new study: finasteride upregulates AR

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baldinglikeamofo

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http://www.ncbi.nlm.nih.gov/pubmed/21229554


Finasteride upregulates expression of androgen receptor in hyperplastic prostate and LNCaP cells: Implications for chemoprevention of prostate cancer.

Hsieh JT, Chen SC, Yu HJ, Chang HC.

Department of Urology, National Taiwan University Hospital and National Taiwan University, College of Medicine, Taipei, Taiwan.
Abstract

BACKGROUND: Although finasteride is recognized for its role as a chemopreventive agent for prostate cancer, higher grades of malignancy have been reported. It is questioned whether blocking of testosterone conversion to dihydrotestosterone (DHT) by finasteride in prostate tissue will change expression of androgen receptor (AR). Therefore, this study evaluated the effects of finasteride on AR expression in prostate tissue and in the LNCaP cell line.

METHODS: Between January and December 2006, we retrospectively selected and evaluated 47 cases of benign prostatic hyperplasia treated with variable duration of finasteride (5?mg QD) before transurethral resection of the prostate. AR expression in prostate tissue was semiquantified by immunostaining and compared with duration of finasteride treatment. An androgen-dependent prostate cancer cell line (LNCaP) was cultured in charcoal/dextran-treated FBS with DHT or testosterone, and treated with finasteride for 1-3 weeks. Samples of total RNA were collected to analyze expression of AR by real-time quantitative reverse transcription polymerase chain reaction.

RESULTS: Immunohistochemical study revealed significant upregulation of ARs by finasteride treatment for 30-180 days. In cell line study, quantitative real-time reverse transcription polymerase chain reaction revealed significant upregulation of ARs treated by finasteride.

CONCLUSIONS: In our study, finasteride influenced AR expression in benign prostate tissue and prostate cancer cell. Before we can use finasteride in chemoprevention with confidence, we still need to clarify the influence of finasteride in ARs and its regulation pathway. Prostate © 2011 Wiley-Liss, Inc.
 
Bryan

Bryan

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Interestingly, this is the first time I've seen anything in support of Sawaya's similar finding in the hair follicles of men taking finasteride.
 
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Rabid

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A little post I wrote a while back on this subject...
Rabid said:
If you're not experiencing those dreaded side effects from finasteride, and it isn't doing a damn thing for your hairloss (for months I thought I was simply receiving bad pills), perhaps you are suffering from a condition so simple and obvious, it's explained in the basic FAQ on this website, yet there seems to be very little discussion elsewhere. I seriously urge everyone to think about the concept of reflex hyperandrogenicity. The FAQ explains it pretty damn quickly and well enough. If the concept of up and down-regulation of receptors makes perfect intuitive sense, which it does, then this concept makes as much sense as anything else posted on this site.

Let me know if these questions have previously been discussed, but is it possible that those who continue to lose hair on finasteride, and especially the ones who claim to get worse, (such as myself- been on 9 months, hair worsening exponentially over past 6) are experiencing a sub-clinical hyperandrogenicity? This concept could explain why side effects often disappear over time, as they did in my case. My sides-effects were terrible, but waned and mostly vanished after a month or two. I'm not saying you couldn't still have reflex hyperand. if you have side effects.

Could reflex hyperandrogenicity be quietly accounting for a significant percentage of the perceived “finasteride sheds� Are there any studies that prove such a "finasteride shed" even truly exists? If so, please post them, because virtually all hairloss sufferers seem to put great faith in this concept. (If it does, than perhaps it's a temporary reflex hyperandrogenicity that successful users are able to eventually counteract?) Obviously, there are countless satisfied finasteride. users out there, and many of them testify to the shed, so I'm not denying it works for them, perhaps most successful users. However, it seems like people could have easily started spinning ideas to convince one another that the drug would eventually start working and said if there’s a minoxidil. shed, and minoxidil. works, why not just assume that any long-term hairloss treatment could cause sheds? Surely Merck wouldn’t mind if users believed this, as people wouldn’t quit treatment right away. Interesting though that Merck doesn’t report this as a side effect, to my knowledge. That seems very fishy. Moreover, Dr. Rassman (He seems to be well respected from what I've seen) writes that he very rarely sees such finasteride. sheds in practice, despite all the hype on these hairloss forums. It’s extremely easy to see why this concept would get so much hype, why something could be so loathed and dreaded, yet such a welcome relief (because that’s a sign that it’s working!), depending on where one happens to find themselves flailing in their own hairgrowth/hairloss cycle.

