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No increase, the finasteride just won't meaningfully reduce NPP's effect on hair loss (because it 5α-reduces to a weakened product, DHN, in scalp and other 5α-reductase rich tissues, like prostate). Finasteride doesn't increase hair loss with any AAS. It only meaningfully reduces testosterone's effect on hair loss (because it 5α-reduces to an amplified product, DHT, in scalp).@Type-IIx does NPP and Fina cause increase in hairloss?
Do any other AAS cause increase haiross with Fina?
Edit -this is assuming you use a test base at all times.
This is my experience also .No increase, the finasteride just won't meaningfully reduce NPP's effect on hair loss (because it 5α-reduces to a weakened product, DHN, in scalp and other 5α-reductase rich tissues, like prostate). Finasteride doesn't increase hair loss with any AAS. It only meaningfully reduces testosterone's effect on hair loss (because it 5α-reduces to an amplified product, DHT, in scalp).
Ahh ok, nice. thank youNo increase, the finasteride just won't meaningfully reduce NPP's effect on hair loss (because it 5α-reduces to a weakened product, DHN, in scalp and other 5α-reductase rich tissues, like prostate). Finasteride doesn't increase hair loss with any AAS. It only meaningfully reduces testosterone's effect on hair loss (because it 5α-reduces to an amplified product, DHT, in scalp).
So i never lose hair on deca, it will just be the same.This is my experience also .
Test more so than deca yes.So i never lose hair on deca, it will just be the same.
But why do people have success with fin on AAS if it only works with test? Is it because test is usually the culprit in this scenario?
Ok greatTest more so than deca yes.
And it lessens the load on hair loss that testosterone has but does not do so with dht compounds so you still lose some hair with those.
Some believe high androgen levels also effect hair and prostate .
Maybe you should read it again !The guy from MPMD seems to think it does increase hairloss: Will Taking Deca With Finasteride Cause Hair Loss?
Wow, you certainly did think and elaborate more. I appreciate you taking the time to do so. It is so very helpful.OK @jJjburton after thinking about this question a bit more, I should modify my earlier statement to make a correction, and to include some context. I try to admit when I’m wrong, so I should state that indeed, nandrolone + 5AR inhibitor use is probably worse than foregoing 5AR inhibitor use in some very select few cases that occur in practice (but this has naught to do with MPMD’s castrated rat prostate size graph).
It is true that inhibiting 5AR of nandrolone logically increases the net flux towards greater concentrations of reactant – the more potent nandrolone – and rationally would seem to decrease the relative concentrations of the weakened DHN with respect to nandrolone. The anticipated consequence of this (though there is a dearth of studies that actually assess human 5AR inhibitor use with nandrolone and effects on hair loss) is that 5ARs (e.g., finasteride, dutasteride) may make hair loss worse in very specific scenarios that I will attempt to illustrate:
✓ Scenario A: Deca + Test (low-medium dose), e.g., 200 mg nandrolone + 250 mg testosterone enanthate weekly...
* 5AR inhibitor use is rational for hair loss prone individuals (due to amplification of T by 5AR, and not quite profound direct nandrolone effects given low-medium doses).
✓ Scenario B: 750 mg nandrolone + 600 mg testosterone enanthate + 450 mg trenbolone + ….
* 5AR inhibitor (topical) use + more advanced hair loss preventive methods are rational (but with anticipated reduced efficacy vs. low dose/endogenous T) for hair loss prone individuals (due to amplification of T by 5AR).
These and various permutations in their themes are the norm for bodybuilding cycle designs in practice. Since Testosterone is a) supportive of sexual function, and b) synergistic (coupled with other AAS) in its anabolic effects by modulating total-body growth a la IGF-I, etc., it is rarely seen in practice that the next scenarios are encountered:
✖ Scenario C: 300 - 400 mg nandrolone + 10 mg daily metandienone (Dianabol):
Here, we have a scenario (low-medium dose nandrolone + a non-5α-reducible drug that supports sexual function and provides IGF-I augmentation via its aromatization sans testosterone) where abstaining from 5AR inhibitor use for the very reason that it is likely (but not assured) to worsen hair loss is seemingly rational. And yet still, it is quite possible that 10 mg daily metandienone so potently induces hair loss in itself that it supersedes any relevance of nandrolone & DHN, regardless of its non-5α-reducibility.
