Anyone got any evolutionary theories for hairloss?

[DammitLetMeIn]

I don't really buy the 'brain cooling' theory. White men are four times more likely to than black men develop premature balding (Setty LR. Hair patterns of the scalp of white and Negro males. Am J Phys Anthropol 1970;33:49­-55.) And as we know lighter skin colour evolved at the higher latitudes (http://en.wikipedia.org/wiki/Image:Map_ ... _equi3.png). So shouldn't lighter-skinned men be less likely to lose their hair?

I can't say I buy into the brain cooling theory either. That said, I haven't been following the thread closely enough to have examined carefully both sides of the argument.

 

[Bryan]

You always end up moving the goal posts when they dont suit you Bryan! You ask for some support for my theory, and i have very clearly provided that. But now you start to demand absolute proof as you always do.

No, Stephen, in this particular case I'm not asking you to "support your theory" (except very indirectly), nor am I demanding "absolute proof" for it. I'm asking you to provide an example of what you earlier claimed to have: an example of contact inhibition altering the way that cells respond to androgens. Are you going to admit, finally, that you cannot provide such an example?

Any half decent scientist could clearly see the relevance of the evidence i have presented Bryan. You seem to have a big problem in understanding what a "BODY" of scientific evidence means! This is probably because all you are used to is cherry picking certain studies to support your biased opinions, then ranting at people who dont agree with you!

I don't care about what you think is the alleged "relevance" of the evidence, and I don't care about what you think is the "body of evidence". I'm asking you to provide an example of what you claimed to have earlier. GIVE US AN EXAMPLE.

Do you feel like a cornered rat, Stephen? :wink:

You have not got the slightest idea about "true" scientific evidence Bryan!

You have not even got "ANYTHING" remotely linked to the mechanisms you make claims for, and you "KNOW IT"! Hence these ranting distractions. 8)

But _I_ never made any claims about having any evidence for the "genetic clock" theory, Stephen. I made it perfectly clear that it was just an IDEA, just a hypothesis. YOU, on the other hand, claimed that there is a biological precedent for contact inhibition altering the way that cells react to androgens. But you SCREWED-UP ROYALLY when you said that, Stephen. I'm calling your bluff: give us an example of such a biological precedent. You can't do it, and you know it. You're not going to squirm out of this. You better just admit that you can't do it.

How does that "rule out" the brain cooling strategy? You're becoming more and more incoherent...

Sigh! :roll:

If you go along with the "idea" proposed by Cabanac, that male pattern baldness is "needed" to compensate for beard growth in order to maintain the bare area necessary to cool the brain through radiation, beard growth and male pattern baldness would have to be in sync. They would both have to happen at the same time, in order to maintain the "radiator" area!

But I do NOT necessarily go along with Cabanac's proposal that male pattern baldness specifically compensates for beard growth. I think it compensates specifically for increased brain function and elevated temperatures in the brain. Period. Full stop. Forget the part about growing a beard.

Right, you have "demanded" i provide you with answers...

I'm demanding you provide proof of something that you said YOU ALREADY HAD: an actual example of cells having their response to androgens altered by contact inhibition. You're about to learn a very valuable lesson: don't make claims that you can't back-up! :wink:

...now i demand you provide "ME" with some answers about the "direct" theory you claim is "safe"! I dont want to hear your usual excuse here of "scientists will figure it out one day".

Oh, you're going to ask me again about that "genetic clock" theory? I'll cut it short with a simple and honest answer: I DON'T KNOW how that works. I never ever said that I did. (There, that was easy! :wink: )

See how things get a lot easier when you're simply HONEST, Stephen? When you make-up crap claims that you can't back-up, I guarantee you that you'll get into trouble every time!

Now let's get back to the main issue here: where is that bioligical precedent of contact inhibition causing a change in the way that cells respond to androgens? :wink: If you admit that you don't have any such example, then I will finally let you off the hook, and this unpleasant episode for you will be over.

Bryan

 

[Bryan]

Wow..I'm pleasantly surprised to see there are some here like me..even those who only believe part of what I do. Pretty brave given the lack of tolerance and open-mindedness shown by quite a few here. Nothing new there though.

