Local vs Systemic DHT

[harold]

Obviously local production is important. I dont think anyone is going to suggest otherwise? But how important is serum levels of DHT? Could one inhibit DHT production locally and treat male pattern baldness without significantly effecting levels in other parts of the body. It has been suggested that the scalp is so well vascularized that DHT in the blood must have an effect.
On the other hand there is a study that shows that while before and after finasteride treatment there was a big reduction in DHT/T ratio in both vertex hair and serum there was no real change in hair from unaffected occipital regions. This was looking at the ammount of DHT and Testosterone in the hair itself - not the folicle or the scalp. So even though the blood ratio of DHT/T dropped heavily there was no real effect in the occipital hair regions where 5-AR activity is reported to be lower than in balding regions. If these hair ratios of DHT/T reflect what is important for hair growth/maintenance then it implies that they are largely independent of serum levels. The dutasteride studies found an improvement in hair counts between the 0.5mg and 2.5mg per day dosage regimes even though both bllock the formation of pretty much all DHT in serum. There is however a difference in the levels of DHT being produced in the scalp in the two dosages.
Thoughts?
hh

 

[michael barry]

I believe Bryan once wrote that 98% of your DHT in serum gets bound by globulin. 3 alpha steroid reductase quickly converts DHT back to testoserone or binds it (forget which) in muscle tissue, making DHT amost a complete non-factor in muscles. Bryan has stated for years that almost all the DHT that gets uptaken at the follicle was made at the follicle, and serum DHT is a much much less important factor.


To be honest...............I feel that focusing on things that could both block and suppress the androgen receptor in addition to inhibiting alpha five reductase would be a great deal better than merely trying to inhibit DHT. If you could stop almost all androgenic uptake for several years, while using a stimulant.....................you might be very suprised at what the body could do a few years down the line in terms of regrowth.


Those soy pictures in the tyrosine kinease patent were very impressive.

 

[goata007]

To be honest...............I feel that focusing on things that could both block and suppress the androgen receptor in addition to inhibiting alpha five reductase would be a great deal better than merely trying to inhibit DHT.

I'm eagerly waiting for ASCJ-9, the stuff that destroys androgen receptors, the trial should finish this month and by end of next month or two they should also release results. If its any good for acne, i'm definitely putting it on my scalp.

 

[harold]

This study shows a difference in both vertex hair and serum DHT levels when compared to non-balding men. Crucially however there is no difference in occipital hair DHT levels between male pattern baldness sufferers and controls. So even though the there was a serum difference it didnt seem to effect local hair follicle levels. This tends to indicate that f there is more DHT in the blood it is merely indicative of greater local activity. This is what the researchers confirm when they say that the increased DHT/T ratio in blood is merely indicative of greater 5AR-2 activity.

J Dermatol Sci. 2004 Feb;34(1):11-6.Click here to read Links
Comparative studies on level of androgens in hair and plasma with premature male-pattern baldness.
Bang HJ, Yang YJ, Lho DS, Lee WY, Sim WY, Chung BC.

Bioanalysis and Biotransformation Research Center, Korea Institute of Science and Technology, PO Box 131, Cheongryang, Seoul 130-650, South Korea.

BACKGROUND: It is well known that male-pattern baldness (male pattern baldness) is not started from occipital, but frontal or scalp of head. We can assume that distribution of androgenic steroids is different for each region of the head. OBJECTIVE: We hypothesize that the levels of androgenic steroids are different not only between vertex hair with male pattern baldness and controls but also between occipital hair with male pattern baldness and controls. Moreover, we want to search for the biochemical indicator in plasma and hair sample (baldness: 22, non-baldness: 13) obtained from dermatology of medical center. After then, we desire to present fundamental data regarding diagnosis, medical cure, and prevention for premature male pattern baldness. METHODS: After hair and plasma were hydrolyzed, and then extracted with organic solvent. To assess androgenic steroids levels, we used gas chromatography-mass spectrometry (GC-MS) system in selected ion monitoring mode. RESULTS: The level of dihydrotestosterone (DHT) and the ratio of testosterone to epitestosterone (T/E ratio) in vertex hair from premature baldness subjects were higher than in the sample of non-baldness subjects (P<0.001, 0.001), whereas the levels of androgens in occipital hair from the same baldness group were not different. In addition, we discovered the levels of DHT, testosterone, and DHT/T ratio in plasma from premature male pattern baldness were higher than in those of control subjects (P<0.001, 0.001, 0.005). CONCLUSION: We verified that the distribution of androgenic steroids is unlike in various regions of individual subjects. Moreover, the increased DHT/T ratio in balding plasma indirectly confirms the high activity of 5alpha-reductase type II.

