For bryan and Foote.

[Bryan]

Doing what exactly????

Dave already explained that to you: you use two different characters (one at the start, the other at the end) when quoting or emphasizing a word or phrase.

I doubt very much that the people who read these boards have the slightest interest in what you consider to be `correct' grammer Bryan.

There you go: just like you did with the word "correct" in that sentence. Just about everybody else in the world would use either 'correct' or "correct", but YOU consistently use `correct'. Why is that?? Is that something you were taught in school, or is it something original with you, or what, exactly? Just curious...

Bryan

 

[michael barry]

This is an article on lipoxidil.com about soy phytoestrogens DECREASING the amount of androgen receptors and why soy may help in baldness here http://www.lipoxidil.com/site/phytoestrogenes.php


If Fluridil works by gumming up androgen receptors, if progesterone cream works by filling androgen receptors up with a female hormone (even if it has to be done about 5 times a day), wouldnt that prove that DHT binding with these receptors is what "kicks off" the miniaturization process? Even if DHT only functioned to "mark" the follicle for superoxide attack from the immune system, it seems that if we could continuously block androgen receptors we'd have much more success in treatment would it not? After all, if scalp hair follilces DONT NEED androgens to grow, why would selection put them there? They are there to make ya' bald in my opinion. They do it where there are the highest concentration of AR's first (the temples, vertex).

Im guessing this is why SOD's like Doctor Proctor puts in his product are successful..........that its the immuno response to DHT in the follicle that does the MOST damage after enough receptors have hosted enough DHT over the years to "mark" the follicle for immuno-attack.

By the way, Dr. Pickart and Dr. Proctor both seem like very nice men who would have no qualms about challenging convention if they thought it was wrong (especially Pickart as Ive gotten a few responses from him on is forum).

 

[Dave001]

I doubt very much that the people who read these boards have the slightest interest in what you consider to be `correct' grammer Bryan. They like me are a lot more interested in content rather than presentation :roll:

I don't care whether your posts are grammatically correct. If it were up to me, you'd aim for brevity and dismiss all else. I asked you a simple question, and look at what you spewed.

As Bryan has expressed, we have noticed a peculiarity in your use of quotes, which you usually delimit by a `backtick` followed by an apostrophe or 'inverted comma'. We've been curious about your reason for the unconventional usage. Do you have one?

 

[Dave001]

Most people reading this would conclude that your concern here is just a distraction from the content of what i say, and they would be right!

I think most people reading this would much prefer a distraction from your content to the real thing.

 

[Bryan]

If Fluridil works by gumming up androgen receptors, if progesterone cream works by filling androgen receptors up with a female hormone... wouldnt that prove that DHT binding with these receptors is what "kicks off" the miniaturization process?

Sort of, but there's a problem with your statement above, Michael, and it shows that you don't really understand Stephen's theory. Let me try to explain it in a nutshell:

You didn't specify WHICH androgen receptors you were talking about, although one could reasonably assume that you were referring to androgen receptors within hair follicle dermal papilla cells. Stephen, OTOH, believes that topical antiandrogens work for balding (like RU58841 in all the stumptailed macaque studies) because the drug becomes SYSTEMIC, and goes deeper into the body than just the hair follicles. He thinks it then affects the parts of the skin and/or circulation in such a way as to relieve the alleged "edema" which he thinks is the true cause of balding.

So his bottom-line continues to be that hair follicles don't react DIRECTLY to androgens (or antiandrogens, for that matter), but they react to more global influences; edema and contact inhibition, to be specific. And THOSE two things are what the antiandrogens are helping to ameliorate (according to his theory).

Bryan

 

[michael barry]

Bryan,
Thanks for your reply. I was speaking about the androgen receptors on the follicle proper. Every study Ive read involving androgens added to various hair cells state that they slow down production of outer root sheath cells, keratinocytes, etc.......

Even if the experiments didnt show that DHT directly affected hair cell production, by "inflaming" or "marking" the follicle, DHT could still direct the immune attack to it as a "direct" result of androgen binding to follicle receptor sites. Dr. Proctors products as well as Pickarts are supposedly primarily SOD and folks report that they work. Ive openly wondered if the weak immunosuppressant caffeine is what the Doctor's over at Alpecin were thinking when designing a product around that (if it does indeed help).

The little article on lipoxidil was the only other compound (other than vitamin B6) that Ive read seems to decrease the amount of androgen receptors being made. There is supposed to be thirty percent more AR's in the temple area of balding men. Thats whats attracted my attention to soy.


