19nor question?

[qscgugcsq]

I didnt read alot on 19nor so it may sounds stupid XD

As I understood the pregesteron/prolactin's side should not be a concern if E is well undercontrol. (correct me if i'm wrong)

so, the safest way(side effect related to progesteron/prolactin I mean) should be to keep a physiological dose of test(exemple 40mg test-p/eod) + the 19nor that we are talking about. (deca-trenbolone would be the most interesting for me).

The deca hardly aromatize. So, 120mg test + 1500mg deca(=300mg test(in term of aromatization) so it would take the same amount of AI than a 400-500 mg test cycle)
So 120mg test + 1 500mg deca would only need .25 arimidex eod(or any other AI with equivalent dosage)
So if this reasoning is right. A VERY HIGH quantity of deca with low test would cause same side(still in term of aromatization) as a beginners cycle of 500mg test. And the E will be under control so progest/prolac should not be a concern.

Plz correct me if I'm wrong.

Second, Trenbolone

By following the same logic, trenbolone do not aromatize. So, taking any amount of trenbolone with a physiological testosterone dose even without AI should cause minimal prolac/progest sides.


It's only a simple understanding and I'm aware that it is not as simple as that. I guess that more 19nor we take more progest/prola we have no matter how much E. But is there any limits where E doesn't matter anymore and where progesteron and prolactin become too important.
I'm not searching a definitive answer just an approximativation.

Thanks

[qscgugcsq]

Bump

[Atomini]

I posted this in my Trenbolone thread when someone asked pretty much the exact same question (post #446 in my Trenbolone thread in response to post #445):

The issue of Progestins and elevated Prolactin is an interesting one.

Increases in Prolactin can be kept in control by keeping Estrogen levels from rising, and can also be controlled from the use of a Prolactin antagonist as you probably already know. What's also strange 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 in varying numbers of users. 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. 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. 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, even in conditions where Estrogen levels are kept to a minimum and controlled. 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'll always run a prolactin antagonist when running Trenbolone regardless. I will take zero chances with this.

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. There isn't a whole lot of data or solid data on Prolactin LEVELS raising from 19-Nors, but it is strongly speculated that the Estrogen receptor is a co-binding factor in Prolactin receptor expression (PRLR). This can make us far more sensitive to Prolactin even if its not increased or wildly out of range. This theory also fits well with the Estrogen receptor being the causitive factor in Prolactin issues. This is also why for the most part, controlling E2 levels should control Prolactin. It is ALSO why Trenbolone's side effects are reported to be far more pronounced when running it in a high Estrogen environment as a result of stacking Tren with high doses of an aromatizable compound, such as Testosterone (rather than keeping Testosterone at a TRT dose). The whole issue of Prolactin and what causes it to rise up and down is a dodgy one and varies between individuals as well.

Even in William Llewellyn's Anabolics book, he states:

Trenbolone is not aromatized by the body, and is not measurably estrogenic. It is of note, however, that this steroid displays significant binding affinity for the progesterone receptor (slightly stronger than progesterone itself). The side effects associated with progesterone are similar to those of estrogen including negative feedback inhibition of testosterone production and enhanced rate of fat storage. Progesterone also augments the stimulatory effect of estrogens on mammary tissue growth. There appears to be a strong synergy between these two hormones here, such that gynecomastia might even occur with the help of progestins, without excessive estrogen levels. The use of an anti-estrogen, which inhibits the estrogenic component of this disorder, is often sufficient to mitigate gynecomastia caused by progestational anabolic/androgenic steroids. Note that progestational side effects are more common when trenbolone is being taken with other aromatizable steroids.

As far as it goes with gyno... Gyno is also such a complex issue and the mechanism behind which it forms has so many different pathways. The causation is very complex, and its precise specifics are largely unknown, and a number of agents including estrogens, progestins, GH, IGF -1, and prolactin may be involved. However, most authorities believe that a decreased (T+DHT)/E ratio is central to the development of gyno, and that blocking the effects of estrogen, or increasing T + DHT levels, is central to amending the problem. Prolactin is not a central issue, but it is one of the contributing factors should other necessary functions be set in place. There are many different factors in the overall complex mechanism that produces gyno. Therefore, if you can eliminate one or more of the gears in the machine that is responsible for the formation of gyno, you can effectively have a high chance of stopping, blocking, and preventing it.

I hope I have helped you to understand these things better.

[Turkish Juicer]

Hmmmm...

If 120mg is the ''physiological dose'' or as we generally call it the ''TRT'' dose, and if Deca doesn't aromatize, ''then why use an AI at all during a cycle like this'' is the first question that popped in my mind before I was able to come up with a solid answer to your question...

[Atomini]

Hmmmm...

If 120mg is the ''physiological dose'' or as we generally call it the ''TRT'' dose, and if Deca doesn't aromatize, ''then why use an AI at all during a cycle like this'' is the first question that popped in my mind before I was able to come up with a solid answer to your question...

Good point. There should be no need for an AI when using TRT doses of Testosterone.

But I do remember seeing some individuals in the TRT section of the forum in the past complain that even at their TRT doses (+/- 100mg weekly), aromatization was still getting to the better of it and these particular individuals required a low AI dose. However, this doesn't seem to occur with most individuals, and the only way to be sure that these things are happening is through bloodwork. This is why I reccomend 100mg as a good range for TRT dosing, as I find it absolutely crazy when I see some people around here claiming that 250mg weekly is a TRT dose... um, NO. The body only produces endogenously approximately 50 - 70mg weekly on its own naturally.

[qscgugcsq]

Wow... Once again you impressed me XD Thanks alot Atomini.