And yes Bryan...it sure IS unique. That was exactly my point.

???

WHAT is unique? Jacob, you need to learn to quote previous posts, so that we can know what you're talking about.

Bryan

 

[Jacob]

Find your previous post. It's not like millions of years and posts have gone by.

 

[Bryan]

Are you CRAZY?? I'm not going to go searching back through previous posts on previous pages just in an attempt to find out what it is you're talking about. It's YOUR job to provide the proper context by quoting a previous post. You click on the "quote" button, Jacob. It's easy, even for you.

Bryan

 

[Jacob]

Sorry Bryan..I don't work for you.

In the time you spent whining about my not quoting you..you could easily have looked it up.

Your memory must not be that great btw.

 

[Dave001]

Its a good theory, however, baldness is consistently linked with other health problems which suggests that perhaps its a reaction to something going wrong inside the body perhaps?

It isn't consistently. Epidemiological studies are inherently weak: every degenerative condition can probably be correlated positively with other diseases, but that says nothing about the cause, nor does it suggest an elevated risk factor for all affected individuals (affected by balding, in this case).

I think it's an indirect effect. Baldness is obviously linked to androgens, and those other health issues are also linked to androgens in some way. Baldness doesn't directly cause (or is caused by) those other health issues. At least, as far as I know!

I don't think there is any good evidence that it has anything to do with androgens, which either haven't consistently been shown to be globally elevated in baldness, or established as a causative factor for the disease in question. (before I hit "post", I should clarify that the antecedent of my "it" is NOT baldness! :wink: )

 

[Jojje]

fight fight fight fight :lol:

 

[S Foote.]

You always end up moving the goal posts when they dont suit you Bryan! You ask for some support for my theory, and i have very clearly provided that. But now you start to demand absolute proof as you always do.

No, Stephen, in this particular case I'm not asking you to "support your theory" (except very indirectly), nor am I demanding "absolute proof" for it. I'm asking you to provide an example of what you earlier claimed to have: an example of contact inhibition altering the way that cells respond to androgens. Are you going to admit, finally, that you cannot provide such an example?

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract[/url]

I also cited a more significant study, where a type of prostate cell "switches its growth response to androgens in-vitro, in the same way as hair follicle cells do in in-vitro testing. This "switch" in androgen response, is clearly linked to changes in gene expression linked to contact inhibition. As every medical scientist knows that cancer cells become non responsive to contact inhibition, "meaning" a change in this genetic pathway.

I lost the link to this study when my computer crashed some time ago, but you know the study "well"!

This body of evidence is what i "CLAIMED" Bryan, and it is all i have "EVER" claimed, despite your usual "spin" when things are not going your way in these debates!!! :roll: :roll:

Now by any recognised scientific standard, this is far more scientific "evidence" to support my interpretation of the in-vitro results, than your random guess work! :wink:

You admit above that you have not even got a damm thing in the scientific evidence to offer a shred of support for "YOUR" claims! :wink: :wink:

People here will also note your avoidence of the points i raised in my last post about the follicle stem cell issue, and how that goes against your personal opinions! :wink:

If you are man enough to debate that, then start another thread about it. But i sense you will just try to sweep this under the carpet as you usually do with facts that dont suit you! 8)

S Foote.

 

[Bryan]

The in-vitro studies show that follicle cell samples known to be future male pattern baldness follicles, are "NOT" in any way growth restricted when dosed with androgens. It is only after "some" effect of androgens in-vivo has "already" growth changed follicle cells, that "then" these cells also show a growth restriction when exposed to androgens in-vitro.

I suggested that the normal growth control of contact inhibition in-vivo, "could" explain this "switch" in the effects of androgens on follicle cells in-vitro.

I don't care about your SUGGESTIONS or what you think COULD explain all this. I want you to answer a direct question that you've been avoiding for a long long time: do you or do you not know of any biological example (a "precedent", as you like to say) in which cells DID IN FACT change the way they respond to androgens because of contact inhibition?

