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Trestolone/Ment significantly increases my hematocrit levels!

4 years ago I had a very similar conversation with PA.
 

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4 years ago I had a very similar conversation with PA.
It is no secret Nandrolone partly aromatizes in the liver, similar to its derivates. But it ALSO aromatizes through aromatase tissue present in adipose. To my knowledge there is no study in humans in vivo, so the ratio of this is not determined. The crux of @gains4000 argument is that it is entirely aromatized in the liver, which is not true at all and is the result from inability to verify his citations as well as a refusal to read the actual scientific literature.

And I will restate, there is no evidence that this applies to MENT.

I generally don't like to turn to anecdotal reports, but I will when the scientific evidence is lacking. I had experimented with this when I was first trialing MENT for clientele usage. Over a 3 week period I had used 1400mg per week of MENT solo (specifically Trestolone Enanthate) and was able to experience low estrogen symptoms from AI usage alone. This at least told me that if any conversion was taking place in the liver, it was negligible.
 
It is no secret Nandrolone partly aromatizes in the liver, similar to its derivates. But it ALSO aromatizes through aromatase tissue present in adipose. To my knowledge there is no study in humans in vivo, so the ratio of this is not determined. The crux of @gains4000 argument is that it is entirely aromatized in the liver, which is not true at all and is the result from inability to verify his citations as well as a refusal to read the actual scientific literature.

And I will restate, there is no evidence that this applies to MENT.

I generally don't like to turn to anecdotal reports, but I will when the scientific evidence is lacking. I had experimented with this when I was first trialing MENT for clientele usage. Over a 3 week period I had used 1400mg per week of MENT solo (specifically Trestolone Enanthate) and was able to experience low estrogen symptoms from AI usage alone. This at least told me that if any conversion was taking place in the liver, it was negligible.

Many medico-scientific journals have noted nandrolone to be a non-aromatizable AAS. Studies using brain cells have shown nandrolone to be more neurotoxic (damaging to nerve cells) because it is not aromatized. It is true that nandrolone is not a candidate for classic aromatization, as the 19-carbon that is missing from nandrolone is the starting point for the entire aromatase reaction. Interestingly, nandrolone stimulates aromatase in rat models, even though it does not participate in the reaction. This would accelerate the conversion of other androgens (testosterone, D-bol, etc).

Yet, the results of a recent study published in the Climacteric prove that nandrolone and other 19-nortestosterone-derived steroids can be converted into estrogenic steroids through a series of enzymatic reactions that take place in the human liver. The catalytic (accelerating) first enzyme, CYP 450arom, is not present in the adult human liver, though CYP 450arom is present in certain liver diseases and tumors. However, another enzyme called CYP 450 monooxygenase is able to attack the 2-carbon of the nandrolone and begin the generation of the phenolic A-ring…the definitive step in converting an androgen (or 19-norandrogen in this case) into an estrogen.

Recall that the CYP 450arom played a catalytic role, speeding up the classic aromatase reaction. CYP 450 monooxygenase is much slower and less efficient. This accounts for the comments that nandrolone aromatizes at a rate of 20 percent of testosterone or androstenediol.

In fact, the rate may be much less. Realizing that Deca is injected intra-muscularly and disperses slowly, and the enzyme system discussed in the Climacteric article was specific to the liver, it is unlikely that standard nandrolone-containing cycles would see a major contribution to feminizing effects from nandrolone being aromatized.
However, oral norandrogen-precursors were prominently marketed during the prohormone glory days and an oral norandrogen (7á-methylnortestosterone) is being developed as a potential male contraceptive. It is possible, especially at abusive doses, that such oral norandrogens may elevate estrogen levels sufficiently to cause gynecomastia or other estrogen-related problems. In women provided with oral norandrogens for menopause, researchers speculate that the drugs may hold the potential of increasing estrogen and thus, risk for blood-clotting problems or estrogen-sensitive cancers.

