anyone take finasteride .05 mg every day?

[hello]

Two years ago, I took it for about a month and panicked after reading about side effects. I maybe experienced some of the sides with 1 mg daily... Im thinking of giving it another go.


Would 0.5 mg per day be a good idea? Maybe less results but less sides Im thinking.


My hair's not bad yet, I just want to maintain what I have.

 

[eth0]

You can take 0.25 if you want, that's what I did.
It'll prevent hair loss just the same as 1mg as finasteride has a flat rate.

 

[decro435]

I think (.25 mg) Finasteride inhibits 60% DHT or something along those lines.

"eth0" did you try (1 mg) Finasteride? Did you notice any side effects?
And if you did, did you see the side effects subside once you began taking (.25 mg)?

 

[Thickandthin]

I think you can take finasteride pretty haphazardly, at varying dosages and intervals and still see results. The studies showed .01 mg having no effect. so just to be safe you should probably take atleast 0.1-0.2 mg.

 

[hello]

hmm, interesting. what about taking 1 mg every other day instead of 0.5 mg every day?

 

[vanheldan]

hmm, interesting. what about taking 1 mg every other day instead of 0.5 mg every day?

from my understanding you need to take finasteride every 24hrs. so you're better off taking a smaller dose everyday than taking a larger dose every two days

 

[vanheldan]

btw, i'm starting finasteride in the next few weeks at 0.125mg and hoping to go up by 0.125mg every month.

once i start, i'll post my story in the 'tell your story' forum and keep everyone up to date.

 

[captain_que]

btw, i'm starting finasteride in the next few weeks at 0.125mg and hoping to go up by 0.125mg every month.

.

by month 20 you´ll be up to 5mg and can take whole proscar pills!

 

[eth0]

"eth0" did you try (1 mg) Finasteride? Did you notice any side effects?
And if you did, did you see the side effects subside once you began taking (.25 mg)?

No, I didn't bother taking 1mg.
I assume the only reason people do is for conveninece, alhough it takes 10 seconds to put a 1mg pill into quarters so it's hardly a chore.

I would have cut it down to 0.05 if I could as that's also just as effective at stopping hair loss, but that was too much work.
I know some guys disolve theirs in alcohol to get it down to this amount.

Read the study here
http://www.physics.upenn.edu/facultyinf ... peciafda2/

 

[vanheldan]

btw, i'm starting finasteride in the next few weeks at 0.125mg and hoping to go up by 0.125mg every month.

.

by month 20 you´ll be up to 5mg and can take whole proscar pills!

at this moment in time i'm planning to stop at around 0.5mg. that's 4 months in. i should know by then whether its having an effect an whether i should up the dose.

 

[captain_que]

btw, i'm starting finasteride in the next few weeks at 0.125mg and hoping to go up by 0.125mg every month.

.

by month 20 you´ll be up to 5mg and can take whole proscar pills!

at this moment in time i'm planning to stop at around 0.5mg. that's 4 months in. i should know by then whether its having an effect an whether i should up the dose.

I understand. I was just joking :innocent:

 

[ryan r]

But if 0,5 or 0,2 mg finasteride is just as effective as 1mg finasteride, why are the chances of side effects lower, if it blocks just as much DHT?

 

[Hecfield]

Someone can correct me if I'm wrong, I'm just hypothesising.

Alpha reductase, which metabolises testosterone to DHT, is present in two forms in the body, type 1 and type 2. Finasteride inhibits type 2, which (I'm not sure of the figures exactly so I'm just rounding for ease) accounts for 1/3 of scalp DHT and 2/3 of serum (blood) DHT. Its a basic rule of enzyme inhibition, once you've inhibited a certain percentage of enzymes the effects of any increase in dose is negligible, because you've blocked as many as you're going to block. You reach that point in the scalp before you do in the blood, so the dose becomes irrelevant in the scalp before it does in the blood. After that, all your doing is decreasing your blood DHT level without significantly changing your scalp DHT level.

With dutasteride it's a different story.

 

[Bryan]

Finasteride inhibits type 2, which (I'm not sure of the figures exactly so I'm just rounding for ease) accounts for 1/3 of scalp DHT and 2/3 of serum (blood) DHT.

For what it's worth, Gisleskog et al, in their exhaustive studies of finasterinde and dutasteride, claim that the type 2 enzyme is responsible for slightly over 80% of serum DHT.

You reach that point in the scalp before you do in the blood, so the dose becomes irrelevant in the scalp before it does in the blood. After that, all your doing is decreasing your blood DHT level without significantly changing your scalp DHT level.

Interesting hypothesis. What do you base that idea on? Can you provide any arguments to support it?

 

[Hecfield]

If you mean studies and that, then no, unfortunately. Just based on what I know of enzyme kinetics/inhibition, which is a decent amount (I'm studying biochemistry/genetics). If finasteride is a typical enzyme inhibitor, which I assume it is, then it should always reach a plateau of effectiveness when its in excess, and any improvement will be so small that its negligible, even if you add more and more and more. Heres just a random example from a google search for 'enzyme inhibition curve, http://www.probior.com/img/product/SODI ... nCurve.gif. That shows 100% inhibition, which is exceptional in physiological conditions, but whatever. The point is there's a peak where the increment becomes so low you can pretty much ignore it.

