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From: Pete - Give me your views Please :)
Date: 3/11/2002
Time: 12:09:54 PM
Remote Name: 195.93.34.187
YOU MUST CHECK YOUR HORMONE LEVLS BEFORE DECIDING ON TREATMENT
You guys checked my link out - go to site map link at the bottom of home page and then to the Hormone test link.
http://www.hairgrowth.co.uk/cgi-bin/at.cgi?a=188527
Hi Peeps,
You should have surely all worked out that all these posts are similar and have been similar for the past few years. Can you read between the lines...cos i can. For me there is only one real development in hair loss besides DHT inhibitors and thats Aromatase inhibitors . DHT inhibitors and Aromatse inhibtors combined together is a treatment that will rasie a few eyebrows. I appreciate all your views.
Pete
I have come across the below articles which suggest the aromatase inhibitor have the following benefits :
1. "This combination reduces excess estrogen, raises free testosterone, and potentiates the hair growth effects of 5-alpha-reductase inhibitors."
2. the concentration-dependent inhibition of VEGF expression by DPC using the cytochrome-p-450-aromatase inhibitor, confirms the involvement of this estrogenic pathway in the regulation of VEGF expression in vitro
3. Most researchers now concede that DHT is not the sole hormonal trigger of hair loss. SHBG increases with age and with the presence of bound estrogen, can act like an additional androgen receptor. Excess estrogen upregulates DHT receptors
4 Aromatase enzyme has some involvement in regulating hair growth cycle and seem have a negative effect in skin surrounding follicles(atrophy).
Article 1
Extract from Messengers work:
Current thinking is that androgens are acting on the Dermal Papilla. The observation that there was no detectable aromatase activity in hair follicle dermal papilla cells would point away from our hypothesis. In contrast to the established line of thinking we believe that aromatase activity in non-follicular skin fibroblasts is more important and could account for the change in skin texture seen in balding sites.
The high levels of aromatase in fibroblasts from frontal scalp is consistent with our original hypothesis. The putative inhibitory effect of oestrogens on hair growth would need to derive from the surrounding dermis as aromatase activity was absent in dermal papilla cells. There is no evidence that androgens act directly on the hair follicle in the balding process and subjective observation of a balding scalp suggests that there is a general alteration in skin texture. It is possible therefore that inhibition of hair growth is a secondary response to more general changes in local biology of the skin.
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).
RECEPTORS and TEMPLE GROWTH
Have you ever pondered that there are receptor differences( more androgen inhibitor receptors as well as ****estrogen inhibitor receptors***** ) in this area and in prescence of "estrogen" is whats making hair growth hard to regrow. Even though DHT is primary cause - Just a theory!
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