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  1. #1
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    Default Does finasteride block dht or cause the body to produce less dht?

    I have been on finasteride now for about a year, though I lowered my dosage to .05mg about 4 months ago when the sides were getting bad. Things have improved slightly since then. I have read that finasteride is only in the system for a matter of hours and in that time it blocks dht production. What I am curious about is why it takes a matter of months to see improvement from side effects were one to stop taking the drug? If it takes months this leads me to believe that not only does finasteride block dht when taken it also causes the body to produce less dht whilst on the drug. Am I correct in assuming this? Blocking dht and causing the body to produce less dht are two different things, are they not?

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    Good question. I await a response from everyone who promotes the safety of Propecia, as I assume they wouldn't do so without knowing the answer.

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    Quote Originally Posted by chrisis View Post
    Good question. I await a response from everyone who promotes the safety of Propecia, as I assume they wouldn't do so without knowing the answer.
    By the same token, you rail against the dangers so shouldn't you know the answer to this yourself. If you do, just answer the question without the diatribe and passive aggressive attacks.

  4. #4
    Senior Member Davey Jones's Avatar
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    Quote Originally Posted by philippe View Post
    I have been on finasteride now for about a year, though I lowered my dosage to .05mg about 4 months ago when the sides were getting bad. Things have improved slightly since then. I have read that finasteride is only in the system for a matter of hours and in that time it blocks dht production. What I am curious about is why it takes a matter of months to see improvement from side effects were one to stop taking the drug? If it takes months this leads me to believe that not only does finasteride block dht when taken it also causes the body to produce less dht whilst on the drug. Am I correct in assuming this? Blocking dht and causing the body to produce less dht are two different things, are they not?
    The body does not produce DHT directly, really. Basically, testosterone in your bloodstream is binded to a substance that prevents it's breakdown. This allows testosterone to get to androgen receptors in a functional state. Once unbinded though (as it must be to bind to receptor sites and enzymes), substances can convert testosterone into other hormones. You're probably familiar with the fact that test converts to estrogen. It also converts to DHT though, once combined with a particular enzyme. Fin, however, is more competative in reacting with this enzyme. Thus, fin sort of uses up all of that substance by binding with it instead of test, allowing testosterone to remain as testosterone. It doesn't do anything to DHT itself.

    So the answer to your question is that yes, those are different processes. Fin does the stop production one.

    (A substance that "blocked" DHT would instead be more competative in binding with the receptor site. But as the site in question is the androgen receptor site, I'd imagine blocking that would be bad news bears even harder than fin is already sometimes bad news bears.)

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    Quote Originally Posted by MackJames View Post
    By the same token, you rail against the dangers so shouldn't you know the answer to this yourself. If you do, just answer the question without the diatribe and passive aggressive attacks.
    If describing my experience with finasteride openly and honestly is "railing against the dangers" then yeah, I rail.

    Also, the onus is on the drug pusher to prove its safety, not the patient or victim. That's why we have clinical trials. The fact Merck and the FDA have been backtracking recently is cause for concern. Clearly not enough is known about how finasteride interacts with the male hormonal system resulting in side effects in an unknown number of men. I believe finasteride promoters ought to act with conscience and consider that fact, and I believe more investigations are needed.

    I maintain that questions like this should be answered by those who promote the safety of finasteride. The brutal fact is no one knows why there are so many reports of side effects and why there's so much variation in terms of when they kick in, whether they're temporary or permanent and the degree of severity. This is undeniably a matter of great concern for all of us.

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    Quote Originally Posted by chrisis View Post
    If describing my experience with finasteride openly and honestly is "railing against the dangers" then yeah, I rail.

    Also, the onus is on the drug pusher to prove its safety, not the patient or victim. That's why we have clinical trials. The fact Merck and the FDA have been backtracking recently is cause for concern. Clearly not enough is known about how finasteride interacts with the male hormonal system resulting in side effects in an unknown number of men. I believe finasteride promoters ought to act with conscience and consider that fact, and I believe more investigations are needed.

    I maintain that questions like this should be answered by those who promote the safety of finasteride. The brutal fact is no one knows why there are so many reports of side effects and why there's so much variation in terms of when they kick in, whether they're temporary or permanent and the degree of severity. This is undeniably a matter of great concern for all of us.
    Once again, I agree. Hormones have so many feedback loops based around various levels of the hormones themselves and other compounds. The endocrine system is so ridiculously complicated that it damn near defies reason. If people would be a little more critical of finasteride and admit "Okay, so it is a little bad," there could be a lot more research into what levels actually cause variations in symptoms and the particular feedback loops and levels could be controlled for.

    Unrestrained defense of a drug is not a good way to handle things.

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    thanks davey for your response--unfortunately what is still unclear is how the body seems to change when on finasteride, i.e., the whole question of why it takes months to get sides to go away (if they do go away at all). clearly there is too little information. i am not a finasteride basher--i, like many of us on this forum, want to know as much as possible about the substances i put into my body to combat hairloss. i do wish the fda would be more forthcoming with finasteride's potential "dark side."

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    And for those who think side effect reports are constrained to these forums.

    You're wrong

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    Senior Member JJacobs152's Avatar
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    Quote Originally Posted by Davey Jones View Post
    The body does not produce DHT directly, really. Basically, testosterone in your bloodstream is binded to a substance that prevents it's breakdown. This allows testosterone to get to androgen receptors in a functional state. Once unbinded though (as it must be to bind to receptor sites and enzymes), substances can convert testosterone into other hormones. You're probably familiar with the fact that test converts to estrogen. It also converts to DHT though, once combined with a particular enzyme. Fin, however, is more competative in reacting with this enzyme. Thus, fin sort of uses up all of that substance by binding with it instead of test, allowing testosterone to remain as testosterone. It doesn't do anything to DHT itself.

    So the answer to your question is that yes, those are different processes. Fin does the stop production one.

    (A substance that "blocked" DHT would instead be more competative in binding with the receptor site. But as the site in question is the androgen receptor site, I'd imagine blocking that would be bad news bears even harder than fin is already sometimes bad news bears.)
    Nicely said, and the enzyme which finasteride works on is 5alpha-reductase. Also, used for the treatment of benign prostatic hyperplasia.

  10. #10
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    The bodys naturally produced enzyme, 5 Alpha-Reductase, binds to Testosterone and in that binding process it "pulls" apart what it has bound and creates other hormones such as Allopregnanolone (a neurological hormone) and Dihydrotestosterone. DHT does not exist in the body, at all, unless 5AR creates it.

    5-AR Type II is the primary enzyme that creates DHT, though Type I is being found to have some effect on hair loss as well (due to dustasteride being found to also help).

    Finasteride basically sticks itself in between 5-AR and Testosterone. Finasteride has binding receptacles that 5-AR Type II binds to so it effectively prohibits a large portion of the conversion of T to DHT.

    Dutasteride has receptacles for 5-AR Type I and Type II and thusly has a greater effect. One could almost say the use of Dut would simulate a 5-AR deficiency.

    Finasteride has a half life of I believe it was 8 hours. So 1mg is .5mg after 8 hours and .5mg would be .25mg after 8 hours etc etc.


    Why a reduced dosage has the potential to lessen side effect symptoms is that the body will have what amounts to a mostly clear period after 8 hours. .5 to 1mg Finasteride "blocks" approximately 70% of 5AR conversions, and it parabolically drops off below .5mg.

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