✖ Scenario D: 1500 mg or higher nandrolone weekly (i.e., “Deca only”) [i.e., high dose necessary to sustain low-normal E2, augment IGF-I, support sexual function, etc.]
The assumptions of these scenarios are that cycle design is always rationally directed towards the use of compounds that: I) provide for an increase to IGF-I, II) support basal estrogenic activity & III) sexual function in men.
Even here, where 5AR inhibitor use is ostensibly most irrational for hair loss prone individuals, it is unclear whether such high doses of nandrolone actually effect hair loss differently given 5AR to DHN versus antagonism thereof by dutasteride or finasteride, because of the increased hair loss resulting from the high levels of nandrolone itself (potentially greater than T amplification to DHT at approximately endogenous or low-medium dose concentrations where 5AR inhibitors are most effective).
MPMD
@Blueman
Derek from MPMD’s extrapolation from growth of rodent ventral prostate to hair loss in humans is entirely untenable.
Despite the constellation of “androgenic” effects, that includes prostate size increases & hair loss, Derek’s use of a graph from Sundaram & colleagues measuring ventral prostate size in castrated rats is inapposite the topic of hair loss in man.
Growth (a biological effect) of (castrated) rat ventral prostate epithelial cells (hypertrophy/size ↑ and/or hyperplasia/# ↑) is qualitatively distinct,to hair loss (a different biological effect) in human dermal papilla cells. Hair loss in human dermal papilla cells is affected by ROS homeostasis, where androgens (but not testosterone†) cause an increase in reactive oxygen species, thereby ↑TGF-β1 secretion – stimulating procollagenous activity & hair loss. This is at best only related tangentially and in small part to hypertrophic or hyperplastic mechanisms in prostate epithelial cells.
†: Interestingly, if we could hypothetically completely blockade 5AR, testosterone would be the most hair safe compound that we know of, because it has been shown to not affect hair loss in scalp.
I think I read somewhere that drug companies are now looking into degrading the 5AR receptors in the scalp, instead of just inhibiting them. That might be the final solution for all these problems.OK @jJjburton after thinking about this question a bit more, I should modify my earlier statement to make a correction, and to include some context. I try to admit when I’m wrong, so I should state that indeed, nandrolone + 5AR inhibitor use is probably worse than foregoing 5AR inhibitor use in some very select few cases that occur in practice (but this has naught to do with MPMD’s castrated rat prostate size graph).
It is true that inhibiting 5AR of nandrolone logically increases the net flux towards greater concentrations of reactant – the more potent nandrolone – and rationally would seem to decrease the relative concentrations of the weakened DHN with respect to nandrolone. The anticipated consequence of this (though there is a dearth of studies that actually assess human 5AR inhibitor use with nandrolone and effects on hair loss) is that 5ARs (e.g., finasteride, dutasteride) may make hair loss worse in very specific scenarios that I will attempt to illustrate:
✓ Scenario A: Deca + Test (low-medium dose), e.g., 200 mg nandrolone + 250 mg testosterone enanthate weekly...
* 5AR inhibitor use is rational for hair loss prone individuals (due to amplification of T by 5AR, and not quite profound direct nandrolone effects given low-medium doses).
✓ Scenario B: 750 mg nandrolone + 600 mg testosterone enanthate + 450 mg trenbolone + ….
* 5AR inhibitor (topical) use + more advanced hair loss preventive methods are rational (but with anticipated reduced efficacy vs. low dose/endogenous T) for hair loss prone individuals (due to amplification of T by 5AR).
These and various permutations in their themes are the norm for bodybuilding cycle designs in practice. Since Testosterone is a) supportive of sexual function, and b) synergistic (coupled with other AAS) in its anabolic effects by modulating total-body growth a la IGF-I, etc., it is rarely seen in practice that the next scenarios are encountered:
✖ Scenario C: 300 - 400 mg nandrolone + 10 mg daily metandienone (Dianabol):
Here, we have a scenario (low-medium dose nandrolone + a non-5α-reducible drug that supports sexual function and provides IGF-I augmentation via its aromatization sans testosterone) where abstaining from 5AR inhibitor use for the very reason that it is likely (but not assured) to worsen hair loss is seemingly rational. And yet still, it is quite possible that 10 mg daily metandienone so potently induces hair loss in itself that it supersedes any relevance of nandrolone & DHN, regardless of its non-5α-reducibility.