On an aside note that I forgot to mention but I think you, Dave, and Stephen would find interesting was an article I read (not online) a couple of years back that had a man smearing on a "cream" steroid on his muscular arms after his shower. He had a little baby boy and would hold his child. The kid started getting acne and a little hair on his arms WAAAAY to early in life. Goes to show that hormones run so much in us whether we like it or not.

 

[Bryan]

Bryan,
Thanks for your reply. I was speaking about the androgen receptors on the follicle proper. Every study Ive read involving androgens added to various hair cells state that they slow down production of outer root sheath cells, keratinocytes, etc.......

I knew that's what you meant, Michael. I was just trying to emphasize the subtleties of Stephen's theory, and point out his peculiar alternate explanation for why antiandrogens benefit balding.

Even if the experiments didnt show that DHT directly affected hair cell production, by "inflaming" or "marking" the follicle, DHT could still direct the immune attack to it as a "direct" result of androgen binding to follicle receptor sites.

Actually, experiments DON'T show such a thing. At least, I've never found any that demonstrated that, and I've been looking for them for a long time. I've even posted in the past on various hairloss sites about how odd it is that I've never been able to find anything about that theory in the medical literature. The only thing I've found which possibly hints at it might be that recent study about human hair follicles transplanted onto immune-deficient mice.

The little article on lipoxidil was the only other compound (other than vitamin B6) that Ive read seems to decrease the amount of androgen receptors being made.

You found a claim somewhere that B6 decreases the production of androgen receptors? Do you have a link to that? And what was the other compound?

Bryan

 

[michael barry]

Bryan,

The soy compound was genistien and I read about it here http://www.lipoxidil.com/site/phytoestrogenes.php

"Retinoic acid (vitamin A derivative), may reduce the number of androgen receptors by 30-40 percent. [29] Vitamin B6 reduces by 35-40% the extent of protien synthesis observed after androgen receptor activation [30]" -------This info is here
http://dermatology.cdlib.org/DOJvol4num ... nkovi.html



Here is a blip on B6 that seems to concur with the above a bit on ....http://www.regrowth.com/hair_loss_treatments/vitamin_b6/vitamin_b6.cfm

 

[S Foote.]

Doing what exactly????

Dave already explained that to you: you use two different characters (one at the start, the other at the end) when quoting or emphasizing a word or phrase.

[quote="S Foote.":d5915]I doubt very much that the people who read these boards have the slightest interest in what you consider to be `correct' grammer Bryan.

There you go: just like you did with the word "correct" in that sentence. Just about everybody else in the world would use either 'correct' or "correct", but YOU consistently use `correct'. Why is that?? Is that something you were taught in school, or is it something original with you, or what, exactly? Just curious...

Bryan[/quote:d5915]

That's just my original style Bryan! :wink:

If it upsets you so much i will "change" OK :roll:

S Foote.

 

[S Foote.]

Most people reading this would conclude that your concern here is just a distraction from the content of what i say, and they would be right!

I think most people reading this would much prefer a distraction from your content to the real thing.

No Dave, "most" people (happy now?) would expect that if someone does not agree with a theory, that they would at least state some scientific reasons "for" their opinions.

That is the norm on these forums. To act as if everyone should just take your personal opinions at face value without question, just proves to people that you just can't back up your arrogant statements. End of story :wink:

S Foote.

 

[S Foote.]

Michael.

There is one important factor that has to be considered about in-vitro testing in this context.

That is that when follicle cells are cultured for these experiments, they lose the ability to produce androgen receptors!

The production of androgen receptors is therefore induced "artificialy" as described in this article.

http://www.fasebj.org/cgi/content/full/16/14/1967

"1. No significant effect of androgen on the growth of KCs cocultured with DPCs from Androgenetic Alopecia
We cocultured KCs and DPCs from Androgenetic Alopecia using transwell culture dishes and examined the effect of R1881 (methyltrienolone, synthetic androgen) on the growth of KCs. The addition of 10-9 M R1881 showed no significant influence on the proliferation of KCs in the coculture. We then assumed that in vitro cultivation of DPCs might alter the expression level of androgen receptor (AR). Semiquantitative RT-PCR showed that AR mRNA in DPCs from Androgenetic Alopecia was decreased during subcultivation from the third to ninth passage. To solve this problem, AR was overexpressed in the DPCs by transfecting the AR expression vector pSG5-AR. "

My concern is that if the cells are "altering" like this by the culturing itself, how accurate is the testing going to be? What else is altering in these cells?