Nandrolone is considered a relatively safe AAS and has been used extensively by recreational bodybuilders and power athletes. It has rarely been considered to increase the risk of estrogen-related problems, as steroids missing the 19-carbon are not substrates for the classic aromatization reaction. However, in addition to its capacity to stimulate progesterone receptors (a related group of feminizing sex steroid hormones), nandrolone may also increase estrogen levels via a secondary aromatase reaction, promoting the development of gynecomastia and prolonging the delay in restoring natural testosterone production post-cycle. Classic aromatization of testosterone or other androgens may also be accelerated by nandrolone. Oral forms of nandrolone, including prohormones, likely have a much higher estrogenic index and a higher risk of estrogenic side effects due to hepatic (liver) first pass clearance.
 
Many medico-scientific journals have noted nandrolone to be a non-aromatizable AAS. Studies using brain cells have shown nandrolone to be more neurotoxic (damaging to nerve cells) because it is not aromatized. It is true that nandrolone is not a candidate for classic aromatization, as the 19-carbon that is missing from nandrolone is the starting point for the entire aromatase reaction. Interestingly, nandrolone stimulates aromatase in rat models, even though it does not participate in the reaction. This would accelerate the conversion of other androgens (testosterone, D-bol, etc).

Yet, the results of a recent study published in the Climacteric prove that nandrolone and other 19-nortestosterone-derived steroids can be converted into estrogenic steroids through a series of enzymatic reactions that take place in the human liver. The catalytic (accelerating) first enzyme, CYP 450arom, is not present in the adult human liver, though CYP 450arom is present in certain liver diseases and tumors. However, another enzyme called CYP 450 monooxygenase is able to attack the 2-carbon of the nandrolone and begin the generation of the phenolic A-ring…the definitive step in converting an androgen (or 19-norandrogen in this case) into an estrogen.

Recall that the CYP 450arom played a catalytic role, speeding up the classic aromatase reaction. CYP 450 monooxygenase is much slower and less efficient. This accounts for the comments that nandrolone aromatizes at a rate of 20 percent of testosterone or androstenediol.

In fact, the rate may be much less. Realizing that Deca is injected intra-muscularly and disperses slowly, and the enzyme system discussed in the Climacteric article was specific to the liver, it is unlikely that standard nandrolone-containing cycles would see a major contribution to feminizing effects from nandrolone being aromatized.
However, oral norandrogen-precursors were prominently marketed during the prohormone glory days and an oral norandrogen (7á-methylnortestosterone) is being developed as a potential male contraceptive. It is possible, especially at abusive doses, that such oral norandrogens may elevate estrogen levels sufficiently to cause gynecomastia or other estrogen-related problems. In women provided with oral norandrogens for menopause, researchers speculate that the drugs may hold the potential of increasing estrogen and thus, risk for blood-clotting problems or estrogen-sensitive cancers.

Nandrolone is considered a relatively safe AAS and has been used extensively by recreational bodybuilders and power athletes. It has rarely been considered to increase the risk of estrogen-related problems, as steroids missing the 19-carbon are not substrates for the classic aromatization reaction. However, in addition to its capacity to stimulate progesterone receptors (a related group of feminizing sex steroid hormones), nandrolone may also increase estrogen levels via a secondary aromatase reaction, promoting the development of gynecomastia and prolonging the delay in restoring natural testosterone production post-cycle. Classic aromatization of testosterone or other androgens may also be accelerated by nandrolone. Oral forms of nandrolone, including prohormones, likely have a much higher estrogenic index and a higher risk of estrogenic side effects due to hepatic (liver) first pass clearance.
Continue to not reference a single study. You’re so dense it’s unbelievable.
 
Nobody was being sarcastic, I don’t see the reason why the author would lie about AI not preventing nandrolone from aromatizing. Simple as that.

The study you attached has nothing to do with nandrolone Aromatization.

Feel free to withdraw from the discussion🤷🏿‍♂️
Who the fuck knows, saw the same sort of thing in R.A.S. Hemat's "Andropathy" textbook, that is a work of science fiction.

