3 months on Fin & it has gotten worse

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Before fin I barely had Norwood 2. But I was thinking all over my scalp. But after fin. I have been shedding so hard that I am on norwood 2 now and my whole scalp is losing hard. I lose like 10 hair follicles whenever I just touch my hair. Wtf is this shit. Wtf is going on like WTF!
Also I don’t have any sides. My dick is actually harder than last time. And I am horny more often and harder. I cum 4-5 times daily. Before fin: 2-3 times. Erection quality is same.
 
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ive red something about intial fin shedding
 
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u shed when u start fin any effective hairloss treatment will make u shed

if ur losing ground on fin then you need other treatments too
 
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u shed when u start fin any effective hairloss treatment will make u shed

if ur losing ground on fin then you need other treatments too
Wdym by ground
 
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oral minox gives you a very brutal shed I've heard

I use topical and the shed from that was bad
I used fin and oral minox but didn't notice any initial shed

look at @Thompsonz
he did what?
Ray peat!?
and he turn norwood clock back
 
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Fin leads to an increase in testosterone, as its conversion to DHT is decreased. Testosterone is a pro-balding hormone, albeit much less potent than DHT.

Forget fin, use the following topicals for 4 hours each if you can afford them. I was on Fin for many years and the balding steadily got worse, switched to these topicals and am experienceing regrowth towards NW1:

Ru58841
topical Dutasteride (doesn't go systemic, unlike topical Fin)
Extra Strength Minox
 
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Fin leads to an increase in testosterone, as its conversion to DHT is decreased. Testosterone is a pro-balding hormone, albeit much less potent than DHT.

Forget fin, use the following topicals for 4 hours each if you can afford them. I was on Fin for many years and the balding steadily got worse, switched to these topicals and am experienceing regrowth towards NW1:

Ru58841
topical Dutasteride (doesn't go systemic, unlike topical Fin)
Extra Strength Minox
I think it's more likely fin just didn't inhibit enough DHT in your follicles rather than a slight increase in T doing any damage
 
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I think it's more likely fin just didn't inhibit enough DHT in your follicles rather than a slight increase in T doing any damage
I wasn't referring to myself, my point was the increase in T is why you were experiencing shedding. That is the scientific cause of "fin shedding".

Not sure why you confused emoji'd my post. It's the most useful balding stack you'll ever see, with no sides. But go ahead and get on fin for 10 years and find out yourself that it will not halt balding and will kill your libido and sperm count in the process.
 
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I wasn't referring to myself, my point was the increase in T is why you were experiencing shedding. That is the scientific cause of "fin shedding".

Not sure why you confused emoji'd my post. It's the most useful balding stack you'll ever see, with no sides. But go ahead and get on fin for 10 years and find out yourself that it will not halt balding and will kill your libido and sperm count in the process.
No, the initial shed is because less of the DHT is binding to the androgen receptor in the hair follicle allowing it to go from its DHT induced telogen phase into the anagen phase.
 
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increase in T is why you were experiencing shedding. That is the scientific cause of "fin shedding".
No it isn’t jfl, it’s cause the change in dht levels interrupts growth cycles and for some people it causes a lot more hairs’ growth cycles to be synced up then they normally would so they all start shedding at the same time before eventually regrowing in
 
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I wasn't referring to myself, my point was the increase in T is why you were experiencing shedding. That is the scientific cause of "fin shedding".

Not sure why you confused emoji'd my post. It's the most useful balding stack you'll ever see, with no sides. But go ahead and get on fin for 10 years and find out yourself that it will not halt balding and will kill your libido and sperm count in the process.
I'm pretty sure the initial shed that some people experience is simply miniaturized hairs falling out and getting replaced with stronger ones due to the decrease in exposure to DHT.

Some topicals might be very effective, but impractical, expensive and hard to get a hold of. Meanwhile, long-term studies on finasteride (10 years) show the incidence of side-effects on fin is comparable to the incidence of side-effects in the overall population.

Also, men born with 5AR deficiency have testosterone, but no DHT and don't seem to get MPB.
 