That's a "yes" or a "no", Stephen. Stop stalling.

I suggested this "possibility" because contact inhibition effects the very basic growth gene expression of cells, and this may then allow other external factors (like androgens) to effect these cells differently.

I see that you are now (wisely) using the cautious words "posiibility" and "may" in that paragraph above. That's a step in the right direction. Now answer the DIRECT QUESTION that I posed to you just above.

I cited a precedent for this explaination from a study that linked the same genes effecting both contact inhibition, and the TGF beta-1 pathway. The TGF beta-1 pathway being known to be involved in the male pattern baldness cell in-vitro studies.

The word "precedent" in the above context is meaningless. ANSWER THE DIRECT QUESTION I ASKED YOU.

You admit above that you have not even got a damm thing in the scientific evidence to offer a shred of support for "YOUR" claims! :wink: :wink:

The "genetic switch" hypothesis? No I don't. I never said I did.

People here will also note your avoidence of the points i raised in my last post about the follicle stem cell issue, and how that goes against your personal opinions! :wink:

I didn't avoid it at all. I gave you a simple, honest, and direct answer, which is that I DON'T KNOW how to answer the points you raised. That's because nobody really understands the molecular reasons for why androgens suppress scalp hair follicles; therefore, I can't comment on what you said about stem cells.

Bryan

 

[DammitLetMeIn]

damn this reminds me of me v docj077

 

[S Foote.]

The in-vitro studies show that follicle cell samples known to be future male pattern baldness follicles, are "NOT" in any way growth restricted when dosed with androgens. It is only after "some" effect of androgens in-vivo has "already" growth changed follicle cells, that "then" these cells also show a growth restriction when exposed to androgens in-vitro.

I suggested that the normal growth control of contact inhibition in-vivo, "could" explain this "switch" in the effects of androgens on follicle cells in-vitro.

I don't care about your SUGGESTIONS or what you think COULD explain all this. I want you to answer a direct question that you've been avoiding for a long long time: do you or do you not know of any biological example (a "precedent", as you like to say) in which cells DID IN FACT change the way they respond to androgens because of contact inhibition?

That's a "yes" or a "no", Stephen. Stop stalling.

Oh bulls**t Bryan :roll:

Your tactic of trying to distort the original debates we had about this, is just not going to work!

I have "NEVER" said that there was an already known "DIRECT" precedent in studies for contact inhibition switching the androgen response. All i have ever "CLAIMED" is that there is evidence that this could be a "POSSIBILITY". You know this, so your constant distraction tactics here are just plain lies :wink:

All you have to do to prove your not just lying to people about this, is to reference my prior posts where i made such a claim? Put up or shut up Bryan :wink:

Not only do you have no precedent whatsoever for the genetic clock idea as you admit, what evidence there "IS" actually goes against this notion!

This is why you want to sweep the stem cell qestion under the carpet. 8)

So is any other supporter of the current androgen theory, prepared to try to explain this major flaw in it?

S Foote.

 

[Bryan]

I have "NEVER" said that there was an already known "DIRECT" precedent in studies for contact inhibition switching the androgen response. All i have ever "CLAIMED" is that there is evidence that this could be a "POSSIBILITY".

WOW!! I think we can finally accept that as the long-lost admission on your part! Congratulations, Stephen, and welcome to the world of simple honesty and forthrightness!

...This is why you want to sweep the stem cell qestion under the carpet. 8)

I already told you that I'm not "sweeping it under the carpet". I don't know the answer to that question and I'm not really even sure what the relevance of it is, so I can't comment.

So is any other supporter of the current androgen theory, prepared to try to explain this major flaw in it?

I'm not sure that what you said about stem cells constitutes a "major flaw" in the standard theory. I know you'd LIKE it to, but that's not terribly surprising! :wink:

Bryan

 

[S Foote.]

I have "NEVER" said that there was an already known "DIRECT" precedent in studies for contact inhibition switching the androgen response. All i have ever "CLAIMED" is that there is evidence that this could be a "POSSIBILITY".

