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Nandrolone increases the Estrogenic Potency of Testosterone

Deca solo for me caused limp penis . After week three or four sex drive became nothing, as in days without any kind of erection,untill I added in dbol, or Cialis or both. Expiriment for yourself.

I've done 225 mgs test, 600 deca and sex drive dropped a lot, limp dick, On hrt after deca solo at 210 mgs a week, added in dbol some days and sex drive raised. Then did 10 mgs test eod or e3d and sex drive returned.

Currently on 600 deca and 10 mgs dbol and sex drive has been high. 3 xs daily last few days, without Cialis. Sex drive is a state of mind, like sex with a partner it's mental more than anything, when you're there ,I say enjoy it and don't suppress it. Kegals have helped as well,lots of them!

Its possible Deca could change brain chemistry by lowering dopamine. Say a person has higher than normal dopamine levels , takes deca for months upon month for years, like any drug it can change brain chemistry.

i am reading this pdf book "Built to survive" it's about the use of anabolic steroids for HIV muscle wasting and it talks about how nandrolone has to be used with another androgen because its too weakly androgenic on its own in lower dosages <200mg week.

"Nandrolone, like other anabolic steroids, is not however, suitable as a substitute for testosterone for the treatment of testosterone deficiency, as it does not produce the effects on libido, quality-of- life and physical hardiness that testosterone itself does.

Nandrolone probably converts to estrogen, not through the action of aromatase, but through the action of organic acids or alkalines in the body that act on nandrolone after it is converted to its 1-beta hydroxylated derivative. This means that estrogen inhibitors like Arimidex, which decrease the activity of aromatase, may not stop nandrolone from aromatizing to estrogen."
 
600mg nandrolone study : highest dosage used in a study created by bodybuilders

Nandrolone decanoate was selected for the possibility that it might be better tolerated than testosterone. Nandrolone is not appreciably aromatized to estrogen (43, 44) and is believed to be associated with less breast engorgement and other androgenic effects that may occur with high doses of testosterone. In fact, nandrolone appeared to be well tolerated in our study. The only common adverse effect was the self-reported testicular shrinkage that would be expected with high doses of androgens suppressing LH and FSH secretion. There were small, but significant, increases in serum hemoglobin of 1.0 and 1.4 g/dL in the two respective treatment groups, but the clinical relevance of this change is uncertain. There was also an approximately 1.5-fold increase in ALT in both groups, which reached statistical significance in the nandrolone only group. There was no clinical evidence of hepatitis, suggesting that these small increases may have been due to the im injections. Of importance, total cholesterol and triglycerides did not increase during the 12 weeks of study therapy. There was actually a significant decrease in total cholesterol documented in the nandrolone only group. However, this does not preclude the possibility that there was a decrease in the high density lipoprotein or an increase in the low density lipoprotein fractions of cholesterol. Although the high doses of nandrolone used in this study did not result in serious adverse events, the safety of such regimens should be confirmed in larger studies, and the risks of longer therapy are uncertain.

 
How fluid is this effect on dopamine receptors? For example, if the use of nandrolone can reduce the number dopamine receptors, would the number of dopamine receptors rebound after cessation of nandrolone use?
Unknown. It's probably transient, i.e., when you come off nandrolone the brain adapts.
 
@Type-IIx didn’t you cover your thoughts on where you fall on the masteron skeletal. Muscle tissue growth?

I can’t remember if you summarized the Peter Bond views.
I basically concur with Peter Bond's view that due to its metabolism in human skeletal muscle by 3α-HSD, it's a relatively weak anabolic. It is still a great complement to many cycles because of its tissue-selective effects on the uptake of estrogens, to increase the androgen/estrogen ratio, and for some mild anabolism per-mg.
 
I basically concur with Peter Bond's view that due to its metabolism in human skeletal muscle by 3α-HSD, it's a relatively weak anabolic. It is still a great complement to many cycles because of its tissue-selective effects on the uptake of estrogens, to increase the androgen/estrogen ratio, and for some mild anabolism per-mg.
Isn't the shifting of the methyl group from the 1 to the 2 position on the steroid backbone meant to prevent its conversion by 3HSD, reaching the cytosolic androgen receptor in decent concentrations?
 