Same group now looking at men before and after finasteride. Interesting to note that neither of these papers are looking at scalp levels - ie other studies on dutasteride/finasteride take a piece of scalp and basically blend it into a bloody liquid and then measure DHT. These guys are looking at androgen concentrations in the hair itself. I dont know if this is a better or worse indicator than scalp levels. Nevertheless it confirms with what others have found about more 5-AR expression and DHT in balding areas.

Br J Dermatol. 2006 Apr;154(4):730-4.Click here to read Links
Evaluation of androgens in the scalp hair and plasma of patients with male-pattern baldness before and after finasteride administration.
Ryu HK, Kim KM, Yoo EA, Sim WY, Chung BC.

Bioanalysis and Biotransformation Research Centre, Korea Institute of Science and Technology, PO Box 131, Cheongryang, Seoul, 130-605, Korea.

BACKGROUND: Finasteride, a competitive inhibitor of the enzyme 5alpha-reductase II, is widely used as a medical treatment for patients with male-pattern baldness (male pattern baldness), which is affected by the distribution of androgenic steroids. It is also notable that the androgenic effect in male pattern baldness is different for each region of the head. OBJECTIVES: To study the effect of the drug finasteride, we quantified androgenic steroids in the vertex and occipital scalp hair and in the plasma of patients with male pattern baldness. METHODS: The patients with male pattern baldness, aged 23-52 years, were treated with finasteride 1 mg daily for 5 months. The hair and plasma samples were hydrolysed, extracted with n-pentane, and derivatized with MSTFA:NH4ITE (1000:4:5, v/w/w). We analysed the concentrations of dihydrotestosterone (DHT) and testosterone (T) in the hair and plasma using gas chromatography-mass spectrometry (GC-MS). RESULTS: In the hair, the ratio of DHT/T was decreased in the vertex scalp hair after the individual received finasteride (P < 0.005). However, we found no significant difference in the ratio of DHT/T in the occipital scalp hair before and after individuals received finasteride. Like the results in the vertex scalp hair, the ratio of DHT/T in the plasma was remarkably decreased after finasteride administration (P < 0.001). CONCLUSIONS: This study supports the effect of finasteride in patients with male pattern baldness by examining the decreased level of DHT/T in scalp hair and in plasma. Thus, in view of the androgenic effect in the different hair regions, the vertex scalp hair plays a more important role for patients with male pattern baldness treated with finasteride than does the occipital hair.

 

[harold]

I believe Bryan once wrote that 98% of your DHT in serum gets bound by globulin. 3 alpha steroid reductase quickly converts DHT back to testoserone or binds it (forget which) in muscle tissue, making DHT amost a complete non-factor in muscles. Bryan has stated for years that almost all the DHT that gets uptaken at the follicle was made at the follicle, and serum DHT is a much much less important factor.


To be honest...............I feel that focusing on things that could both block and suppress the androgen receptor in addition to inhibiting alpha five reductase would be a great deal better than merely trying to inhibit DHT. If you could stop almost all androgenic uptake for several years, while using a stimulant.....................you might be very suprised at what the body could do a few years down the line in terms of regrowth.


Those soy pictures in the tyrosine kinease patent were very impressive.

Lately I have come to the conclusion that for me at least inhibting DHT would be enough. My hair maintains fine with finasteride but the sides are just not acceptable really. These studies suggest that local DHT inhibition is possible. Given the "irreversible" nature of finasteride 5-AR2 binding I am tempted to consider that it may even be possible to just use an ultra-low dose finasteride/dutasteride topical. As close as possible as just enough to bind with all the 5-AR in the scalp leaving as little as possible left over to wash into the bloodstream. The idea is to reverse the ratio of scalp/serum DHT inhibition seen with oral dosing.
hh
Would love to see those pics by the way but that link to the patent seems to be down.

 

[SoThatsLife]

To be honest...............I feel that focusing on things that could both block and suppress the androgen receptor in addition to inhibiting alpha five reductase would be a great deal better than merely trying to inhibit DHT.

I'm eagerly waiting for ASCJ-9, the stuff that destroys androgen receptors, the trial should finish this month and by end of next month or two they should also release results. If its any good for acne, i'm definitely putting it on my scalp.

Thats sounds good in one way, but destroying the androgen receptors must have a negative effect someway? anyone?