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No it isn’t jfl, it’s cause the change in dht levels interrupts growth cycles and for some people it causes a lot more hairs’ growth cycles to be synced up then they normally would so they all start shedding at the same time before eventually regrowing in
No, the initial shed is because less of the DHT is binding to the androgen receptor in the hair follicle allowing it to go from its DHT induced telogen phase into the anagen phase.
ya I guess I was wrong about it causing the "fin shedding". Either way, Fin's weakness is that it increases T which has a miniaturization effect.
 
ya I guess I was wrong about it causing the "fin shedding". Either way, Fin's weakness is that it increases T which has a miniaturization effect.
i've used topical fin for 6 months and it was really great but felt overwhelmed by the idea "I need to use this drug for years" and quit.

now I want to get HT and then use topical dut for a while. why dut is not FDA proven yet? is there any prostate,testicle related harmful side effect?
Because I've already have 1 undescended testicle which makes me high risk group for testicle cancer.
 
I'm pretty sure the initial shed that some people experience is simply miniaturized hairs falling out and getting replaced with stronger ones due to the decrease in exposure to DHT.

Some topicals might be very effective, but impractical, expensive and hard to get a hold of. Long-term studies on finasteride (10 years) show the incidence of side-effects on fin is comparable to the incidence of side-effects in the overall population.

Also, men born with 5AR deficiency have testosterone, but no DHT and don't seem to get MPB.
How are topicals impractical? They take 1 min to rub int the scalp. I can give you the links to where to get them: anageninc, minoxidilexpres.

Studies about its side effects bs, every single person I know on Fin has decreased libido. It's just normies answering the polling in studies are subjectively answering and are not as aware of their libido decline. Look at the studies on Fin's effects on sperm count. They are brutal.

Obviously no DHT will lead to a lack of balding. But you will not kill DHT with Fin, only like 50% reduction of scalp DHT, and testosterone most certainly plays an additional role given you are not a non-DHT god. Ru58841 is so effective because it blocks both DHT and Test's effects on the scalp greatly.

 
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I'm pretty sure the initial shed that some people experience is simply miniaturized hairs falling out and getting replaced with stronger ones due to the decrease in exposure to DHT.

Some topicals might be very effective, but impractical, expensive and hard to get a hold of. Meanwhile, long-term studies on finasteride (10 years) show the incidence of side-effects on fin is comparable to the incidence of side-effects in the overall population.

Also, men born with 5AR deficiency have testosterone, but no DHT and don't seem to get MPB.
When will it get replaced with stronger hair?
 
ya I guess I was wrong about it causing the "fin shedding". Either way, Fin's weakness is that it increases T which has a miniaturization effect.
Not even close to how potent DHT is at causing miniaturization compared to Test.
 
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No, the initial shed is because less of the DHT is binding to the androgen receptor in the hair follicle allowing it to go from its DHT induced telogen phase into the anagen phase.
This.

15% increase in T (because its not converted into DHT) will not be the cause your hairlost. DHT its much more androgenic in the scalp than T.
If its shedding, than its working, don't overthink and continue the treatment. Wait a few more months to conclude if it works for you.
I wouldn't start topicals just because i am shedding from a 2 month fin treatment. I would prefer to wait, and if it works, i will just pop a pill for the rest of my life, easy.
 
ya I guess I was wrong about it causing the "fin shedding". Either way, Fin's weakness is that it increases T which has a miniaturization effect.
I just don't think that's true brah. DHT rapes your follicles simply because its concentration in hair follicles is waaaay higher (as it doesn't circulate in the body to the degree that T does) PLUS it binds to the androgen receptors more than T does. T probably does fuck all to your hair. Just my 2 cents from reading a lot on the issue.
 
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i've used topical fin for 6 months and it was really great but felt overwhelmed by the idea "I need to use this drug for years" and quit.

now I want to get HT and then use topical dut for a while. why dut is not FDA proven yet? is there any prostate,testicle related harmful side effect?
Because I've already have 1 undescended testicle which makes me high risk group for testicle cancer.
topical fin goes systemic, so it is essentially useless. you should try topical Dut and minox first. You will likely find you don't need an HT after a few months of that combo. Throw in Ru and you're golden.
 
