Pillows, Pillows, Pillows..??..

[Armando Jose]

Michael barry wrote:
"I believe much like Bryan does that your head hair has a varrying sensitivity to male hormones generally from front to back."

have you any reference?
But, please, don´t send studies with affected persons, I want this issue with healthy people.

Armando





Stenn and Paus, a very good and free article
Controls of hair follicle cycling.
Physiol Rev. 2001 Jan;81(1):449-494. Review.
PMID: 11152763 [PubMed - indexed for MEDLINE]

Armando

 

[docj077]

Michael barry wrote:
"I believe much like Bryan does that your head hair has a varrying sensitivity to male hormones generally from front to back."

have you any reference?
But, please, don´t send studies with affected persons, I want this issue with healthy people.

Armando

It is assumed and correct as the androgen receptor concentration, and thus the sensitivity, is different from front to back in normal vs. balding scalp.

 

[michael barry]

Doctor,

You'll notice Armando just completely ignores these pictures:
http://www.hairsite.com/hair-loss/forum ... ast_answer

Of a man who had plugs back in the eighties, combed em' forward and kept em short, while the hair behind them fell out as they were geneticially predetermined to do, thus refuting his hypothesis utterly and completely.


Ive provided Armando with plenty of photos that demonstrate this; but he never admits he's wrong, and keeps asserting that sebum back up (despite the lack of success of alpha five type one inhibitors that drammaticaly reduce sebum secretion like MK386) is actually the cause of pattern baldness.




It would be a waste of time to re-link links for Armando that also show that there are more androgen receptors on hair follicles in the front of the scalp than the back, and that balding scalp has 3-3.5 times more DHT. An utter waste of time, because he will simply act as if he didn't see it and go on asserting that he is correct just like the anti-shampoo idiots used to.

 

[S Foote.]

Michael.

Those are interesting pics, but it's a pity that they are not close enough to show any "doughnutting" in those old large grafts.

Was there any mention of this in the text?

I don't wish to become involved in any more pointless debates. We have gone over the same ground many times now, and my personal arguments should be clear to people now.

I think however that this study is relevant to the sebum argument, as it measured sebum excretion in female Androgenetic Alopecia.

http://www.blackwell-synergy.com/doi/ab ... 05.06953.x

Quote:

"Conclusions Our results show that sebum excretion is not elevated in women with female pattern hair loss. This may indicate that different androgen-response pathways operate in controlling hair growth and sebum excretion. The alternative explanation is that nonandrogenic mechanisms are involved in mediating hair loss in some women."

S Foote.

 

[Armando Jose]

Hi guys;

Its is easy to convice me, if anyone post a real study where in Healthy persons (not affected with common hair loss) there is a difference among scalp hairs. Only a link.

Have a nice day.

Armando

 

[michael barry]

Healthy people with full heads of hair dont get their scalps studied Armando.

Scientist only study men who are balding.



Im practiacally certain you'd find increased amounts of receptors on temporal hair follicles in YOUNG men who will later have Androgenetic Alopecia, but it isn't time yet.




You know Armando, the vertex bald spot on men rests on pillows at night.............................why is it the second place to lose hair after the temples on the Norwood scale? WHy do men keep that "band" over the top of their head and the "tuft" for so long in male-pattern-baldness, but lose the temples......................neither rests on a pillow..///////////////
Why do wreaths thin over time?

Why..................................well, its pointless forget it.







Stephen, do you know much about the lateral-slit technique in preparing recipeint sites in hair transplantation? You should, because if Im reading it right, a slit is made at a severe angle THAT DOES NOT REMOVE ANY TISSUE and does not go deep, anywhere near as deep as the dermal papilla is probably going to dive when the hair goes into its first anagen phase-----thus no tissue scaffold would be at anagen-level depth, and even if it was it would be only as thick as a razor blade due to the instrument that made it is that small. Here is a video demonstration by Joetronic on a melon:
http://hairtransplanttv.com/mediagaller ... e+Creation


You can read and see more pictures here:
http://www.plusmedsaglik.com/english/in ... eral_kesit

 

[Armando Jose]

Dear Michael Barry;

You say: "Healthy people with full heads of hair dont get their scalps studied Armando.

Scientist only study men who are balding. "


Ja, ja, ja.

The truth is here. Scientist and pharamaceuticals are only interested in the cure, only in the cure, not in prevention.

¿Why? probably because a good preventive method need fix exactly the trigger of the event, and it is very difficult????.

A lot of scientist, who only study people who are balding, are not real researchers.

Do you know if Merck's scientist have studied this issue? They championished the androgenetic theory and they developed finasteride to treat common baldness,

is true or not the statement " prevention better than cure".


have a nice day

Armando

 

[docj077]

Dear Michael Barry;

You say: "Healthy people with full heads of hair dont get their scalps studied Armando.

Scientist only study men who are balding. "


Ja, ja, ja.

The truth is here. Scientist and pharamaceuticals are only interested in the cure, only in the cure, not in prevention.

¿Why? probably because a good preventive method need fix exactly the trigger of the event, and it is very difficult????.