The reason for their misrepresentations is more often than not due to basic misunderstanding ("never attribute to malice that which can just as readily be attributed to stupidity"). Also, we see this often from fitness professionals that market themselves on their "pet concepts," based either on fraudulently produced scintillating findings, or on misreprentations of published research (e.g., effect size manipulations, ignoring insignificant differences & casting them as trends) that generate controversy & newsworthiness, using these "pet concepts" as a distinguishing mark of their work.
 
It is no secret Nandrolone partly aromatizes in the liver, similar to its derivates. But it ALSO aromatizes through aromatase tissue present in adipose. To my knowledge there is no study in humans in vivo, so the ratio of this is not determined. The crux of @gains4000 argument is that it is entirely aromatized in the liver, which is not true at all and is the result from inability to verify his citations as well as a refusal to read the actual scientific literature.

And I will restate, there is no evidence that this applies to MENT.

I generally don't like to turn to anecdotal reports, but I will when the scientific evidence is lacking. I had experimented with this when I was first trialing MENT for clientele usage. Over a 3 week period I had used 1400mg per week of MENT solo (specifically Trestolone Enanthate) and was able to experience low estrogen symptoms from AI usage alone. This at least told me that if any conversion was taking place in the liver, it was negligible.
I'll get back to this later. Not to talk about liver "aromatization" via CYP450, but about aromatase. P.S., this additional "aromatization" in liver is more rapid than via aromatase in vivo because it occurs in the liver (early/acute increases).

We know the rates of aromatization (via aromatase) for all the major aromatizable androgens, T, Nand, Bold, MENT, Metandienone (though I don't have this data in hand for Dbol, it exists, from two German language studies by Lutzmann and Gerhards in 1961 in rat liver and Breuer and Schikowski in 1963 in a placental enzyme system), & MT.
 
From my article, titled "Primobolan / Equipoise Crashed My E2 – Help!," accessed 1 Jan 2024 from https://thinksteroids.com/articles/primobolan-equipoise-crashed-my-e2-help/:

T =[Aromatase]=> E2, Κm = 1.83 nM, following Michaelis-Menten kinetics [1].

We do not know the [precise] Km for in vivo Aromatase activity with respect to EQ (boldenone undecylenate; BU). However we do know that the Aromatase enzyme is saturable, such that above some dose, that depends on Aromatase expression³ or protein number (and binding hormone profile¹), that more will not cause any further elevations to active estrogens (free E2 and E1). Since EQ (boldenone undecylenate; BU) is subject to hindered aromatization, its reaction rate (Vmax) must be relatively slowed. As such, its in vivo Km must be shifted to the right (vs. that for T/E2) requiring greater concentrations than T for saturation of Aromatase. This tells us that, versus T, higher boldenone doses are needed before Aromatase is saturated (not subject to any increases to E2 at doses above a saturation point).

reaction-rate-vs-substrate-concentration.png


From [1] we know too that the 40% greater Vmax of Aromatase vis-à-vis T in aged vs. young men was virtually entirely explained by body fat mass and SHBG (i.e., binding hormone profile¹).

However, we can infer it from [2] which tells us that boldenone acts as a substrate to Aromatase, producing estrone & estradiol at 58% rate of T [2].

We know that nandrolone acts as a substrate to Aromatase, producing estradiol at 20% the rate of testosterone [3].

As already mentioned here [link], we know that MENT acts as a substrate to Aromatase, producing 7α-methylestradiol; 7α-ME, a potent methylestrogen that is more than 4X (!) as potent ("efficacious," a bad thing here) than estradiol (E2) in ER-containing cells [4]. Efficacy is determined by measuring the effect, e.g., growth (here, in breast cancer cells). The EC₅₀ (EC50) is determined by the concentrations at which the ligand triggers growth (this may be confirmed by measurements of cell cycle progression (i.e., the S-phase entry during the cell cycle).