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How are topicals impractical? They take 1 min to rub int the scalp. I can give you the links to where to get them: anageninc, minoxidilexpres.

Studies about its side effects bs, every single person I know on Fin has decreased libido. It's just normies answering the polling in studies are subjectively answering and are not as aware of their libido decline. Look at the studies on Fin's effects on sperm count. They are brutal.

Obviously no DHT will lead to a lack of balding. But you will not kill DHT with Fin, only like 50% reduction of scalp DHT, and testosterone most certainly plays an additional role given you are not a non-DHT god. Ru58841 is so effective because it blocks both DHT and Test's effects on the scalp greatly.

how u know topical dut has no sides? everything gets absorbed eventually
 
I just don't think that's true brah. DHT rapes your follicles simply because its concentration in hair follicles is waaaay higher (as it doesn't circulate in the body to the degree that T does) PLUS it binds to the androgen receptors more than T does. T probably does fuck all to your hair. Just my 2 cents from reading a lot on the issue.
sorry, that's incorrect. Refer to the article I linked in my previous post.
 
how u know topical dut has no sides? everything gets absorbed eventually
500 Dalton law of molecule absorption. Topical Dut's is 535 or so. Also confirmed by ppl who got their serum DHT measured.
 
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500 Dalton law of molecule absorption. Topical Dut's is 535 or so. Also confirmed by ppl who got their serum DHT measured.
dafuq:feelsuhh: which number is topical fin? also google says it has exception. but interesting you should make a thread tbh
 
dafuq:feelsuhh: which number is topical fin? also google says it has exception. but interesting you should make a thread tbh
under 400 I believe.

Not even close to how potent DHT is at causing miniaturization compared to Test.
Doesn't matter if it's not as close to as potent, it still has an effect on balding, and that is why you will slowly lose hair over time even on Fin. It's also why Ru is so effective (significantly more than oral Fin). That extra effect of blocking T's binding on scalp receptors does a lot. Also, ppl have different sensitivities to each hormone, some ppl's hair might be especially affected by T.
 
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under 400 I believe.


Doesn't matter if it's not as close to as potent, it still has an effect on balding, and that is why you will slowly lose hair over time even on Fin. It's also why Ru is so effective (significantly more than oral Fin). That extra effect of blocking T's binding on scalp receptors does a lot. Also, ppl have different sensitivities to each hormone, some ppl's hair might be especially affected by T.
so topical dut to block dht and RU to block test. how do u apply this shit if you have long thick hair tho?
 
Before fin I barely had Norwood 2. But I was thinking all over my scalp. But after fin. I have been shedding so hard that I am on norwood 2 now and my whole scalp is losing hard. I lose like 10 hair follicles whenever I just touch my hair. Wtf is this shit. Wtf is going on like WTF!
Also I don’t have any sides. My dick is actually harder than last time. And I am horny more often and harder. I cum 4-5 times daily. Before fin: 2-3 times. Erection quality is same.
Because you are ugly and you will be forever ugly
 
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it's so not tested, how can you trust that drug for long term effects?

it's systemic metabolites are fairly ineffective and have no effect on endogenous hormone production. Also, the idea that anti-androgens are bad for your heart is bro-science given the extensive studies on mtf trans, who are undergoing 1000x the systemic AR effect that RU would produce (minimal).
 
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so topical dut to block dht and RU to block test. how do u apply this shit if you have long thick hair tho?
wash your hair first, then use a dropper (I use .75 ml) directly touching your scalp and squeeze a little in various areas.
 
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under 400 I believe.


Doesn't matter if it's not as close to as potent, it still has an effect on balding, and that is why you will slowly lose hair over time even on Fin. It's also why Ru is so effective (significantly more than oral Fin). That extra effect of blocking T's binding on scalp receptors does a lot. Also, ppl have different sensitivities to each hormone, some ppl's hair might be especially affected by T.
I agree, but you can hold on to your hair for a lot longer than without it. RU58841 is interesting but it's not FDA approved as of now, not sure if it ever will be, they stopped their stage trials? Also RU is an anti-androgen which means if it goes systemic it will not only bind to DHT but also all other androgen receptors. I mean it's a research chemical at the end of the day, but looking at anectodal evidence it is highly effective but also a lot of horror stories obviously considering it's not researched enough in my opinion.

