Nandrolone increases the Estrogenic Potency of Testosterone

[1fst400]

I've always used a small amount of mast to combat deca sides.. works well..

What works well for you?

 

[OuchThatHurts]

I tried several runs with deca and NPP and did not respond well hormonally at all. Then I was introduced to tren and loved it. It doesn’t have the sides for me that nandrolones did. Winstrol does boost my libido. I was thinking of switching to proviron since many seem to like it more. Perhaps just try a higher dose. I have more than enough for 5 weeks 100mgs qd. Mast I will try again. Mast did a number on my liver enzymes but I think I can keep that to a minimum now.

 

[LATS]

What works well for you?

Generally I like to run about 200mgs of mast enth a week if I'm running g a nandrolone.. studies show that mast decreases prolactin and modulates estrogen.. so in addition to adding a bit more punch to a cycle it makes the cycle a bit more tolerable ..

 

[Type-IIx]

Why does science direct say this?
"19-NT has been shown to suppress LH and FSH effectively with full maintenance of androgen-dependent functions. With the combination of both androgenic and progestational activity, the potential for 19-NT to provide contraception as a single agent has been considered. Small trials with 19-NT alone or in combination with depot medroxyprogesterone acetate (DMPA, see below) have confirmed that azoospermia is induced without any symptoms of androgen deficiency (despite low T levels)."

Anyway i'm not advocating for deca only. i just haven't found any study on why nandrolone, a male sex hormone, would cause impotence. i understand that the common answer is nandrolone is a less androgenic drug but a lot of AAS(winstrol, mast, proviron, drol, dbol) are less androgenic than Test on paper.

There are always sources of disagreement among studies that investigate matters that are not taught as subject matter in textbooks (so called theories, that are well-supported and reasoned constructs that explain some phenomenon). Basically, when it comes to uncertain hypotheses (those worthy of funding & scientific work for investigation), you'll always find uncertainty in the results, and eventually there will arise what may be fairly considered as exceptions to the general rule in the recent literature (remember the axiom of what the exception does to the rule).

Similarly, there are inconsistent findings with MENT supporting sexual function. Small studies (often n<10 subjects) might show it fully supports sexual function and libido. Others, the opposite. From Walton & colleagues (doi:10.2164/jandrol.107.002683), 2 of 13 (15%) MENT subjects withdrew after 8 weeks of treatment due to low libido & erectile dysfunction...Adverse events included reduced libido & erectile function in 4 *additional* subjects in the MENT group who completed treatment (6/13, or 46%) [these adverse effects were not reported by any subject in the testosterone group]...Due to the incidence of reports of low libido and early withdrawal in the MENT group, it was decided in consultation with the study Data Monitoring and Safety Committe to shorten the MENT treatment period to 24 weeks whereas men in the testosterone group completed 48 weeks of treatment.

My view (a hypothesis supported by the bulk of the literature; a construct), is that 5α-reductase amplification (e.g., T ⇒ E₂) is a discrete function (similar to aromatization) of testosterone. That modern synthetic AAS fail (the bulk of work in synthesis thereof having ended in the 1960s for all intents and purposes), without T. Hypothetically, other androgens may conceivably be designed that amplify androgenic action in the 5α-reductase rich gonadal tissues; e.g., Halo may, but its 5α-reductase product has never been investigated to either confirm or refute whether its action is amplified or is merely sufficiently androgenic to serve as a satisfactory therapy in sexual dysfunction due to androgen deprivation (e.g., TRT). Actually, come to think of it, 1-Testosterone ("DHB") fits this criteria, acting ostensibly as a prohormone to DHT. Peter Bond thinks that 1-Testo metabolizes to DHT perhaps by some unknown enzyme that subjects 1-Test to 1,2-dihydrogenation during its metabolism. The only plausible other explanation I've been able to think of is that perhaps this occurs by inhibition of 17β-HSD1 (thereby increasing DHT & lowering E₂), and there is some support from modeling of inhibitors of 17β-HSD.

I believe that an AAS must be profoundly androgenic (e.g., metandienone [Dbol]) to sufficiently overcome a lack of 5α-reductase amplification, and that only T can reliably (the exception proving the rule; of course some weirdos may report a libido increase on Deca only, but it would be very unusual) support sexual function as a general rule.

