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Winny & Finasteride (Propescia)
- Thread starter e-man2
- Start date
“Yeah, my main beef is with the idea that Deca and finasteride don't mix (test not being an issue). It's not based on any eveidence or even on logic. I just think it's gotten to be one of those things we "know" and take for granted without really thinking about. And also, Bill Roberts seems to think, as many do, that all androgens that agonize the AR have the potential to cause AGA. Not based in fact, as I've also posted.“
You don’t think the evilness of dht on the hair is because it’s has strong binding affinity?
What about those androgens with poor binding affinity? Do you think they accelerate aga?
Maybe telogen effluvium while on and accelerating androgenetic alopecia?
Just brainstorming
You don’t think the evilness of dht on the hair is because it’s has strong binding affinity?
What about those androgens with poor binding affinity? Do you think they accelerate aga?
Maybe telogen effluvium while on and accelerating androgenetic alopecia?
Just brainstorming
300-400mg of Deca
The dosage I am reffering to is 300-400mg/wk of Deca. What impact does this dosage have on MPB if used inconjunction with Finasteride??
In other words, since Finasteride prevents Nondrolone converting to DHN, then at what dosage does Nandrolone (not DHN) become of significant impact to hair loss? Is my dosage of 300-400mg/week of any significance?
Thanks,
Peace
The dosage I am reffering to is 300-400mg/wk of Deca. What impact does this dosage have on MPB if used inconjunction with Finasteride??
In other words, since Finasteride prevents Nondrolone converting to DHN, then at what dosage does Nandrolone (not DHN) become of significant impact to hair loss? Is my dosage of 300-400mg/week of any significance?
Thanks,
Peace
You don’t think the evilness of dht on the hair is because it’s has strong binding affinity?
What about those androgens with poor binding affinity? Do you think they accelerate aga?
Maybe telogen effluvium while on and accelerating androgenetic alopecia?
Just brainstorming [/B][/QUOTE]
Good question. I don't know the answer to it. But here's something to chew on. The people with congenital absence of 5- AR can make no DHT, but they have normal levels of testosterone. They never develop AGA, and testosterone certainly has a strong binding affinity for the AR.
What about those androgens with poor binding affinity? Do you think they accelerate aga?
Maybe telogen effluvium while on and accelerating androgenetic alopecia?
Just brainstorming
[/B][/QUOTE]Good question. I don't know the answer to it. But here's something to chew on. The people with congenital absence of 5- AR can make no DHT, but they have normal levels of testosterone. They never develop AGA, and testosterone certainly has a strong binding affinity for the AR.
OK, BuffDoc is correct! And here is the study to prove it( I know you do not like across the board references to studies but here it is anyway!) Note that the Note that in this study, the binding affinity of the reduced 19-nor was the same as the 19-nor but the androgenic effect was increased, hence if we assume that the alopecia is androgenic in nature( and most do), the reduced 19-nor would be more detrimental than the 19-nor.
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J Steroid Biochem Mol Biol 1997 Jan;60(1-2):121-9 Related Articles, Links
5alpha-reduction of norethisterone enhances its binding affinity for androgen receptors but diminishes its androgenic potency.
Lemus AE, Enriquez J, Garcia GA, Grillasca I, Perez-Palacios G.
Department of Reproductive Biology, UAM-Iztapalapa, Mexico City, Mexico.
Norethisterone (NET), a 19-nor synthetic progestin, undergoes enzyme-mediated 5alpha-reduction and exerts potent androgenic effects in target organs. To investigate its mode of androgenic action we examined, in a comparative manner, the in vitro metabolism of NET and testosterone (T), as well as the binding affinities to androgen receptors (AR) and the androgenic potency of NET, T, and their 5alpha-reduced derivatives. Bioconversion of [3H]-NET and [3H]-T was studied in rat prostate homogenates, AR binding affinity was assessed in rat ventral prostates using [3H]-mibolerone as the radioligand, and the androgenic potency was evaluated by the increase of beta-glucuronidase activity in the mouse kidney, and by the growth of accessory sex organs in castrated male rats. The results demonstrated that 5alpha-NET displayed a higher AR binding affinity but a significantly lower androgenic potency than unchanged NET. The bioconversion studies indicated that the metabolism of NET was similar to that of T, although to a lesser extent, thus ruling out the possibility that the synthetic progestin metabolizes rapidly into less active derivatives. To investigate the nature of the paradoxical effect of 5alpha-reduction upon the NET molecule, the interaction with AR and the androgenic potency of T, 19-nortestosterone (19norT), 17alpha-ethynyl testosterone (ET) and their 5alpha-reduced derivatives were examined. The results of AR binding studies revealed that 5alpha-reduction of T and ET significantly enhanced their affinities, and that the 5alpha-derivative of 19norT displayed a similar binding affinity to that exhibited by 19norT. In terms of biological activity, the results showed that 5alpha-reduction of T and 19norT significantly increased their androgenic potency , whereas 5alpha-reduction of ET resulted in a significant diminution of its androgenicity in a manner similar to that observed with the 5alpha-reduction of NET. When NET and 19norT were simultaneously administered with 5alpha-dihydrotestosterone they exhibited a potent synandrogenic activity, an effect that was cancelled by their 5alpha-reduction. Interestingly, ET displayed an antiandrogenic activity, an effect that was also suppressed by its 5alpha-reduction. The overall results demonstrated a distinctive, paradoxical effect of 5alpha-reduction upon the NET molecule, which was different from that seen in naturally occurring androgens, and which suggests that the presence of the 17alpha-ethynyl group plays a key role in this phenomenon. The data provided further evidence that the metabolism of synthetic contraceptive progestins modulates the expression of their hormone-like actions.
