0.25 mg Finasteride

[Ende]

1 mg finasteride a day, wouldn't be superior to 0.2 mg a day, in terms of visible results.

Sure it would. Why wouldn't it? The early "dose-ranging" study of finasteride by Merck clearly showed that the larger the dose, the better the haircounts were. Up to a certain point, anyway.

That's my point. If 0.05, 0.2, 0.5 and 1 mg are equal when it comes to DHT suppression, large doses and better results proves that the enzymes are only blocked for a certain amount of time.

 

[Bryan]

Those studies you're referring to, how where they done?

Oh please! I have STACKS of finasteride and dutasteride studies. There's no way I could explain them all!

Since finasteride and dutasteride are known to reduce the prostate size, which probably is the place where most DHT is produced, I assume a reduction in the amount of enzymes is possible, but only in that area. The enzymes which are located at the top of your head, are only blocked for a certain time - and they're the main concern regarding hair loss.

I'm not sure what you mean.

 

[Ende]

I will agree that DHT is mainly paracrine hormone, but it obviously has endocrine properties. When all the receptors in the local area are saturated, it'll travel around your body, and it counters estrogen and its effects.

DHT doesn't "travel around the body" very much. Read that Gisleskog et al study that I cited for you ealier; it'll tell you more about why it isn't much of an endocrine hormone. One of the important reasons seems to be that the body eliminates it from the bloodstream fairly rapidly; more rapidly than testosterone, for example.

Then why does severe side effects occur, and why does some people develop secondary hypogonadism? I've experience with Andractim too, and I assure you that DHT is able to move throughout your body when all the receptors in the target area are saturated. It does so until it finds something to bind to. It suppresses estrogen, and thereby maintains- or shifts the testosterone/estrogen ratio in favor of testosterone.

 

[Bryan]

1 mg finasteride a day, wouldn't be superior to 0.2 mg a day, in terms of visible results.

Sure it would. Why wouldn't it? The early "dose-ranging" study of finasteride by Merck clearly showed that the larger the dose, the better the haircounts were. Up to a certain point, anyway.

That's my point. If 0.05, 0.2, 0.5 and 1 mg are equal when it comes to DHT suppression, large doses and better results proves that the enzymes are only blocked for a certain amount of time.

They're not equal when it comes to DHT suppression, they're NEARLY equal when it comes to DHT suppression. That's why larger doses are a bit more effective than smaller ones (up to a certain point).

 

[Ende]

Since finasteride and dutasteride are known to reduce the prostate size, which probably is the place where most DHT is produced, I assume a reduction in the amount of enzymes is possible, but only in that area. The enzymes which are located at the top of your head, are only blocked for a certain time - and they're the main concern regarding hair loss.

I'm not sure what you mean.

The prostate contains a lot of 5AR type 2 enzymes, no? Since finasteride and dutasteride are able to reduce the prostate size by cell death (stated by Mew), I assume that it's possible that they may destroy the enzymes as well. If the studies you're referring to where done at the prostate, it could explain why some claim it's a SI.

 

[Ende]

Sure it would. Why wouldn't it? The early "dose-ranging" study of finasteride by Merck clearly showed that the larger the dose, the better the haircounts were. Up to a certain point, anyway.

That's my point. If 0.05, 0.2, 0.5 and 1 mg are equal when it comes to DHT suppression, large doses and better results proves that the enzymes are only blocked for a certain amount of time.

They're not equal when it comes to DHT suppression, they're NEARLY equal when it comes to DHT suppression. That's why larger doses are a bit more effective than smaller ones (up to a certain point).

Yes, of course, but how many percentages are we talking about... It's not significant IMO. I believe that the results are based on half lifes.

 

[Bryan]

Then why does severe side effects occur, and why does some people develop secondary hypogonadism? I've experience with Andractim too, and I assure you that DHT is able to move throughout your body when all the receptors in the target area are saturated. It does so until it finds something to bind to.

Sorry, but I think that's pure baloney! I think finasteride and dutasteride cause problems in some people by suppressing the formation of DHT at the sites themselves where 5a-reductase is produced. DHT doesn't "move throughout the body" doing various things, and the problems are then caused when some other drug keeps that from happening. Problems are caused when finasteride/dutasteride block 5a-reductase locally in susceptible tissues.

 

[Bryan]

The prostate contains a lot of 5AR type 2 enzymes, no? Since finasteride and dutasteride are able to reduce the prostate size by cell death (stated by Mew), I assume that it's possible that they may destroy the enzymes as well. If the studies you're referring to where done at the prostate, it could explain why some claim it's a SI.

A lot of this work (the work showing that finasteride/dutasteride bind to 5a-reductase irreversibly) has also been from purely in vitro experiments. Are you still doubting this claim which has been calmly discussed and pointed out for years?

 

[Ende]

Then why does severe side effects occur, and why does some people develop secondary hypogonadism? I've experience with Andractim too, and I assure you that DHT is able to move throughout your body when all the receptors in the target area are saturated. It does so until it finds something to bind to.

Sorry, but I think that's pure baloney! I think finasteride and dutasteride cause problems in some people by suppressing the formation of DHT at the sites themselves where 5a-reductase is produced. DHT doesn't "move throughout the body" doing various things, and the problems are then caused when some other drug keeps that from happening. Problems are caused when finasteride/dutasteride block 5a-reductase locally in susceptible tissues.