✖ Scenario D: 1500 mg or higher nandrolone weekly (i.e., “Deca only”) [i.e., high dose necessary to sustain low-normal E2, augment IGF-I, support sexual function, etc.]
The assumptions of these scenarios are that cycle design is always rationally directed towards the use of compounds that: I) provide for an increase to IGF-I, II) support basal estrogenic activity & III) sexual function in men.
Even here, where 5AR inhibitor use is ostensibly most irrational for hair loss prone individuals, it is unclear whether such high doses of nandrolone actually effect hair loss differently given 5AR to DHN versus antagonism thereof by dutasteride or finasteride, because of the increased hair loss resulting from the high levels of nandrolone itself (potentially greater than T amplification to DHT at approximately endogenous or low-medium dose concentrations where 5AR inhibitors are most effective).
MPMD
@Blueman
Derek from MPMD’s extrapolation from growth of rodent ventral prostate to hair loss in humans is entirely untenable.
Despite the constellation of “androgenic” effects, that includes prostate size increases & hair loss, Derek’s use of a graph from Sundaram & colleagues measuring ventral prostate size in castrated rats is inapposite the topic of hair loss in man.
Growth (a biological effect) of (castrated) rat ventral prostate epithelial cells (hypertrophy/size ↑ and/or hyperplasia/# ↑) is qualitatively distinct,to hair loss (a different biological effect) in human dermal papilla cells. Hair loss in human dermal papilla cells is affected by ROS homeostasis, where androgens (but not testosterone†) cause an increase in reactive oxygen species, thereby ↑TGF-β1 secretion – stimulating procollagenous activity & hair loss. This is at best only related tangentially and in small part to hypertrophic or hyperplastic mechanisms in prostate epithelial cells.
†: Interestingly, if we could hypothetically completely blockade 5AR, testosterone would be the most hair safe compound that we know of, because it has been shown to not affect hair loss in scalp.
yeah if we still have hair by thenI think I read somewhere that drug companies are now looking into degrading the 5AR receptors in the scalp, instead of just inhibiting them. That might be the final solution for all these problems.
So, taking finasteride is generally effective during a testosterone and nandrolone cycle, wherein the test dose is higher than the nand? Also, will dissolving my finasteride tablets in my minoxidil solution and applying it topically allow for adequate absorption on the scalp? I am considering this approach to minimize the potential unwanted systemic effects of finasteride. ThanksOK @jJjburton after thinking about this question a bit more, I should modify my earlier statement to make a correction, and to include some context. I try to admit when I’m wrong, so I should state that indeed, nandrolone + 5AR inhibitor use is probably worse than foregoing 5AR inhibitor use in some very select few cases that occur in practice (but this has naught to do with MPMD’s castrated rat prostate size graph).
It is true that inhibiting 5AR of nandrolone logically increases the net flux towards greater concentrations of reactant – the more potent nandrolone – and rationally would seem to decrease the relative concentrations of the weakened DHN with respect to nandrolone. The anticipated consequence of this (though there is a dearth of studies that actually assess human 5AR inhibitor use with nandrolone and effects on hair loss) is that 5ARs (e.g., finasteride, dutasteride) may make hair loss worse in very specific scenarios that I will attempt to illustrate:
✓ Scenario A: Deca + Test (low-medium dose), e.g., 200 mg nandrolone + 250 mg testosterone enanthate weekly...
* 5AR inhibitor use is rational for hair loss prone individuals (due to amplification of T by 5AR, and not quite profound direct nandrolone effects given low-medium doses).
✓ Scenario B: 750 mg nandrolone + 600 mg testosterone enanthate + 450 mg trenbolone + ….
