Anyone got any evolutionary theories for hairloss?

[Bryan]

Interesting there is a relation between metabolism of fatty acids (sebum) and hair growth.

Why am I not surprised that you would try to attribute that to SEBUM, specifically? :wink:

Bryan

 

[Armando Jose]

Sebum
The oil on the surface of skin is a complex mixture of sebum, lipids (from the surface skin cells), sweat and environmental material.

Clearly phospholipases are part of the system.

Armando

 

[Bryan]

Oh, I don't doubt that problems with phospholipases are in fact associated with hair loss like that study indicated, but I question your assumption that it's through phospholipases associated specifically with sebum.

 

[Beethoven]

Oh, I don't doubt that problems with phospholipases are in fact associated with hair loss like that study indicated, but I question your assumption that it's through phospholipases associated specifically with sebum.

Hey! this is an Evolution vs God debate, don't distract it to minor things like hair and sebum...

created by who, the Miller / Urey experiments prove that atoms naturally form organic compounds

I support everything Bryan and docj said here, and I always amused by the silly arguments against evolution, they try to attack earth as life supporting planet (already been answered in this debate) or to attack development by mutation (also been answered).
What bubka said is still our weakest link in my opinion, the spontaneous creation of the first living cell from organic compounds is really hard to believe. Once I except mutation it's not to hard to see the very long line between one living cell to a human, but the creation of the first one is still a subject to many theories. I remember reading that scientists are trying to duplicate in labs the process in which a live cell was formed.

 

[Jacobo]

I think as humans we have a common spiritual core. A core that cares for each other, looks out for the preservation of our species, etc. .

I like to think that. But also there is the possibility that caring for each other, etc, are learned behaviour. Humans cooperate more than any other specie (spel?) because, due to longevity, the older generation knows that cooperation and caring is good for the community as a whole, and punish the other alternatives. Something like we are good because we were taught to be, against basic selfish survival instincts. What would happen with children no educated at all, will they care? Moral evolution as well as physical? Some animals care, some abandon their offspring if they don't like them (I guess if they think that they are not fit for survival). I would like to know the answer. Or maybe not.

 

[Jacobo]

Hey! this is an Evolution vs God debate, don't distract it to minor things like hair and sebum...

Yep, let's go on, even if goes to off topic

 

[Armando Jose]

Thank you jacob, cultural evolution form part of the Evolution.
My idea is that problems in sebum flow is the initial and triggering cause of common baldness.


I see in this web (*) that oleic acid “aeratedâ€￾ can produce irritation and hair loss.

BTW, Free fatty acids form part of Revivogen, Is it neccesary close the bottle very well to avoid the peroxide formation?


My idea is that fresh sebum is good and vital for a healthy hair, but if this sebum gets oxidiced could be a great problem. If the sebum flow is altered, problems wit hair.

Armando



(*)
http://www.intox.org/databank/documents ... cie385.htm


A single application of 0.3-2 mL oleic acid (which had been aerated for 1 week to facilitate peroxide formation) was rubbed into the skin for 20 seconds. Marked irritation and hair loss was observed in rabbits, guinea pigs and mice.(3) No conclusions can be made from this study.

(3) Flesch, P. Hair loss from sebum. A.M.A. Archives of Dermatology and Syphilology. Vol. 67, no. 1 (January, 1953). p. 1-9

 

[S Foote.]

I may not be able to explain the "genetic switch" hypothesis to your satisfaction (who COULD?), but then neither can YOU provide an explanation for how contact inhibition could change a cellular response to androgens from stimulation to suppression. I've asked you repeatedly to give me another biological precedent for that occurrence, and you have utterly failed. You haven't given me so much as a single example.

I "HAVE" provided you with the known precident for that "switch" many times, so your continued claim that i have not just shows your a liar :wink:

Sorry, Stephen, but I'm going to show everyone just who the "liar" is here.

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

The word "androgen" doesn't even APPEAR in that abstract, dumbbell! You're giving me NOT what I asked for, but something only very very tangentially related, hoping that everybody would think you've answered my challenge! If the word "androgen" doesn't even appear in that abstract, then how could that be an example of contact inhibition altering the way that cells respond to androgens??

Now just try to allow this precedent to enter your thick skull, and stop lying on these forums claiming i have not referenced this before! :roll:

OH REALLY?? Who's the liar NOW?? :lol:[/quote:e35c7]

You know very well that i have answered "ALL" these points before Bryan, yet still every now and again you try to claim i haven't.