A lot of scientist, who only study people who are balding, are not real researchers.

Do you know if Merck's scientist have studied this issue? They championished the androgenetic theory and they developed finasteride to treat common baldness,

is true or not the statement " prevention better than cure".


have a nice day

Armando

What are you talking about now, Armando? There is no such thing as a genetic disease containing a gene mutation with a drug or technique that provides a complete cure unless you're talking about certain diseases that require the removal of environmental factors. Finasteride is a preventitive drug and it was developed as such. It prevents the progression and allows for reversal in some patients.

There really is not point in studying Finasteride as a drug for hair loss, because hair loss is not necessarily a life-threatening illness. On the other hand, studying the use of finasteride for benign prostatic hyperplasia is necessary as that disease can cause severe complications.

Scientists simply don't study people to see what makes them healthy. They study those with a particular disease, because that is all they have the time and the money to do.

 

[Armando Jose]

Hi Doctor;

You say that finasteride was developed as a preventive method,

Sincerelly, do you would recommend this medicine to your own son (moreless 20 years old), without any aparent problem with hair, only to prevent future common baldness??

Me, don't.

By the way, thank you for your points. I always read your messages.

Armando

 

[michael barry]

Doctors proscribe proscar and propecia every day to young men


If I were a young'n again, just starting to lose it..............I'd give Revivogen a year to 18 months with a little saw palmetto (and with what Ive recently read a glass of black tea) a shot first, and if I kept fallin', I'd probably switch to finas.


If I even THOUGHT I had hairloss genes, I'd probably pick a topical out BEFORE I saw any recession.

 

[powersam]

Michael barry wrote:
"I believe much like Bryan does that your head hair has a varrying sensitivity to male hormones generally from front to back."

have you any reference?
But, please, don´t send studies with affected persons, I want this issue with healthy people.

Armando

i think this is a good point though. people should be looking at the androgen receptors on a male pattern baldness unaffected person. the information would have to be useful, if only for elimination purposes.

 

[S Foote.]

Stephen, do you know much about the lateral-slit technique in preparing recipeint sites in hair transplantation? You should, because if Im reading it right, a slit is made at a severe angle THAT DOES NOT REMOVE ANY TISSUE and does not go deep, anywhere near as deep as the dermal papilla is probably going to dive when the hair goes into its first anagen phase-----thus no tissue scaffold would be at anagen-level depth, and even if it was it would be only as thick as a razor blade due to the instrument that made it is that small. Here is a video demonstration by Joetronic on a melon:
http://hairtransplanttv.com/mediagaller ... e+Creation


You can read and see more pictures here:
http://www.plusmedsaglik.com/english/in ... eral_kesit

I think you are reading that wrong Michael.

From your second link:

http://www.plusmedsaglik.com/english/in ... eral_kesit

Quote:


"The depth of the incisions are aligned with the length of the grafts’ roots, therefore there is no risk of opening the incisions too deeply."

Look at the pictures in that article showing the grafts to be transplanted. These are follicles that are already in "full" anagen, that are producing terminal scalp hair. The surgeons dont go for follicles that are in the miniaturised resting state, they want "proven" terminal hair producers.

It doesn't matter what the recipient site preperation is, what matters is the scar "scaffold" that forms around these transplanted "large anagen" follicles in my opinion. This then preserves this space during future normal shrinkage in the resting phase, and future anagen re-enlargements.

S Foote.

 

[S Foote.]

Michael barry wrote:
"I believe much like Bryan does that your head hair has a varrying sensitivity to male hormones generally from front to back."

have you any reference?
But, please, don´t send studies with affected persons, I want this issue with healthy people.

Armando

i think this is a good point though. people should be looking at the androgen receptors on a male pattern baldness unaffected person. the information would have to be useful, if only for elimination purposes.

It is a very important point, because the current theory depends on some kind of follicle differences before androgens come into the equation.

To date the actual hard evidence says there is no such difference.

In the macaque studies, follicle cells known to be "future" male pattern baldness follicles, are "NOT" turned into male pattern baldness cells through direct "soaking" in androgens.

In order to try and explain this, mechanisms that go against all we know about hormone effects on cells have to be "invented".

S Foote.

 

[michael barry]

Stephen,

First read this short piece on "junk" DNA:


Article:
So-called junk DNA might regulate the activity of the genes they surround

Anjana Ahuja:


Itstrickytounderstandthissentenceisntit? If you pluck the punctuation out of a sentence, it becomes much harder to read. Biologists now suspect that some stretches of DNA in the human genome that were previously thought to be useless might serve as punctuation between genes.

Your genome – the genetic material that makes you, you – is made up of genes and so-called junk DNA. Genes are the instruction manuals that your body uses to make proteins. But genes constitute only 4 per cent of the genome. The rest – the junk DNA – appears to serve no useful purpose. In the jargon, it doesn’t code for anything. This is puzzling, because scientists thought that evolution would fine-tune the human genome to preserve the essential bits and discard the rest.

