Am I a Norwood 2 or 3? (or 2A or 3A?)

[mpb47]

completely false. Most of that 30% would have been neutralized by your natural androgen binding proteins so whatever tiny amount was left over wouldn't cause you to lose any more hair...




you can't just suppress one of your most important hormones and expect your body not to do anything. Your body will try to reach homeostasis at any cost whether you like it or not.

5AR inhibitors over time WILL CAUSE HYPERANDROGENISM. THAT'S A FACT. AND HERE'S THE PROOF:

http://www.ehrs.org/conferenceabstracts/2000marburg/guestlectures/s04-sawaya.htm

what now? Still a theory? I can dig up a bunch of studies on prostate issues where they found that 5AR inhibitors stop working after some time with definite AR upregulation

Don't know if you realize this or not, but you are quoting someone that got busted a couple of times by the feds and the FDA. She faked a medical lic and got barred from the FDA to do trials. She may know what she is doing but it''s hard to be sure after this. Read the link below for more details. Just because it's written down does not make it true. I guess that is why they push peer review so hard.

Hyperandrogenism was a buzz word you heard thrown about back in the late 90's early 00's. It may be true but even back then most thought it was pretty rare. Or at least that was the impression I got.

http://www.gpo.gov/fdsys/pkg/FR-2009-06-12/pdf/E9-13929.pdf

[2020]

why would she fake the results of that particular study?

Also, why is it so hard to believe that your body will fight your attempts at suppressing certain hormones?

[mpb47]

why would she fake the results of that particular study?

Also, why is it so hard to believe that your body will fight your attempts at suppressing certain hormones?

On December 11, 2003, the U.S.
District Court for the Middle District of
Florida accepted Dr. Mary E. Sawaya’s
plea of guilty and convicted her of one
count of making a false statement to a
Federal agency, a Federal felony offense
under 18 U.S.C. 1001. This offense was
committed when Dr. Sawaya created a
medical license by obtaining a copy of
a colleague’s Florida medical license,
altered that license using a photocopy
machine to reflect that the license was
issued in her name, and submitted the
false and fraudulent Florida medical
license to the sponsor of a clinical trial,
for which she was a clinical
investigator. The sponsor submitted that
license to FDA as part of the drug
approval process. When the false license
was due to expire, Dr. Sawaya once
again created a false and fraudulent
medical license with a different
expiration date and submitted that
license to the clinical trial sponsor.

For your second question:
I am not agreeing or disagreeing, just saying you need better sources.

[2020]

http://www.ncbi.nlm.nih.gov/pubmed/21557276

.. Immunohistochemical study revealed significant upregulation of ARs by finasteride treatment for 30-180 days....


seriously, how else would you explain that even though finasteride brings your DHT to castrate levels, yet you still continue to bald overtime when castrates don't

[25 going on 65]

Are you sure castrates have similar DHT levels to non-castrated fin users? Castration would also drop testosterone dramatically if I'm not mistaken, which finasteride doesn't

Also I'm trying to read up on hyperandrogenism and it seems it applies to excess secretion of androgens, but not to an increase in androgen receptor sites. My mind is buzzing with questions.....
If the AR sites increase in number, but your body produces the same amount of 5a-reductase enzymes (and fin binds to the same amount, thus maintaining a consistently low level of DHT), is it necessarily the case that a greater amount of DHT is being absorbed after x amount of time on fin?

It might be that there is less opportunity for the protein binding 2020 mentions, therefore more DHT would reach AR sites. But that reminds me of another question: if most of the remaining 30% of DHT (for fin users) binds to protein and not AR sites, why does dutasteride give significantly better results for some of us? Especially for males who lose ground on fin but not dut? If the amount of absorbed DHT is so low with fin alone, should dut really make that much of a difference?

I'm not denying that the body naturally tries to achieve homeostasis, but that's the point of fin (and some other hormone medications). It's basically intervening in our endocrine system to induce certain physiological changes (in our case, stopping MPB). It's not necessarily the case that the male body is able to truly "offset" for the effects of fin, just like the female body isn't able to offset the effects of birth control/
Also it seems finasteride keeps working after any number of years, i.e. it still binds to the 5a-r enzyme and thereby reduces DHT. Does anyone here really think Spencer would have that much hair after 2+ decades of premature MPB if fin wasn't working for him?
The cosmetic result fades with time but to me it seems plausible that this is the result of cumulative damage; even if you suppress 90% of serum DHT (as with dut) there will always be some amount of the hormone reaching receptor sites in your follicles, no?