It doesn't seem to be an acurate reflection of the in-vivo cell condition does it?

S Foote.

 

[S Foote.]

Bryan,
Thanks for your reply. I was speaking about the androgen receptors on the follicle proper. Every study Ive read involving androgens added to various hair cells state that they slow down production of outer root sheath cells, keratinocytes, etc.......

Even if the experiments didnt show that DHT directly affected hair cell production, by "inflaming" or "marking" the follicle, DHT could still direct the immune attack to it as a "direct" result of androgen binding to follicle receptor sites. Dr. Proctors products as well as Pickarts are supposedly primarily SOD and folks report that they work. Ive openly wondered if the weak immunosuppressant caffeine is what the Doctor's over at Alpecin were thinking when designing a product around that (if it does indeed help).

The little article on lipoxidil was the only other compound (other than vitamin B6) that Ive read seems to decrease the amount of androgen receptors being made. There is supposed to be thirty percent more AR's in the temple area of balding men. Thats whats attracted my attention to soy.


On an aside note that I forgot to mention but I think you, Dave, and Stephen would find interesting was an article I read (not online) a couple of years back that had a man smearing on a "cream" steroid on his muscular arms after his shower. He had a little baby boy and would hold his child. The kid started getting acne and a little hair on his arms WAAAAY to early in life. Goes to show that hormones run so much in us whether we like it or not.

Michael.

I think the immunology in male pattern baldness is due to the lymphedema i suggest is causing the miniaturisation through "early" contact inhibition.

The conditions in the male pattern baldness scalp of immune sensitivity and fibrosis, have long been recognised in lymphedema.

http://www.lymphoedema.org.au/

Click on "What is lymphedema"

I don't think the immunology directly effects follicles, but the fibrosis it causes in the longer term will resist any attempts to re-enlarge the follicles. So the immunology will have to be targeted in treatments as people are now realising.

S Foote.

 

[michael barry]

Stephen,

I see that other experiments like this http://www.ehrs.org/conferenceabstracts ... -itami.htm had to artificially culture androgen receptors to put with the keratinocyte and dermal papilla cells, and I assume that this always has to be done becuase culturing DPC's, KC's, and EC's proboably all inhibit AR expression for petri-dish purposes. I dont know if Bryan or Dave would accept that labratory standard operating procedure invalidating the ensuing experiments.......be anxious to hear their take on that.

Bryan refers to your belief that topical anti-androgen receptor indications like fluridil and RU58841 work because the adhere to receptors further down (to the suprise of their inventors I'd imagine), what receptors are there in the lymph nodes for them to adhere to?


I know you've stated that DHT's primary role in a male is to govern the pumping of the lymphaitic system and too much of it seems to slow the pumping down, hence the edema on the top of the scalp. I wasnt aware that there are AR's on lymph nodes?


My initial hesitations of your idea still persists.
ONE. Scalp edema, as a function of plain ol' gravity, should'nt happen as much as Androgenetic Alopecia should it? I mean, wow, HALF Caucasoid men's scalp just have lymph pumps that are backed up with stagnant protiens and lymph fluid, causing high fluid pressure and an immuno-response that causes fibrosis on their skulls? Thats hard to swallow, but I'll accept anything science conclusively proves.

TWO. We all know that androgens stimulate beard, auxilary, body hair growth...........since a man gets hairier from the eyebrows down as he ages, it just stands to reason that since he balds up top that these same hormones are causing the baldness in a similar way up there (i.e. by direct influence on the follicle just as it works on the body hair). Youre stating that DHT makes body hair grow directly, but making head hair fall out indirectly.

THREE. The biggie. Sebaceous glands get BIGGER in male pattern baldness even in the front of the scalp. How can they enlarge if fluid pressure is too high to allow it?

FOUR. Things like proanthocyanidrins, laminria extract, etc. supposedly excite certain cells in the follicle to speed up production. Too much Insulin-like Growth Factor supposedly slows production in parts of the follicle. Why not DHT?

Question. Im assuming you use cold water rinses and a form of massage on your own scalp to induce the lymph to drain back down. If this is all you use........what has your success been like? Are you keeping the hair you have?

 

[Dave001]

No Dave, "most" people (happy now?)

