, moisture and ash. Implanted animals also tended to have a smaller deposition of carcass and kidney fat, but significantly heavier kidneys and less wool when the latter three weights were related to empty body weight. The mean values for plasma urea and serum total protein as indicators of protein metabolism were significantly decreased and increased respectively in treated lambs, but no other significant differences in blood metabolites and hormones were recorded. A significant increase in teat length of implanted lambs indicated the oestrogenic nature of the anabolic preparation.


It's in lambs but what do you do? The interesting thing in this study is that they administered estrogen + trenbolone and didn't find an increase in prolactin.

[jimmyinkedup]

Estradiol binds to shbg ....lower esdtradiol = higher shbg ...higher shbg = lower free test. As we all know lower shbg = higher sex drive / higher shbg = lower sex drive.
dr marianco has writeen about this somewhere..I forget where i read it.

[Sworder]

Yes, but if you have normal testosterone levels (or supra as on cycle) the SHBG issue is solved. Once again, I am just arguing the statement that low-normal/below range estrogen affects libido as Swifto claimed he always has a reference. If you have 0 estrogen, your libido is gonna be the last thing on your mind.

[Atomini]

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.

I'd just like to point out the validity of these statements here. I'm a man of evidence and science, and 85% of the time I will ask for studies and references to back up claims made by someone. I will also provide studies and references when explaining something, if they are needed wherever.

HOWEVER... there are just some things that are very basic knowledge in a particular field of study that do not require 'studies' or 'references' to understand. For example, I was recently talking to some guy in the gym who is your typical worry wart concerning growth hormones that are pumped into chickens and cows, and how he is deathly afraid of consuming the growth hormones and it having an effect on his body. I proceeded to explain to him how basic molecular biology works whereby these growth hormones are peptide hormones, and should you consume them through your GI tract, they will be ripped apart into individual amino acids by digestive enzymes and stomach acids, thereby effectively eliminating the growth hormone via deconstruction of the peptide. Therefore, the growth hormone ingested cannot possibly have any transferrance in its useable form from the meat you eat into your body and have any effect. He proceeded to say "show me some studies that prove this is true", at which point I got really pissed off and told him "this is BASIC GRADE 10 BIOLOGY, there are no studies, and I am not obligated to reference you to ANYTHING because all you need to do is go and pick up a basic grade 10 highschool biology textbook and look up 'amino acids and proteins' in the index, flip to that page, and start reading!".

With that being said, the excessive lowering of E2 levels in the body resulting in a loss of libido in males IS A FACT. Although, like Swifto, there are no studies (that I know of) that I can present here, I have one of my 2nd year university textbooks, Molecular And Cellular Biology by Stephen L. Wolfe that states in the hormones and receptors subchapter of an endocrine chapter, that loss of libido in males in fact does occur in lieu of excessive drops of E2 levels. If you really really want, I can read through it when I have some free time and locate the specific sentence/paragraph and scan it for you to see.



And a side note here, it is going to be difficult for you to find all of the studies you want on these subjects. The use of AAS for the purpose of physique and performance enhancement is not an officially recognized use by the medical community or the FDA, and therefore there are few studies that exist where test subjects are administered the compounds and stacks that we use, at the doses we use them as well. You'll find them, but there are not many and there is not very much variety in these studies to boot. Unfortunately there is instead a lot of personal experience and anecdotal evidence we must go by with a keen eye instead, and although I wish this were not the case, this is the research environment that has been created by the current legal and moral status of anabolic steroid use for the purpose of performance enhancement. There's nothing you or I can really do about that right now, and clamoring and banging your fists on the table demanding more studies for certain things that may be too basic or things that just have not been covered, are not going to make them just appear.

[Swifto]

Yes, but if you have normal testosterone levels (or supra as on cycle) the SHBG issue is solved. Once again, I am just arguing the statement that low-normal/below range estrogen affects libido as Swifto claimed he always has a reference. If you have 0 estrogen, your libido is gonna be the last thing on your mind.

Don't put words in my mouth.

I said "too low", you have extrapolated that to mean, "...low-normal/below range estrogen affects libido as Swifto claimed he always has a reference." to suit your stupid argument.