[2020]

Are you sure castrates have similar DHT levels to non-castrated fin users? Castration would also drop testosterone dramatically if I'm not mistaken, which finasteride doesn't

T by itself doesn't cause hair loss as proven by:

http://en.wikipedia.org/wiki/5-alpha-reductase_deficiency

Also I'm trying to read up on hyperandrogenism and it seems it applies to excess secretion of androgens, but not to an increase in androgen receptor sites. My mind is buzzing with questions.....

it isn't that complicated.... your body has detected lesser levels of 5AR, so it tries to compensate for that in whichever way it can -> more receptors or more sensitive receptors.

Same thing happens with low T. Since there is less of that male hormone, your body tries to compensate by making more DHT since it's much more potent anyways.

This is all 100% true.

If the AR sites increase in number, but your body produces the same amount of 5a-reductase enzymes (and fin binds to the same amount, thus maintaining a consistently low level of DHT), is it necessarily the case that a greater amount of DHT is being absorbed after x amount of time on fin?

I'm thinking your body start upregulating AR activity until it reaches normal levels(before fin)

It might be that there is less opportunity for the protein binding 2020 mentions, therefore more DHT would reach AR sites. But that reminds me of another question: if most of the remaining 30% of DHT (for fin users) binds to protein and not AR sites, why does dutasteride give significantly better results for some of us? Especially for males who lose ground on fin but not dut? If the amount of absorbed DHT is so low with fin alone, should dut really make that much of a difference?

because there is even less DHT then? Much harder and it takes much longer for your body to upregulate all that to normal?

Also it seems finasteride keeps working after any number of years, i.e. it still binds to the 5a-r enzyme and thereby reduces DHT. Does anyone here really think Spencer would have that much hair after 2+ decades of premature MPB if fin wasn't working for him?

he doesn't have that much hair.... it's mostly hairspray and topik
I'm pretty sure he has been slowly losing ground for many years now despite being on fin.

The cosmetic result fades with time but to me it seems plausible that this is the result of cumulative damage; even if you suppress 90% of serum DHT (as with dut) there will always be some amount of the hormone reaching receptor sites in your follicles, no?

maybe your body starts making more 5AR? Not sure, but your body is definitely responding to 5AR blockers by some sort of upregulation.

[Tracy C]

^ you're pretty much back at the baseline after 5 years...

You are misrepresenting what that chart says. That chart does not say that nor does it show that.

[25 going on 65]

Ok. So this article does strongly suggest AR count increases with fin use. But that isn't technically hyperandrogenism (which would mean excess secretion of androgens rather than an increasing # of receptor sites) and I'm not convinced it would lead to the same symptoms, or to hair loss, nor am I convinced it is the sole reason why one can lose ground while on fin--if it is a reason. I think jumping to these conclusions isn't doing guys like Kirby any favors. It still requires a lot of guesswork on our part to fill in all these blanks, and guesswork has its place but it doesn't substitute for proper studies.
It still doesn't add up that fin actually does continue working for as long as 17 years (most likely longer, that's just the longest example I know of). Spencer himself admits he uses spray and concealer, but he is still a NW3v. He started balding in his early 20s and is now 47. There's no way he wouldn't be at least a NW5 by now without fin, and that's being highly generous. If he quit the drug tomorrow he'd be a bald man in less than 16 months. And there are users on hair loss forums who report over a decade of keeping their hair on fin or fin/dut.
I'd say this notion of the body compensating/overcompensating for finasteride is worth looking into with more, different and bigger studies, but I'm not ready to embrace it yet--certainly not as a cause of hair loss--any more than I'm ready to embrace the idea of Gho multiplying follicles.
(btw I agree T doesn't cause hair loss, I only brought it up because it's needed for DHT to form and thought that might be another contributing factor to DHT reduction in castrates)

[Tracy C]

Spencer himself admits he uses spray and concealer, but he is still a NW3v. He started balding in his early 20s and is now 47. There's no way he wouldn't be at least a NW5 by now without fin, and that's being highly generous.

If he quit the drug tomorrow he'd be a bald man in less than 16 months.

I doubt that it would happen anywhere near that fast - but it would happen. You can use the curve in that chart that 2020 misread to extrapolate a much more probable time frame, which would be a heck of a lot longer than 16 months.