Now an international team of scientists has discovered that junk DNA might regulate the activity of the genes they surround. While genes do the hard work of making proteins, the junk DNA could be responsible for starting and stopping protein production. “Some of the junk DNA might be considered punctuation marks – commas and full stops that help make sense of the coding portion of the genome,†says Dr Victoria Lunyak, of the University of California, San Diego, School of Medicine, one of the authors of a paper published in Science. Another analogy is to think of genes as building labourers, and the surrounding pieces of junk DNA as foremen.



This could explain why gene therapy has had limited success: scientists have tended to transfer genes without the junk DNA. And we know what happens when a foreman doesn’t turn up on a building site: you get the tea-drinking and wolf-whistling, but not much building.


==========================

When you discount that there could be a "DNA clock" or that such a notion is ridiculous, keep in mind that genetics are apparently far more complex than we might have previously thought. For instance what tells melanocyte cells to stop producing enough melanin to stain a hair follcile, thus some folks with full heads of hair go grey.........................while some balding men dont grey, but instead just lose the living hell out of their hair. One gene surely isn't responsible for all this, or is it.................is so much junk DNA there giving instructions that one gene can do more than ever thought possible. The most pathetically bald guy I know at our company is in his mid-thirties with jet black hair. He is a NW7. His head gleams literally. You can comb your hair in the shiny reflection off his pate. But no immune response or no inflammation is visible to me. He is white as a sheet with jet black hair. No grey at all. I work with another man who is mostly salt with a little pepper up there. Super thick head of hair with a teenage hairline. No loss. Mostly grey in his fifties.





Stephen you also didnt comment on Cole's observation. You see Cole used to get bitched at in online forums for always using a full 1.0 needle (Woods uses needles, I think Cole has moved on to sometimes using the razor-like "slits"). Cole uses nape of the neck hairs for hairlines because those hairs are so much smaller in diameter, thus they mimick hairline hairs much more realistically rather than big thick donor area follicles. But the hairs stay smallish, and DO NOT get thicker in circumference despite the same sized "hole" being made as a tissue scaffold (when done with a needle).

The whole point of my posting about the lateral slit technique wasn't all about the depth either, but the size. THESE ARE RAZOR THIN INSTRUMENTS Stephen. They don't "remove" flesh, just cut or "peel" skin up, so the follicle can be jammed in the "slit", and the flesh pushed back down over them. There really shouldn't be much of a scaffold at all.........but even if there is.................all the scaffolds would be the same size. Why then is there still a difference between the size of the hairs based on what part of the donor area they were harvested from? Hairs from the sides typically are not as large as the area in the very back , but are also larger than nape hairs. Surgeons use the side and nape hair for the hairline and side-of the head traspnantations to rebuild the sides in people whose sides have receeded all the way back to their ears.



There really is no other trouble spot I haven't been over in regards to your theory that I can think of other than that one, but I will say this......................surely there is an instrument that can be inserted in the skin that would measure the pressure around it. If you could do this in someone's donor area and then the vertex (if signs of miniaturization were starting to take place) and document higher pressure in that would-be classic bald spot, you'd be doing alot to assert you theory in others eyes. Basically Stephen you are asking people to take you word for their being higher fluid pressure in the classic male pattern baldness areas of men's heads although no one ever has documented this. The burden of proof will be on you. Otherwise I dont see your idea ever picking up traction even if it was true.

 

[S Foote.]

Stephen,

First read this short piece on "junk" DNA:


Article:
So-called junk DNA might regulate the activity of the genes they surround

Anjana Ahuja:


Itstrickytounderstandthissentenceisntit? If you pluck the punctuation out of a sentence, it becomes much harder to read. Biologists now suspect that some stretches of DNA in the human genome that were previously thought to be useless might serve as punctuation between genes.

Your genome – the genetic material that makes you, you – is made up of genes and so-called junk DNA. Genes are the instruction manuals that your body uses to make proteins. But genes constitute only 4 per cent of the genome. The rest – the junk DNA – appears to serve no useful purpose. In the jargon, it doesn’t code for anything. This is puzzling, because scientists thought that evolution would fine-tune the human genome to preserve the essential bits and discard the rest.

Now an international team of scientists has discovered that junk DNA might regulate the activity of the genes they surround. While genes do the hard work of making proteins, the junk DNA could be responsible for starting and stopping protein production. “Some of the junk DNA might be considered punctuation marks – commas and full stops that help make sense of the coding portion of the genome,†says Dr Victoria Lunyak, of the University of California, San Diego, School of Medicine, one of the authors of a paper published in Science. Another analogy is to think of genes as building labourers, and the surrounding pieces of junk DNA as foremen.



This could explain why gene therapy has had limited success: scientists have tended to transfer genes without the junk DNA. And we know what happens when a foreman doesn’t turn up on a building site: you get the tea-drinking and wolf-whistling, but not much building.


