Ok, dustateride was not the miracle we expected, whats next?

[CCS]

answer for haRM1 and question for bryan

Harm1,

only dutasteride,which is not prescribed for hairloss, inhibits type1 and2. propecia only inhibits type2, and it was made by merk. i Don't know why you keep asking why merk fights type 1 when they have not and they only fought type 1 this whole time. They did make a type 1 inhibitor to do tests with, but they are not selling it.

in answer to my own question about whether type1 plays a tiny role, i recall that transplanting a non-balding hair into a balding zone does not affect it's life at all compared to the hairs on the back, even though it is now next to high DHT hairs. ANd transplanting a balding hair to a non-balding zone or to the arm does not make it live any longer than the hairs it was origional next to. it dies on time with them. this shows that blood DHT has little effect.

however, i wondered if it was very small compared to the high dht inside the follicle, and might play a larger role by comparison if the follicle had propecia in it. we do know that 1mg finasteride regrows 83% as much hair as 5mg finasteride, and this is probably because of a difference in DHT inhibition of some size. The question is whether the blood DHT levels that could enter the cell are anywhere close to the DIFFERENCE in the DHT levels of propecia and proscar. BRIAN, did the scientists who did the transplant studies have groups who were taking finasteride when they had the transplant, to cut out the "background noise" and get an even better look at the effect of blood dht? Or did the life times of the hairs have enough precision to not need that test?

 

[Bryan]

So is THERE no official answer? Can we ask a professional, or merc ?

I think everybody realizes by now (especially Merck! ) that the type 2 enzyme is more strongly associated with hairloss than type 1.

What I ment to ask is this: Could the reason hair loss is still battled against with type 1 inhibition even tough people with just type 1 never grow bald, be the folowing: Using DHT inhibitors such as propecia increases DHT levels by more DHT receptors in the body, and more prodacrion of 5ARD--> This brings up 5AR1 to a higher level than it is found in those people with a genetic lack of type 2, and in the high numbers it gets to CAN result in harming the hair. DO you think this could be the reason?

No. I don't know of any evidence that the use of finasteride causes an increase in the production or activity of the type 1 enzyme. In fact, Imperato-McGinley (the doctor who did the original research into the "pseudohermaphrodites" in the 1970's) did a test showing that finasteride use had no effect on the production of sebum. If type 1 increased for some reason, an increase in sebum would be an obvious and expected result.

Why do you dislike AZELIC? I use it on my zits and i see great resaults.

Sure. Azelaic acid is good for acne, because it has antiabacterial and other properties which make it good for zits. All I'm saying is that it probably doesn't work as a topical 5a-reductase inhibitor.

I use 20 precent for my zits, What is the danger using 20 precent on my scalp?

Nothing at all. I just doubt that it'll do any good.

I tried it and nothing bad had happend. Zits are also caused be type 2 5ar like, that was proven when they just tried a type 1 inhibitor for acne.

Uh, no...that's not the reason!

Nobody really knows yet why MK386 didn't seem to work for acne.

What does it have to do with age, and anyway think of it as a general question for all users. Is it a fact that inhibiton of DHT raises DHT receptors in the body and also the amount of 5AR? And is it knows if those paremeters come back to nornal when propecia is stopped? IF NOT it could end in cancer and rapid hair loss WHEN PROPECIA IS DROOPED.ANybody ever adress this important issue?

I suggest tapering-off slowly when stopping finasteride.

LAST THING: What do you use friend?

Not much of anything, at the moment. A little Proxiphen every now and then.

Bryan

 

[Bryan]

Re: answer for haRM1 and question for bryan

however, i wondered if it was very small compared to the high dht inside the follicle, and might play a larger role by comparison if the follicle had propecia in it. we do know that 1mg finasteride regrows 83% as much hair as 5mg finasteride, and this is probably because of a difference in DHT inhibition of some size. The question is whether the blood DHT levels that could enter the cell are anywhere close to the DIFFERENCE in the DHT levels of propecia and proscar.

The problem with that general idea is that not only are follicle levels of DHT suppressed slightly more when you go from Propecia to Proscar, so are blood levels of DHT, so it doesn't really clarify the situation any.