============================
J Steroid Biochem Mol Biol 1997 Jan;60(1-2):121-9 Related Articles, Links
5alpha-reduction of norethisterone enhances its binding affinity for androgen receptors but diminishes its androgenic potency.
Lemus AE, Enriquez J, Garcia GA, Grillasca I, Perez-Palacios G.
Department of Reproductive Biology, UAM-Iztapalapa, Mexico City, Mexico.
Norethisterone (NET), a 19-nor synthetic progestin, undergoes enzyme-mediated 5alpha-reduction and exerts potent androgenic effects in target organs. To investigate its mode of androgenic action we examined, in a comparative manner, the in vitro metabolism of NET and testosterone (T), as well as the binding affinities to androgen receptors (AR) and the androgenic potency of NET, T, and their 5alpha-reduced derivatives. Bioconversion of [3H]-NET and [3H]-T was studied in rat prostate homogenates, AR binding affinity was assessed in rat ventral prostates using [3H]-mibolerone as the radioligand, and the androgenic potency was evaluated by the increase of beta-glucuronidase activity in the mouse kidney, and by the growth of accessory sex organs in castrated male rats. The results demonstrated that 5alpha-NET displayed a higher AR binding affinity but a significantly lower androgenic potency than unchanged NET. The bioconversion studies indicated that the metabolism of NET was similar to that of T, although to a lesser extent, thus ruling out the possibility that the synthetic progestin metabolizes rapidly into less active derivatives. To investigate the nature of the paradoxical effect of 5alpha-reduction upon the NET molecule, the interaction with AR and the androgenic potency of T, 19-nortestosterone (19norT), 17alpha-ethynyl testosterone (ET) and their 5alpha-reduced derivatives were examined. The results of AR binding studies revealed that 5alpha-reduction of T and ET significantly enhanced their affinities, and that the 5alpha-derivative of 19norT displayed a similar binding affinity to that exhibited by 19norT. In terms of biological activity, the results showed that 5alpha-reduction of T and 19norT significantly increased their androgenic potency , whereas 5alpha-reduction of ET resulted in a significant diminution of its androgenicity in a manner similar to that observed with the 5alpha-reduction of NET. When NET and 19norT were simultaneously administered with 5alpha-dihydrotestosterone they exhibited a potent synandrogenic activity, an effect that was cancelled by their 5alpha-reduction. Interestingly, ET displayed an antiandrogenic activity, an effect that was also suppressed by its 5alpha-reduction. The overall results demonstrated a distinctive, paradoxical effect of 5alpha-reduction upon the NET molecule, which was different from that seen in naturally occurring androgens, and which suggests that the presence of the 17alpha-ethynyl group plays a key role in this phenomenon. The data provided further evidence that the metabolism of synthetic contraceptive progestins modulates the expression of their hormone-like actions.
JB,
Thanks for the nice study. It reminds me of an important principle that we all forget sometimes: binding affinity does NOT necessarily translate into a positve agonist (activator) effect.
A great example is found in the opioid (narcotic) receptors. Naloxone, an opioid antagonist, binds very avidly to the receptor, so avidly that it may displace morphine and other potent agonists (activators). Yet it exerts NO opioid effect whatsoever!
Likewise, there may be substances that bind very strongly to the AR, but exert minimal biological effect.
Thanks for the nice study. It reminds me of an important principle that we all forget sometimes: binding affinity does NOT necessarily translate into a positve agonist (activator) effect.
A great example is found in the opioid (narcotic) receptors. Naloxone, an opioid antagonist, binds very avidly to the receptor, so avidly that it may displace morphine and other potent agonists (activators). Yet it exerts NO opioid effect whatsoever!
Likewise, there may be substances that bind very strongly to the AR, but exert minimal biological effect.
