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Topic starter
16/03/2020 11:52 pm
This discussion started again on that board I don't want to talk about anymore, and I thought it might be an interesting idea to see what intelligent people had to say on the matter :
androgens and prolactin.
After estrogenic and progestagenic activity was dismissed, the whole issue of prolactin being the culprit started up. Same BS as always and a lot of people recommending grandma's homegrown remedies against something that has never even been established.
Fact : androgens decrease prolactin and prolactin activity.
Theory : Prolactin is the culprit in gyno caused by deca/tren
questions :
1.Is there any evidence an androgen can cause an increase in prolactin or prolactin signalling in HEALTHY tissue/individuals ?
2.Is there any evidence that prolactin can cause gyno in estrogen-deprived media/conditions ?
So far all I've found only confirms that this is the so manieth scaremongering tactic, same as it was with AI's and the lot.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
17/03/2020 12:16 am
I've been monitoring my prolactin levels since I started using androgens, and it never changed.
"The medals don't mean anything and the glory doesn't last. It's all about your happiness. The rewards are going to come, but my happiness is just loving the sport and having fun performing" ~ Jackie Joyner Kersee.
Topic starter
17/03/2020 12:38 am
ever used deca/tren in that time ?
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
17/03/2020 1:06 am
in the past when i have extensively used tren, my prolactin levels were normal. i agree, this is some of the worst fear mongering.
17/03/2020 1:29 am
ever used deca/tren in that time ?
Yes BC, both, but never used high doses.
"The medals don't mean anything and the glory doesn't last. It's all about your happiness. The rewards are going to come, but my happiness is just loving the sport and having fun performing" ~ Jackie Joyner Kersee.
17/03/2020 1:46 am
.
deca alone at 800 mg weekly, last 2 weeks at 1000 mg weekly.
respect to Androgens and Prolactin specifically (I not dismiss estrogenic or/and progestogenic effects conclusivel yet, -from genetic predisposition-)
from
nandrolone and aromatase
http://www.cuttingedgemuscle.com/Forum/showthread.php?threadid=1913 4" target="_blank" rel="noopener"> http://www.cuttingedgemuscle.com/Fo...?threadid=19134
at 09-17-2008
well well well mr boldman
congratulations....... great.the values.
....................before cycle---------on cycle (week 5)
estradiol--------30.2 pg/ml----------74.9 pg/ml
prolactin--------11.1 pg/ml----------11.2 pg/ml
free t4-----------1.2 ng/dl------------1.3 ng/dlat the end of the month i will take a blood test again (i continue on cycle)
.
and again
at 09-29-2008
.Today.
estradiol------- 68.30-------pg/ml
prolactin--------.9.70-------pg/ml
free T4---------.1.10-------ng/dlwell, no prolactin increase, estradiol stabilized (but supraphysiological) and free T 4 normal.
job done (but still on cycle), next job, next year, methandrostenolone (used time ago, but with stanozolol).
.
now on 50 mg daily, methandrostenolone, next week plus 100 mg stanozolol every day.
.
dr frankenstein
Topic starter
17/03/2020 2:07 am
keep us posted on that one as well. Do you have scans of these sections of the lab results ? (all personal info blanked out of course). I wouldn't mind using it in an article.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
17/03/2020 2:29 am
Isn't Tren An androgen?
Seabiscuit Hogg is a fictious internet character. It is not recommended that you receive medical advice from fictious internet characters.
SBH :)
Topic starter
17/03/2020 2:52 am
Isn't tren an androgen?
Hence the question. There is no evidence or even reason to believe tren can increase prolactin. yet its frequently claimed. Quite the opposite :
quote:
1: J Vet Med A Physiol Pathol Clin Med. 2002 Feb;49(1):13-7. Links
Effects of anabolic implants of oestradiol alone or in combination with trenbolone acetate on the ultrastructure of mammary glands in female lambs regarding their interference in prolactin secretion.Blanco A, Moya L, Flores R, Agüera E, Monterde JG.