The binding affinity (IC₅₀) of MENT's aromatic product (7α-methylestradiol) is 102% that of estradiol [4], which is typically used as the reference compound for ER binding given its noteworthy efficacy, potency, and affinity for the ERα receptor, in the literature.

Given the findings of Attardi et al, in comparing the rate of aromatization, in recombinant human aromatase, between MENT and Nandrolone, that "At 180 min, about 23% of MENT was converted to 7α-ME and about 13% of [Nandrolone] to E2," knowing that Nandrolone produces estradiol via its acting as a substrate to Aromatase at 20% the rate of T [5], we can deduce that MENT aromatizes at roughly 35% the rate of T... to 7α-ME (an aromatic product with four-fold E2's potency, i.e., for causing growth in breast cancer cells). Simple multiplication of the rate of aromatization (35%) * EC50(7α-methylestradiol) * RBA(7α-methylestradiol) ≈ a 40% greater growth potential in ER-containing cells than T. We still must account for potency of metabolites and their rates of metabolism (i.e., breakdown) to precisely describe in vivo effects.

At this point I'd surmise you're as bored as I am, but I can continue trotting out studies about Dianabol & Methyltestosterone, but what's the Goddamn point, when I am now arguing with people on the defensive that interpret the world through authorities like subreddit admins & hardcore drug addicts, and don't even understand that they're even misapplying those people's statements to argue something else altogether, but not with any evidence that falsifies the statement at issue, that:

MENT, by acting as a substrate to Aromatase, produces 7α-ME at 35% the rate that testosterone produces E2.

References
[1] Lakshman, K. M., Kaplan, B., Travison, T. G., Basaria, S., Knapp, P. E., Singh, A. B., … Bhasin, S. (2010). The Effects of Injected Testosterone Dose and Age on the Conversion of Testosterone to Estradiol and Dihydrotestosterone in Young and Older Men. The Journal of Clinical Endocrinology and Metabolism, 95(8), 3955–3964. doi:10.1210/jc.2010-0102
[2] Gual, C., Morato, T., Hayano, M., Gut, M., & Dorfman, R. I. (1962). Biosynthesis of Estrogens. Endocrinology, 71(6), 920–925. doi:10.1210/endo-71-6-920
[3] Ryan, K. J. (1960). Estrogen formation by the human placenta: Studies on the ... Acta Endocrinologica Supplementum, 1960, 51, 697.
[4] Attardi BJ, Pham TC, Radler LC, Burgenson J, Hild SA, Reel JR. Dimethandrolone (7alpha,11beta-dimethyl-19-nortestosterone) and 11beta-methyl-19-nortestosterone are not converted to aromatic A-ring products in the presence of recombinant human aromatase. J Steroid Biochem Mol Biol. 2008;110(3-5):214-222. doi:10.1016/j.jsbmb.2007.11.009
[5] Ryan, Kenneth J. “Biological aromatization of steroids.” Journal of Biological Chemistry 234.2 (1959): 268-272.
 
What’s your thoughts about how much proviron affects hematocrit levels. It’s my understanding that proviron can slightly increase hematocrit levels, but nothing significant.
Proviron at 100 mg/d is nonerythropoietic (has no significant effect on HCT/Hb).
 
Because really what difference does it make what science says and how it happens - for 99% of users it doesn't matter... the only thing that matters is that for most people even small doses of ment aromatize like the devil's bitch lol
Thanks luki, it's good to know science is irrelevant, and I'm wasting my time by using it for its explanatory & predictive power. TIL.

I'm sure that none of what you apply in bodybuilding is rooted in science, nah. It's just "practice" no need for "theories."

Yet you post shit like this "experiment": https://www.professionalmuscle.com/...mprove-insulin-sensitivity-experiment.176756/

Your New Years Resolution should be try to appreciate things you're not good at, like science. Just because something isn't a strength of yours doesn't mean it's useless; it just means it's an area of yours that needs improvement.
 