WOW!! I think we can finally accept that as the long-lost admission on your part! Congratulations, Stephen, and welcome to the world of simple honesty and forthrightness!

So you cannot prove your accusation in this thread that i have made different claims about my argument in the past?

Well then Bryan, you are now a proven liar :wink:

...This is why you want to sweep the stem cell qestion under the carpet. 8)

I already told you that I'm not "sweeping it under the carpet". I don't know the answer to that question and I'm not really even sure what the relevance of it is, so I can't comment.

[quote="S Foote.":aec42]So is any other supporter of the current androgen theory, prepared to try to explain this major flaw in it?

I'm not sure that what you said about stem cells constitutes a "major flaw" in the standard theory. I know you'd LIKE it to, but that's not terribly surprising! :wink:

Bryan[/quote:aec42]

If you are not sure how the stem cell issue is a major flaw in the current theory you support, you just shouldn't get involved in scientific debates!

I explained to you how this is a major flaw, go back and read the posts!

If you are not prepared to answer those very clear arguments against your own on the record claims, then don't ever call my theory "eccentric" again!

You come on these forums shouting about how safe the old idea's are, and how "wacky" other theories are.

So put up or shut up Bryan! :wink:

S Foote.

 

[Bryan]

So you cannot prove your accusation in this thread that i have made different claims about my argument in the past?

Of course I can. I just don't particularly feel like wasting my time going back and quoting your old posts, only to have you quibble about this word or that, and what you supposedly REALLY meant. I know how you operate, Stephen! I know you like a book! :wink:

 

[S Foote.]

So you cannot prove your accusation in this thread that i have made different claims about my argument in the past?

Of course I can. I just don't particularly feel like wasting my time going back and quoting your old posts, only to have you quibble about this word or that, and what you supposedly REALLY meant. I know how you operate, Stephen! I know you like a book! :wink:

Not good enough Bryan :roll:

If you are going to accuse people of lying, as you have here in respect of my old posts, you had better prove your accusations.

People on these boards get fed up of how you always make these sort of "side stepping" accusations, when you just can't answer the scientific arguments. :wink:

Get digging through the old posts or apologise Bryan. :wink:

Still no comment about the stem cell issue then? How very typical of you! :roll:

S Foote.

 

[michael barry]

Stephen,

With all the time you have spent quippling with Bryan over apologies,


you could have made one long post that describes in detail exactly what happens with your theory and why from the cellular level as it relates to molecular pathways to the dermal papilla level.

It would probably be rather long, and might take you half an hour to type out.


I'd particularily like you to explain how the perifollicular fibrosis always seen in male pattern baldness around the root sheath seems to effect the dermal papilla so much when migrating up and down at the end of catagen and the beginning of anagen phases and also like to see you SHOW CONCLUSIVELY THAT THE SAME STREAMERS OF COLLAGEN APPEAR UNDERNEATH HAIR FOLLICLES AND AROUND THEM IN BOTH EDEMA ON THE LEG AND MALE PATTERN BALDNESS.

If you could do that, maybe more than one person would be attracted to your theory. Just having fibrosis in common in NOT ENOUGH TO CONVINCE people that lymphedema form drainiage backup is what is happening on the scalp much like non-working lymph vessels cause it on the leg. The type of fibrosis has to be perifollicular in the same way (under the hairs, and around them, pushing the vellus hairs to the top of the dermis where they remain doormant foreverafter) to get people to really look at your idea in detail.

Everything would have to be the same also.....................does long term edema have the liver spots and skin discoloration like we see on old men's scalps? Do the body hairs often turn grey and grow more weakly before they are shed for good? etc. It would have to look exactly alike if the same process is going on.

Thats a tall order, but trading insults with Bryan over the issue is an empty procedure for advancing your idea in anyone's mind. These debates look like semantics to me. One side is claiming the other said X, and the other is saying, "I never said X, I said Y". Then "I want an apology because I never said X", etc.

 

[S Foote.]

Stephen,

With all the time you have spent quippling with Bryan over apologies,


you could have made one long post that describes in detail exactly what happens with your theory and why from the cellular level as it relates to molecular pathways to the dermal papilla level.