Topical Dut does go systemic but to a lesser extent than oral, I think 20-40% reduction in DHT blood levels but very high reduction in the scalp.
 
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I agree, but you can hold on to your hair for a lot longer than without it. RU58841 is interesting but it's not FDA approved as of now, not sure if it ever will be, they stopped their stage trials? Also RU is an anti-androgen which means if it goes systemic it will not only bind to DHT but also all other androgen receptors. I mean it's a research chemical at the end of the day, but looking at anectodal evidence it is highly effective but also a lot of horror stories obviously considering it's not researched enough in my opinion.

Topical Dut does go systemic but to a lesser extent than oral, I think 20-40% reduction in DHT blood levels but very high reduction in the scalp.

Look at the link I posted, it's systemic metabolites are weak and any binding of receptors is likely countering by an increase in endogenous production. The horror stories are by dumbshit normies who are experiencing crazy psychosomatic placebo sides. Mtf trans have no heart issues, how da fuq would the weak ass metabolites of Ru do anything bad? It's high-inhib to not take something that already has a few studies on it. It's not FDA approved because it ran out of marketing and support for who knows what financial reasons.

No way in hell topical dut blocks 20-40%. According to the article I linked it's more like 15% at most.
 
Look at the link I posted, it's systemic metabolites are weak and any binding of receptors is likely countering by an increase in endogenous production. The horror stories are by dumbshit normies who are experiencing crazy psychosomatic placebo sides. Mtf trans have no heart issues, how da fuq would the weak ass metabolites of Ru do anything bad? It's high-inhib to not take something that already has a few studies on it. It's not FDA approved because it ran out of marketing and support for who knows what financial reasons.

No way in hell topical dut blocks 20-40%. According to the article I linked it's more like 15% at most.
I've read it before but looking at this:
"This means that even if RU58841 goes systemic, by creating a blockade of the androgen receptor, RU58841 prevents the negative feedback androgens would normally create via the hypothalamic–pituitary–gonadal axis (HPG axis) in men. By binding to androgen receptors, RU58841 will induce anti-androgen effects without reducing serum androgen levels in the body."

It doesn't decrease blood levels of androgens but what does this mean? I need to do more reasearch but if I read it correctly, it can block androgen receptors in the other tissues of the body? Muscles and brain of instance? How does this play out, if the free test can't bind to these androgen recepters as it does go systemic?

Also regarding the 20-40% systemic reduction, check the video I linked above at around 13:30 and forward, he talks about a study.
 
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I don't really care much what he says tbh. Let's look at some science...

According to wikipedia article on 5AR deficiency:
5ar


They have testosterone, but no DHT and get no MPB.

Furthermore:
DHT signals mainly in an intracrine and paracrine manner in the tissues in which it is produced, playing only a minor role, if any, as a circulating endocrine hormone. Circulating levels of DHT are 1/10th and 1/20th those of testosterone in terms of total and free concentrations, respectively, whereas local DHT levels may be up to 10 times those of testosterone in tissues with high 5α-reductase expression such as the prostate gland.

In addition, the biological importance of DHT was not realized until the early 1960s, when it was found to be produced by 5α-reductase from circulating testosterone in target tissues like the prostate gland and seminal vesicles and was found to be more potent than testosterone in bioassays. The biological functions of DHT in humans became much more clearly defined upon the discovery and characterization of 5α-reductase type II deficiency in 1974. DHT was the last major sex hormone, the others being testosterone, estradiol, and progesterone, to be discovered, and is unique in that it is the only major sex hormone that functions principally as an intracrine and paracrine hormone rather than as an endocrine hormone.

Dhtt


from:


In a nutshell, T has a binding affinity that is multiple times lower than that of DHT + T circulates in your body multiple times more so than DHT does. DHT stays where it's produced (follicles, prostate).