By "too low" I mean when we experience side effects, such as loss of labido. This "too low" statistic of estrogen will vary from individuals, just like some will get gynecomastia on high estrogen and others will not. Yet I have to give you a reference backing my claims. Sometimes a theory backed by indirect data is sufficient IMO. Not some wild theory at all, as I said, run a large dosage of Letro and let me know what happens to your sex drive, and we know Letro lowers E moreso than most other AI's...

[Sworder]

I'd just like to point out the validity of these statements here. I'm a man of evidence and science, and 85% of the time I will ask for studies and references to back up claims made by someone. I will also provide studies and references when explaining something, if they are needed wherever.

HOWEVER... there are just some things that are very basic knowledge in a particular field of study that do not require 'studies' or 'references' to understand. For example, I was recently talking to some guy in the gym who is your typical worry wart concerning growth hormones that are pumped into chickens and cows, and how he is deathly afraid of consuming the growth hormones and it having an effect on his body. I proceeded to explain to him how basic molecular biology works whereby these growth hormones are peptide hormones, and should you consume them through your GI tract, they will be ripped apart into individual amino acids by digestive enzymes and stomach acids, thereby effectively eliminating the growth hormone via deconstruction of the peptide. Therefore, the growth hormone ingested cannot possibly have any transferrance in its useable form from the meat you eat into your body and have any effect. He proceeded to say "show me some studies that prove this is true", at which point I got really pissed off and told him "this is BASIC GRADE 10 BIOLOGY, there are no studies, and I am not obligated to reference you to ANYTHING because all you need to do is go and pick up a basic grade 10 highschool biology textbook and look up 'amino acids and proteins' in the index, flip to that page, and start reading!".

With that being said, the excessive lowering of E2 levels in the body resulting in a loss of libido in males IS A FACT. Although, like Swifto, there are no studies (that I know of) that I can present here, I have one of my 2nd year university textbooks, Molecular And Cellular Biology by Stephen L. Wolfe that states in the hormones and receptors subchapter of an endocrine chapter, that loss of libido in males in fact does occur in lieu of excessive drops of E2 levels. If you really really want, I can read through it when I have some free time and locate the specific sentence/paragraph and scan it for you to see.

And a side note here, it is going to be difficult for you to find all of the studies you want on these subjects. The use of AAS for the purpose of physique and performance enhancement is not an officially recognized use by the medical community or the FDA, and therefore there are few studies that exist where test subjects are administered the compounds and stacks that we use, at the doses we use them as well. You'll find them, but there are not many and there is not very much variety in these studies to boot. Unfortunately there is instead a lot of personal experience and anecdotal evidence we must go by with a keen eye instead, and although I wish this were not the case, this is the research environment that has been created by the current legal and moral status of anabolic steroid use for the purpose of performance enhancement. There's nothing you or I can really do about that right now, and clamoring and banging your fists on the table demanding more studies for certain things that may be too basic or things that just have not been covered, are not going to make them just appear.

The use of AAS to increase libido is officially recognized by the medical community and the abundance of FDA approved testosterone shows consent. I believe estrogen to be important in sexual desire and libido as well. This is a personal theory though which I firmly stand by. Swifto says he always has references for every statement he makes. I was curious about the low estrogen = low libido statement as I have struggled to find a reference for that notion as well. Once again, I am not saying that you will have a functioning libido with 0 estrogen. I am saying that the low-normal or even low estrogen as shown in the study jimmy provided will yield in a functioning libido. Again, I believe in estrogen's importance in libido...

Saying that it is "too basic" to conduct studies on is false Atomini! There are plenty of "basic" studies out there, testosterone to show increase in muscle mass is very basic and there are TONS of studies on that topic. The best argument for why there is no studies on the libido/estrogen subject would be somewhere along the lines that libido doesn't empirically exist and to try to discredit the questionnaires they use or something. I am not trying to have a discussion about the topic, I have been searching for a reference for low libido/low estrogen myself and was hoping to find it as Swifto always has one!

