Minimum finasteride dose that works (oral)

Jack_Daniels

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Hello,

I would like to ask you, which is the mimimum dose of finasteride that can work with the less side effects? I have seen some studies say that even 0.05 mg of finasteride can decrease scalp skin dht by 61.6% and serum dht by 49.5%. So whats the point of getting 1mg per day if less than 1 mg can also work with less chance of side effects? Tell me your experiences, if you have tried minimum doses of finasteride to avoid side effect and what were your results?

Here is the study that i'm talking about:



Also some doctors reccomend 1mg / 3 times a week to avoid side effects. What do you think about that?

 

Norwoody

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My thoughts are that 1mg a day is probably more than necessary for most people. I believe in other countries the standard dose is a bit less. Of course, it all comes down to how much you're willing to risk with side effects. But I think that people likely take too much (and probably too frequently) most of the time. Finasteride has a pretty short half life, however, the systemic effects last longer than that. Guys are probably building up so much in their system that the body doesn't have much of a use for it, and so what's left over is likely utilized in a way which is mostly contributing towards side effects. In my opinion, if you are going to take finasteride, you're probably better off taking less of a dose and sacrificing a few percentages of blockage. IMO it's better to take the minimal effective dose of any given treatment, and spread out different types of treatments that address the issue via multiple pathways.
 

Michael1986

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Guys are probably building up so much in their system that the body doesn't have much of a use for it, and so what's left over is likely utilized in a way which is mostly contributing towards side effects. In my opinion, if you are going to take finasteride, you're probably better off taking less of a dose and sacrificing a few percentages of blockage. IMO it's better to take the minimal effective dose of any given treatment, and spread out different types of treatments that address the issue via multiple pathways.
That's not how it works. The side-effects are caused by the DHT suppression itself, and there is no evidence that finasteride does anything else other than suppress DHT. All doses of around 0.2mg and upwards suppress DHT by almost the exact same amount, due to the fact that finasteride has an essentially flat dose response curve once you go above 0.2mg. The exception to this is a small number of people who are outliers, and who need a higher dose than usual in order to potently inhibit their DHT. Merck decided on a dose of 1mg in order to take account of all the outliers.
 

jamesbooker1975

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Go topical at 0.1 % .
It really don't have much sense on use it oral, cause, after all, more dht you eliminate more chances to work . So the key is to use it at low dose , but topical, the key is to eliminate more on the scalp than in the rest of the body and not the oppotive like it is doing it with it is take it orally.
Keep in mind that the only reason on why Merck realease it as oral pill instead of topical is cause they do a focus group an people thought it will be easy to pop a pill than apply a lotion. Nobody put in question " what if topical have less side effects ?"
 

Norwoody

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there is no evidence that finasteride does anything else other than suppress DHT
By inhibiting 5AR, finasteride increases T which in turn aromatizes to E. This isn't a direct effect, but it is a side effect and it presents other implications.
 

Jack_Daniels

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i dont understand why merck does not make clinical studies on topical finasteride at a dose around 0.1% , so it get FDA aproved as well? Why people who care for hairloss should take a pill that is normally for prostatic hyperplasia treatment and decreases more the dht in the system rather than in the scalp, so changing your hormonal balance?

i think that someone who wants to get the pill, should go for the minimum dose around 0.2 to 0.25 mg per day, or decrease the frequency of getting the pill during the week. Like taking finasteride for about 3-4 times per week. Because by getting high dose every day, then you keep building up so much in your system, and so body does not have enough dht to work normally.
 

Michael1986

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By inhibiting 5AR, finasteride increases T which in turn aromatizes to E. This isn't a direct effect, but it is a side effect and it presents other implications.
Yes, but as you say, that still happens as a result of the DHT suppression. I was just trying to say that finasteride's only direct mode of action is suppressing DHT by inhibiting 5AR.
 

Michael1986

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Go topical at 0.1 % .
It really don't have much sense on use it oral, cause, after all, more dht you eliminate more chances to work . So the key is to use it at low dose , but topical, the key is to eliminate more on the scalp than in the rest of the body and not the oppotive like it is doing it with it is take it orally.
Keep in mind that the only reason on why Merck realease it as oral pill instead of topical is cause they do a focus group an people thought it will be easy to pop a pill than apply a lotion. Nobody put in question " what if topical have less side effects ?"
Topical finasteride seems to always go systemic, and it might be that the main reason it has a chance of working is due to it going systemic to begin with. Finasteride is a smaller molecule than dutasteride, which is why it is thought that topical dutasteride has a better chance of not going systemic. Topicals are also a hassle to use, and topical finasteride is very dangerous to use if your partner is pregnant or you are trying to conceive, or if you have a child who is going through puberty. Oral finasteride is more convenient, and has a proven track record as a highly effective treatment for hair loss.
 
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Norwoody

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My contention is simply that most people are probably taking more than they need relative to the side effects, which is probably why we see people either loving or hating this drug.
 