We are talking about relevant "precedents" Bryan, not yet to be proven facts!

Still i have clearly shown that it is perfectly logical for prior contact inhibition to interact with the TGF beta-1 pathway, to change how cells may "THEN" respond to external stimuli including androgens! :roll:

I have also before given you a known precedent of androgens effecting cell growth in an "opposite" manner, "after" the influence of changes in genetic expression linked to changes in contact inhibition!

This was that prostate cancer cell study you "KNOW" we discussed before! :wink:

The change in the way androgens effected the growth of those cells, was directly linked to the transformations induced in those cells by cancer. The very well known basic effect of cancer is to change the expression of genes related to the normal "contact inhibition" of cell growth. This is the very nature of the cancerous transformation, and is why cancer is so dangerous! :roll:

You want more? 8)

There is then the Fuchs study in mice, that proved if you alter some of the factors known to be related to contact inhibition, (Wnt's beta catanin), you can grow much larger follicles. But then you also get tumors!

http://www.hhmi.org/fuchs/index.html


These are the logical precedents in support of my theory, that i have explained to you many times before Bryan. I can't help the fact that you just don't understand the scientific relevance!

You on the other hand have nothing, zero, zilch, to support your claim of "genetic clocks" in follicles, or any other explaination for the androgen driven transformation in follicle response.

In the example i have quoted, the "switch" in androgen response is mediated by a second party (the cancer). According to you, the switch in androgen response is "directly caused" by androgens themselves?

This goes against every known precedent in physiology. Hormones either cause an action on a cell type, or they don't. Hormones are just not known to directly change a cells response "TO" them!

If you have any precedents to the contrary post them? Put up or shut up Bryan! :wink:

[quote="S Foote.":e35c7]If as you claim here, follicles in the male pattern baldness area have evolved to be directly shrunk by androgens for cooling purposes along with beard growth, why aren't "ALL" men capable of growing a beard then bald??

Quit trying to make it so black-and-white. It's just a tendency in that direction. It doesn't mean that if you grow a beard, you're automatically DOOMED to start losing your scalp hair!

So yet another u turn then Bryan :roll:

How is that a "u-turn"?

Earlier in this thread you clearly tried to claim that a direct action of androgens on follicles, was in line with a brain cooling requirement. But you can't answer the evidence to the contrary, so this is now only a "tendency".

What "evidence to the contrary" are you talking about?[/quote:e35c7]

The evidence of the obvious time delay between beard and baldness, that clearly rules out this as a brain cooling evolved strategy. That was clear from my first response Bryan! :roll: :roll: :roll:

S Foote.

 

[S Foote.]

Why are such debates pointless? I fail to understand such reasoning. Minoxidil is indeed a selective arterial dilator. If it does increase NO, then I'd like to truly know what the effect is on lymphatics. Lymphatics at the level of the hair follicle don't have anything put endothelial cells lining them. They can't expand or contract unless the muscles around them allow them to do so, because they don't have a muscular layer in order to change their diameter. NO should have no real effect at this level, because there is nothing to affect.

I'm sorry, but I just can't accept that as the mechanism of action of minoxidil. Especially, with the recent discovery of its effect upon TGF-beta and keratinocyte apoptosis.

Also, if minoxidil is shifting fluid aware from peripheral tissues, then it should also shift nutrients aware from that area decreasing the available nutrients for the follicles. That seems to be a negative result.

My theory involves the local "general" lymphatics that govern the local tissue fluid levels and pressures, not just the lymphatics around the follicles.

Here are some studies you may find interesting.

The first confirms the influence of NO2 in lymphatic vessel "pumping".


http://www.annalssurgicaloncology.org/c ... suppl/275S

Quote:


"Biological properties of lymph microvessels include characteristics of spontaneous contractions of lymph vessels, nitric oxide (NO)-mediated modulation of active lymph pump activity, flow-induced production and release of NO from lymphatic endothelial cells, and localization of NO synthase in cultured lymphatic endothelial cells."

The second is about the link with lympedema, and all the factors we know are found in the male pattern baldness area, inflammation hypoxia etc.


http://www.ncbi.nlm.nih.gov/entrez/quer ... s=16834456

The third is a comfirmation of the PO2 status of the male pattern baldness scalp.


http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=8628793

S Foote.