[2020]

Ok. So this article does strongly suggest AR count increases with fin use. But that isn't technically hyperandrogenism (which would mean excess secretion of androgens rather than an increasing # of receptor sites) and I'm not convinced it would lead to the same symptoms, or to hair loss, nor am I convinced it is the sole reason why one can lose ground while on fin--if it is a reason. I think jumping to these conclusions isn't doing guys like Kirby any favors.

fine but that's still proof that your body does do some sort of upregulation to make existing DHT more potent in order to establish homeostasis....
This also explains how side effects go away for most people as long as they stay on it long term.

It still doesn't add up that fin actually does continue working for as long as 17 years (most likely longer, that's just the longest example I know of). Spencer himself admits he uses spray and concealer, but he is still a NW3v. He started balding in his early 20s and is now 47. There's no way he wouldn't be at least a NW5 by now without fin, and that's being highly generous.

his MPB is slow then and his hair loss still continued despite being on fin. WHY? 70% DHT reduction is pretty much castration. What is going on? Ideas?

If he quit the drug tomorrow he'd be a bald man in less than 16 months.

I wonder why... Your body has upregulated itself to make existing DHT more potent. If you go off fin, suddenly all that extra DHT will ravage all your androgen receptors causing massive hair loss. Btw, there is no proof that going off fin will ACTUALLY get you exactly back at where you would have been... most of the time it's worse and sometimes it's not.

And there are users on hair loss forums who report over a decade of keeping their hair on fin or fin/dut.

so what then? Eventually they will start losing hair again though.... why?

[2020]

You are misrepresenting what that chart says. That chart does not say that nor does it show that.

I see a downward trend starting from year two which SHOULDN'T BE THERE!!! 70% reduction is more than enough to stop all androgen interactions ever! Something else is happening and I know what. I can't believe it's taking 20 years to figure this crap out.

[Tracy C]

I see a downward trend starting from year two which SHOULDN'T BE THERE!!!

You are misreading that chart because you do not know what you are doing.

[2020]

You are misreading that chart because you do not know what you are doing.

how am I misreading it? Hair count starts to go down after year two and it keeps going down... sure, you're still above the baseline but after some time you won't be....

The point is that this downward trend shouldn't happen! 70% reduction in DHT is more than enough to permanently stop all androgen interactions but with 5AR inhibitors it isn't for reason I explained above.

What's the problem?

[25 going on 65]

70% reduction in serum DHT wouldn't prevent all DHT from binding to follicular AR sites. What you're saying is that the DHT which does get through, is too little to continue the MPB process, which is something I'm not so sure about. Do castrates and non-castrated fin users really have the same DHT levels? Can I read about this somewhere?
btw I did consider the possibility that quitting fin leads to over-reception of DHT due to increased AR sites combined with pre-fin DHT levels. I'm just not ready to assume that's the sole cause of the "catch-up loss" phenomenon or if it's even a major contributing factor. (Maybe we don't know that quitting fin returns you to where you would have been in terms of lost hair, but if not then we similarly can't say it leaves you worse or better off.)

[2020]

70% reduction in serum DHT wouldn't prevent all DHT from binding to follicular AR sites. What you're saying is that the DHT which does get through, is too little to continue the MPB process, which is something I'm not so sure about.

no... I'm saying that most of your DHT (> 90%) is already being "deactivated" by your body's own androgen binding proteins so I'm sure fin should be able to take care of the rest but it doesn't....

Do castrates and non-castrated fin users really have the same DHT levels? Can I read about this somewhere?

http://www.ncbi.nlm.nih.gov/pubmed/1699965

control DHT levels: 4.5 ng/g
DHT levels after finasteride: 0.302 ng/g
DHT levels after castration: 1.14 ng/g

Castrates don't lose hair even though they have higher DHT levels than people on finasteride!!!

Castration-resistant prostate cancer exists for a reason.... castration is not enough!

^ lol I should post this in a separate thread: Finasteride - more effective than castration!

btw I did consider the possibility that quitting fin leads to over-reception of DHT due to increased AR sites combined with pre-fin DHT levels. I'm just not ready to assume that's the sole cause of the "catch-up loss" phenomenon or if it's even a major contributing factor.

how would you explain it then?

(Maybe we don't know that quitting fin returns you to where you would have been in terms of lost hair, but if not then we similarly can't say it leaves you worse or better off.)

^ exactly. We don't even know. Some people end up worse, some better.