* 5AR inhibitor (topical) use + more advanced hair loss preventive methods are rational (but with anticipated reduced efficacy vs. low dose/endogenous T) for hair loss prone individuals (due to amplification of T by 5AR).
These and various permutations in their themes are the norm for bodybuilding cycle designs in practice. Since Testosterone is a) supportive of sexual function, and b) synergistic (coupled with other AAS) in its anabolic effects by modulating total-body growth a la IGF-I, etc., it is rarely seen in practice that the next scenarios are encountered:
✖ Scenario C: 300 - 400 mg nandrolone + 10 mg daily metandienone (Dianabol):
Here, we have a scenario (low-medium dose nandrolone + a non-5α-reducible drug that supports sexual function and provides IGF-I augmentation via its aromatization sans testosterone) where abstaining from 5AR inhibitor use for the very reason that it is likely (but not assured) to worsen hair loss is seemingly rational. And yet still, it is quite possible that 10 mg daily metandienone so potently induces hair loss in itself that it supersedes any relevance of nandrolone & DHN, regardless of its non-5α-reducibility.
✖ Scenario D: 1500 mg or higher nandrolone weekly (i.e., “Deca only”) [i.e., high dose necessary to sustain low-normal E2, augment IGF-I, support sexual function, etc.]
The assumptions of these scenarios are that cycle design is always rationally directed towards the use of compounds that: I) provide for an increase to IGF-I, II) support basal estrogenic activity & III) sexual function in men.
Even here, where 5AR inhibitor use is ostensibly most irrational for hair loss prone individuals, it is unclear whether such high doses of nandrolone actually effect hair loss differently given 5AR to DHN versus antagonism thereof by dutasteride or finasteride, because of the increased hair loss resulting from the high levels of nandrolone itself (potentially greater than T amplification to DHT at approximately endogenous or low-medium dose concentrations where 5AR inhibitors are most effective).
MPMD
@Blueman
Derek from MPMD’s extrapolation from growth of rodent ventral prostate to hair loss in humans is entirely untenable.
Despite the constellation of “androgenic” effects, that includes prostate size increases & hair loss, Derek’s use of a graph from Sundaram & colleagues measuring ventral prostate size in castrated rats is inapposite the topic of hair loss in man.
Growth (a biological effect) of (castrated) rat ventral prostate epithelial cells (hypertrophy/size ↑ and/or hyperplasia/# ↑) is qualitatively distinct,to hair loss (a different biological effect) in human dermal papilla cells. Hair loss in human dermal papilla cells is affected by ROS homeostasis, where androgens (but not testosterone†) cause an increase in reactive oxygen species, thereby ↑TGF-β1 secretion – stimulating procollagenous activity & hair loss. This is at best only related tangentially and in small part to hypertrophic or hyperplastic mechanisms in prostate epithelial cells.
†: Interestingly, if we could hypothetically completely blockade 5AR, testosterone would be the most hair safe compound that we know of, because it has been shown to not affect hair loss in scalp.
Yes but i read from back when i was trying same thing that you have to use a super low dose amount if finastride or else it just absorbs through the skin anyway. It was like .1 mg. Or something low.So, taking finasteride is generally effective during a testosterone and nandrolone cycle, wherein the test dose is higher than the nand? Also, will dissolving my finasteride tablets in my minoxidil solution and applying it topically allow for adequate absorption on the scalp? I am considering this approach to minimize the potential unwanted systemic effects of finasteride. Thanks
cool it worked for you? `Only .1 mg? wow didn't realize the absorption would be that efficient through the scalp. What is ur minoxidil solution made of? thxYes but i read from back when i was trying same thing that you have to use a super low dose amount if finastride or else it just absorbs through the skin anyway. It was like .1 mg. Or something low.
I did not try it due to circumstances. But there is a chart that shows the amount of finastride that would absorb through scalp vs not. And if you went over the dose, it was the same as just taking it orally.cool it worked for you? `Only .1 mg? wow didn't realize the absorption would be that efficient through the scalp. What is ur minoxidil solution made of? thx
So you can use very small amounts topically to get same effect to prevent sidescool it worked for you? `Only .1 mg? wow didn't realize the absorption would be that efficient through the scalp. What is ur minoxidil solution made of? thx