==========================

When you discount that there could be a "DNA clock" or that such a notion is ridiculous, keep in mind that genetics are apparently far more complex than we might have previously thought. For instance what tells melanocyte cells to stop producing enough melanin to stain a hair follcile, thus some folks with full heads of hair go grey.........................while some balding men dont grey, but instead just lose the living hell out of their hair. One gene surely isn't responsible for all this, or is it.................is so much junk DNA there giving instructions that one gene can do more than ever thought possible. The most pathetically bald guy I know at our company is in his mid-thirties with jet black hair. He is a NW7. His head gleams literally. You can comb your hair in the shiny reflection off his pate. But no immune response or no inflammation is visible to me. He is white as a sheet with jet black hair. No grey at all. I work with another man who is mostly salt with a little pepper up there. Super thick head of hair with a teenage hairline. No loss. Mostly grey in his fifties.

You just dont get the point Michael!

There is no evidence "whatsoever" for any pre-existing genetic differences in the various hair follicles, this notion is pure assumption.

The in-vitro tests that you largely base your assumptions on, clearly show that androgens are not directly converting alledged male pattern baldness disposed follicles "into" male pattern baldness follicles!

This is a "DIRECT" test of your assumptions, and it fails the theory you support!

Where are these pre-existing extra or different androgen receptors in these known future male pattern baldness follicles, that you claim is the cause of male pattern baldness?

This argument is "tooth fairy" science Michael!

You put an extracted tooth under your pillow, and in the morning there is no tooth but money instead. This "PROVES" that the tooth fairy exists!!!!

If a particular theory relies upon an impossible process, the theory is wrong!

You have to show step by step processes that make scientific sense of your argument?

The whole point of my posting about the lateral slit technique wasn't all about the depth either, but the size. THESE ARE RAZOR THIN INSTRUMENTS Stephen. They don't "remove" flesh, just cut or "peel" skin up, so the follicle can be jammed in the "slit", and the flesh pushed back down over them. There really shouldn't be much of a scaffold at all.........but even if there is.................all the scaffolds would be the same size. Why then is there still a difference between the size of the hairs based on what part of the donor area they were harvested from?

Because it is the size of the inserted transplant that determines the size of the fibrose shell that forms around it. The "mould" is made by the stucture placed in the tissue. Not the size of any hole made in the tissue.

There really is no other trouble spot I haven't been over in regards to your theory that I can think of other than that one, but I will say this......................surely there is an instrument that can be inserted in the skin that would measure the pressure around it. If you could do this in someone's donor area and then the vertex (if signs of miniaturization were starting to take place) and document higher pressure in that would-be classic bald spot, you'd be doing alot to assert you theory in others eyes. Basically Stephen you are asking people to take you word for their being higher fluid pressure in the classic male pattern baldness areas of men's heads although no one ever has documented this. The burden of proof will be on you. Otherwise I dont see your idea ever picking up traction even if it was true.

Now you are resorting to "Bryan" type double standards Michael!

You claim i have no direct evidence for higher tissue fluid pressures in the male pattern baldness area, so i shouldn't be taken seriously. The "indirect" evidence for my claim however is based in known and recognised physiology, as i have referenced many times.


The theory you support claims a pre-existing difference in scalp follicles that causes male pattern baldness when these follicle cells are directly exposed to androgens.

The in-vitro tests "actually" give us hard evidence that this is wrong. It requires some kind of "tooth fairy" mechanism to be explained, but you still expect scientificaly minded people to take "YOUR" opinion seriously?

I have said i dont wish to get involved in any more pointless unscientific debates on internet forums Michael.

If you insist on pushing this point, just stick to one simple question.

How do you explain the proven fact that androgens are "NOT" changing known future male pattern baldness follicles you claim are "directly" effected by androgens, "INTO" male pattern baldness follicles in-vitro?

Please try to explain this using the very well known hormone/cell interaction processes, and not some wild assumption!

S Foote.

 

[michael barry]

Well, lemme see..............


You just dont get the point Michael!

There is no evidence "whatsoever" for any pre-existing genetic differences in the various hair follicles, this notion is pure assumption.===============Pre-existing differences in genetic hair follicles you ask? Well eyebrow hairs show no change when androgens are added in experiments, but beard hairs grow BETTER when androgens are added to them. Scalp hairs that are male pattern baldness hairs grow more weakly when androgens are added to them, but non-male pattern baldness hairs are not affected. Underarm hairs are also not effected by androgens. We have several different types of hairs Stephen. Nose hair, ear hair, beard hair, eye-lash hair, eyebrow hair, head hiar outside the hippocratic wreath, head hair inside the hippocratic wreath, arm hair, leg hair, finger hair, toe hair.................all these are a little different. AND WHEN THEY ARE TRANSPLANTED TO DIFFERENT AREAS OF THE BODY THEY MERELY WILL GROW EITHER SHORTER OR LONGER, BUT THEY WILL NOT CHANGE THEIR PRE-EXISTING DIAMETER OR CURL OR STRAIGHTNESS. Thats pretty different wouldn't you say?