No. I don't care what characters you choose to quote with. It is, however, disrespectful to the reader to intentially disregard convention. Your quirky style does not make you come across as the "mad genius", but rather the "stupid idiot".

would expect that if someone does not agree with a theory, that they would at least state some scientific reasons "for" their opinions.

You wouldn't know science if it bit you in the ***. Neither biology nor medicine are theoretical sciences. If you had anything novel of value to contribute you would publish or patent (good luck getting your "original" style accepted by a peer reviewed publication that takes itself seriously). Your so-called theory is not provable because it is a load of sh*t and you haven't a clue what you're talking about.

 

[S Foote.]

Stephen,

I see that other experiments like this http://www.ehrs.org/conferenceabstracts ... -itami.htm had to artificially culture androgen receptors to put with the keratinocyte and dermal papilla cells, and I assume that this always has to be done becuase culturing DPC's, KC's, and EC's proboably all inhibit AR expression for petri-dish purposes. I dont know if Bryan or Dave would accept that labratory standard operating procedure invalidating the ensuing experiments.......be anxious to hear their take on that.

Bryan refers to your belief that topical anti-androgen receptor indications like fluridil and RU58841 work because the adhere to receptors further down (to the suprise of their inventors I'd imagine), what receptors are there in the lymph nodes for them to adhere to?

I don't think you are clear about my theory Michael, so i'll try to clear up this points.

I don't think the inventors of anti-androgens would be suprised, because as far as i know the only anti-androgens to show any effect upon male pattern baldness in humans, are known to have a more systematic effect.

I know you've stated that DHT's primary role in a male is to govern the pumping of the lymphaitic system and too much of it seems to slow the pumping down, hence the edema on the top of the scalp. I wasnt aware that there are AR's on lymph nodes?

First, it has been shown that regular contractions of lymphatic vessels, play a role in pumping lymph through the vessels.

http://www.healthy.net/asp/templates/ar ... cle&ID=993

This mechanism has to involve the contractions of muscle fibers in the vessel walls. Muscle is known to contain androgen receptors.

http://muscle.ucsd.edu/musintro/steroids.shtml

So a pathway exists for androgens to effect lymphatic pumping. I would add that the nervous system is going to be involved in the signaling necessary for any androgen induced muscle contractions, and androgens are known to effect the nervous system.

http://www.mesomorphosis.com/articles/a ... nction.htm

I think there is an important reason in evolution for androgens "TO" increase lymphatic drainage. This is a "performance" enhancing effect. This increase in tissue fluid turnover would increase nutrient supply and waste removal in tissues to aid tissue performance in line with general androgen effects in men.

My initial hesitations of your idea still persists.
ONE. Scalp edema, as a function of plain ol' gravity, should'nt happen as much as Androgenetic Alopecia should it? I mean, wow, HALF Caucasoid men's scalp just have lymph pumps that are backed up with stagnant protiens and lymph fluid, causing high fluid pressure and an immuno-response that causes fibrosis on their skulls? Thats hard to swallow, but I'll accept anything science conclusively proves.

TWO. We all know that androgens stimulate beard, auxilary, body hair growth...........since a man gets hairier from the eyebrows down as he ages, it just stands to reason that since he balds up top that these same hormones are causing the baldness in a similar way up there (i.e. by direct influence on the follicle just as it works on the body hair). Youre stating that DHT makes body hair grow directly, but making head hair fall out indirectly.

No Michael this is not what i have said.

Gravity has very little to do with the conditions that i propose develope in "some" men to create male pattern baldness.

I have said that i believe body hair growth and male pattern baldness are "BOTH" indirect effects of DHT based upon local changes in lymphatic drainage. DHT as you say grows hair over the larger part of the body. I suggest that in increasing lymphatic pumping, DHT reduces tissue fluid pressures particularly in areas rich in lymphatic vessels. When this happens near hair follicles, the reduced tissue pressure reduces the resistence to the growth of larger follicles through normal contact inhibition. So where there are increased concentrations of lymph vessels near follicles, the effect is more hair growth.

This matches with the increased concentrations of lymph vessels near the surface in the groin (pubic) area, the armpits and beard area.

The corrolation can even be seen in scalp hair growth, take a look at this.

http://137.222.110.150/calnet/DeepNeck/ ... m#section6

Note how the level of the surface collection nodes, (where the vessels start to go deep) represents the base of the hairline. Also note that the vessels at the end of the system (the male pattern baldness area), are few compared with the lower vessels these have to drain through. I think this is important in understanding the development of male pattern baldness in "some" people.