Leading me to believe that the leftover DHT you get even while on dutasteride probably has more of an effect on your hair than T ever will, as it's not nearly as present in your follicles + has a way lower binding affinity than DHT.
 
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I've read it before but looking at this:
"This means that even if RU58841 goes systemic, by creating a blockade of the androgen receptor, RU58841 prevents the negative feedback androgens would normally create via the hypothalamic–pituitary–gonadal axis (HPG axis) in men. By binding to androgen receptors, RU58841 will induce anti-androgen effects without reducing serum androgen levels in the body."

It doesn't decrease blood levels of androgens but what does this mean? I need to do more reasearch but if I read it correctly, it can block androgen receptors in the other tissues of the body? Muscles and brain of instance? How does this play out, if the free test can't bind to these androgen recepters as it does go systemic?
The metabolites are weak and have very partial binding effect. Prob countered by a slight increase in endogenous androgen production, as is typical when receptors are slightly desensitized.

I don't really care much what he says tbh. Let's look at some science...

According to wikipedia article on 5AR deficiency:
View attachment 1583285

They have testosterone, but no DHT and get no MPB.

Furthermore:
DHT signals mainly in an intracrine and paracrine manner in the tissues in which it is produced, playing only a minor role, if any, as a circulating endocrine hormone. Circulating levels of DHT are 1/10th and 1/20th those of testosterone in terms of total and free concentrations, respectively, whereas local DHT levels may be up to 10 times those of testosterone in tissues with high 5α-reductase expression such as the prostate gland.

In addition, the biological importance of DHT was not realized until the early 1960s, when it was found to be produced by 5α-reductase from circulating testosterone in target tissues like the prostate gland and seminal vesicles and was found to be more potent than testosterone in bioassays. The biological functions of DHT in humans became much more clearly defined upon the discovery and characterization of 5α-reductase type II deficiency in 1974. DHT was the last major sex hormone, the others being testosterone, estradiol, and progesterone, to be discovered, and is unique in that it is the only major sex hormone that functions principally as an intracrine and paracrine hormone rather than as an endocrine hormone.

View attachment 1583294


from:


In a nutshell, T has a binding affinity that is multiple times lower than that of DHT + T circulates in your body multiple times more so than DHT does. DHT stays where it's produced (follicles, prostate).

Leading me to believe that the leftover DHT you get even while on dutasteride probably has more of an effect on your hair than T ever will.
You just copy pasta'd a wikipedia article about DHT. The article I linked directly compares Fin to RU:

"The 5% strength RU58841 solution induced the most hair growth after only 2 months of treatment.

RU58841 was given less time to work and still significantly outperformed Finasteride in this study.

Although Finasteride significantly reduced DHT levels, DHT remaining and produced by Type I 5α-reductase isoenzyme still contributed to hair follicle miniaturization.

Because Testosterone and DHT both bind to the androgen receptor, a locally sufficient dose of an "AR blocker" (topical anti-androgen) appears to suppress Testosterone and DHT induced follicular regression more effectively than 5α-reductase inhibition. "
 
The metabolites are weak and have very partial binding effect. Prob countered by a slight increase in endogenous androgen production, as is typical when receptors are slightly desensitized.


You just copy pasta'd a wikipedia article about DHT. The article I linked directly compares Fin to RU:

"The 5% strength RU58841 solution induced the most hair growth after only 2 months of treatment.

RU58841 was given less time to work and still significantly outperformed Finasteride in this study.

Although Finasteride significantly reduced DHT levels, DHT remaining and produced by Type I 5α-reductase isoenzyme still contributed to hair follicle miniaturization.

Because Testosterone and DHT both bind to the androgen receptor, a locally sufficient dose of an "AR blocker" (topical anti-androgen) appears to suppress Testosterone and DHT induced follicular regression more effectively than 5α-reductase inhibition. "
I don't know much about RU. I'm just saying that if fin does not work for you then it has to be because of insufficient DHT inhibition, rather than an increase in T. It just wouldn't make sense when you look at the numbers in regards to binding affinity and presence in hair follicles of both DHT and T.