The in-vitro tests that you largely base your assumptions on, clearly show that androgens are not directly converting alledged male pattern baldness disposed follicles "into" male pattern baldness follicles! +++++++++++++++++++++++++++++++++++++++++Yup, Stephen.............scientist have never been able to pluck hairs and cultivate them for the nine or so days that hairs can be cultivate them and catch them at the perfect point in time that they are going to become sensitive to testosterone. You have this rock on a cliff's edge to hang onto, no matter what happens. And even if it did happen, you'd probably complain about the methodology of the professional scientists who were conducting the tests.

This is a "DIRECT" test of your assumptions, and it fails the theory you support! ++++++++++++see above

Where are these pre-existing extra or different androgen receptors in these known future male pattern baldness follicles, that you claim is the cause of male pattern baldness? +++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++To my knowledge doctors have noticed that there are extra androgen receptors in balding scalp hair follicles, but as Ive told Armando, doctors seldom run tests on people with full heads of hair. Im pretty certain temporal hair of men who will later lose that hair probably does contain higher numbers of androgen receptors, but the hairs haven't flipped their response to androgens yet. However Stephen, as the "Junk DNA" article above might lead you to consider, its very possible that the DNA instructs an upregulation of androgen receptors in male pattern baldness follicles "when the time comes". As the article made pretty clear, DNA might be even more complicated that we know as of yet.

This argument is "tooth fairy" science Michael! +++++++++++++++++++++++++++++++++++++++++++++++++++++++If its tooth fairy science Stephen, its the science that Ralf Paus, Kurt Stenn, Ken Washenik, Hideo Uno, Paul Kemp, Jerry Cooley, Colin Jahoda, the rest of the people at Aderans, Phoenixbio, INtercytex, Shishedo, the National Institutes of Health, the American Medical Association, the European Hair Research Society, Tricologists and Dermatologists everywhere think. I guess they all believe in tooth fairy science then.

You put an extracted tooth under your pillow, and in the morning there is no tooth but money instead. This "PROVES" that the tooth fairy exists!!!!

If a particular theory relies upon an impossible process, the theory is wrong! +++++++++++++++++++++++++++++++++++++++++++++++++++++You believe its "impossible" for hairs to have a negative response to male hormones through uptaking them in androgen recepotors and negative growth factors being released due to mitochondrial DNA instructions over time makes it so? We know body hair has a "positive" response to androgens as does beard hair, and if you take androgen away and soak the system with estrogens, the hair grows weakly. Thats a direct response.

You have to show step by step processes that make scientific sense of your argument?




Stephen wrote:
"Because it is the size of the inserted transplant that determines the size of the fibrose shell that forms around it. The "mould" is made by the stucture placed in the tissue. Not the size of any hole made in the tissue"


If the above statement is true, then according to your theory Stephen follicular units that have any resting hairs in them should never be able to grow or expand because they were small when implanted. We know thats not the case.





Lets go on:
Now you are resorting to "Bryan" type double standards Michael!

You claim i have no direct evidence for higher tissue fluid pressures in the male pattern baldness area, so i shouldn't be taken seriously. The "indirect" evidence for my claim however is based in known and recognised physiology, as i have referenced many times. +++++++++++++++++++++++++++++++++++++++++++++++++++++++++++Im not saying you shouldn't be taken seriously, however I did say the burden of proof is on you to forward your theory. I tried to test if for a couple of months with an icepack on my leg and got.............less hair there, and gave up. Arguing your theory on the internet has yielded no fruit since 2001 or so. However a tissue pressure test in balding vs. non-balding scalp should be something a doctor could perform on you or someone else. This would be a chance for you to prove your idea had merit.


The theory you support claims a pre-existing difference in scalp follicles that causes male pattern baldness when these follicle cells are directly exposed to androgens. ......................................++++++++++++++++++++++++++++++++++++++not exactly, the theory I support is that follicles exposed to androgens over time begin to grow more weakly in response to them after years and years of more androgenic stimulation just as body hair grows stronger and stronger after years of androgenic stimulation. Alpha five reductaste is known to increase after many years as a man gets older in its activity, and DHT levels rise as Testsoterone levels fall. Its perfectly normal. The tele-evangelists whose ex-wife is dying of cancer was on the TV screen in a news segment the other day. His name is Jim Baker. He had pretty decent hair in the eighties in his early forties. He's chrome-dome bald in his sixities. Lost all that hair, and he had decent hair. DHT increased over time, and the androgenic stimulation for his hair apparently became too much.

The in-vitro tests "actually" give us hard evidence that this is wrong. It requires some kind of "tooth fairy" mechanism to be explained, but you still expect scientificaly minded people to take "YOUR" opinion seriously? ========================================================================================================what about that RU58841 study that put human hair follicles on mouse-backs and found that only 2% of untreated hairs had a second growth phase, vs. 28% of hairs that were treated with RU58841 (not enough of it in my opinion)? Tissue scaffolds were formed as you described.........................they should have all grew then right? This is a contested point between us. This in vitro study would disprove your theory in most peoples estimation and would be far more conclusive than the 22 week study that Oreintriech did with just a few follicles. I dont care about the pre-pubertal macaque studies Stephen, pre-pubsecents dont go bald..........................adult males do. Thats what we are interested in.