Department of Comparative Anatomy and Pathological Anatomy, Veterinary Faculty, University of Cordoba, Spain.The side-effects of anabolic steroid implants on mammary gland ultrastructure were evaluated in female lambs treated with oestradiol (n = 10) and with oestradiol plus trenbolone acetate (n = 10). Ten non-implanted lambs were used as controls. Apart from the ultrastructural study of the mammary gland, an assessment of the prolactin pituitary cell population was carried out by immunological methods. Our results showed that oestrogenic implants exert stimulating effects on mammary gland development, both by activating the synthesis process at mammary gland cell levels and by increasing prolactin pituitary production. Nevertheless, there was no evidence of secretory products in the lumen of the gland. Implants containing trenbolone acetate counteracted the mammary stimulus of oestrogens showing ultrastructural images of cell autolysis and necrosis.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
17/03/2020 3:15 am
Re: next topic : androgens and prolactin
Fact : androgens decrease prolactin and prolactin activity..
see this is not a fact. and thats where the problem begins. constructing your theory based on false assumptions. Also not sure how you came to the conclusion that progestenic activity was dismissed. Not so. Progestins modulate ER-a+b, PRL, PRLR, not to mention AR and others, and have often vastly different effects from progesterone. It seems from reading some of your posts that you are unaware of how it is that progestin agonist/antagonist and estrogen agonist/antagonist actions occur (you are aware that both trenbolone and nandrolone are mixed agonist antagonists of the PgR, just as tamoxifen is a mixed agonist/antagonist. While there are many aspects to it, quite often its related to receptor subtype distribution (in the case tamoxifen- an easy one since this has been clearly delineated- if erbeta expression is greater then antagonist- if eralpha expression is greater agonist.)-- btw- if you think this through and relate to paracrine prolactin actions on ER you will see why tamoxifen is not reccomended-- or effective)- also if you look at your heifer study, you will see why this does not apply or translate (dose dependent-hint).
and seriously, just because something is an androgen does not in anyway shape or form mean that it will have the same effect as all other androgens. and here its even more convoluted because these are not just androgens but progestins as well. (and being a progestin certainly not discounted)
you really need to look at the data and study findings more closely because your extrapolations are not supported. You also need to delineate between autocrine and paracrine actions as well as the impact of low and high doses. (as relates to the studies in which androgens lower prolactin and PRLR).
and most importantly, in practical use, prolactin suppression works. there may be room for debate as to why and even over the mechanisms that make estrogen suppression relatively inneffective alone, but effectiveness of prolactin suppression in cases where estrogen suppression alone is not effective, is not really up for debate. Unless you have tried it. (even then not up for debate-- just saying-- actual experience (which includes stepping outside your own experience to understand why others have similar or different results) in relation to the underlying science is always helpful (well most of the time, sometimes it can lead the wrong way, but usually helpful)
Topic starter
17/03/2020 3:43 am
I'll answer more in depth when I have the time, but a few short things to note : whether or not the action is systemic or paracrine (and we know its not systimec, courtesy of oswaldo and many others blood panels), a systemic anti-estrogen treatment would stop the needed estrogen from being available to cause gyno. We also know that when mammals are ovariectomized, adrenalectomized or castrated, the prime organs that produce estrogen, that prolactin production is severely hampered in all tissues. We also know courtesy of the study cited in nandi's article on the matter that estrogen is needed for prolactin to cause gyno.
All of these together show that conventional anti-e's would still work even if you wanted to believe in some sort of voodoo paracrine prolactin action. Hence no need for anti-prolactin medication of any kind. This is also backed by the fact that in most cases the treatment for type 1 gyno (type 2 is larger and always treated with surgery) is anti-estrogens. no research is being done into other therapies, which I would assume means endocrinologists are still pleased with the results. There are two exceptions. Hyperprolactinaemia (usually caused by a carcinoma and clearly showing elevated systemic levels of prolactin) and hypogonadism (which is treated with ANDROGEN THERAPY of all things). In any and all case a strong link between Androgen to estrogen ratio has been demonstrated with gyno.
Someone other than macro, correct me if i'm wrong in any of my logic here.
And while you may believe deca and tren are some sort of weird alien drugs that fall outside the realm of androgens (which they would have to, since its androgen action through the AR that lowers prolactin) I have at least one study in a mammal that clearly shows trenbolone offsets the effects of estrogen on mammary tissue, causing clear shrinkage through lysis and apoptosis. Meaning trenbolone behaves exactly like all other androgens in this regard.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
17/03/2020 4:07 am
keep us posted on that one as well. Do you have scans of these sections of the lab results ? (all personal info blanked out of course). I wouldn't mind using it in an article.
of course. i will.
.
dr frankenstein
17/03/2020 4:37 am
I have at least one study in a mammal that clearly shows trenbolone offsets the effects of estrogen on mammary tissue, causing clear shrinkage through lysis and apoptosis. Meaning trenbolone behaves exactly like all other androgens in this regard.