I believe Bryan once wrote that 98% of your DHT in serum gets bound by globulin. 3 alpha steroid reductase quickly converts DHT back to testoserone or binds it (forget which) in muscle tissue, making DHT amost a complete non-factor in muscles. Bryan has stated for years that almost all the DHT that gets uptaken at the follicle was made at the follicle, and serum DHT is a much much less important factor.

If this is a fact, wouldn't that kill the myth that weight training speeds up hair loss? Or at least the effect is very minimal?

Harold, do you mean this one http://v3.espacenet.com/origdoc?DB=EPOD ... =EP1915997 ? it works

 

[michael barry]

The more Ive thought about it, it looks like the amount of CAG repeats on the androgen receptor gene and how strongly you express it is really the biggest difference.


Think about it, you have a mutated receptor gene and excessive amounts or receptors or better working receptors sitting there on your hair just calling for androgenic stimulis, more than they are getting. Would it not be just like the human body from what we have read, to get the alpha five reductase enzymes in the root sheath and other parts of the follicle to get "busier" and convert more T-to DHT locally to serve this end? If a man had lower globulin, and thus more free unbound testosterone, it would just be sped up.


People with androgen insensitivity never bald, despite making all the testosterone they want. If we could both block and downreg androgen receptors topically....................that would be the way to go. Science could then have decades to work on all that is downstream of androgenic uptake (truly small micro-scientific inquiry) while the rest of humanity enjoyed keeping their hair.

 

[chancer]

The more Ive thought about it, it looks like the amount of CAG repeats on the androgen receptor gene and how strongly you express it is really the biggest difference.


Think about it, you have a mutated receptor gene and excessive amounts or receptors or better working receptors sitting there on your hair just calling for androgenic stimulis, more than they are getting. Would it not be just like the human body from what we have read, to get the alpha five reductase enzymes in the root sheath and other parts of the follicle to get "busier" and convert more T-to DHT locally to serve this end? If a man had lower globulin, and thus more free unbound testosterone, it would just be sped up.


People with androgen insensitivity never bald, despite making all the testosterone they want. If we could both block and downreg androgen receptors topically....................that would be the way to go. Science could then have decades to work on all that is downstream of androgenic uptake (truly small micro-scientific inquiry) while the rest of humanity enjoyed keeping their hair.

what a great post.... almost poetic!

 

[harold]

The more Ive thought about it, it looks like the amount of CAG repeats on the androgen receptor gene and how strongly you express it is really the biggest difference.

From that Sawaya study on differences in Androgen Recptors and 5AR distribution amongst scalp regions in balding men and women there was a 1.5 times as many androgen receptors in frontal vs occipital regions whilst I think 3.5 times as much 5-AR between the two regions. I think its possible/probable that the difference in AR number is due to androgen receptors being upregulated in the face of greater androgenic stimuli. Was looking at a study in mice and when they were castrated there was a large drop in the expression of androgen receptors.

Think about it, you have a mutated receptor gene and excessive amounts or receptors or better working receptors sitting there on your hair just calling for androgenic stimulis, more than they are getting. Would it not be just like the human body from what we have read, to get the alpha five reductase enzymes in the root sheath and other parts of the follicle to get "busier" and convert more T-to DHT locally to serve this end? If a man had lower globulin, and thus more free unbound testosterone, it would just be sped up.


People with androgen insensitivity never bald, despite making all the testosterone they want. If we could both block and downreg androgen receptors topically....................that would be the way to go. Science could then have decades to work on all that is downstream of androgenic uptake (truly small micro-scientific inquiry) while the rest of humanity enjoyed keeping their hair.

If we could block and downregulate topically then that would be fantastic. I dont think we can though and just as an instinct from my own personal experiments it seems that even drugs/compounds with very local activities can and do have systemic effects. Given this I would rather mess about with 5-AR inhibitors and try to minimise their effect systemically. I guess I am getting older and I also and am no longer the testosterone filled teenage I once was. If I want to keep as much hair as I can though I also need something that works now. If local 5-AR inhibition is enough thenm that is something to aim for.
hh

 

[michael barry]

From that Sawaya study on differences in Androgen Recptors and 5AR distribution amongst scalp regions in balding men and women there was a 1.5 times as many androgen receptors in frontal vs occipital regions whilst I think 3.5 times as much 5-AR between the two regions. I think its possible/probable that the difference in AR number is due to androgen receptors being upregulated in the face of greater androgenic stimuli. Was looking at a study in mice and when they were castrated there was a large drop in the expression of androgen receptors.