I have said i dont wish to get involved in any more pointless unscientific debates on internet forums Michael. +++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++Does a debate magically become unscientific when someone doesn't believe what you want them to believe? Thats like an atheist (like your friend Bryan) being un-religious when he tells a prosetylizing missionary that he doesn't beleive in Jesus based on his disagreement with the historical evidence. This does not mean that Bryan beleives in the tooth fairy, or may not hold any religious beleifs (Hell, Bryan might believe that butterflies are divine for all I know).

If you insist on pushing this point, just stick to one simple question.

How do you explain the proven fact that androgens are "NOT" changing known future male pattern baldness follicles you claim are "directly" effected by androgens, "INTO" male pattern baldness follicles in-vitro? ++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++==They have never been able to cull a hair follicle in the nine day or so period that they can keep it alive and be able to soak it in androgens and make it have a measurable bad response. It would be interesting to attempt to do this with hairs that are just behind a receeding hairline, but still of normal size. However, only being able to keep hairs alive out of the body for such a short time is probably never going to see such an experiment take place. But we KNOW THAT male pattern baldness follicles DO respond negatively to androgens..................and grow just as well as non-male pattern baldness follicles if the androgens are taken away. So whats the fuss?

Please try to explain this using the very well known hormone/cell interaction processes, and not some wild assumption!




You are the one claiming that increased tissue fluid pressure is what is causing a "flip" in the direct response to androgens. I DEFY you to get with a lymphedema specialist and attempt to measure tissue fluid pressure levels in your own balding scalp vs. your donor area. I bet they would be about the same. If you could show me that they weren't, I bet the same Doctor would be very interested in testing two or three other people to see if he got the same inconsistency. If he DID, he'd no doubt try and publish it somewhere...............................then Stephen Foote would actually be in business as far as his assertions go. Until then, you merely are "that guy who believes lymphedema is happening on balding scalps" who pretty much gets ignored on most forums. Youve been at it since 2001 that I know of Stephen, and still seem no closer to having any proof.

To dismantle the current theory is going to take more that your obvservations on hypoxia in large 4 mm grafts and a macaque study, and one 22 week mouse study.

 

[Armando Jose]

My question was regarding studies with healthy persons, not affected by common hair loss. I want to kinow how is our biology in healthy persons. And the answer were:

Stephen Foote wrote:
“It is a very important point, because the current theory depends on some kind of follicle differences before androgens come into the equation.

To date the actual hard evidence says there is no such difference.â€￾

PowerSam wrote:
“I think this is a good point though. people should be looking at the androgen receptors on a male pattern baldness unaffected person. the information would have to be useful, if only for elimination purposes.â€￾

Thank you guys. We are in the right road. This work can be realiced by pharm industry with no problem.



Michael Barry wrote to my question if he would recommend finasteride as a preventive method:
“ If I were a young'n again, just starting to lose it..............I'd give Revivogen a year to 18 months with a little saw palmetto (and with what Ive recently read a glass of black tea) a shot first, and if I kept fallin', I'd probably switch to finas.


If I even THOUGHT I had hairloss genes, I'd probably pick a topical out BEFORE I saw any recession.â€￾

Thank you for your honest answer. My bet is jojoba oil or better Oropelum lotion (jojoba plus essential oils and aloe, spirulina and saw palmeto among others)

Armando

 

[S Foote.]

Well, lemme see..............


You just dont get the point Michael!

There is no evidence "whatsoever" for any pre-existing genetic differences in the various hair follicles, this notion is pure assumption.===============Pre-existing differences in genetic hair follicles you ask? Well eyebrow hairs show no change when androgens are added in experiments, but beard hairs grow BETTER when androgens are added to them. Scalp hairs that are male pattern baldness hairs grow more weakly when androgens are added to them, but non-male pattern baldness hairs are not affected. Underarm hairs are also not effected by androgens. We have several different types of hairs Stephen. Nose hair, ear hair, beard hair, eye-lash hair, eyebrow hair, head hiar outside the hippocratic wreath, head hair inside the hippocratic wreath, arm hair, leg hair, finger hair, toe hair.................all these are a little different. AND WHEN THEY ARE TRANSPLANTED TO DIFFERENT AREAS OF THE BODY THEY MERELY WILL GROW EITHER SHORTER OR LONGER, BUT THEY WILL NOT CHANGE THEIR PRE-EXISTING DIAMETER OR CURL OR STRAIGHTNESS. Thats pretty different wouldn't you say?

Well no Michael, you still miss the relevant points here!

Androgens do "NOT" cause any "CHANGE" in-vitro, to the pre-existing growth characteristics of "ANY" kind of hair follicle!

You claimed in this thread that androgens are directly "CHANGING" healthy follicles into male pattern baldness follicles, because these follicles have a pre-existing "DIFFERENCE" in androgen receptors.

But the in-vitro tests prove that "KNOWN" future male pattern baldness follicles, do not react by showing any growth restriction when dosed with androgens!

The old excuse that in time this will happen, is the impossible mechanism i refer to.

