Does finasteride block dht or cause the body to produce less dht?

[philippe]

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?

[chrisis]

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.

[MackJames]

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.

[Davey Jones]

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.)

[chrisis]

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.

[Davey Jones]

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.

[philippe]

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."

[chrisis]

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

You're wrong

[JJacobs152]

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.

[NotBelievingIt]

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.

[chrisis]

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.

If that's the case, it means after 3 months I should be fine, unless something else is going on. Any ideas on what the "something else" is? Then we can figure out how to resolve it.

[sausage]

Well apparently some people believe side effects are in peoples heads.....but to be honest I have never heard so much tosh in all my life.

[oOKawaiiOo]

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.

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.

Finally some biological mechanism. I always thought fin was a competitive inhibitor to 5-AR (enzyme) that catalyzes testosterone to DHT. So by increasing the substrate levels [concentration], it would have a better chance in binding to the enzyme and preventing further increase in DHT levels.

What is an competitive inhibitor? Binds substrate that competes for the binding at the active site of the enzyme where the reaction occurs.

http://en.wikipedia.org/wiki/Competitive_inhibition

But from what your saying, it looks like an uncompetitive inhibitor which binds to the enzyme and testosterone. Meaning you slow down the production of DHT but not as effective as competitive inhibitors.

http://en.wikipedia.org/wiki/Uncompetitive_inhibitor

Most of the drugs out there are competitive inhibitors, and are more effective in preventing reactions from occuring than uncompetitive.

http://www.drugs.com/pro/propecia.html

The link above claims fin is a competitive inhibitor.....so it doesnt bind to testosterone at all. Just the 5-AR.

I also have a B.S in Biological Sciences.

[the_charger]

Isnt the FDA medication approval process a pretty thorough way of determining if a medication is fit for public consumption or not? even if it isnt, there have been a ton of studies done on finasteride after the fact that all show it is tolerated well and I don’t think any permanent or severe side effects resulted from those... the fact that all this talk of severe side effects is so recently compared to how long the medication has been on the market really shows how very rare this is!

of course after a drug is released and millions of people start taking it, you will start to see very rare side effects that weren’t found initially. This isn’t unique to finasteride and it happens with literally any prescription medication out there. Merck and the FDA aren’t backtracking like you are saying, if anything it shows they continue to monitor adverse side effects to watch for these rare events and updates their labels to warn of these changes. Just like how they noticed in extremely rare cases it can cause male breast cancer or prostate cancer or depression.

finasteride isn’t perfect, I don’t even think its near perfect. but it is a very effective treatment for hair loss but you risk some very rare symptoms if you take it. On the other side of the coin, there isn’t much else to treat hair loss right now, and hair loss itself can be extremely hard on some people, so anyone thinking about taking it really needs to weigh out the pro’s and con’s.

everyone seems to make propecia out to be some sort of horrible devil drug, but has anyone ever looked at antidepressants? sexual side effects from antidepressants effect somewhere around 20% of all users, and this is very well documented. Not to mention about another dozens of common side effects. Just to name a few: nausea, vomiting, headache, fatigue, dizziness, insomnia, diarrhea, weight loss, weight gain, mania, tremors, cardiovascular problems, severe withdrawal symptoms, and even sexual dysfunction that can last years after stopping the treatment. And MILLIONS of people take these treatments, usually without a second thought. Whats worse is kids are getting treated with antidepressants more and more often. I think I read that over 50 million people have taken or are currently taking antidepressants! Its weird to me that

So yeah, finasteride isn’t perfect, and it can cause very rare and severe symptoms. But when you put it into perspective and compare it to other drugs like antidepressants, which are one of the most commonly prescribed types of medications, finasteride isn’t really that bad. Unfortunately this doesn’t help the people that ended up with bad side effects.. Hopefully we can get some better studies that give us a full understanding of whats happening and how these people can be treated.

[gmonasco]

Also, the onus is on the drug pusher to prove its safety, not the patient or victim.

But since finasteride did pass the required safety protocols of those clinical trials, the onus is really now upon those who claim it is unsafe to prove their case.