BRIAN, did the scientists who did the transplant studies have groups who were taking finasteride when they had the transplant, to cut out the "background noise" and get an even better look at the effect of blood dht? Or did the life times of the hairs have enough precision to not need that test?

I don't think that would clarify the situation, for the reason I stated above. When you take finasteride, BOTH blood and follicles levels of DHT are reduced in parallel.

Bryan

 

[CCS]

bryan, bryan, i think you are not on the ball. the graphs you sent me show that when proscar is used for 28 days, 5ar1 levels are not affected. dht levels and 5ar2 levels are. if that study is credible, then you don't need to look at acne as a measure of whether 5ar1 is affect; we already have the graphs.

Second off, even if azelic acid did inhibit DHT, and that caused acne reduction, the sebum glands have type 1, not 2, so this would mean that type 1 was affected, and does not mean it would work on hair loss. however, since M386 did not affect acne, i think that proves that the azelic acid's acne benifits are not necessarily from DHT inhibition. it seems people assume that just because something treats a condition which is agrivated by androgens that it must be an androgen inhibitor.

we know that topical spironolactone stops hair on women, but that is hair, not acne.
has spironolactone or flutamide or any androgen blockers affected acne? has topical finasteride been tested on acne? I really doubt it, but i still wonder.

 

[CCS]

and i forgot to add. in the graphs, when proscar was discontinued, DHT levels returned to normal. they came up and approached normal. they did not go past it. So if 5ar2 does go into hyperdrive, it leaves it easily.

the only thing the graphs don't show is whether the androgen receptor numbers increased in response to proscar. However, on propecia.com, there is a graph of placebo, propecia, people who switched from placebo to propecia, and people who switched from propecia to placebo. since receptor numbers are probably related to hairloss, that graph may shed some light.

 

[CCS]

http://www.drugs.com/PDR/Propecia_Tablets.html

scroll 1/3 the way down.

the drop off is fast, but not faster than how fast the placebo group eventually falls. also, when back on it, they climbed higher than the people who stayed on it but started a year later. this graph shows that people who started late not only did not get as high, but climbed less even from their lower starting level.

looking at the placebo, I would not be worried about finasteride dependence. they did not fall further than their placebo counterparts, and they got more benifit from getting back on than their late starting counter parts.

 

[Bryan]

bryan, bryan, i think you are not on the ball. the graphs you sent me show that when proscar is used for 28 days, 5ar1 levels are not affected. dht levels and 5ar2 levels are. if that study is credible, then you don't need to look at acne as a measure of whether 5ar1 is affect; we already have the graphs.

Those graphs are the results of calculated data points, based on the average results of careful blood measurements of DHT in all their test subjects who took various doses of finasteride and dutasteride.

In particular, they assumed that finasteride has no significant effect on 5a-reductase type 1, it wasn't a result of actual experimentation. Here's what they say on the final page of the study in the Discussion section:

"No effect of finasteride on 5a-reductase type 1 was included in the current model. However, finasteride has been shown to interact with 5a-reductase type 1 in vitro with a second-order rate about 2.2% of the rate constant for the GI198745-5a-reductase type 1 interaction. If the same relation between the rate constants of the 5a-reductase type 1 interaction with finasteride and GI198745 is true in vivo, a steady-state finasteride concentration of about 1200 ng/mL would be needed to suppress 5a-reductase type 1 by 50%. Assuming linear pharmacokinetics, daily doses of about 270 mg finasteride would be required to achieve average concentrations of this magnitude. Because this is more than 50-fold higher than the dose used clinically, exclusion of the finasteride-5a-reductase type 1 interaction should not affect predictions with the current model."

Second off, even if azelic acid did inhibit DHT, and that caused acne reduction, the sebum glands have type 1, not 2, so this would mean that type 1 was affected, and does not mean it would work on hair loss.

Correct. However, Dr. Lee himself claims that topical azelaic acid reduces DHT by up to 98% (or whatever the number is that he uses) wherever it's applied, and that it affects BOTH versions of the 5a-reductase enzyme. That "98%" figure is extremely unlikely to be correct, in my opinion.

however, since M386 did not affect acne, i think that proves that the azelic acid's acne benifits are not necessarily from DHT inhibition.