You believe that what's bullshit? DHT deficiency and elevated estrogen level are the problem when you get severe side effects from finasteride. How do you explain that? Excessive estrogen is known to induce secondary hypogonadism. DHT and some of its derivatives like mesterolone, are know to suppress the estrogen level, and thereby shifting the testosterone/estrogen ratio in favor of testosterone, and you still believe that DHT doesn't have any effects on the endocrine system?

 

[Ende]

The prostate contains a lot of 5AR type 2 enzymes, no? Since finasteride and dutasteride are able to reduce the prostate size by cell death (stated by Mew), I assume that it's possible that they may destroy the enzymes as well. If the studies you're referring to where done at the prostate, it could explain why some claim it's a SI.

A lot of this work (the work showing that finasteride/dutasteride bind to 5a-reductase irreversibly) has also been from purely in vitro experiments. Are you still doubting this claim which has been calmly discussed and pointed out for years?

I don't know what in vitro means, and yes, I don't believe that finasteride is a SI, and I do believe that half life is important.

 

[Bryan]

That's my point. If 0.05, 0.2, 0.5 and 1 mg are equal when it comes to DHT suppression, large doses and better results proves that the enzymes are only blocked for a certain amount of time.

They're not equal when it comes to DHT suppression, they're NEARLY equal when it comes to DHT suppression. That's why larger doses are a bit more effective than smaller ones (up to a certain point).

Yes, of course, but how many percentages are we talking about... It's not significant IMO.

There were about as many doses as you mention above.

I believe that the results are based on half lifes.

Okay. Whatever.

 

[Ende]

I believe that the results are based on half lifes.

Okay. Whatever.

That's your answer? Don't f*** around. You're saying that the information which Merck states about how finasteride works, is false?

 

[Bryan]

You believe that what's bullshit?

I've already explained to you numerous times what I think is bullshit! I don't think that DHT does very much by moving throughout the body in the bloodstream. It only does things AT THE SITES WHERE IT'S ACTUALLY GENERATED by 5a-reductase. How many times do I have to repeat that?

 

[Ende]

Howcome the serum concentration of DHT is measurable, and the suppressed DHT level continues to raise one or two weeks after using 1 mg of finasteride then? It's measurable because excessive amounts travels around your body, from one place which is loaded with 5AR type 2 enzymes, to another.

 

[Bryan]

I don't know what in vitro means, and yes, I don't believe that finasteride is a SI, and I do believe that half life is important.

The term in vivo means done in a living animal, like a human being, or some laboratory animal (rats, guinea pigs, mice, monkeys, etc.) In vitro, on the other hand, refers to an experiment done just in laboratory equipment. For example, subjecting tissue samples to a 5a-reductase inhibitor like finasteride in a test-tube for a long period of time (days or weeks) at body temperature and coming back to find that the 5a-reductase in the samples is still permanently disabled by the finasteride would be an in vitro experiment. Experiments like that have actually been done with finasteride/dutasteride, which is why they're considered to be irreversible inhibitors.

 

[Bryan]

That's your answer? Don't f*ck around. You're saying that the information which Merck states about how finasteride works, is false?

No I'm not. What are you talking about? :dunno:

 

[Bryan]

Howcome the serum concentration of DHT is measurable, and the suppressed DHT level continues to raise one or two weeks after using 1 mg of finasteride then? It's measurable because excessive amounts travels around your body, from one place which is loaded with 5AR type 2 enzymes, to another.

It's certainly measurable, because we've developed good laboratory tests whcih are capable of detecting it. But that doesn't mean that the tiny amounts of DHT in the bloodstream actually do very much to the parts of the body where they aren't actually produced!

 

[Ende]

I don't know what in vitro means, and yes, I don't believe that finasteride is a SI, and I do believe that half life is important.

The term in vivo means done in a living animal, like a human being, or some laboratory animal (rats, guinea pigs, mice, monkeys, etc.) In vitro, on the other hand, refers to an experiment done just in laboratory equipment. For example, subjecting tissue samples to a 5a-reductase inhibitor like finasteride in a test-tube for a long period of time (days or weeks) at body temperature and coming back to find that the 5a-reductase in the samples is still permanently disabled by the finasteride would be an in vitro experiment. Experiments like that have actually been done with finasteride/dutasteride, which is why they're considered to be irreversible inhibitors.

Observations and statements like that are hard to deny, but if it's true, Merck is stating false information. You need more to convince me. This discussion began when you expressed that my proposal, which is based on information from the drug manufacturer, is bullshit.

 

[Ende]

That's your answer? Don't f*ck around. You're saying that the information which Merck states about how finasteride works, is false?

No I'm not. What are you talking about? :dunno:

You're stating that finasteride is a SI. Merck states;

CLINICAL PHARMACOLOGY
Finasteride is a competitive and specific inhibitor of Type II 5?-reductase (...)

 

[Bryan]

Observations and statements like that are hard to deny, but if it's true, Merck is stating false information. You need more to convince me. This discussion began when you expressed that my proposal, which is based on information from the drug manufacturer, is bullshit.

Merck isn't stating false information. They simply didn't say anything one way or the other in that PDF file that you presented about whether or not finasteride is an irreversible inhibitor. If you want to do more research on that, I suggest starting with the study I cited. There are others which discuss that issue, too.