That pretty much says it all doesn't it?


A great topical anti-androgen would really need to do both, but also (in my opinon) be not be inflammatory in any way. It would be even better if something in the forumulation got androgen receptors do downregulate their expression like various things Ive read about (selenium, certain flavonoids, something in lavender, tocopherol succinate, a couple of other things) so that perhaps blocking the receptors doesn't get them to mutate and accept other substances as androgens




This is why Ive been harping on trying various topicals on our beard hair....................and see if this or that really reduces it as a way of telling if something has the potential to be helpful in vivo with a human being. Im worried that peppermint might do something harmful to hair period, and thus why Im kinda still searching. Im currently testing topcial green tea, cedarwood, and recently have decided to try beta sitosterol on half of where a moustace would be if I grew one......
Fluridil is tempting..................I wish someone would try that and report back to us if they had any success.



So far the green tea isn't doing a great deal to be honest. I'd love to think we could counteract a negative growth factor or two, but that is trusting that it will be the entire answer, and it truly may not be. We know that stopping androgens at the follicle site would be an adequate answer in the meantime, hence why I focus on it. The dangerous things about the folks you read about on her thinking they are having mucho success with certain stimulants only (caffeine, carnetine, etc.) is that the first couple of years on minoxidil-----a man would probably be tempted to feel the same way, only to find out ultimately cellular damage is still taking place. I think anti-androgens are the base which to start a response given what we know at this point and other things should be additives to that base.



If someone stuck a gun to my head and said "give me the best regimine with the least amount of side effects possible" I'd tell them Finasteride, fluridil, prox-n, and nizoral 2X a week. I'd like to see beta sis be a big-success, as one can easily drain the capsules into their daily shampoo (while in their hand) and wash in................that would be great.

 

[Bryan]

Lately I have come to the conclusion that for me at least inhibting DHT would be enough. My hair maintains fine with finasteride but the sides are just not acceptable really. These studies suggest that local DHT inhibition is possible.

For years I've always argued for the probable effectiveness of topical 5a-reductase inhibitors (assuming you can find one that actually works in the first place) by pointing to the apparent success in both animals and humans at inhibiting sebaceous glands and sebum production with such agents. For example, the application of a small amount of GLA to the forehead of a human subject was able to significantly reduce his sebum production, just like it inhibited flank-organs in a hamster study (both tests were done by the same scientists).

So the point I'm making here is this: if serum DHT has a significant effect on hair follicles, wouldn't you also expect it to have a significant effect on the nearby and closely-related sebaceous glands?? But it clearly DOESN'T, because the application of GLA has a very significant "local" effect on sebaceous glands in both humans and animals; therefore, I conclude that serum DHT isn't likely to have much of an effect on hair follicles, either.

 

[Bryan]

Think about it, you have a mutated receptor gene and excessive amounts or receptors or better working receptors sitting there on your hair just calling for androgenic stimulis, more than they are getting. Would it not be just like the human body from what we have read, to get the alpha five reductase enzymes in the root sheath and other parts of the follicle to get "busier" and convert more T-to DHT locally to serve this end?

I've posted before a few times the study by Happle & Hoffmann in which they stimulated in vitro cultures of human scalp hair follicles with varying amounts of extra testosterone, and then measured the changes in their production levels of androgen receptors and the 5a-reductase enzymes (both types).

Interestingly, the changes were inconsistent: the extra testosterone sharply UP-regulated levels of the type 2 enzyme, mildly DOWN-regulated levels of androgen receptors (supporting Sawaya's finding about finasteride and androgen receptors), and had no real effect at all on the type 1 enzyme. That would appear to be an attempt on the part of the cell to maintain an androgenic homeostasis ONLY when it comes to androgen receptors, but NOT when it comes to the 5a-reductase enzymes. I find that both fascinating and puzzling.

 

[Bryan]

From that Sawaya study on differences in Androgen Recptors and 5AR distribution amongst scalp regions in balding men and women there was a 1.5 times as many androgen receptors in frontal vs occipital regions whilst I think 3.5 times as much 5-AR between the two regions. I think its possible/probable that the difference in AR number is due to androgen receptors being upregulated in the face of greater androgenic stimuli. Was looking at a study in mice and when they were castrated there was a large drop in the expression of androgen receptors.