Correct. It has antibacterial and anti-hyperkeratinization properties (say that rapidly 10 times). That's what makes it useful for acne.

we know that topical spironolactone stops hair on women, but that is hair, not acne.
has spironolactone or flutamide or any androgen blockers affected acne?

Yes, topical spironolactone has been tested for acne at least a time or two. It's shown some success at that.

has topical finasteride been tested on acne? I really doubt it, but i still wonder.

Only indirectly, as far as I know. I cited Imperato-McGinley's study in another thread in which she tested finasteride's effect on sebum production. There wasn't any.

Bryan

 

[Bryan]

http://www.drugs.com/PDR/Propecia_Tablets.html

scroll 1/3 the way down.

the drop off is fast, but not faster than how fast the placebo group eventually falls.

Err...I'm going to assume that you're referring to the finasteride--->placebo group. The drop off IS faster than any other group! That is, the downward slope is STEEPER. I think that probably is the result of discontinuing the drug after the follicles have become somewhat "sensitized" by the relative lack of androgenic stimulation (like the infamous AR upregulation, or whatever). For that reason, I always recommend that if you ever decide to stop taking finasteride, you should taper-off SLOWLY, not go cold-turkey.

Bryan

 

[Guest]

you really should mix some 5% minoxidil in with the isopropyl rubbing alcohol if you can tolerate it. the propylene glycol will slow the evaporation time so that the finasteride has more time to be absorbed before it dries. Once it dries, anything on the skins surface will stay there. Also, minoxidil does more than just grow hair: it stops scaring and other stuff that lead to permenant hair loss later. If you use more than one tablet per month, consider making smaller batches every two weeks, just incase the finasteride breaks down faster in liquid. Unlike dutasteride, which has a 5 week half life in the human body, finasteride has a 4 hour half life. While the liver is responsible for metabolizing it and your bottle does not have a liver, I'd still take the precaution. My knowledge of chemistry and functional groups tells me that nothing in minoxidil should react with finasteride, but I'd still play it safe, unless you are really busy and just want to make it once a month. You should be fine.

Oh, and most of the studies that say topical finasteride does not work used ground pill paste on the head. If I would have known about the studies before the finished, I would have bet all my college financial aid that they were going to fail, and I'd be rich now.

LOL - see I'm right, check how friends you have at MySpace. They all ran off once they knew the balding situation.

:lol:

I'm just playing mate. A joke.

 

[CCS]

cat,

that is not my myspace account. it is a second account I just threw up for this web site. i think i mentioned that on the site, under the "who i want to meet section"

 

[CCS]

bryan, i asked about acne because I was wondering if type 2 could be responsible for acne. not that I care too much about a disease I no longer have, but i'm always curious, especially when spironolactone treated acne and m386 did not. it is possible one of the inactive ingredients in the spironolactone delivery treated acne, so now i wonder if they had a placebo that just lacked the spironolactone.

as for the azelic acid, i can't imagine how it would stop dht production, and must point out that if it stops 98% of scalp dht, then we would not need finasteride or spironolactone. tests were done in vitro, and I wonder if a pH change caused the cell function of dht production to shut down. it is not safe to change our pH.

http://www.baldingblog.com/2005/09/19/d ... hair-loss/
here is a little more, though i notice that all transplant docs seem to be against topicals, and only recommend rogaine and propecia, probably because we already know they work. it means more bald people, but i guess it is not in their best interest for their patients to look like freaks later in life and no one wanting to get transplants. however, propecia stops hair loss for most poeple, and some others may need only a few follow up grafts, and docs don't do transplants on people who don't respond to propecia. good new topics would kill the transplant business.