 

[michael barry]

Stephen


1) Its unlikely DHT effects muscles much at all, because it gets taken apart by an ezyme in the muscles caleld 3 alpha-hydroxysteroid reductase, Look:
______________________________________________________________
quote:
Skeletal muscle is unique from other androgen dependent tissues in the body. It actually contains little or no 5-AR, so little or no DHT is actually formed in the muscle. In addition to this, any DHT that is formed, or that is already present in the blood and travels to the muscle, is quickly deactivated by an enzyme called 3alpha-hydroxysteroid reductase (3a-HSD).

So at least as far as muscle is concerned, testosterone is the primary active androgen. This is not to say that administering exogenous DHT is not without any anabolic effect. It actually does have some anabolic activity in the muscle, albeit significantly weaker than that of an equal amount of testosterone. This is due to its quick breakdown by 3a-HSD into the weak metabolite 5alpha-androstan-3a,17b-diol. If this enzyme were somehow blocked, it is likely that DHT would exhibit very potent anabolic effects on muscle.
_____________________________________________________________



Stephen Foote,

If what you claim is true, that DHT is made in the root sheath by the present 5 alpha reductase type 2 enzyme, and "falls" down all the way to the lymphatics and supercharges them to pump, causing a back up of hairloss on the scalp...................then that edemal should spread to the sideburns and forehead area, and also down the neck. But we see that bald men often have thick sideburns, no edema on their foreheads, and hairy necks. Also this precludes 3 HSD being absent in the skeletal muscle tissue where they lymphatics above the skeletal muscle of the skull are.


2) And Stephen, MOST IMPORTANTLY, why does FLURIDIL, which is designed to degrade in water and could in no way reach down to the lymphatics work as those pictures of users I posted a while back attest to? There were three pics of men who all regrew some hair on it...................and there is no way it effected the lymphatic pumps. This is in addition to the two well-known fluridil photos that show efficacy that we have. Revivogen should work just fine for hairloss as its fatty acids only have to get to the root sheath to stop DHT from being made.



3) By the way........................that RU58841 study I posted was relevant to the fact that the mice had no edema, tissue scaffolds WERE formed, yet the hairs only grew for one cycle and miniaturized in the control mice except for 2 hairs. I thought tissue scaffolds should have protected these hairs according to your theory?




You ought to attempt to test your theory yourself with an ice pack on some forearm or leg hair twice a day for about 20 minutes. If in six months you could show us a picture of an "hairier" patch of skin, some people might give your theory a second look. Just arguing with Bryan will never garner it any attention.

And Stephen....................................If your theory is wrong, just think of how many men tried it for a year or so (cold water, inversion) and had NO success who lost hair because of you.

And think about all the men who have listened to Bryan and tried finasteride, spironolactone, and nizoral and kept their hair. If youre NOT right, youve probably hurt alot of people, not helped them.




Im burned out as all get out by alternative baldness theories like hair cutting (the stupidest one of all), large pillows, lack of blood flow (cured by magnets---there is a website and its awful), shampoo, magnetic fields (I loved that one, hysterical), and "X'" shaped scalp pressuere caused by the downward push of the galea, a thickened galea, excessive hormones during puberty (disporoven by transexuals), stress, etc.


Yours is the only theory that can answer the success of transplanatation, but it obviously has flaws.


4) What I cannot get for the life of me is how you claim there is no biological precedent for testosteron altering how tissue responds over time when you have seen the AWFUL effects of testosterone on skin of women who have used testosterone therapy. Didnt you look at the before picture of the once beautiful "Buck Angel" that I posted? http://ringmybell.tv/BuckBefore.jpg She is an ugly guy with no penis now, all because of testosterone.:::
http://images.google.com/imgres?imgurl= ... n%26sa%3DN

SHe had lovely skin just a few years ago. I posted a pictures of two females on testosterone on Oprhah, one's face aged 15-20 years faster than her sisters, she has a beard, she has lost hair. Does edema extend to her face? It aged the living sh*t out of it and greyed her beard (and thinned her hairline if you look close).

We have a scientific precedent of oodles of just testosterone or DHT being added to wreath hair and it became sensitive to it and slowed cellular division which you casually dismissed for whatever reason. Perhaps there is not a "genetic clock" but a threshold of androgen tolerance before head hair becomes sensitive to it, and THEN It gets effected by androgens and oxides.