The only problem with that theory is that two separate pieces of evidence (Sawaya's finding about finasteride and androgen receptors, and the Happle & Hoffmann study I mentioned in my reply just above to Michael Barry) indicate that it's just the OPPOSITE of that: greater androgenic stimulation DOWN-regulates androgen receptors in human scalp hair follicles, it doesn't UP-regulate them. It may be different in other tissues and in other species, like in that mouse study you mentioned. You can't just assume that what happens in mice also happens in human scalp hair follicles.

 

[michael barry]

Interestingly, the changes were inconsistent: the extra testosterone sharply UP-regulated levels of the type 2 enzyme, mildly DOWN-regulated levels of androgen receptors (supporting Sawaya's finding about finasteride and androgen receptors), and had no real effect at all on the type 1 enzyme. That would appear to be an attempt on the part of the cell to maintain an androgenic homeostasis ONLY when it comes to androgen receptors, but NOT when it comes to the 5a-reductase enzymes. I find that both fascinating and puzzling.

Bryan,
If extra testosterone gets a sharply UP-regulated level of type 2 DHT as a response, then lower amounts of globulin (insulin resistance) really might be something that would speed up extra DHT being made by the type two enzyme in the root sheath would it not? Interesting stuff, thank you for posting it.

 

[goata007]

So the point I'm making here is this: if serum DHT has a significant effect on hair follicles, wouldn't you also expect it to have a significant effect on the nearby and closely-related sebaceous glands?? But it clearly DOESN'T, because the application of GLA has a very significant "local" effect on sebaceous glands in both humans and animals; therefore, I conclude that serum DHT isn't likely to have much of an effect on hair follicles, either.

ok...I'm a little confused here, isn't sebum production affected by type-I dht? since finasteride only inhibits type-II it shouldn't have any effect on sebum production. :dunno:

 

[Bryan]

ok...I'm a little confused here, isn't sebum production affected by type-I dht? since finasteride only inhibits type-II it shouldn't have any effect on sebum production. :dunno:

Sure, but it's just the PRINCIPLE that we're discussing here! We're discussing what effect (if any) that serum DHT has, versus "locally-produced" DHT!

Let me try to explain my point again using slightly different words: we know from actual experimentation by legitimate scientists that you can significantly reduce the production of sebum by using a TOPICAL 5a-reductase type 1 inhibitor (GLA). Serum DHT clearly doesn't stop that from happening, proving that serum DHT must have only a relatively minor effect, at best. So the point I'm making is that if that's the case in sebaceous glands, doesn't it seem very likely to also be the case in hair follicles (using type 2 inhibitors, of course)??

.

 

[harold]

From that Sawaya study on differences in Androgen Recptors and 5AR distribution amongst scalp regions in balding men and women there was a 1.5 times as many androgen receptors in frontal vs occipital regions whilst I think 3.5 times as much 5-AR between the two regions. I think its possible/probable that the difference in AR number is due to androgen receptors being upregulated in the face of greater androgenic stimuli. Was looking at a study in mice and when they were castrated there was a large drop in the expression of androgen receptors.

The only problem with that theory is that two separate pieces of evidence (Sawaya's finding about finasteride and androgen receptors, and the Happle & Hoffmann study I mentioned in my reply just above to Michael Barry) indicate that it's just the OPPOSITE of that: greater androgenic stimulation DOWN-regulates androgen receptors in human scalp hair follicles, it doesn't UP-regulate them. It may be different in other tissues and in other species, like in that mouse study you mentioned. You can't just assume that what happens in mice also happens in human scalp hair follicles.

Well I wasnt assuming it did happen. Just saying that in the absence of other evidence and given what I had seen it seemed possible/probable that this was the case. It would have been nice if it did because then we would have a clear explanation of why both increased DHT and increased androgen receptors in balding areas go hand in hand. Otherwise I find it hard to work out how it might be working.
Though if this is true
"The investigation of a large
number of genetic variants covering the AR locus suggests
that a polyglycine encoding GGN repeat in exon one is
a plausible candidate for conferring the functional effect.
The polyglycine tract is located in the transactivating domain
of the androgen receptor protein (AR), "
Then it would seem that if Androgenetic Alopecia is driven primarily by such a mutation then the ARs of Androgenetic Alopecia people are not more sensitive as I believed was the case but possibly more prone to be expressed leading to higher levels of ARs in androgen target tissues. If this is the case and the behaviour you describe above occurs then this could explain why there is more DHT in such areas as well as more ARs (there would be even more if they were not being downregulated by testosterone/DHT).
Do you have any links to those studies? It sounds interesting.
Here is something about rats and the effect of androgens/castration on AR levels for what its worth. Not much I guess
hh

J Appl Physiol. 1999 Dec;87(6):2016-9.Click here to read Links
Effects of castration and androgen treatment on androgen-receptor levels in rat skeletal muscles.
Antonio J, Wilson JD, George FW.