It would probably be rather long, and might take you half an hour to type out.


I'd particularily like you to explain how the perifollicular fibrosis always seen in male pattern baldness around the root sheath seems to effect the dermal papilla so much when migrating up and down at the end of catagen and the beginning of anagen phases and also like to see you SHOW CONCLUSIVELY THAT THE SAME STREAMERS OF COLLAGEN APPEAR UNDERNEATH HAIR FOLLICLES AND AROUND THEM IN BOTH EDEMA ON THE LEG AND MALE PATTERN BALDNESS.

If you could do that, maybe more than one person would be attracted to your theory. Just having fibrosis in common in NOT ENOUGH TO CONVINCE people that lymphedema form drainiage backup is what is happening on the scalp much like non-working lymph vessels cause it on the leg. The type of fibrosis has to be perifollicular in the same way (under the hairs, and around them, pushing the vellus hairs to the top of the dermis where they remain doormant foreverafter) to get people to really look at your idea in detail.

Everything would have to be the same also.....................does long term edema have the liver spots and skin discoloration like we see on old men's scalps? Do the body hairs often turn grey and grow more weakly before they are shed for good? etc. It would have to look exactly alike if the same process is going on.

Thats a tall order, but trading insults with Bryan over the issue is an empty procedure for advancing your idea in anyone's mind. These debates look like semantics to me. One side is claiming the other said X, and the other is saying, "I never said X, I said Y". Then "I want an apology because I never said X", etc.

Michael.

First off just read the posts, and you will clearly see that instead of answering the scientific points i made, Bryan created a distraction by called me a liar!

If someone had called you a liar on these forums, i am sure you would object to that and ask for proof of the accusation.

So please dont try to say i am not justified in complaining about this.

Secondly, this has not distracted from a very serious point that no one seems willing to comment on?

This is the simple fact that each new hair cycle, stem cells re-create the follicle structure that is "claimed" to then respond in "many" different ways to androgens. This notion demands that different follicles must have "different" stem cells for the "direct" theory to be true!

It's funny that all the self elected science "experts" on these forums when confronted with this major hole in their own beliefs, just refuse to comment and distract from the issue by having a go at my theory!

If these internet forum "scientists" are so certain that i am wrong, and the current theory is correct, why are they all so frightened of responding to the stem cell question?

Would you like to comment on this stem cell issue issue Michael?

S Foote.

 

[docj077]

Secondly, this has not distracted from a very serious point that no one seems willing to comment on?

This is the simple fact that each new hair cycle, stem cells re-create the follicle structure that is "claimed" to then respond in "many" different ways to androgens. This notion demands that different follicles must have "different" stem cells for the "direct" theory to be true!

It's funny that all the self elected science "experts" on these forums when confronted with this major hole in their own beliefs, just refuse to comment and distract from the issue by having a go at my theory!

If these internet forum "scientists" are so certain that i am wrong, and the current theory is correct, why are they all so frightened of responding to the stem cell question?

Would you like to comment on this stem cell issue issue Michael?

S Foote.

I don't know what Michael has to say about the stem cells, but I had no idea that you added that to your theory.

To be honest, re-creation of the hair follicle structure does not demand new stem cells. Even if there are new stem cels, they will be direct descendants of the previous stem cell lineage, so they'll have the same genetic structure and function.

However, I've never read that there is a renewal of stem cells within the follicular unit with each hair cycle. I'd actually learn something new if you posted a link to an article that demonstrated that phenomenon. I'd appreciate it a lot.

Michael does have a point regarding what is required if there is indeed edema in the scalp. The microscopic appearance would have to be the same or at least have similar characteristics to edema in other tissues. Perifollicular fibrosis would be a big help to you, but collagen streamers would help your cause even more.