Deca dosed at 600 mg/w is the lowest dose that can plausibly support sexual function, and bloodwork supports its yielding low-normal E₂ (see Nandrolone Data (including joint pain relief mechanisms [by Type-IIx]); this would tend to line up with the basal potency of DHN in those 5α-reductase rich gonadal tissues.

The fact that well into supra-physiologic dosing & resultant concentrations of Deca is required to adequately support sexual function bolsters my view or hypothesis.

Proviron is yet another, albeit interesting, exception, in that it augments libido and sexual drive by acting on the brain & CNS. Electroencephalographic profiles of varying dosages of mesterolone (as low as 1 mg) were found to be very similar to those seen with psychostimulants such as dextroamphetamine (a well known potent stimulator of sexual behavior in animals including humans). In this regard, it acts oppositely Deca as well.

 

[OuchThatHurts]

If you're saying dosages as low as 1mg mesterolone exert a measurable psychotropic effect, then perhaps it's just as equally possible that 25-50mg was too much rather than too little. However, as mesterolone is weakly bound at the AR, I've often considered this somewhat analogous to ER modulators (SERMs) - in essence blocking the more potent AR receptor binding of T, DHT, Tren, et al, thus attenuating overall anabolism within a specific polypharmaceutical AAS course of "therapy".

So while modestly increasing free T through SHBG binding, it will still not reduce the bulk of bound T via albumin (which represents the bulk of protein bound T). It seems difficult to assess the net effect of any physiological (in terms of anabolism) effects of mesterolone other than its measurable psychotropic/psychostimulant nootropic properties.

 

[Love_to_Bodybuild]

I've been on an hrt run last five weeks, it was deca 25 mgs, and test 20 mgs eod. Then sex drive dropped too low and feeling low. After months of nandrolone deca use, i have felt more sluggish and a low dopamine feeling, test just feels way better and doesn't cause depression, so I went back to trt dose untill next blast.

I can do a deca cycle at 600 mgs and be fine with 10 mgs dbol. This is the last "blast" done that ended around Christmas, twas six weeks. @Type-IIx are these studies saying or indicating that 600 plus mgs deca restores sex drive?

Regardless, low, moderate dosed dbol, 10- 20 mgs is enough for sexual function on deca, on 600 mgs or less, from experience.

 

[OuchThatHurts]

I believe that an AAS must be profoundly androgenic (e.g., metandienone [Dbol]) to sufficiently overcome a lack of 5α-reductase amplification, and that only T can reliably [...] support sexual function as a general rule.

I could not agree more. With 0 androgenicity there is 0 anabolism. (one begets the other)

 

[Ranchhand]

What works well for you?

Generally I like to run about 200mgs of mast enth a week if I'm running g a nandrolone.. studies show that mast decreases prolactin and modulates estrogen.. so in addition to adding a bit more punch to a cycle it makes the cycle a bit more tolerable ..

That's a 5 to 1 ratio of Nandrolone to Masteron. That's where I'm at as well with my Test to Mast ratio. I've noticed if I go up in ratio, say closer to 3 to 1 of Test to Mast I start to notice symptoms of low E2. Sorry guys, I don't have a direct comparison of nandro to Mast but thought my experience with Test and Mast ratios could be a helpful gauge.

 

[TheRoid]

That's a 5 to 1 ratio of Nandrolone to Masteron. That's where I'm at as well with my Test to Mast ratio. I've noticed if I go up in ratio, say closer to 3 to 1 of Test to Mast I start to notice symptoms of low E2. Sorry guys, I don't have a direct comparison of nandro to Mast but thought my experience with Test and Mast ratios could be a helpful gauge.

I would tend to say that when using Masteron your E2 level is basically a mere, not really revealing figure.
In the past I've been pushing Mast far above my Test dose. My E2 reading was high but I sure as hell was experiencing low estrogen symptoms.

 

[Ranchhand]

I would tend to say that when using Masteron your E2 level is basically a mere, not really revealing figure.
In the past I've been pushing Mast far above my Test dose. My E2 reading was high but I sure as hell was experiencing low estrogen symptoms.

That's a better way of saying it, experiencing low estrogen symptoms when Mast dose is too high. Thanks

 

[OuchThatHurts]

Some AAS have lowered my E2 levels but none at any dose has ever crashed my estrogen while using T also. But without T, non-aromatizing steroids like Deca and others have been very HPTA suppressive and without T, estrogen levels are sure to plummet.