5) You yourself were able to show that male pattern baldness-Dermal papilla cells showed oxidative stress much easier than Non-Balding dermal papilla cells, this is further evidence that they have been changed in some fashion.


6) Nizoral should not be able to get deep enough to effect male pattern baldness, but it obviously does and now there are three experiments detailing its efficay. Piroctone olamine shampoo grew hair even slightly better than nizoral did, and it also had an effect on sebum secretions that I didn't even notice until just the other day.............................Im suprised it can get down deep enough in the dermis to effect the lymphatic pumps.


You might go over these links that describe some "mild" perifollicular firbosis with some edemas vs. the constant obvious perifollicular firbosis in male pattern baldness, http://www.google.com/search?sourceid=n ... lymphedema



They look like two differentl animals to me.
We are on the cusp of one company, Anaderm, formulating a topical that can end androgen receptor expression in dermal tissue.............which should keep young men from ever losing their hair in the first place. WE are also on the cusp of ICX successfully cloning hair and being able to give those of us who have lost some full heads of hair back again. When these things happen, science will ignore all further inquiry into male baldness as it will be more or less solved and they will move onto other stuff. You'd better get that edema experient going and have some pics you can send to docs now if you want it reviewed.

 

[Bryan]

You know very well that i have answered "ALL" these points before Bryan, yet still every now and again you try to claim i haven't.

You have NEVER answered that question before. Not one single time. As you long as you keep claiming that you have, I will be here to demonstrate to everyone how you're lying about it.

We are talking about relevant "precedents" Bryan, not yet to be proven facts!

Still i have clearly shown that it is perfectly logical for prior contact inhibition to interact with the TGF beta-1 pathway, to change how cells may "THEN" respond to external stimuli including androgens! :roll:

I don't care how "logical" you think it is. CITE ME AN ACTUAL BIOLOGICAL PRECEDENT IN WHICH IT ACTUALLY HAPPENED. You can't do it, and you know it. I'm not letting you slip out of this, Stephen, no matter how much you huff and puff and try to change the subject to something else.

I have also before given you a known precedent of androgens effecting cell growth in an "opposite" manner, "after" the influence of changes in genetic expression linked to changes in contact inhibition!

This was that prostate cancer cell study you "KNOW" we discussed before! :wink:

The change in the way androgens effected the growth of those cells, was directly linked to the transformations induced in those cells by cancer.

ROTFLMAO!! I don't CARE about any changes induced by CANCER, Stephen!! For the umpteenth time, give me what I asked you for: give me an example where CONTACT INHIBITION (not cancer) caused a change in the cellular response to androgens! :wink:

You want more? 8)

Do I want "more"??? You haven't yet given me even ONE! :wink: :lol:

There is then the Fuchs study in mice, that proved if you alter some of the factors known to be related to contact inhibition, (Wnt's beta catanin), you can grow much larger follicles. But then you also get tumors!

http://www.hhmi.org/fuchs/index.html

You're stalling again, Stephen! I don't care about contact inhibition and beta catenin, I'm asking you to back-up your claim about contact inhibition and the cellular response to androgens.

Don't you get what's happening here?? THIS ISSUE ISN'T GOING AWAY. I'm going to hold your nose to the grindstone until you admit that you can't back-up that rash claim you made long ago. I suggest that you go ahead and admit it right now, and save yourself further embarrassment.

You on the other hand have nothing, zero, zilch, to support your claim of "genetic clocks" in follicles, or any other explaination for the androgen driven transformation in follicle response.

That's right, and neither do YOU have any explanation for the transformation in follicle response. Better go ahead and admit it right now, because I guarantee you that if you keep lying about it, this issue isn't going away! :wink:

What "evidence to the contrary" are you talking about?

The evidence of the obvious time delay between beard and baldness, that clearly rules out this as a brain cooling evolved strategy. That was clear from my first response Bryan! :roll: :roll: :roll:

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

Bryan

 

[Guest]

YEAH GO BRYAN! KICK S FOOTES ***!

 

[mumuka]

You ought to attempt to test your theory yourself with an ice pack on some forearm or leg hair twice a day for about 20 minutes. If in six months you could show us a picture of an "hairier" patch of skin, some people might give your theory a second look. Just arguing with Bryan will never garner it any attention.
...................................................................................

When these things happen, science will ignore all further inquiry into male baldness as it will be more or less solved and they will move onto other stuff. You'd better get that edema experient going and have some pics you can send to docs now if you want it reviewed.