Lastly, I think you might have missed a few important features of the scalp of male pattern baldness when compared to the scalp of men without male pattern baldness. The same holds true for scalp of men with male pattern baldness compared to the rest of the integument in these same individuals. Areas with hairloss in male pattern baldness have a higher density of androgen receptors and 5-alpha-reductase activity. From there, everyone else can be explained scientifically. There is an increase in IGF-1 in balding scalp and an increase in TGF-beta. IGF-1 will promote keratinocyte proliferation, prevent apoptosis, prevent keratinocyte differentiation/function, and eventually cause hyperkeratinization. TGF-beta will inhibit collagenase, increase collagen deposition, cause keratinocytes near dermal fibroblasts to undergo apoptosis, and eventually cause the perifollicular fibrosis that occurs.

Like Michael said, there is also a development of a collagen streamer and the upward movement of the structure into the nutrient poor and generally poorly perfused epidermis.


Your theory fits Stephen, but I don't think it's the cause. If there is indeed an inhibition of stem cell function due to TGF-beta (or whatever other factor you might find), then it's quite likely that it's a secondary event that adds to the overall pathology that we can see microscopically.

Like I said, post what you've found with regards to the stem cells sometime and post whatever you've found with regards to lymphedema. I already know about the androgen receptors on some epithelial cells and the possibility of muscle hypertrophy causing lymphatic obstruction. I'd be interested to see what else you've found to back up your ideas.


I think we need to stop arguing about who has what theory and whether or not someone is wrong. People need to start posting what they find along with a direction that we can take it and their opinion, so we can put something decent together for people that post here.


Michael contributes, Bryan contributes, and heck, even Dammitletmein has brought up some interesting dietary dilemmas. Do the same. It's not like any of us will make money with theories. We can help people, but the theories can be stolen and patented in the form of drugs and there would be nothing that any of us could do about it.

 

[michael barry]

Alright Stephen,

I'll put my oars in the water and explain why at this time I believe the direct theory of baldness to be true, and why.


First, look at these (some are NEW!) pictures of Revivogen's success,
http://www.revivogen.com/pictures/

I tested Revivogen on my arm way back, and it produced a veritable "hole" in my wrist hair growth. All I had were some vellus-type hairs in the middle of the arm, surrounded by big thick arm hairs where I wasn't applying it. Pine oil did something similar on the back of my right hand at about 3 months, but to a lesser extent. Cedarwood (or pine) oil appears in many old essential oil remedies for baldness.


Look at these fluridil photos: http://www.menspharma.com/results.htm

We know that fluridil is designed to degrade in water, and thus many of us are aftraid that it cant really reach the scalp's follicles because of having to pass through a water layer in the scalp before getting to the papilla with good efficacy. We KNOW that there are no sides with fluridil, but yet it obviously has "some" efficacy. There are problems however, like not being able to shampoo with it but a couple of times a week without really compromising its effectiveness and the inability to use other topicals with it because they will degrade it also. I think its probably helpful, but not as good as topical spironolactone applied twice a day.



Google results for topical spironolactone and hirsuitism: Via Bryan's site,
http://www.geocities.com/bryan50001/spironolactone.html

We see that even with a cream vehicle that makes hirsutism WORSE, spironolactone, the receptor blocker, still can overcome it and reduce hairweight by some 49 percent in one patient.

..................and we know spironolactone is used in male pattern baldness for the perfectly opposite reason. Dr. Proctor puts it in proxiphen, Dr. Lee sells it, genhair.com sells it. They believe it helps scalp hair for the precisely opposite reason that it REDUCES body hair growth, namely it keeps androgens from acting on hair.

Byryan has one very blurry spironolactone regrowth photo, but other than that, nobody seems to have taken a before and after of hair growing better on the head as a resullt of spironolactone usage. However, we can assert that it should because we do have some photos of fluridil and revivogen working up there on the scalp.


WARNING, PERSONAL OPINION AHEAD. I re-read something Bryan wrote about GLA applied to a flank organ, and how much it inhibited its growth. Revivogen's instructs tell you that after a good while, you can start using it every other day or so after stabilization is achieved. In other words, Khadhavi thinks it hangs around a good while. Well, we KNOW that spironolactone's half-life is 85 minutes, and canrenone's half-life is about 10 hours. So spironolactone really is probably only effective for 12-14 hours. In the flank organ study, spironolactone reduced the organs growth by 39.-something-percent, and GLA reduced it by 66 percent. I think that it would be safe to assume that if you used sprio twice a day, every 12 hours, your anti-androgenic activity would be roughly twice what the once a day application would be. That works out to 78-79 percent or so.