 

[CCS]

bryan, i realize that proscar reduces serum dht. but according to sum studies, it reduces scalp dht by only 38%. i think that is when they measure blood. that new measurement, which includes the cells (i'm guessing) says it reduces 60-70%.

serum dht is like the air breath. shut down all the cheminies in town, and the air does get clearer. but what about the air near where some cheminies are still going? i did not read the studies, but correct me if i'm wrong when i think the dht in the blood in the scalp is only reduced by 38% dht is freshly dumped out of the sebacious cells, and is diluted when it gets to the rest of the body. the same may be true of the rest of the skin in the body, though i suspect the greatest dht activity exists in the armpits, growin, and other areas where there is a lot of hair. while the skin has much volume, it is small compared to the full body's volume.

so perhaps the dht in the skin does have some small effect. what if all dht inhibition up to 57% had no effect on hair loss, and there was a transition range from 90% to 57%, and any inhibition greater than 90% had the same effect? the transplant to the arm would not measure this. the use of oral proscar and topical m386 on the arm would compare 5% dht concentration on the arm to 20-40% in the scalp, and answer this question for us.

 

[powersam]

"the only thing the graphs don't show is whether the androgen receptor numbers increased in response to proscar." - collegechemistry student

is that even possible? can androgen receptor numbers increase in response to introduced factors such as finasteride?

 

[CCS]

i don't know. i did read that when spironolactone (or was it some other androgen blocker) was used orally to fight prostate cancer, the androgen receptors mutated so that they could still be activated by other chemicals. i read that second hand, not in a study. the receptors did not multiply, but they did become more sensitive.

as bryan recently pointed out, the graphs that show 5ar activitiy are just estimated, not actually from measured data. i wondered how they could know how much 5ar was inhibited.

 

[Bryan]

"the only thing the graphs don't show is whether the androgen receptor numbers increased in response to proscar." - collegechemistry student

is that even possible? can androgen receptor numbers increase in response to introduced factors such as finasteride?

Uhh...they don't increase in response to the presence of finasteride, they increase as a response to the absence of DHT! In other words, there's obviously a feedback control of the synthesis of androgen receptors. When the cell sees a sharp decline in DHT, it signals the manufacture of more androgen receptors in an attempt to restore that androgenic stimulation. It has nothing to do with finasteride per se.

Bryan

 

[Bryan]

as bryan recently pointed out, the graphs that show 5ar activitiy are just estimated, not actually from measured data.

Let's put it this way: they're interpolated and extrapolated from the measured blood levels of DHT of all their test subjects who took various doses of dutasteride.

Bryan

 

[Felk]

BUT there are biological questions about cutting the type 1 DHT production because its in YOUR BRAIN. WE have a biological model for men without type 2 alpha five reductase, but not type 1. I wouldn't want cancer in my 40s to have hair in my twenties would you?

In other words, Id stick with propecia if I were young. Avodart, Dutasteride, was made for older men with prostate hyperplasia so bad that they have to get up 4 times a night to piss, not 22 year olds losing their hairline.

This attitude was always the one I shared regarding finasteride and dutasteride. However this is an interesting point on the other side...

I think it's clear that the younger you are when you start taking 5a-reductase inhibitors, the closer you approach the experience of the pseudohermaphrodites, who never get prostate enlargement or (apparently) prostate cancer. Starting them much later in life, however, is a different story, and may not be so benign.

I guess that is more relevant to finasteride users though, as the pseudohermaphrodites still have type 1.

Bah, i never know what to think about these things!

 

[powersam]

also as to the inhibiting type 1 . i think if you are on a 2 or 3 pills a week Avodart dosing schedule you wont have any problems. simply because it only lowers type 1 by something like 15% which would be well within the natural range of variation between men.

 

[ecs]

Guys, Even if you get CASTRATED and have almost no testosterone..........................all you do is pretty much stop losing hair and regain just a bit of what youve lost.........

I have heard about realtionship between castration and hairloss for years, I wonder if this is true or just a rumor, are there any medical records back this up?
I am asking this just out of curiosity, of course I am not leaving my baby in exchange of hairs lol.

 

[bubka]

Guys, Even if you get CASTRATED and have almost no testosterone..........................all you do is pretty much stop losing hair and regain just a bit of what youve lost.........

I have heard about realtionship between castration and hairloss for years, I wonder if this is true or just a rumor, are there any medical records back this up?
I am asking this just out of curiosity, of course I am not leaving my baby in exchange of hairs lol.

pretty sure that males that are castrated pre puberty will not experience male pattern baldness... but i am sure there are exceptions

castration after puberty does little for mbp