Human Performance Laboratory, University of Nebraska, Kearney, Nebraska 68849, USA. antonioj@unk.edu

The effects of castration and dihydrotestosterone (DHT) treatment on levels of skeletal muscle androgen receptor (AR) were examined in three groups of adult male rats: 1) intact normal rats, 2) rats castrated at 16 wk of age, and 3) rats castrated at 16 wk of age and given DHT for 1 wk starting at week 17. All animals were killed at 18 wk of age. Castration caused a decrease (P < 0.05) in the weights of the levator ani and bulbocavernosus muscles. The administration of DHT to the castrated rats increased (P < 0.05) the weights of the levator ani and bulbocavernosus muscles. Castration caused a significant downregulation of AR levels in the bulbocavernosus (P < 0.05) but had no significant effect on AR levels in the levator ani muscle. DHT administration to the castrated group upregulated AR levels in the bulbocavernosus and levator ani muscles. The plantaris muscle did not significantly (P > 0.05) change for any of the treatments. These findings suggest that the effects of castration and androgen replacement differentially affect skeletal muscle mass and AR levels.

 

[first]

These studies suggest that local DHT inhibition is possible. Given the "irreversible" nature of finasteride 5-AR2 binding I am tempted to consider that it may even be possible to just use an ultra-low dose finasteride/dutasteride topical. As close as possible as just enough to bind with all the 5-AR in the scalp leaving as little as possible left over to wash into the bloodstream. The idea is to reverse the ratio of scalp/serum DHT inhibition seen with oral dosing.

Topical finasteride has proven to have a very positive effect in recent studies.

Clinical Study

The effect of the novel combination was observed in a study. The subjects were divided into three groups.

* Group I (Placebo Group) plain lotion was applied
* Group II (Minoxidil Group) 5% Minoxidil lotion was applied
* Group III (Combination Group) 5% Minoxidil lotion, 0.025% Tretinoin and 0.1% Finesteride were applied.

The important aspect of the study was the fact that none of the parties involved viz. the clinical / research staff, the study sponsors or the subjects in the three groups were aware of the various groups until the data was collected in the verified database. The subjects were evaluated every six months with the help of a subjective questionnaire, objective examination and close-up photographs.

Results

In the Placebo Group, there was neither any improvement nor deterioration. In the Minoxidil Group 25% of the subjects showed hair growth. In the Combination Group as much as 75% of the subjects showed improvement. Further, the quality of the newly grown hair was also better in the combination group.

 

[Bryan]

Though if this is true
"The investigation of a large
number of genetic variants covering the AR locus suggests
that a polyglycine encoding GGN repeat in exon one is
a plausible candidate for conferring the functional effect.
The polyglycine tract is located in the transactivating domain
of the androgen receptor protein (AR), "
Then it would seem that if Androgenetic Alopecia is driven primarily by such a mutation then the ARs of Androgenetic Alopecia people are not more sensitive as I believed was the case but possibly more prone to be expressed leading to higher levels of ARs in androgen target tissues.

Hmmm....maybe I'm misreading it, but it sounds to me like they ARE talking about more sensitive (or less sensitive) ARs. They're talking about certain encoding repeats "conferring the functional effect", which sounds to me like they mean the overall sensitivity of each AR.

Do you have any links to those studies? It sounds interesting.

Sorry, but I don't. As far as I know, Sawaya has STILL not actually published her infamous finding about the "intense upregulation" of androgen receptors in finasteride users. She only happened to mention that at a news conference at a medical conference several years ago.

The Happle & Hoffmann study was published in the book Hair Research fo the Next Millenium. As far as I know, it hasn't been published in a medical journal. I've cited that study several times over the years, because it has some very interesting and useful stuff in it. I've even used it more than once as ammunition against Stephen Foote! :mrgreen: I really should scan it and post it so that the rest of you can read the whole thing...it's not terribly long, and it reads fast.

 

[abcdefg]

A substance reducing beard hair though is not really a definitive test. It hasnt really been proven that DHT is the only thing responsible for facial hair growth. It is possible dht triggers hair to grow but testosterone keeps it growing. So inhibiting dht on the face as a test might only work if you did it before you ever grew any facial hair. Propecia and dht inhibitors do not remove facial or body hair in most people so it takes more then dht to sustain body or facial hair.