I basically concur with Peter Bond's view that due to its metabolism in human skeletal muscle by 3α-HSD, it's a relatively weak anabolic. It is still a great complement to many cycles because of its tissue-selective effects on the uptake of estrogens, to increase the androgen/estrogen ratio, and for some mild anabolism per-mg.

i honestly can't tell a difference between Proviron and Masteron.

Both are weak anabolics and are solely used for Androgenic activity.

I have a lot of Mast E and i don't really use since Proviron gives me the same effects - Increased libido and Anti-gyno effects. I don't really see this use of injecting masteron when i can take a non toxic oral proviron tab.
 
Nandrolone WITHOUT testosterone as a base has been well researched and tolerated in humans up to 600mg/week.

Nandrolone without a doubt is Superior to Testosterone for Muscle Wasting Diseases and Increasing Lean Body mass.

Body mass index (BMI) of subjects in the nandrolone group had a significantly greater increase (mean = 1.28) compared to both testosterone (post hoc P < .05) and placebo (post hoc P < .01). Waist circumference and triceps skinfold thickness of patients on nandrolone showed similar results. Nandrolone also ensured a better quality of life. Patients with low testosterone level (<3 ng/mL) benefited immensely from nandrolone therapy, which increased their weight and BMI significantly compared to placebo (P < .05).

Patients with a low testosterone level benefited immensely from nandrolone therapy.


Source : https://www.tandfonline.com/doi/pdf/10.1310/hct1104-220
 
Isn't the shifting of the methyl group from the 1 to the 2 position on the steroid backbone meant to prevent its conversion by 3HSD, reaching the cytosolic androgen receptor in decent concentrations?
No, first because it fails at this, per Schanzer drostanolone is rapidly and extensively metabolized by 3α-HSD: "The parent steroid is excreted as a conjugate that can be hydrolysed with β-glucuronidase. The main metabolite is the 17-keto-oxidized 3α-hydroxy-reduced product 3α-hydroxy-2α-methyl-5α-androstan-17-on, which in comparison with T metabolism, is the 2α-methyl androsterone analog." Second, because per Vida the effect of 2α-methylation on metabolism was fairly inferred just to serve to inhibit reduction of the Δ⁴-3-ketone system; and on activity, to reduce activity, primarily androgenic. I think that there's an idealized view of the process of 1950s & 60s chemists to "design" these drugs "for a specific purpose" and "make modifications to achieve an outcome," but the process was not at all like this. Rather, this novel drug class of interest was haphazardly played around with, different compounds synthesized en masse (by different chemists in laboratories across the world), and then sense was tried to make of how they might work. Vida did a great job at this, his Theory of Binding being entirely vindicated by more modern techniques used to study structure/activity relationships.
 
No, first because it fails at this, per Schanzer drostanolone is rapidly and extensively metabolized by 3α-HSD: "The parent steroid is excreted as a conjugate that can be hydrolysed with β-glucuronidase. The main metabolite is the 17-keto-oxidized 3α-hydroxy-reduced product 3α-hydroxy-2α-methyl-5α-androstan-17-on, which in comparison with T metabolism, is the 2α-methyl androsterone analog." Second, because per Vida the effect of 2α-methylation on metabolism was fairly inferred just to serve to inhibit reduction of the Δ⁴-3-ketone system; and on activity, to reduce activity, primarily androgenic. I think that there's an idealized view of the process of 1950s & 60s chemists to "design" these drugs "for a specific purpose" and "make modifications to achieve an outcome," but the process was not at all like this. Rather, this novel drug class of interest was haphazardly played around with, different compounds synthesized en masse (by different chemists in laboratories across the world), and then sense was tried to make of how they might work. Vida did a great job at this, his Theory of Binding being entirely vindicated by more modern techniques used to study structure/activity relationships.
Thanks.
Then they synthesized it to get a patent on the compound and its applications while it offers no real advantage over DHT?
 
Thanks.
Then they synthesized it to get a patent on the compound and its applications while it offers no real advantage over DHT?
No problem brother. I do think it is advantageous over DHT because of the fact that 2α-methylation does protect the Δ⁴-3-ketone system by inhibiting reduction to an extent, very likely yielding more active metabolites. It's certainly more anabolic than DHT in man, just not as anabolic as the Hershberger Assay data suggests. But you really see a pronounced effect of 2α-methylation in Superdrol (basically methyl masteron) to protect the Δ⁴-3-keto structure, by its virtual complete resistance to metabolism.
 
