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Topic 519 - Oral Hair Loss Medications  - Propecia, Proscar, Loniten, Finasteride, Minoxidil, Spironolactone etc - forum 14

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Propecia Androgen Receptor Upregulation #3

katmandoo

From: katmandoo
Date: 07 Jan 2008
Time: 03:31:34
Remote Name: 213.139.194.86

Comments

Great work! It very impressive. Your web site is helpful. All the best!

From: Ephemeral Blackjack
Date: 12/20/2001
Time: 5:26:55 PM
Remote Name: 165.247.162.14

Comments

Bryan,

Thank you for your responses to my two previous posts on this issue. They were well written and informative (as he disarmingly says as he gets ready to disagree with some of the response and ask even more irritating questions on other points) :-).

I am going to have to "disagree" with some of your post and ask you some additional questions and raise additional theories due to another study pointed out to me by Zippy in the dutasteride forum. For those of you just following the thread, here are the two studies.

STUDY 1 - Provided by Bryan Shelton

"ANDROGEN RESPONSIVE GENES AS THEY AFFECT HAIR GROWTH"

Marty E. Sawaya, MD, PhD, ARATEC (Alopecia Research & Associated Technologies) Clinics & University of Miami School Medicine, Florida, USA.

"Androgens have profound affects on scalp hair follicles causing growth inhibitory activity hence, miniaturization of hair follicles in the case of men with Androgenetic alopecia (AGA). In human scalp hair follicles, androgens are thought to be growth inhibitory, whereas on beard and body hair, androgens upregulate hair growth. The biochemical activity and immunohistochemical expression of 5a-reductase isoenzymes type I and II has been assessed in scalp of men with AGA, as well as the cytochrome P-450 aromatase enzyme, androgen receptor (AR), estrogen receptor (ER) alpha and beta. Studies in 10 men with AGA where scalp biopsies are obtained before and after 6 months treatment with finasteride (a specific type II 5a-reductase inhibitor) reveal interesting results with regard to the effects of suppressing DHT and how it affects these androgen associated factors. Differences in expression were found for some of the enzymes as well as transcription proteins, AR, ER-alpha and beta. All scalp biopsies from patients obtained 6 months after finasteride treatment revealed intense upregulation of AR expression in comparison to pre-treatment biopsies of the same patient, whereas ERs were not affected, indicating that AR is very sensitive to the affects of 5a-R type II suppression of DHT. Results suggest that as the hair growth returns in these previously miniaturized follicles, DHT suppression also alters the expression of specific Caspase genes inhibiting programmed cell death, apoptosis. Therefore, we can learn alot about the multiple effects of DHT by looking at its suppression in human scalp hair follicle to gain a better understanding of the many androgen responsive genes involved in hair growth regulation."

STUDY 2 - Provided by "Zippy"

http://www.propeciadoctors4hairloss.net/news7.htm

I'll have to ask you all to go here for the study, I was tempted to copy it directly for ease of viewing but that might have been illegal.

O.K. These are the studies.

To summarize the studies in hopefully an accurate manner:

(1) Study 1 - There is an "intense" upregulation - read increase - in androgen receptors that occurs sometimes within the 1st six months of propecia usage (it would have been nice if Merck had taken those measurements at prior and post time intervals and with more than 10 subjects including non-responders. Why don't those damn people think - don't they all know how important this is to us !!!!) :-)

Study 2 - There are two types of androgen receptors type A and type B. Type A causes inhibition of hair growth while type B promotes normal growth (or at least doesn't stop it - my addition). Different receptor forms can have the different actions when binding with the same hormone. In men with androgenic alopecia, men have more of type A in the balding areas than type B. Propecia may work by reversing this ratio, i.e. decreasing A and increase B.

O.K. So here are the questions and concerns. In the first study, which type of androgen receptors is being upregulated, the type A or the type B or both?

If it is type A, then it would seem to be a net negative that needs to be addressed. If it is type B, then it would seem to good or at least harmless. It is also possible that it is both, with the retio of type A to type B changing from more B and less A, thereby maintain the positive response. It should also be remembered that the ratio of type A to type B that propecia changes will not be the same in everyone. Someone who does not get as much change from type A to type B is likely to be more affected by the upregulation than someone who has more type B (This sentence is a theory not a fact). It should also be noted that the two receptors may not have equal effect for the purposes of hair loss (i.e. more than one type B receptor may be needed to cancel the inhibitory effects of one type A receptor).

Now on to your statements. Bryan wrote:

"Again in my opinion, no. I think the increase in androgen receptors is a rather futile effort by the cell to maintain an androgenic stimulus. If you reduce the DHT inside a cell by upwards of 90% or so, I don't think even a major increase in androgen receptors is going to do that much to restore the balance. I still think that the other factors involved in hairloss are what cause the lack of response in some individuals, like the inflammation and fibrosis that have to be overcome as the MPB process is coasting to a stop, and/or the DHT from 5a-R type 1 that seems to play at least some role."

Finasterides average is only 70% with a range of +-20%. Also I'm not sure we know about the equality of the receptors in terms of the effects on MPB. I still think it may be beneficial for some people to work on androgen receptor downregulation via a solution of green tea extract, at least prior to dutasteride which does have the reduction amount that you refer to. I also won't suggest that it is a total solution in the sense that growth agents and SODS are also important. If you are looking for maximum regrowth these would seem to be mandatory and should speed the healing effect. Another thought that I would share is that if the type A androgen receptors upregulate and since finasteride does not stop DHT due to type I 5AR, then the DHT produced due to this version of 5AR might have more of a damaging effect than normal. Since green tea extract helps inhibit type I 5AR, this may be another reason to use the green tea extract.

"It's a net negative, but it's not that big a deal. After all, if it had a significant effect, then finasteride or dutasteride wouldn't work at all."

I think the key point I would make here is a more precise definition of a significant effect. If you are in the minority percentile where finasteride does not work and you continue to lose your hair, and this is a significant effect for you. If you respond with only keeping your hair and not with moderate regrowth, and you needed moderate regrowth to not feel like a freak who is embarrassed to go outside, than this is a significant effect for you.

O.K. That was a long enough post. Hopefully I have not set the hairsite record. :-) Bryan and anyone else who is willing go ahead and tear it apart please do so at your earliest convenience. Thanks.

Ephemeral Blackjack

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