But AI's are the only drugs that have single-handedly crashed my estro. Specifically Arimidex and Femara. (anastrozole and letrozole)

edit: Also want to add that MENT was earmarked as a prophylactic it's so suppressive. But it was thought that its testosterone mimicking effects would overcome the loss is endogenous T production. They were wrong. This only further confirms my theory that a superior form of T has not yet been formulated.

 

[TheRoid]

Some AAS have lowered my E2 levels but none at any dose has ever crashed my estrogen while using T also. But without T, non-aromatizing steroids like Deca and others have been very HPTA suppressive and without T, estrogen levels are sure to plummet.

But AI's are the only drugs that have single-handedly crashed my estro. Specifically Arimidex and Femara. (anastrozole and letrozole)

edit: Also want to add that MENT was earmarked as a prophylactic it's so suppressive. But it was thought that its testosterone mimicking effects would overcome the loss is endogenous T production. They were wrong. This only further confirms my theory that a superior form of T has not yet been formulated.

Hard to beat what Nature perfectioned in eons, at least when considering ALL the main natural androgen functions.

 

[OuchThatHurts]

Hard to beat what Nature perfectioned in eons, at least when considering ALL the main natural androgen functions.

Agreed. Science always builds on nature. Always has. But never in reverse. At least not yet.

 

[LATS]

I would tend to say that when using Masteron your E2 level is basically a mere, not really revealing figure.
In the past I've been pushing Mast far above my Test dose. My E2 reading was high but I sure as hell was experiencing low estrogen symptoms.

We have to remember that mast may not effect e2 blood levels but can affect e2 at the receptor. So if we have competition at the receptor and e2 is losing the estrogen is still staying present in the blood .. but joints.. sex drive.. mood can give signs of low e2

 

[OuchThatHurts]

We have to remember that mast may not effect e2 blood levels but can affect e2 at the receptor. So if we have competition at the receptor and e2 is losing the estrogen is still staying present in the blood .. but joints.. sex drive.. mood can give signs of low e2

Good point. That would lead to false blood readings on plasma E2 levels/concentrations with compounds like Masteron acting as an estrogen receptor modulator (ERM).

Then it only stands to reason that bloodwork may be misleading and we would have exactly zero other ways to know other than "FEELZ".

And feelz is impossible to gauge relatively.

 

[LATS]

Good point. That would lead to false blood readings on plasma E2 levels/concentrations with compounds like Masteron acting as an estrogen receptor modulator (ERM).

Then it only stands to reason that bloodwork may be misleading and we would have exactly zero other ways to know other than "FEELZ".

And feelz is impossible to gauge relatively.

Exactly.. take into account the receptors even in our joints.. then a compound like mast may win in the competition for those receptors. We assume our e2 is low.. blood work says otherwise.. so then we try to blame other things for the issue.. so if taking mast for estrogen modulation a little goes a long way..

 

[TheRoid]

We have to remember that mast may not effect e2 blood levels but can affect e2 at the receptor. So if we have competition at the receptor and e2 is losing the estrogen is still staying present in the blood .. but joints.. sex drive.. mood can give signs of low e2

No more no less, exactly what I meant.

 

[OuchThatHurts]

Does anyone in this thread have a link to a study or article showing Primo, Mast, Win really and truly lowers serum E2? If so, would you please send it to me?

Thanks in advance,
O.T.Hurts

 

[OuchThatHurts]

Exactly.. take into account the receptors even in our joints.. then a compound like mast may win in the competition for those receptors. We assume our e2 is low.. blood work says otherwise.. so then we try to blame other things for the issue.. so if taking mast for estrogen modulation a little goes a long way..

No more no less, exactly what I meant.

Got it. This is good info. I plan pretty diligently. I'm not loose with the sauce.

Dial that shit in!

 

[LATS]

Does anyone in this thread have a link to a study or article showing Primo, Mast, Win really and truly lowers serum E2? If so, would you please send it to me?

Thanks in advance,
O.T.Hurts

I've never seen one.. I have seen people post blood work where e2 has taken a hit from dht derivatives buy there is no literature that woukd show as to why. Now if you look at studies on masteron it had good capabilities as a estrogen modulator At the receptor.. hence its ability to reduce breast tumors affected by estrogen etc. Now mast etc does have mild AI benefit but very mild.. so this reduction in e2 when primo etc is present is hard as to why when the literature just doesn't show that it has that ability.. victor black has addressed this numerous times with his research into it and also cannot find the correlation