INT

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What else does finasteride do directly besides inhibit 5AR?
That's not what I said, not what you said. You said:

That's not how it works. The side-effects are caused by the DHT suppression itself, and there is no evidence that finasteride does anything else other than suppress DHT

The role of 5AR not that well understood yet, saing that side effects are caused by only the drop in DHT is something that is still up for debate.
 

jamesbooker1975

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Topical finasteride seems to always go systemic, and it might be that the main reason it has a chance of working is due to it going systemic to begin with. Finasteride is a smaller molecule than dutasteride, which is why it is thought that topical dutasteride has a better chance of not going systemic. Topicals are also a hassle to use, and topical finasteride is very dangerous to use if your partner is pregnant or you are trying to conceive, or if you have a child who is going through puberty. Oral finasteride is more convenient, and has a proven track record as a highly effective treatment for hair loss.
The studies are, at list mixed. Also, the " you must lower your systemic DHT , not your local DHT " was just propaganda from Merck . If you want to understand how merck work, read the Vioxx scandal .
 

jamesbooker1975

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That's not how it works. The side-effects are caused by the DHT suppression itself, and there is no evidence that finasteride does anything else other than suppress DHT. All doses of around 0.2mg and upwards suppress DHT by almost the exact same amount, due to the fact that finasteride has an essentially flat dose response curve once you go above 0.2mg. The exception to this is a small number of people who are outliers, and who need a higher dose than usual in order to potently inhibit their DHT. Merck decided on a dose of 1mg in order to take account of all the outliers.
"The side-effects are caused by the DHT suppression itself"
No, at least, no only. Since you are supprecing an enzyme that works in other reactions, for example, on the creation of other neurosteroids like allopregnolone . That is what Merck never told us .
 

jamesbooker1975

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My contention is simply that most people are probably taking more than they need relative to the side effects, which is probably why we see people either loving or hating this drug.
Well, for example, when I passed from Finasteride to Dutasteride, I really not saw much more growth. When you have a receding hairline. What it should be done since the first date, without the Propaganda from Merck, is to check DHT and find the lower amount that you can have in your body, without side effects . For many people that will work, for other, not.

Keep in mind , that there not a single study, incredible, that show if to the people that are genetic subsectible to get male pattern baldness, it is the accumulation effect of DHT or are the levels of DHT, or both, what it cause the activation of baldness .
 

Michael1986

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That's not what I said, not what you said. You said:



The role of 5AR not that well understood yet, saing that side effects are caused by only the drop in DHT is something that is still up for debate.
"The side-effects are caused by the DHT suppression itself"
No, at least, no only. Since you are supprecing an enzyme that works in other reactions, for example, on the creation of other neurosteroids like allopregnolone . That is what Merck never told us .
What I was trying to say is that the 5AR inhibition is the only thing that finasteride does directly (at least as far as I'm aware). The other things it causes such as its effect on neurosteroids are still a result of the initial 5AR inhibition. Therefore, since finasteride inhibits virtually the same amount of 5AR for all doses of around 0.2mg upwards, I don't see how increasing the dose much higher than this would be likely to result in a significantly greater risk of side-effects or any additional side-effects. That was all I was trying to say. I am open to correction, however, if there is research that has shown finasteride to have a direct effect on other reactions that is independent of its inhibition of 5AR.
 

INT

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What I was trying to say is that the 5AR inhibition is the only thing that finasteride does directly (at least as far as I'm aware). The other things it causes such as its effect on neurosteroids are still a result of the initial 5AR inhibition. Therefore, since finasteride inhibits virtually the same amount of 5AR for all doses of around 0.2mg upwards, I don't see how increasing the dose much higher than this would be likely to result in a significantly greater risk of side-effects or any additional side-effects. That was all I was trying to say. I am open to correction, however, if there is research that has shown finasteride to have a direct effect on other reactions that is independent of its inhibition of 5AR.

We know that there is little difference between 0.05 mg and 1 mg daily when it comes to serum DHT inhibition but we don't know if the same is the case for the 5 AR enzyme. This has never been tested to my knowledge.
 

JohnSmith21

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We know that there is little difference between 0.05 mg and 1 mg daily when it comes to serum DHT inhibition but we don't know if the same is the case for the 5 AR enzyme. This has never been tested to my knowledge.
You get lower dht bc your blocking the enzyme. .2mg blocks as much as 1mg of 5ar. He’s right. If it didn’t block as much 5ar, it wouldn’t lower dht the same amount
 

jazz1

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Go topical at 0.1 % .
It really don't have much sense on use it oral, cause, after all, more dht you eliminate more chances to work . So the key is to use it at low dose , but topical, the key is to eliminate more on the scalp than in the rest of the body and not the oppotive like it is doing it with it is take it orally.
Keep in mind that the only reason on why Merck realease it as oral pill instead of topical is cause they do a focus group an people thought it will be easy to pop a pill than apply a lotion. Nobody put in question " what if topical have less side effects ?"
I been using Topical Finasteride with added Anti Androgen additives for years, I get mine from a Compound Pharmacy they give discount to forum members.

I use:

15% Minoxidil
0.1% Finasteride
5% Azelaic Acid
0.25% Progesterone
0.025% Tretinoin
0.1% Hydocortisone

check here:

 

Michael1986

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I've discovered that there is one other known enzyme that finasteride directly inhibits, which is the 5-beta reductase enzyme. This enzyme produces 5-beta DHT, which has some important functions in our bodies and which doesn't seem to play any role in hair loss. Interestingly, dutasteride doesn't inhibit this enzyme.

An incubation study showed that finasteride only very weakly inhibits 5-beta reductase, with an affinity for this enzyme that is even weaker than its affinity for 5-alpha reductase type 1 (which finasteride at the standard dosage inhibits by no more than 1%). I found a thread on Tressless about this, which I've linked below. The guy who posted the thread was trying to work out if the results of the incubation study can be assumed to be an accurate determination of the amount of 5-beta reductase that finasteride would inhibit within the human body, but nobody was able to answer that specific question.

Basically, the less 5-beta reductase that finasteride inhibits, the better, as this enzyme has some important functions in our bodies and it doesn't appear to play any role in hair loss.

Here is the Tressless thread: https://www.reddit.com/r/tressless/comments/jm3sm9
 
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