In other words, while it lasts, spironolactone is damned effective in my opinion.




Now, all three of the things Ive mentioned are good for baldness. Ive supplied some pics showing that they help. We know fluridil in particular in NO WAY can make it down to the lymphatics and probably isn't as effective as spironolactone twice a day because of it breaking down some before it gets to the follicle proper. Yet the pic says it works. I GUARANTEE you that all three of these things put on your arm or chest or face will reduce hair growth there. That fits right along with the standard theory of baldness. Namely head hair hates androgens and does not need them for growth at all (as people with androgen-insensitivity syndrome conclusively prove) and body hair loves androgens and if denied them will not grow.





Here is further proof that head hair can only stand so much androgen stimuli OR ANY OF IT WILL BALD,

: Skin Pharmacol Physiol. 2006;19(6):311-21. Epub 2006 Aug 23. Links
Effect of 5alpha-dihydrotestosterone and testosterone on apoptosis in human dermal papilla cells.Winiarska A, Mandt N, Kamp H, Hossini A, Seltmann H, Zouboulis CC, Blume-Peytavi U.
Department of Dermatology and Allergy, Charite-Universitatsmedizin Berlin, Berlin, Germany.

Pathogenetic mechanisms in androgenetic alopecia are not yet fully understood; however, it is commonly accepted that androgens like testosterone (T) and 5alpha-dihydrotestosterone (5alpha-DHT) inhibit hair follicle activity with early induction of the catagen. Thus, we investigated the influence of T and 5alpha-DHT on proliferation, cell death and bcl-2/bax expression in cultured dermal papilla cells (DPC) from nonbalding scalp regions of healthy volunteers. T and 5alpha-DHT induced apoptosis in DPC in a dose-dependent and time-related manner; in addition a necrotic effect due to T at 10(-5) M was found. Interestingly, bcl-2 protein expression was decreased in T- and 5alpha-DHT-treated cells, leading to an increase in the bax/bcl-2 ratio. In addition, T and 5alpha-DHT induced proteolytic cleavage of caspase 8 and inhibited proliferation of DPC at 10(-5) M. High concentrations of T and 5alpha-DHT were needed to induce apoptotic effects in DPC. These data suggest that DPC from nonbalding scalp regions do have the capacity to undergo apoptosis, but need a high androgen stimulus. The present study provides an interesting new pathogenetic approach in androgenetic alopecia.

PMID: 16931898 [PubMed - indexed for MEDLINE





All they did in that experiment was make enough testosterone available to head hair EVEN FROM THE WREATH AREA to make it miniaturize. And it did. So we know, as Doctor has pointed out, that T and DHT unlock the same genetic instructs from the DNA of the follicles to make hairs become sensitive to testosterone.




SO now we get to ol' Michael Barry's "theory" of baldness, and why there is more of it now amongst certain populations.

I think human head hair is different from human body hair. I think body hair (with the exception of eyebrow and armpit and pubic hair) has to have some androgens to grow. We know that because women have armpit, pubic, and eyebrow hair that they either dont need androgens or need very very very small amounts of them. Transexuals who take flutamide still have eyebrow hair, and pubic hair, and have to shave their underams. Ive read up on transexuals because they are the perfect people to study as far as baldness is concerned and what happens when androgens are chemically taken away. Ive yet to read of any transexual who is a male living as a woman taking flutamide reporting that further hairloss is a problem. Taking flutamide (and many apparently taking estrogen with it) seems to stop further hairloss in its tracks. Some of these "women" get transplant surgery in order to create a "female" looking hairline because they have lost some hair before they decided to try and be a female.