This is where it gets slightly complicated.

If DHT is generaly increasing lymphatic pumping, the ends of the system can be vunerable. Say DHT is increasing the contraction rate of the lymph vessels in the surface tissue of the head, this is increasingly closing the one way valves against flow from the end of the "pipework" (the male pattern baldness area).

This slight reduction of drainage from the end of the system would not cause problems under normal circumstances. But the human brain has had to evolve a very complex blood circulation system in order to enlarge. To cut a long story short, blood feeds into the scalp from all directions, and if you cut your scalp you soon are aware of the high blood pressure here!

If an individual has a higher pressure blood feed to the scalp, there is more chance of the reduced drainage caused by DHT creating edema and male pattern baldness. Individuals with a lower "basic" blood pressure to the head may not develope this edema. I suggest this feed side of the equation is what predisposes an individual to male pattern baldness for the same level of DHT.

This would also explain the recognised corrolation with male pattern baldness and heart problems, it's the "core" blood pressure that makes the difference.

THREE. The biggie. Sebaceous glands get BIGGER in male pattern baldness even in the front of the scalp. How can they enlarge if fluid pressure is too high to allow it?

But they don't Michael, this is a myth! Show me some hard evidence?

The sebaceous glands in the scalp remain the "same" size they were before male pattern baldness. These were large glands serving large follicles, when the follicles have shrunken the sebaceous glands remain the same size. This is consistant with my theory.

Hair follicles naturally shrink during the resting phase of the hair cycle. This makes them more "adjustable" through normal contact inhibition.

Sebaceous glands don't go through a growth cycle, so it is more likely that a decrease in external pressure will increase their size through contact inibition being "lifted", as happens particularly in the beard area. It is going to be harder for an increase in pressure in the male pattern baldness area to reduce their size, because they are not having to "re-enlarge" like anagen follicles. As pre-existing "large" structures they will not be shrunken by the normal contact inhibition of growth. (They are already grown as it were).

FOUR. Things like proanthocyanidrins, laminria extract, etc. supposedly excite certain cells in the follicle to speed up production. Too much Insulin-like Growth Factor supposedly slows production in parts of the follicle. Why not DHT?

Question. Im assuming you use cold water rinses and a form of massage on your own scalp to induce the lymph to drain back down. If this is all you use........what has your success been like? Are you keeping the hair you have?

The point is Michael, that if contact inhibition of organ growth is involved in androgen related hair growth, this is going to be the governing "overrulling" factor.

I will say it again, there is just no way when you consider "ALL" the facts that DHT can be "directly" reducing hair growth in male pattern baldness. Why?, because the scientific method, rules this out!

For example, the current theory just cannot explain the immunology in male pattern baldness, and that is just one problem it has!

As far as my own situation is concerned, i can maintain what i have left. Although as i have gone on the record about before, my previous treatment for, and the effects of cancer i am left with, rules out much experimentation in my case because of my immune status.

Thanks for your interest and courtesy in discussing these issues.

S Foote.

 

[S Foote.]

No Dave, "most" people (happy now?)

No. I don't care what characters you choose to quote with. It is, however, disrespectful to the reader to intentially disregard convention. Your quirky style does not make you come across as the "mad genius", but rather the "stupid idiot".

[quote="S Foote.":67622]would expect that if someone does not agree with a theory, that they would at least state some scientific reasons "for" their opinions.

You wouldn't know science if it bit you in the ***. Neither biology nor medicine are theoretical sciences. If you had anything novel of value to contribute you would publish or patent (good luck getting your "original" style accepted by a peer reviewed publication that takes itself seriously). Your so-called theory is not provable because it is a load of sh*t and you haven't a clue what you're talking about.[/quote:67622]

So just your usual hot air then Dave!

You really are pathetic.

For your information, i have had two papers published on my theory in the journal designed for the purpose "Medical Hypotheses". I have followed all the rules in pursuing my theory, including contacting accepted experts in the field for their opinions.

I have posted the replies i have had so far as you know, and these "expert" opinions on my theory show just how sadly out of sync you are with "true" science.

I would add that during the course of my correspondence about my theory, i was asked to be a referee for papers submitted to a leading dermatology journal.

I would also say that i was warned by professional scientists about getting involved in pointless debates on internet forums, with sad attention seeking "cut and paste" psuedo scientists.