Now, I’ve read some posts that seem to indicate a true clinical hyperand., but these cases seem very rare. The distinguishing feature there seems to be that the scalp becomes very inflamed and painful. Those people lose hair very quickly. But what about the rest of us who could possibly have subclinical cases, meaning no overt physical symptoms, except for hairloss. Couldn’t that be possible? For instance, I don’t seem to have any more acne or oily skin than usual. I do have increased libido, and increased facial hair. This brings me to my next point. Do not most people think of finasteride as decreasing libido? Yet there are wide ranging reports of increased libido. What causes this? True, there are certainly sexual side effects, but these evidently need not necessarily decrease libido.

Anyhow, just because I don’t have the acne/oily skin/other symptoms, why does that mean I cannot still have a mild case of hyperandrogenicity? Given the extreme sensitivity of hair follicles to the damaging effect of DHT in those with male pattern baldness such as myself, it seems like the hair might rather be the thing most easily affected by small hormonal fluctuations. The point many have made I think is that hairloss would only occur after obvious symptoms of hyperandr. occur in someone taking finasteride., because hair follicles would be much more resistant because of the DHT blocking effect of the drug. This point is very important, and must be examined. I wonder if this DHT blocking continues to remain successful even when the sensitivity and number of DHT receptors has greatly increased as with reflex hyperandr.? Again, my question is, how do we know that acne or oily skin would be evident before hairloss. I hope there’s a simple answer to this, but right now I’m really wondering if those who are trying to help their hairloss but not responding to finasteride. are not responding because of a reflex DHT receptor upregulation resulting in mild, relatively undetectable hyperandrogenicity, which always leads in the other direction to hairloss?

If so, how would you reverse it without quitting finasteride?
Click to expand...


ASJ-19?
 
R

Rabid

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finfighter said:
Rabid said:
A little post I wrote a while back on this subject...
Rabid said:
If you're not experiencing those dreaded side effects from finasteride, and it isn't doing a damn thing for your hairloss (for months I thought I was simply receiving bad pills), perhaps you are suffering from a condition so simple and obvious, it's explained in the basic FAQ on this website, yet there seems to be very little discussion elsewhere. I seriously urge everyone to think about the concept of reflex hyperandrogenicity. The FAQ explains it pretty damn quickly and well enough. If the concept of up and down-regulation of receptors makes perfect intuitive sense, which it does, then this concept makes as much sense as anything else posted on this site.

Let me know if these questions have previously been discussed, but is it possible that those who continue to lose hair on finasteride, and especially the ones who claim to get worse, (such as myself- been on 9 months, hair worsening exponentially over past 6) are experiencing a sub-clinical hyperandrogenicity? This concept could explain why side effects often disappear over time, as they did in my case. My sides-effects were terrible, but waned and mostly vanished after a month or two. I'm not saying you couldn't still have reflex hyperand. if you have side effects.

Could reflex hyperandrogenicity be quietly accounting for a significant percentage of the perceived “finasteride sheds� Are there any studies that prove such a "finasteride shed" even truly exists? If so, please post them, because virtually all hairloss sufferers seem to put great faith in this concept. (If it does, than perhaps it's a temporary reflex hyperandrogenicity that successful users are able to eventually counteract?) Obviously, there are countless satisfied finasteride. users out there, and many of them testify to the shed, so I'm not denying it works for them, perhaps most successful users. However, it seems like people could have easily started spinning ideas to convince one another that the drug would eventually start working and said if there’s a minoxidil. shed, and minoxidil. works, why not just assume that any long-term hairloss treatment could cause sheds? Surely Merck wouldn’t mind if users believed this, as people wouldn’t quit treatment right away. Interesting though that Merck doesn’t report this as a side effect, to my knowledge. That seems very fishy. Moreover, Dr. Rassman (He seems to be well respected from what I've seen) writes that he very rarely sees such finasteride. sheds in practice, despite all the hype on these hairloss forums. It’s extremely easy to see why this concept would get so much hype, why something could be so loathed and dreaded, yet such a welcome relief (because that’s a sign that it’s working!), depending on where one happens to find themselves flailing in their own hairgrowth/hairloss cycle.

Now, I’ve read some posts that seem to indicate a true clinical hyperand., but these cases seem very rare. The distinguishing feature there seems to be that the scalp becomes very inflamed and painful. Those people lose hair very quickly. But what about the rest of us who could possibly have subclinical cases, meaning no overt physical symptoms, except for hairloss. Couldn’t that be possible? For instance, I don’t seem to have any more acne or oily skin than usual. I do have increased libido, and increased facial hair. This brings me to my next point. Do not most people think of finasteride as decreasing libido? Yet there are wide ranging reports of increased libido. What causes this? True, there are certainly sexual side effects, but these evidently need not necessarily decrease libido.