Ive been able to post three pictures of women who took testosterone who gained body hair, thick beards that are just like men's beards, and went Male Pattern Bald. Ive posted a study that showed women who do this were going bald at a 50 percent clip in various states of Norwood after 13 years, going steadily bald just like men do. However, one of them in particular lost all her hair rather quickly and went NW5 very fast.

I think the DNA in head hair is simply different that what it is in body hair. Period. And if you spray enough DHT topically to Brad Pitt, even he, a guy with his full hairline at 43 years of age, will go bald.

I think there are differences in receptor expression, numbers of receptors, how effective the receptors work based on mutations of the androgen receptor genes just like Doctor describes. Dammitletmein has posted that increased IGF-1 seems to increase receptor expression and had studies to back it up. He also was able to show that increased IGF-1 is associated in studies with higher alpha five reductase activity. If alpha five reductase is more acitve or there are more of em' in the root sheath, of course there will be more androgens binding with the receptor sites.



I think men who go very bald very fast with inflammed scalps will in the future be found to have an upregulated receptor genetic expression, their alpha five reductase activity in their skin and hair ONLY Might be elevated a tad also. But their individual hair's threshold for DHT and T will be found to be lower also than men who dont have baldness. I believe just like the majority of scientists looking into baldness that some people are just born with hair that is extremely sensitive to male hormone for whatever reason, and they will have to protect that hair from male hormone if they want to keep it. Thats the biggie. I simply believe there is a difference in the hairs. I also believe that it will be found that certain men who exhibit alot of inflammation will be found to have very active immune systems that perhaps "over-react" to the hair a bit, thus sending some excessive amounts of inflammatory enzymes at their hairs that other balding men who dont have much inflammation dont have. This is much like some men get sick more than others. Some guys immune systems simply work more actively than other guys.


We know that body hair transplants grow on the scalp, BUT NOT ALL MEN who get them have good growth, or even longer growth. Dr. Poswal has reported that many of the men who he has transplanted body hair to the scalp for find that the hair will only grow about twice as long as it does on the body. It doesn't grow long like head hair in MOST cases. In a few men though, it does. Regular hair transplants ALWAYS result in hairs that grow as long as it grows in the back of the head. Topical anti-androgens will suppress the body hair thats moved to the scalp also, and they are not recommended. Internal finasteride is the strongest anti-androgen Ive seen that worked with a body hair transplant. The hair you still have after getting on finasteride is about what will still grow. Ive seen many posts of men who claimed a little lessening of hair growth on the body with dutasteride. Finas, as we both know, doesn't "get" all the DHT, so the body hairs still have enough stimuli to grow pretty well. I simply stopped getting hairier on my body after getting on finas, but I seen a little lessening of body hair while I was piddling with dutasteride after about one year. Im back on finas, as I dont feel like my cranky-old self on dutasteride.


Why the immune response? Ive seen two very plausible theories. Doctor has stated that overexpression of TGFbeta is associated with autoimmune disorders all over the body, and then there is the old one whereby when negative growth factors being released by the dermal papilla outnumber positive growth factors, you have a mini-organ with more negative growth factors than positive ones, and the immune system naturally sees it as a foreign body and begins to attack. Ive seen a "line" of inflammation in my own head by a microscopic camera that blew up the image very large at a clinic. I use treatments to try and fight it, but a receptor blocker should make it stop also after time. Ive seen one other theory, but I dont think it fits the facts, but it is as the hairs begin to miniaturize, they are too small to use all the sebum that lubricates them and excessive sebum is hanging around the opening in the dermis where the hair emerges from the skin, and it has mircobials and other fugni etc, and they elicit an immuno response after a time. It is interesting to not that the first inflammation seen in baldness is right at the opening of the skin where the follicle emerges according to one long medical article I read, but I'd still be suprised if this was the case.


Thats pretty much what I think based on everything Ive read over the past few years.
I think cloning, anaderm, and a great receptor blocker like RU, will be the answers long term in stopping male pattern baldness and making men's head hair like women's head hair. I htink a hair healthy diet can also help lessen inflammation and excessive androgenic actions in the skin to a smaller extent also. I FEAR things like Curis, and beta catenin pathways becuse they really might be able to cause cancer.