Thanks luki, it's good to know science is irrelevant, and I'm wasting my time by using it for its explanatory & predictive power. TIL.

I'm sure that none of what you apply in bodybuilding is rooted in science, nah. It's just "practice" no need for "theories."

Yet you post shit like this "experiment": https://www.professionalmuscle.com/...mprove-insulin-sensitivity-experiment.176756/

Your New Years Resolution should be try to appreciate things you're not good at, like science. Just because something isn't a strength of yours doesn't mean it's useless; it just means it's an area of yours that needs improvement.

Luki is far more knowledgeable than you’ll ever be. I think most of us here will agree to that. Luki has helped soooo many people. You’re just a bizarre tweaker who will never post a physique pic 🤣

Good luck selling your programs, clown. 🤡
 
Thanks luki, it's good to know science is irrelevant, and I'm wasting my time by using it for its explanatory & predictive power. TIL.

I'm sure that none of what you apply in bodybuilding is rooted in science, nah. It's just "practice" no need for "theories."

Yet you post shit like this "experiment": https://www.professionalmuscle.com/...mprove-insulin-sensitivity-experiment.176756/

Your New Years Resolution should be try to appreciate things you're not good at, like science. Just because something isn't a strength of yours doesn't mean it's useless; it just means it's an area of yours that needs improvement.
Man... tell me what's wrong with you...

Do you see any word where I wrote anything against science or your posts? I only wrote the truth, which is that most people don't care about the chemical process behind it, only what effect it gives - does this mean that I have something against scientific explanations? Fuck no

I see that you still have a hard time with me - let it go because I have no intention of getting into unnecessary quarrels with anyone, life is too short for that - and this is my New Year's resolution... but yours should be to start having more distance to yourself and more slack, instead of getting up in your ass about every word you don't like
 
Luki is far more knowledgeable than you’ll ever be. I think most of us here will agree to that. Luki has helped soooo many people. You’re just a bizarre tweaker who will never post a physique pic 🤣

Good luck selling your programs, clown. 🤡

Maybe post a few client transformations made from all the highly technical word salad. There must be 100's to chose from.
 
Man... tell me what's wrong with you...

Do you see any word where I wrote anything against science or your posts? I only wrote the truth, which is that most people don't care about the chemical process behind it, only what effect it gives - does this mean that I have something against scientific explanations? Fuck no

I see that you still have a hard time with me - let it go because I have no intention of getting into unnecessary quarrels with anyone, life is too short for that - and this is my New Year's resolution... but yours should be to start having more distance to yourself and more slack, instead of getting up in your ass about every word you don't like
Actually, luki, I do like ya. If I saw you at the Olympia or another show, I'd want to shake your hand, and am used to having larger guys' hands totally swallow mine. I'm not sure that'd be reciprocated; but I enjoy your contributions.

I like messing with you; I do not dislike you.
 
Maybe post a few client transformations made from all the highly technical word salad. There must be 100's to chose from.
I will not do so, but in a few months don't be surprised when you start to see posts from guys' shows that include photos. I don't even encourage clients to share their results publicly but some do. I certainly don't care about satisfying you, bro. While I like luki, I think you're a fucking moron.
 
Luki is far more knowledgeable than you’ll ever be. I think most of us here will agree to that. Luki has helped soooo many people. You’re just a bizarre tweaker who will never post a physique pic 🤣

Good luck selling your programs, clown. 🤡
That's not very nice.

I would say that you're welcome for the insights shared about MENT aromatization, but it seems you decided to bite the hand that feeds you and kill the messenger.

Character is your weakness to improve on this New Year.

Bit of a scumbag...
 
I think this guy has potential myself.
🤔
The recent cluster of new (and resurfaced old) members does not give me cause for optimism.
Buuuut one never knows, he might be ok 🤷🏻‍♂️

I seem to recall having to drag a backstory out of another science-y guy……..and he turned out to be alright
 

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