Anyhow, just because I don’t have the acne/oily skin/other symptoms, why does that mean I cannot still have a mild case of hyperandrogenicity? Given the extreme sensitivity of hair follicles to the damaging effect of DHT in those with male pattern baldness such as myself, it seems like the hair might rather be the thing most easily affected by small hormonal fluctuations. The point many have made I think is that hairloss would only occur after obvious symptoms of hyperandr. occur in someone taking finasteride., because hair follicles would be much more resistant because of the DHT blocking effect of the drug. This point is very important, and must be examined. I wonder if this DHT blocking continues to remain successful even when the sensitivity and number of DHT receptors has greatly increased as with reflex hyperandr.? Again, my question is, how do we know that acne or oily skin would be evident before hairloss. I hope there’s a simple answer to this, but right now I’m really wondering if those who are trying to help their hairloss but not responding to finasteride. are not responding because of a reflex DHT receptor upregulation resulting in mild, relatively undetectable hyperandrogenicity, which always leads in the other direction to hairloss?

If so, how would you reverse it without quitting finasteride?
Click to expand...


ASJ-19?
Click to expand...


ASC-J9.
Click to expand...

Technically, I believe AndroScience lists its full name as:
ABC-EZ AS-123?




:eek:nfire:
 
el_duterino

el_duterino

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Intersting study - which proves again that using finasteride + RU is very effective since RU will block any excess testosterone and DHT at the AR level.

If ASC-J9 really works that would be even better to add it to the mix but I have my doubts about ASC-j9..androscience never published any studies on hairloss/effects on hair follicles and seems to have halted any plans for male pattern baldness testing.
 
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toivonen

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That study, only confirms some posts and theories of some users, that for ages linked that to the possible unsucess of finasteride with some people..in my case, i always believed to be one of the causes for my poor results.
 
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Rabid

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finfighter said:
Rabid said:
Technically, I believe AndroScience lists its full name as:
ABC-EZ AS-123?




:eek:nfire:
Click to expand...


I wasn't trying to be rude man, I just thought you might benefit from the info, in case you were interested in it...
Click to expand...

Thanks for the info. I was just being silly. I'd love to hear results of this stuff from suspected RHA people, or anyone for that matter. Interesting that it's said to downregulate receptors rather than block them, very unique property that could be exploited if used properly.
 
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thomasD

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Quite some people on the dutch hairloss forum are using it now including myself(First month). Some people say their hair looks thickers and lose less hairs, also less/no sebum production. But I think it's to early to say it works because the people of the first batch started only 3 months ago. We also are experimenting with the dose, because most people use the safe "acne trial" dose(0,025%). But maybe for Androgenetic Alopecia we need a higher dose.

The most common side effects are, dry skin, more active (some people quitted because they couldn't fall asleep).
 
el_duterino

el_duterino

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Are these Dutch guys using ASC-J9 on its own ?
I remember seeing Wesley's list of daily drugs,

which is pretty extensive..unless he uses ASC-j9 alone we won't really know how effectvie it really is.
 
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thomasD

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el_duterino said:
Are these Dutch guys using ASC-J9 on its own ?
I remember seeing Wesley's list of daily drugs,

which is pretty extensive..unless he uses ASC-j9 alone we won't really know how effectvie it really is.
Click to expand...


No, most use it in combination with Minoxidil and/or finasteride. So yeah your right it's hard to tell which one works. But i think Wesley's idea was to quit his oral medications(avodart) and replace it with ASC-J9. That was his plan i think but i haven't seen him for a while .

But the reduction of sebum which almost all users experience with ASC is a good sign no?
 
optimus prime

optimus prime

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Does ASC-J9 work in the same was as Fluridil? When I same same way, I mean do they both downregulate receptors?
 
el_duterino

el_duterino

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yes both produce the same end-result less AR.

But inhibiting AR is not easy and the dosage needed to stop male pattern baldness will be a lot higher than just for acne, therefore you can get side effects unless the drug is designed to break-down in blood fast.
 
R

Rabid

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thomasD said:
But the reduction of sebum which almost all users experience with ASC is a good sign no?
Click to expand...

Yes, that is a good sign that it is having a positive effect, imo. In my case, I wouldn't notice a difference though because I don't have a problem with excess sebum.


Are you aware of anyone on the Dutch site who hadn't had success with finasteride or other anti-androgens, perhaps due to RHA (reflex hyper-androgenicity), who is now seeing improvement after switching to ASC? Would be very interesting to know.
 
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