It seems commonly accepted now that progestagenic steroids like nandrolone and trenbolone elevate prolactin levels and it is by this mechanism they are meant to produce produce certain side effects.
I would like to ask where exactly the evidence for this proposed mechanism is? Are there some research papers regarding these steroids and prolactin levels, in which case I’d love some references.
Or if not, how many people have actually had blood work done during a cycle and actually measured their prolactin levels. If anyone does have any hard data, I’d love to hear about it.
No hard data but from experience from previous cycles involving Nandrolone, I did experience harsh ED, which may or may not have been prolactin-induced.
However, prolactin being the only logical explanation.
Bill Roberts has convincing arguments against the idea that Trenbolone increases prolactin. However, there are plenty of people that have experience prolactin gyno while using Tren. But this is most likely because their Tren has been cut with some other compound.
In the case of nandrolone, I think theres a good chance that the fact that the 5-alpha reduced DHN is such a weak androgen could easily explain ED symptoms. Its also interesting that Bill Roberts makes the case against prolactin with tren, as It seems to me that there is very little evidence in favour of the prolactin mechanism, hence me posting this thread.
Its just that with people being so confident about reccomending drugs like bromocriptine and caberologine, you’d expect there to be some strong evidence for this being beneficial.
There is some evidence of being beneficial, but that evidence doesn’t prove anything with regard to prolactin.
Namely, cabergoline or bromocriptine can be pro-sexual in individuals with completely normal prolactin levels. This is from increasing dopamine.
So experiencing a prosexual effect while suffering from lack of libido following or concurrent with steroid use does not show anything as to whether high prolactin was the cause of the lack of libido.’
A prolactin test is what would show that. But results of such tests are apparently never required, or seemingly even wanted, by those writing that trenbolone (supposedly) causes high prolactin.
As for nandrolone, I expect that any steroid that can increase estrogen can increase prolactin. There is literature evidence of nandrolone increasing prolactin in some substantial percentage of subjects: I don’t recall the percentage but on the order of 30-50%. Incidentally, testosterone performed similarly in this regard, which calls into further question the entire concept.
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The fact that testosterone would raise prolactin levels just as well as nandrolone is really interesting, and that definately throws cold water over the prolactin theory for gyno and other sides from tren and nandolone, since everyone who has ever had a problem with testosterone, has solved it with SERMs or AIs.
I remember reading somewhere that nandrolone does aromatise, but only by a small amount. Looking at nandrolone’s molecular structure though, it is hard to see why it doesn’t aromatise fully. Surely the lack of a methyl group at c10 would reduce the chemical barrier to aromatisation?
Actually it’s the other way around: the aromatase enzyme “expects” the 19-methyl to be there, or rather it is part of the normal mechanism and it might well be the case that binding is better when it is present, as the enzyme is optimized for aromatization of testosterone and androstenedione.
Thinking about it that makes sense, since if the catalytic site on the enzyme is optimised for the presence of the methyl group, then removing it will make it a worse substrate for aromatisation. From a strictly chemical perspective, you would expect the nandrolone molecule to aromatise more easily, since removing a hydrogen atom is going to be easier than removing a methyl group.
Yes, without a suitable enzyme aromatization of any steroid would be impossible under physiological conditions with the presence of the 19-methyl.
(For the sake of whatever interest there might be in it: enzymatically, it becomes possible as a result of double hydroxylation of the 19-methyl, which allows it to become a leaving group as CO2. But under physiological conditions without aromatase, that will never occur.)
What would you say about the case for a non aromatase mediated aromatisation in the case of nandrolone? Since CO2 is such an excellent leaving group, that is obviously the driving force in the case of aromatase. Outside of that though, I wonder what another mechanism for aromatisation could be, perhaps some form of conjugate addition? I’m just speculating here. And do you agree that nandrolone does aromatise to some small extent? I found an interesting paper somewhere about the naturally occuring nandrolone in the body to be a side product of the aromatase reaction, and they had some good evidence for it. Its hard to see how this could work the other way, since there is no obvious driving force for the reaction, but it is interesting information nonetheless.
Bill I read your profile on meso about Anadrol… has anything changed in regards to the occurance of gyno with this compound? I’ve read that prolactin may be a cause, but that it’s more likely that the molecule is similar enough to Estrogen to activate the receptor.
Oxymetholone is in no way more structurally similar to estradiol than other androgens are, and there is zero scientific evidence of estrogenic activity.
Maybe there is another, better explanation, but the observation that Anadrol seems commonly problematic when estrogen levels are high but not when that is not so is the best that I’ve been able to come up.
Being as we have effectively ruled out prolactin as the cause of side effects with progestagenic drugs like deca and tren, would that mean that the standard ancillairies such as nolva would be first line of defence in the event of gyno?
Trenbolone isn’t progestagenic. Or more precisely, its potency is 1% that of progesterone itself, which will be absolutely negligible in effect.
Nandrolone can increase prolactin levels.
The number 1 concern with regard to gyno protection needs to be either keeping estrogen normal or using a SERM.
In addition, controlling prolactin can be of value if it’s possible that prolactin may be elevated. I know of no reason to think that this is the case with actual trenbolone, e.g. that made from Finaplix – it may well be the case with some powders and preparations sold as being trenbolone.
so what would one do if they had high progesterone readings on there bloods? what would trigger that?