There is no precedent at all for any such time delay in the recognised actions of any hormone on any cell type! Cells either respond to a hormone or they don't!

There is no known mechanism that requires a period of exposure to a hormone, "before" there is a direct response "TO" that hormone.

In fact your own claim that the in-vitro tests prove your own argument, relies upon an "INSTANT" reaction between androgens and the alledged different androgen receptors.

This is what i mean by double standards.

Just lets concentrate on one issue at a time here, and explain to me why future male pattern baldness follicles with "alledged" "mutant" androgen receptors (according to you), do not respond as your theory says they will??

I am away untill Sunday, so take the time to think about this question Michael?

S Foote.

 

[docj077]

Mr. Michael Barry,

Arguing with Mr. Foote is pointless. Current research clearly demonstrates what you believe to be true. Not only does current research demonstrate an increase in androgen receptor in balding scalp, but it also demonstrates differences at the receptor level and at the gene level when you compare balding scalp to non-balding scalp follicles and scalp follicles to beard follicles.

It is ridiculous to think that there isn't an intrinsic difference in follicles from different regions of the body. Especially, once a person reaches puberty. Scalp hair, body hair, and beard hair all obviously grow at different rates, so there is an obvious intrinsic difference at both the gene level and at the level of their response to androgens.

The following paper clearly demonstrates that androgens obviously have differing effects depending upon which follicle they influence.

J Invest Dermatol. 2006 Dec;126(12):2583-95. Epub 2006 Jun 29. Links
Differences in expression of specific biomarkers distinguish human beard from scalp dermal papilla cells.Rutberg SE, Kolpak ML, Gourley JA, Tan G, Henry JP, Shander D.
Gillette/P&G Technical Center, Needham, Massachusetts 02492, USA. susan_rutberg@gillette.com

Androgen exposure stimulates the growth of beard hair follicles. The follicle dermal papilla appears to be the site of androgen action; however, the molecular mechanisms that regulate this process are not well understood. In an attempt to identify genes that contribute to the androgen-responsive phenotype, we compared gene expression patterns in unstimulated and androgen-treated cultured human dermal papilla cells isolated from beard (androgen-sensitive) and occipital scalp (androgen-insensitive) hair follicles. Through this analysis, we identified three genes that are expressed at significantly higher levels in beard dermal papilla cells. One of these genes, sfrp-2 has been identified as a dermal papilla signature gene in mouse pelage follicles. Two of these genes, mn1 and atp1beta1, have not been studied in the hair follicle. A fourth, fibulin-1d, was slightly upregulated in beard dermal papilla cells. The differences in the expression of these genes in cultured beard and scalp dermal papilla cells reflected similar differences in microdissected dermal papilla isolated from intact beard and scalp follicles. Our findings introduce potentially novel signaling pathways in dermal papilla cells. In addition, this study supports that cultured dermal papilla cells provide a cell-based model system that is reflective of the biology of in vivo hair follicle cells.


The next study clearly demonstrates a difference in androgen receptor co-activator activity in balding vs. normal scalp hair follicles.


J Invest Dermatol. 2007 May 17; [Epub ahead of print] Links
Androgen Receptor Co-Activator Hic-5/ARA55 as a Molecular Regulator of Androgen Sensitivity in Dermal Papilla Cells of Human Hair Follicles.
Inui S, Fukuzato Y, Nakajima T, Kurata S, Itami S.
1Department of Regenerative Dermatology, Graduate School of Medicine, Osaka University, Osaka, Japan.
Androgen site-specifically affects human hair growth after puberty through androgen receptors in the dermal papilla, which transactivate target genes acting in conjunction with co-activators. To examine the regulation of androgen sensitivity in hair follicles, we focused on androgen receptor co-activator Hic-5/ARA55. Its interaction with transfected androgen receptor in beard dermal papilla cells was confirmed with mammalian two-hybrid assays. The semiquantitative reverse transcriptase-polymerase chain reaction showed that Hic-5/ARA55 mRNA expression was high in dermal papilla cells from the beard and bald frontal scalp but low in cells from the occipital scalp. To determine whether Hic-5/ARA55 mRNA level correlates with its endogenous activity, we studied the effect of dominant negative Hic-5/ARA55 on transfected androgen receptor transactivation induced by R1881 using mouse mammary tumor virus-luciferase assays. We found that it suppressed the transactivation by 64.5 and 71.4% in dermal papilla cells from the beard and bald frontal scalp, respectively, whereas it showed no significant effect in cells from the occipital scalp. Our findings suggest that Hic-5/ARA55 is a molecular regulator for androgen sensitivity in human hair follicles.Journal of Investigative Dermatology advance online publication, 17 May 2007; doi:10.1038/sj.jid.5700883


These studies don't even begin to describe the plethora of genes and proteins that are influenced by androgens.

This is a conversation that isn't even worth having right now. There is obviously a regulatory difference between scalp hair and hair from other regions of the body both before and after puberty and the regulation is directly influenced by androgen receptor mutation/concentration in normal/balding scalp.