No problem brother. I do think it is advantageous over DHT because of the fact that 2α-methylation does protect the Δ⁴-3-ketone system by inhibiting reduction to an extent, very likely yielding more active metabolites. It's certainly more anabolic than DHT in man, just not as anabolic as the Hershberger Assay data suggests. But you really see a pronounced effect of 2α-methylation in Superdrol (basically methyl masteron) to protect the Δ⁴-3-keto structure, by its virtual complete resistance to metabolism.

do you think it is possible Nandrolone probably converts to estrogen, not through the action of aromatase, but through the action of organic acids or alkalines in the body that act on nandrolone after it is converted to its 1-beta hydroxylated derivative. This means that estrogen inhibitors like Arimidex, which decrease the activity of aromatase, may not stop nandrolone from aromatizing to estrogen?
 
A line of research links nandrolone's depressive effect and alterations in neuropeptide Y content in blood and hippocampus. The issue seems to be very multifaceted.
 

Testosterone + Progestin vs Nandrolone + Progestin

More Men suffered from loss of libido in the Nandrolone group than the Testosterone group.

Both groups had reached azoospermia in most men (95%+)

This study further supports @Type-IIx claim that Nandrolone can't replace Sexual functioning in men - although i do have studies showing no loss of libido at 600mg/nandrolone a week.
 

19NT-HPP (Anadur; Pharmacia Arzneimittel GmbH, Ratingen, Germany) is a long-acting testosterone derivative. Injection of 200 mg 19NT-HPP every 3 weeks has been shown to support sexual function in male volunteers with hormonally suppressed endogenous testosterone secretion (Knuth et al., 1985; Behre et al., 1992).

I am finding conflicting information. Some Men can use nandrolone while others can't. This all comes down to self experimentation.


200mg Nandrolone greatly reduces Sperm count and Maintained Sexual function
 

19NT-HPP (Anadur; Pharmacia Arzneimittel GmbH, Ratingen, Germany) is a long-acting testosterone derivative. Injection of 200 mg 19NT-HPP every 3 weeks has been shown to support sexual function in male volunteers with hormonally suppressed endogenous testosterone secretion ...

I am finding conflicting information. Some Men can use nandrolone while others can't. This all comes down to self experimentation.


200mg Nandrolone greatly reduces Sperm count and Maintained Sexual function
The correct interpretation of the data on this subject is that nandrolone in combination with a GnRH antagonist is comparable to testosterone alone in suppressing spermatogenesis (for use as a male contraceptive). The data writ large shows that nandrolone is consistently unfavorable versus testosterone for supporting sexual function & potency. This can really only be determined by those studies that report dropouts of subjects and collect data on tolerability with respect to sexual function and potency. Hell, tolerance to decreased sexual function is far greater in Asian men than European men. Asian men are basically "A-OK" without libido and effects on sexual function can practically only be determined in this population by attaching an instrument to their penis while they sleep to measure nocturnal erections.
 
The correct interpretation of the data on this subject is that nandrolone in combination with a GnRH antagonist is comparable to testosterone alone in suppressing spermatogenesis (for use as a male contraceptive). The data writ large shows that nandrolone is consistently unfavorable versus testosterone for supporting sexual function & potency. This can really only be determined by those studies that report dropouts of subjects and collect data on tolerability with respect to sexual function and potency. Hell, tolerance to decreased sexual function is far greater in Asian men than European men. Asian men are basically "A-OK" without libido and effects on sexual function can practically only be determined in this population by attaching an instrument to their penis while they sleep to measure nocturnal erections.
Cultural influences are a huge confounder when it comes to anything sex-related.
 
The correct interpretation of the data on this subject is that nandrolone in combination with a GnRH antagonist is comparable to testosterone alone in suppressing spermatogenesis (for use as a male contraceptive). The data writ large shows that nandrolone is consistently unfavorable versus testosterone for supporting sexual function & potency. This can really only be determined by those studies that report dropouts of subjects and collect data on tolerability with respect to sexual function and potency. Hell, tolerance to decreased sexual function is far greater in Asian men than European men. Asian men are basically "A-OK" without libido and effects on sexual function can practically only be determined in this population by attaching an instrument to their penis while they sleep to measure nocturnal erections.

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.
 

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