Michael ,you are so right but after reading a lot of Foote's posts i concluded that he will never say a word about how could we use his theory to grow hair... He is always arguing with Bryan but never says `` Bryan i`m right, you could do this or that and see that you will keep/regrow your hair'' ,instead all he does is that scientific yada yada. I wish Bryan would like you Michael (trying new stuff all the time searching for the magic treatment, or at least giving his opinion on herbals like curcumin topical etc .

Anyways ,Michael,thanks for your very intersting and easy to understand(for the normal human being) posts. Always a pleasure to read what you post. Peace.

 

[Armando Jose]

To Mr. Foote;

Have you see this link?
http://dermatology.cdlib.org/122/case_r ... tosti.html

Quote:
The association of lipedematous scalp and androgenetic alopecia in our two patients is, in our opinion, coincidental and resulting from the high frequency of androgenetic alopecia in men. The fact that the lipedematous scalp coincided with the areas affected by androgenetic alopecia is possibly related to the fact that both conditions tend to be localized in the vertex. The casual correlation of lipedematous scalp and androgenetic alopecia in our patients is furthermore suggested by results of treatment with finasteride 1 mg. One year of finasteride treatment in fact induced improvement of androgenetic alopecia in one patient and stabilization in the other, but it did not affect the lipedematous scalp, which remained unchanged in both cases.


Peace

Armando

 

[Bryan]

Stephen has talked about lipedematous scalp before, but I don't think he was aware of that specific study.

How about them apples, Stephen? There was an improvement in the hairloss of that one subject (and a stabilization in the other), without the finasteride affecting the lipedematous scalp condition. How do you explain THAT?? :wink:

Bryan

 

[S Foote.]

Michael.

First let me be clear about something that it seems i have to clear up every now and then.

I came to these forums because of the scientific info and studies people post, and to see if there was anything that would convince me that my theory was flawed. I am "NOT" in the business of convincing people to stop treating their hair loss in any way they want to!

In fact, the emerging evidence of the effective treatments people are reporting tends to support what i am saying. The effectiveness of the systematic 5ARis against the topicals. The increased effect if you also treat the inflammation. The emerging benefits of laser treatments.

I have said before that i really don't care what people want to believe, i am not trying to win "friends" here like some people obviously are! As someone who has suffered long term male pattern baldness, i have a personal interest like everyone else here.

So please don't try to accuse me of tying to mislead people as you have in this quote:

"And Stephen....................................If your theory is wrong, just think of how many men tried it for a year or so (cold water, inversion) and had NO success who lost hair because of you."

Thats just plain unfair Michael!

I have not got the time to answer all your points, and i must say that i have given you my reasoning on most of these before anyway. You dont agree, thats fine i wish you luck.

Just one thing in your argument.

You are just plain wrong about DHT being unable to effect lymphatic pumping! Lymphatic pumping has been "proven" to be mediated by nitric oxide derivitives.

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=15192027

http://www.annalssurgicaloncology.org/c ... suppl/275S

DHT has been proven to be "THE" androgen that effects nitric oxide mediated processes


http://cat.inist.fr/?aModele=afficheN&cpsidt=1682622

http://endo.endojournals.org/cgi/conten ... 495?ck=nck


I am not going to keep on arguing points i have made many times before. If people dont agree, thats fine.

S Foote.

 

[S Foote.]

You know very well that i have answered "ALL" these points before Bryan, yet still every now and again you try to claim i haven't.

You have NEVER answered that question before. Not one single time. As you long as you keep claiming that you have, I will be here to demonstrate to everyone how you're lying about it.

[quote="S Foote.":dc576]We are talking about relevant "precedents" Bryan, not yet to be proven facts!

Still i have clearly shown that it is perfectly logical for prior contact inhibition to interact with the TGF beta-1 pathway, to change how cells may "THEN" respond to external stimuli including androgens! :roll:

I don't care how "logical" you think it is. CITE ME AN ACTUAL BIOLOGICAL PRECEDENT IN WHICH IT ACTUALLY HAPPENED. You can't do it, and you know it. I'm not letting you slip out of this, Stephen, no matter how much you huff and puff and try to change the subject to something else.

I have also before given you a known precedent of androgens effecting cell growth in an "opposite" manner, "after" the influence of changes in genetic expression linked to changes in contact inhibition!