Anyway, I would just assume that since this saturation would occur beforehand in the areas where less enzyme is, simply because less substrate is required to saturate less enzyme. So, in the blood, where there's more type II reductase, finasteride would be more effective at a higher concentration, whereas in the scalp adding more is doing sweet nothing because there's nothing left to do. It would explain why people can get rid of side effects without losing effectiveness, and to my knowledge its a plausible explanation.

I'm surprised that nobody has looked into it. Hold fire for a year or so, I might have found my dissertation.

 

[Bryan]

Anyway, I would just assume that since this saturation would occur beforehand in the areas where less enzyme is, simply because less substrate is required to saturate less enzyme. So, in the blood, where there's more type II reductase, finasteride would be more effective at a higher concentration, whereas in the scalp adding more is doing sweet nothing because there's nothing left to do.

Type II reductase doesn't occur in the blood. It's strictly a CELLULAR enzyme. It's tightly-bound to certain internal cellular membranes, and doesn't go anywhere else. Therefore, your fundamental premise is incorrect. Was that your only reason for believing your stated hypothesis?

 

[Hecfield]

Type II reductase doesn't occur in the blood. It's strictly a CELLULAR enzyme. It's tightly-bound to certain internal cellular membranes, and doesn't go anywhere else. Therefore, your fundamental premise is incorrect. Was that your only reason for believing your stated hypothesis?

Right, sorry, cellular. Intracellular results should be exactly the same as matrix, so it doesn't really effect the conclusion, even if the presmise was a little off. I'm not as knowledgeable as you are regarding the specifics of hair loss, I just know biochemistry.

Its a pretty solid reasoning, its one of the fundamental rules of enzyme inhibiton, just applied to finasteride. I'll look into it more after my exams are over next week, because I really don't see any rational reason for what I said to be off the mark. Its backed up by hundreds of experiments, I've done similary in vitro experiments myself. The only difference is that no experiments that I know of were carried out on testosterone to DHT interactions in vivo. Unless its some kind of exception to the rule, which Popper would be wonderfully proud of, then what I said should hold true.

 

[Bryan]

Right, sorry, cellular. Intracellular results should be exactly the same as matrix, so it doesn't really effect the conclusion, even if the presmise was a little off.

What do you mean by "matrix" in this context?

Its a pretty solid reasoning, its one of the fundamental rules of enzyme inhibiton, just applied to finasteride.

Now you've completely lost me! Now that we've established that 5a-reductase doesn't occur in the blood, what is your current justification for believing that DHT suppression in the scalp is maximized before DHT suppression in the blood?

 

[Hecfield]

By matrix I mean extracellular fluids, as in blood, as in I'm tired, reading about social policy on climate change and am probably typing sloppy generic terms when I should be more precise, thus meaning you don't need to ask such questions.

My reasoning is exactly the same as I explained before. Assuming that finasteride is not specific in whereabouts in the body it inhibits DHT, then inhibition should reach near enough maximum levels in areas where there are less enzymes first. Perhaps a macro-analogy would help me illustrate my point? If not, at least I'll have a huge amount of fun typing it.

Think of finasteride molecules, or whatever its metabolites are that inhibit reductase (again, tiredness), as men. Thats right, little finasteride men. On a galivant around the neighbourhood. Lets say there are 100 men. Now, II reductase can be something that men like, like women or ice cream or something like that. On the way around the neighbourhood, the men see lots of women in some areas, too many for them to all occupy - some of the women therefore end up ignored/unmolested. They then come around a corner where there are less women, and (such is life) all of the women/ice creams get occupied/bought (take it as you will), leaving some of the men to carry on their journey alone. You can add more men, and more women on the streets which had lots of women on can get 'occupied', but all that happens on the less womany streets is a bit more competition between men. Male banter, tomfoolery, fighting, 'I'm better at having muscles than you', that kind of alpha male machismo jazz. That made perfect sense. Maybe not. But hopefully you catch my entirely questionable drift.

I'll really look into this next week, its going to be one of those go out every night/try and do something to fill the day weeks, so I have nil problem in researching more. If you have any studies which would help me with that then please share, I get that you're quite the male pattern baldness library. Anyway, hope that helps. In one sentence, a smaller amount of something means it gets saturated quicker.

 

[Bryan]

By matrix I mean extracellular fluids, as in blood, as in I'm tired, reading about social policy on climate change and am probably typing sloppy generic terms when I should be more precise, thus meaning you don't need to ask such questions.

If I don't know what you mean when you use a certain word, then I need to ask such questions!

My reasoning is exactly the same as I explained before. Assuming that finasteride is not specific in whereabouts in the body it inhibits DHT, then inhibition should reach near enough maximum levels in areas where there are less enzymes first.

And AGAIN I'm asking you: what makes you think that there's less 5a-reductase activity (on average, and for its size) in the scalp than in all the other body tissues that contain it? Is that just an assumption on your part? I don't doubt that the prostate, for just one example, is a very significant source of DHT (especially for its size), but it's certainly not the only other source besides the scalp. I still think it's pretty speculative to say that DHT-producing activity in the scalp is minimized before DHT levels in the blood are minimized. I'd like to know what evidence you have for that, or what argument you can make in support of your hypothesis.