NO. YOU DO NOT. the fact that you cant understand this is baffling. pretty sure that this was already disabused in your other thread. rather enjoyed watching that one.
low doses have considerably different effects than high ones. you surely have seen this in a number of models. and while not 100% agreeing with the math laid out in your other thread 2-3mg of tren per day, is a lot different than the 25-200mg/day. you are aware that concentrations will affect receptor subtype affinity as well as allosteric and promiscuous binding?
and who else is going to take you to task.
look am only jabbing you because it seems to takes some knocks on that thick skull to get you thinking outside your little box.
Topic starter
17/03/2020 5:04 am
NO. YOU DO NOT. the fact that you cant understand this is baffling. pretty sure that this was already disabused in your other thread. rather enjoyed watching that one.low doses have considerably different effects than high ones. you surely have seen this in a number of models. and while not 100% agreeing with the math laid out in your other thread 2-3mg of tren per day, is a lot different than the 25-200mg/day. you are aware that concentrations will affect receptor subtype affinity as well as allosteric and promiscuous binding?
and who else is going to take you to task.
look am only jabbing you because it seems to takes some knocks on that thick skull to get you thinking outside your little box.
Actually I'm only having these discussions on prolactin because I do want to give it a chance. If there is some logical, acceptable model by which this fits, I'm all ears. In fact, that's all i want out of these threads. If all I'm getting out of it is conjecture and more crazy theories, then i'm happy to stay with the facts though and dismiss it entirely.
on low doses and high doses, they do play a role in reaching threshold to activate certain receptor. We know nandrolone can bind the ER and in severely high doses (more than any sensible human would take) will actually activate it as well. This is a case of dose-responsiveness. Likewise with limiting factors. Testosterone is more likely to cause gyno in low doses because the androgen to estrogen ratio is lower, and relative to the dose of testosterone, there is more estrogen.
I'm not aware of any classic steroid actually changing its relative RBA's though. Trenbolone androgenic RBA is still going to exceed its Progestagenic RBA far and large at any given dose (Ojasoo and Raynaud, 1978 and 1995). After all that's what an RBA is, a RELATIVE binding affinity, as in it has to be relative to something, such as binding affinities of other steroids, or binding to alternate receptors by the same steroid.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
17/03/2020 5:25 am
Actually I'm only having these discussions on prolactin because I do want to give it a chance. If there is some logical, acceptable model by which this fits, I'm all ears. In fact, that's all i want out of these threads. If all I'm getting out of it is conjecture and more crazy theories, then i'm happy to stay with the facts though and dismiss it entirely.on low doses and high doses, they do play a role in reaching threshold to activate certain receptor. We know nandrolone can bind the ER and in severely high doses (more than any sensible human would take) will actually activate it as well. This is a case of dose-responsiveness. Likewise with limiting factors. Testosterone is more likely to cause gyno in low doses because the androgen to estrogen ratio is lower, and relative to the dose of testosterone, there is more estrogen.
I'm not aware of any classic steroid actually changing its relative RBA's though. Trenbolone androgenic RBA is still going to exceed its Progestagenic RBA far and large at any given dose (Ojasoo and Raynaud, 1978 and 1995). After all that's what an RBA is, a RELATIVE binding affinity, as in it has to be relative to something, such as binding affinities of other steroids, or binding to alternate receptors by the same steroid.
well have been perhaps a bit harsh with you. you need to stop looking at those old studies. they dont account for the thing that stopping you from seeing at least part of this equation and thats receptor subtypes. hence alpha and beta reference. depending on the compound quite often low doses will initiate very different, even opposite effects because of preferential binding for one subtype at low dose that is ablated at higher dose. this is just one paradigm. if you look at the DHT E primed prolactin release study, beleive it was posted here. low dose dht inhibited prolactin release where high dose had no effect.
and some molecules allosterically, not all of them. in point of fact, TAM does bind to some allosteric sites. but not neccessarily with the same affinity as it does with the ER. you cant correlate one with the other.
did give you a link that should be rather illuminating. perhaps after you read it, the discussion can be more of a discussion. because right now, with you not understanding those factors. as well as not taking into account that there are multiple receptor sites and modulation of multiple sites, its not very fruitful.
did just look at your estrogen and role in fat loss article and there are some things that are just off. for instance using a ppargamma antagonist is a very bad idea. Modulators of ppargamma, both direct and via pparalpha are a good idea. Though you really overstate the role of estrogen in fat loss, and its role in countering fat loss is actually generally more significant. though modulation can impact this.
btw- in case you were not aware, the action of TAM in the hypothalamus is estrogenic, hence why its a primer and not a stimulator the axis. This is why when there is high level suppression of the axis tamoxifen is generally not effective.