This was that prostate cancer cell study you "KNOW" we discussed before! :wink:

The change in the way androgens effected the growth of those cells, was directly linked to the transformations induced in those cells by cancer.

ROTFLMAO!! I don't CARE about any changes induced by CANCER, Stephen!! For the umpteenth time, give me what I asked you for: give me an example where CONTACT INHIBITION (not cancer) caused a change in the cellular response to androgens! :wink:[/quote:dc576]

It seems you have reached your ranting stage earlier than usual Bryan! 8)

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.

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!

Scientists have established that black holes exist in space, by a body of "indirect" evidence. Why don't you make the same demands on "THEM" that you are on me? Why dont you tell them they are wrong because they can't "prove" it? :roll:

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)

What "evidence to the contrary" are you talking about?

The evidence of the obvious time delay between beard and baldness, that clearly rules out this as a brain cooling evolved strategy. That was clear from my first response Bryan! :roll: :roll: :roll:

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

Bryan

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 quite obviously male pattern baldness happens some time "AFTER" beard growth in the vast majority of humans. So such a "neccesary in evolution" mechanism is just "NOT" is it!

Sometimes Bryan, your inability to think these things through amazes me! :freaked:

Right, you have "demanded" i provide you with answers, 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". Something you usually run to when you are cornered. :roll:

This is a point any "real" scientificaly minded person would want an answer to?

We know that the structure of the hair follicle that is effected in male pattern baldness, dissapears every hair cycle, and is rebuilt from stem cells the next anagen phase.

Stem cells have "NO" predisposition to "ANY" influence, hence the term "stem cells". They have the ability to produce any kind of cells depending upon the external signals.

So there is just no way that follicles can be predisposed to respond differently to androgens, unless "some" external signals are "different"!

You have very clearly claimed Bryan, that androgens are directly causing a "switch" in the way hair follicles respond to them over time. But androgens are "androgens". No different signal here! :wink:

Also to be valid, such a time period of any direct "opposite" androgen "switch" would have to be years, as this is the known period of male pattern baldness developement.

Going along with this idea would mean that every new hair cycle in the male pattern baldness area, would mean "NORMAL" scalp growth for a long period, until androgens had at least enough time (according to your genetic clock) to start to shrink these "new" androgen un-exposed follicles?

But we all know this is clearly wrong, and follicles shrink cycle by cycle in male pattern baldness! 8)

The only alternative then is that some other signaling factor is "priming" follicle cells produced from the stem cells each cycle, to "then" react differently to androgens?

But such a third party influence (such as contact inhibition) is not possible in the "direct" theory you support Bryan! You are trying to tell us that "somehow" follicle stem cells that are not predisposed to anything, manage to produce follicle cells with an "opposite" predisposision to the effects of a hormone! :roll: :roll:

It is clear that some posters in this thread are "fooled" by your use of scientific terminology, and are ignorant of the fact that you talk rubbish wrapped up in fancy words!

So just for once, address a valid scientific question with some "valid" science Bryan! :wink:

S Foote.

 

[S Foote.]

Stephen has talked about lipedematous scalp before, but I don't think he was aware of that specific study.

How about them apples, Stephen? There was an improvement in the hairloss of that one subject (and a stabilization in the other), without the finasteride affecting the lipedematous scalp condition. How do you explain THAT?? :wink:

Bryan

I have seen this study Armando linked, and quoted it before.

As usual Bryan, your desperate need for credibility on hair loss forums leads you to miss the relevant facts :wink:

There are "TWO" known conditions here called lipedematous scalp, and lipedematous alopecia. One effects hair loss, and the other doesn't. The available studies show that the edema can exist on different levels in the tissue (read the histology in the various studies).

The two involve differences in the level of edema in the scalp, "AND" the involvement of damaged ectatic "LYMPHATIC" vessels!! :roll:

http://alopecia.researchtoday.net/archive/1/2/66.htm

Quote:

" The presence of ectatic lymphatic vessels in the two cases with hair loss was particularly emphasized."

Some coincidence yeah :roll:

I really get fed up of trying to explain to scientificaly ignorant people like you Bryan, what a "BODY" of evidence means. :roll:

S Foote.

 

[Jacob]

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.

And no..no need to feel sorry for me at all. I've read the posts here..the responses to me- and non-responses for that matter. Keep at it with your theories

 

[Pondle]

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?