But i just can't resist putting retards like you in their place :wink:

S Foote.

 

[Bryan]

Vitamin B6 reduces by 35-40% the extent of protien synthesis observed after androgen receptor activation [30]" -------This info is here
http://dermatology.cdlib.org/DOJvol4num ... nkovi.html

Here is a blip on B6 that seems to concur with the above a bit on .... http://www.regrowth.com/hair_loss_treat ... min_b6.cfm

Yes, I figured that you were probably referring to the study that was cited and referred to at both of those links. I have that full paper right here. It didn't find that B6 has any effect on the numbers of androgen receptors, just that it reducs the transcriptional/translational activity of androgen receptors, in response to androgens. BTW, that's why I've always said that there may be a decent scientific rationale for including a reasonable B6 supplement in the diet of anyone with male pattern baldness.

BTW, there is also an in vitro study which found that EGCG (the main polyphenol in green tea) downregulates the production of androgen receptors in a certain line of prostate cancer cells; however, the relevance of that to hairloss (if any) is unknown.

Bryan

 

[Bryan]

[quote="michael barry":473df]THREE. The biggie. Sebaceous glands get BIGGER in male pattern baldness even in the front of the scalp. How can they enlarge if fluid pressure is too high to allow it?

But they don't Michael, this is a myth! Show me some hard evidence?[/quote:473df]

I believe I have previously shown you evidence for that, but not surprisingly, you just ignored it.

Bryan

 

[michael barry]

Im going to quote Loren Pickart on Cyclosporin....."Cyclosporin is an immunosuppresive drug used in organ transplants to prevent the body from rejecting a new organ. It is used topically in the treatment of immune-associated severe skin conditions. In humans, cyclosporin is very effective orally (80% positive hair growth response) but only marginally effective (20%) whn used topically for aiding hair growth. It promotes hair growth in animal models and promotes human hair growth in virto.

That info was here http://www.skinbiology.com/hairregrowth ... yclosporin

That, along with the experiment of taking miniaturizing hairs from balding guys and putting them on the backs of immuno-deficient mice is why I believe the immune system attack is integral to baldness. Proctor and Pickart seem to believe this. Im guessing the makers of Tricomin and American Crew (peptides again) have invested faith in it too.

If cyclosporin is working "in another way", what do any of you think that it would be?



Stephen, have you gotten any scientists youve talked to express privately why a cure for male pattern baldness is taking so long? What do they say they are stuck on? I was assuming it was finding a topical anti-androgen that didnt break down, competed successfully for androgen receptors with DHT, and only had to be applied once a day, and was cost effective (nobody is gonna pay $200 a month for anything).

Im going to look back into the enlargening sebaceous glands. Ive read that in a few different places.



By the way.......on "internet scientists".......alot of people on forums are like me........just mystified that male pattern baldness is still "unsolved". When minoxidil came out in 1988, my derm told me "its just a matter of time now" and baldness would be "cured forever". This is what gives rise to alternative theories, etc. in my opinion. When computers really became advanced, I just assumed that DNA, RNA models would be run with sophisiticated software showing mathematically and chemically the effects of drugs in such an efficient way that cures for most diseases, anti-virals, vaccines, anti-biotics would ensue and old maladies would all be conquered unless new ones evolved resistances etc. Obviously it hasnt worked out that way. Stephen has stated that Dave, Bryan, (and proboably me) would disappear off forums when HM research gained more info invalidating current thought on male pattern baldness. Hey, when/if HM becomes reality and I can have my 19 year old hair back........I promise you wont see me on any forums concerning hair. I'll be enjoying it and not worrying about it like Brad Pitt proboably does.

 

[Dave001]

I don't think the inventors of anti-androgens would be suprised, because as far as i know the only anti-androgens to show any effect upon male pattern baldness in humans, are known to have a more systematic effect.

That's only true if you choose to believe that studies in which topically applied antiandrogenic agents have been successful were so because of systemic absorption, even despite evidence to the contrary (e.g., lack of endocrine changes or locally observed effect only [e.g., when compared with contralateral site]).

THREE. The biggie. Sebaceous glands get BIGGER in male pattern baldness even in the front of the scalp. How can they enlarge if fluid pressure is too high to allow it?

But they don't Michael, this is a myth! Show me some hard evidence?

Oh, yes, they most certainly *are* enlarged in male pattern baldness subjects compared to nonbalding counterparts.