[jimmyinkedup]

Yeah sex drive is low on the list of importance when it comes to the critical roles e plays..no one knows that more than swifto - read his ai thread. Nonetheless the sex drive issue is a real one , that does exist. I will find marianos article ..it references patients, on trt with normal or slightly above normal t levels with low e levels experiencing sexual dysfunction as a result. His point was e2 levels when it comes to trt need to be dealt with on an individual basis and too low is just as bad as too high.
It is also well know that the androgen / estrogen ratio plays a crucial role in sex drive as well as sexual function/dysfunction. So I dont get why this is being argued ?

[Sworder]

By "too low" I mean when we experience side effects, such as loss of labido.

So you know that your estrogen is too high when you start experiencing side effects as well? You claim in the thread that you should stay in normal range implying that "too high" is above normal range and that "too low" is below range.. You are not making sense.

[Sworder]

So I dont get why this is being argued ?

I was just asking for a reference! Thought it was a simple inquiry, ask for a reference, reference is shown. End of discussion! High e2 has been shown to have an effect on libido, this I don't need a reference for.

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.

[Swifto]

So you know that your estrogen is too high when you start experiencing side effects as well? You claim in the thread that you should stay in normal range implying that "too high" is above normal range and that "too low" is below range.. You are not making sense.

"Too high" is above normal range is when side effects become apparent.

"Too low" is below normal range, because "normal range" for that said individual isnt going to yield side effects. That figure will vary. "Too low" for one person may not be "too low" for someone else, so I call it "too low". Apologies I didnt give a specific figure you utter twat. If normal range is 59, it doesnt mean 58 = "too low".

Are you for f*cking real?

Your not making sense, f*ck off and over analyse this shit at think steroids .com.

[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.

Sorry, I don't really know how to respond to insults unless they include some kind of information I can go off. I apologize if I made you upset but I was very excited at the prospect to finally have a reference for that claim. It appears I am going to have to accept that you don't always have references to the claims you make. Your definition of high/low is making much more sense now, thanks. It's really sad to see a thread which can be filled with so much good information derailed by immature name-calling.

[Sworder]

The prolactin responses to active and passive heating in man
http://onlinelibrary.wiley.com/doi/1...05.031294/full

Abstract

The aim of this study was to compare the prolactin and blood pressure responses at identical core temperatures during active and passive heat stresses, using prolactin as an indirect marker of central fatigue. Twelve male subjects cycled to exhaustion at 60% maximal oxygen uptake (inline image) in a room maintained at 33°C (active). In a second trial they were passively heated (passive) in a water bath (41.56 ± 1.65°C) until core temperature was equal to the core temperature observed at exhaustion during the active trial. Blood samples were taken from an indwelling venous cannula for the determination of serum prolactin during active heating and at corresponding core temperatures during passive heating. Core temperature was not significantly different between the two methods of heating and averaged 38.81 ± 0.53 and 38.82 ± 0.70°C (data expressed as means ±s.d.) at exhaustion during active heating and at the end of passive heating, respectively (P > 0.05). Mean arterial blood pressure was significantly lower throughout passive heating (active, 73 ± 9 mmHg; passive, 62 ± 12 mmHg; P < 0.01). Despite the significantly reduced blood pressure responses during passive heating, during both forms of heating the prolactin response was the same (active, 14.9 ± 12.6 ng ml−1; passive, 13.3 ± 9.6 ng ml−1; n.s.). These results suggest that thermoregulatory, i.e. core temperature, and not cardiovascular afferents provide the key stimulus for the release of prolactin, an indirect marker of central fatigue, during exercise in the heat.

[Brohim]

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.

Maybe you could be the human experiment! Take Tren and a HRT test dose and small amount of AI and monitor prolactin. Then your next cycle take same amount of Tren and higher test dose with no AI and see what happens.

[Sworder]

Maybe you could be the human experiment! Take Tren and a HRT test dose and small amount of AI and monitor prolactin. Then your next cycle take same amount of Tren and higher test dose with no AI and see what happens.

The independent variable is the estrogen(produced by the testosterone and managed by AI).. If you would test for the trenbolone to be the deciding factor then that would be the independent variable.

[Sworder]

This is from high prolactin. I posted it in PCT thread too, you don't have to think that you are "lactating" because you get some oily substance discharged when you are squeezing your nipple. Controlling e2 is in your best interest, don't worry about caber. Keep it on hand if you really feel you need to(which you don't) but avoid using it as it will mess with your dopamine.