That said, whatever works for anyone to keep their hair is awesome. I'm just arguing that fin probably works fine for most people and they don't need to rely on unapproved/off-label compounds.
 
Also, the idea that anti-androgens are bad for your heart is bro-science given the extensive studies on mtf trans, who are undergoing 1000x the systemic AR effect that RU would produce (minimal).
That depends on if they're using androgen receptor inhibitors. Decreasing testosterone production is not the same as inhibiting receptors. The heart relies on androgen receptors to function. Lower testosterone may not damage the heart (women have lower testosterone, obviously), but preventing androgen receptor activity definitely could.

I microdose RU58841, by the way.
 
I don't know much about RU. I'm just saying that if fin does not work for you then it has to be because of insufficient DHT inhibition, rather than an increase in T. It just wouldn't make sense when you look at the numbers in regards to binding affinity and presence in hair follicles of both DHT and T.

That said, whatever works for anyone to keep their hair is awesome. I'm just arguing that fin probably works fine for most people and they don't need to rely on unapproved/off-label compounds.
Ya it's probably a combo of both insufficient DHT reduction, and the fact it does nothing to counter the effects of T. Even if T has multiple times lower binding affinity, 100% of it is still hurting your hair when on Fin. Also, someone's hair can have greater sensitivity to T than average.

Fear of "unapproved" compounds that already have studies on them is high-inhib, especially when Fin is known to nuke your sperm count and systemically destroy your serum DHT. There is no mechanism by which these topicals can produce anywhere near the systemic damage that Fin causes. It's pure fear-mongering by normies.

Fin works for nearly everyone to slow balding, but also does not halt it for nearly everyone. And so by the time you get to late 20's, you will have lost quite a bit of hair even if you were on Fin most of your 20's. And by that point, it's already a cosmetic issue. As you can see, that is extremely unsatisfactory. You can get HT's I guess, and then have your sperm count in the gutter as well. I've been through the experience man. I understand the drive to take the FDA approved substance. But that is the road you are likely looking at unless you are a Fin hyper-responder and lucky enough to avoid tolerance.
 
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That depends on if they're using androgen receptor inhibitors. Decreasing testosterone production is not the same as inhibiting receptors. The heart relies on androgen receptors to function. Lower testosterone may not damage the heart (women have lower testosterone, obviously), but preventing androgen receptor activity definitely could.

I microdose RU58841, by the way.
androgen receptors are only activated by androgens, so a reduction in endogenous production will still produce an effect similar to desensitizing the receptors.
 
The metabolites are weak and have very partial binding effect. Prob countered by a slight increase in endogenous androgen production, as is typical when receptors are slightly desensitized.


You just copy pasta'd a wikipedia article about DHT. The article I linked directly compares Fin to RU:

"The 5% strength RU58841 solution induced the most hair growth after only 2 months of treatment.

RU58841 was given less time to work and still significantly outperformed Finasteride in this study.

Although Finasteride significantly reduced DHT levels, DHT remaining and produced by Type I 5α-reductase isoenzyme still contributed to hair follicle miniaturization.

Because Testosterone and DHT both bind to the androgen receptor, a locally sufficient dose of an "AR blocker" (topical anti-androgen) appears to suppress Testosterone and DHT induced follicular regression more effectively than 5α-reductase inhibition. "
which is the cheapest source to buy ru with decent quality?
 
which is the cheapest source to buy ru with decent quality?
I get mine from anageninc because it's known to have the best quality control. MinoxidilMax also carries it but I've avoided them as some ppl say their quality is shit.
 
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androgen receptors are only activated by androgens, so a reduction in endogenous production will still produce an effect similar to desensitizing the receptors.
As I explained, significantly inhibiting the androgen receptors won't allow even a smaller amount of androgenic activity. That's why inhibiting androgen receptors can be more damaging than decimating testosterone production.
 
As I explained, significantly inhibiting the androgen receptors won't allow even a smaller amount of androgenic activity. That's why inhibiting androgen receptors can be more damaging than decimating testosterone production.
That’s fuzzy logic masquerading as math but I’m too lazy to explain. There’s a feedback loop between them. Weak RU metabolites probably do jack-all anyways.
 

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