By the way, Michael. The response to androgens is dose dependent and time dependent. I think that I've already posted this study before.

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, Charité-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.




Lastly, I think an important study to note is the following as it clearly demonstrates that there is a clear difference with regards to the external hormonal environment when it comes to particular regions of the scalp. There are only two ways that there can be such a clear difference. There is either more five alpha reductase in areas of the scalp that are more sensitive to balding or finasteride produces more SHBG in areas where it has its greatest effects. Personally, I believe both to be true.

Br J Dermatol. 2006 Apr;154(4):730-4. Links
Evaluation of androgens in the scalp hair and plasma of patients with male-pattern baldness before and after finasteride administration.Ryu HK, Kim KM, Yoo EA, Sim WY, Chung BC.
Bioanalysis and Biotransformation Research Centre, Korea Institute of Science and Technology, PO Box 131, Cheongryang, Seoul, 130-605, Korea.

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

 

[michael barry]

Doctor,

You have been a huge boost for this board, as Im sure you realize.



This study that you have found:

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



....................says a ton about baldness that Ive privately wondered about. So there IS apparently more DHT produced by balding area hair follicles. They said follicles, not scalp. Occipital scalp follicles apparently just have less active alpha five reductase enzymes (and less receptors). Those studies are some terrific new information that show gene-level differences, just as you have asserted.





Stephen wrote:

"Well no Michael, you still miss the relevant points here!

Androgens do "NOT" cause any "CHANGE" in-vitro, to the pre-existing growth characteristics of "ANY" kind of hair follicle!

You claimed in this thread that androgens are directly "CHANGING" healthy follicles into male pattern baldness follicles, because these follicles have a pre-existing "DIFFERENCE" in androgen receptors.

But the in-vitro tests prove that "KNOWN" future male pattern baldness follicles, do not react by showing any growth restriction when dosed with androgens! "


+++++++Stephen, I'm going to state this one more time-----------and if you dont acknowledge it, and act as if I didn't answer it, just forget it.

IN VITRO WHOLE HAIR FOLLICLES CAN ONLY LIVE FOR LESS THAN TWO WEEKS. Reaserchers will probably NEVER be able to cull them right before they become negatively sensitive to androgens. Alpecin's researchers at the University of Jena could only keep follicles alive ex vivo for something like 10 days or so (I'd have to check). If you are waiting on such an experiment to take place, you might be waiting for the rest of your life. It will probably not happen before a real countermeasure to baldness anyway.



Stephen also wrote:

"There is no precedent at all for any such time delay in the recognised actions of any hormone on any cell type! Cells either respond to a hormone or they don't!

There is no known mechanism that requires a period of exposure to a hormone, "before" there is a direct response "TO" that hormone. "


I have a different "view" of this, that isn't necessarily a disagreement, but consider this: Young men's beard hair is obviously responsive to androgens, but men in their thirties who get five o'clock shadow by 3 in the afternoon vs. a 19 year old who shaves every fourth day obviously have a different DEGREE of response dont they? There may be no "known mechanism that requires a period of exposure", but the older man has much coarser, longer body hairs.................but less testosterone in all probability and he may or may not have any more DHT being made, right? Time apparently has primed the DNA pump at the receptor level or the DNA response to androgen uptake level or the alpha five level or all three.




Let me put it this way..........................Ive posted pictures of four women who have taken testosterone to be like men. Buck Angel and Van Diesel, two transexual porno actors and two women on an Ophrah show. They ALL have beards now, and all have body hair (although Angel shaves her chest apparently, she has some chest hair in some photos). Do you think that their body got as hairy at one year as it was at year five? Van Diesel has a much thicker beard than most all men. One of the Ophrah women, the one with more hair, had a very nice beard also, but the other woman only had a regular beard's growth. Both of the women's beard hair obviously reacted positively to testoseterone, but one woman's beard growth was much more intense than the other. More DHT? Better androgen-receptors? And again...................TIME is a consideration.




Stephen wrote:

"In fact your own claim that the in-vitro tests prove your own argument, relies upon an "INSTANT" reaction between androgens and the alledged different androgen receptors.

This is what i mean by double standards"


You keep coming up with "instant reaction" Stephen. Do men usually go bald overnight? NO. It usually takes years and years and years. Some men go bald pretty quickly and are bald by 25 and some dont start till 35-45 and are bald in 20 more years. Like the body hair and beard hair on a teenage boy not getting fully thickened until he is in his mid-forties the androgenic response gets more and more with time. More and more apoptosis of cells in the follicle happens and weakens it to oxides in the dermis and premature ageing. Perhaps more DHT is made by the follicle over time as well as more androgen receptors get expressed in ensuing hair cycles over the years. These are things left unfound by science as of yet. But that doesn't mean all the researchers are wong and edema is causing the baldness.


Let me put it this way....................................we know women will have beard hair and body hair just like a man with testosterone.............so would you expect six months of testosterone therapy with a cream to give them the beard hair that they'd have with five years of the cream? Id' bet the same gal after five years would have a hell of a lot thicker beard and body hair growth. Time is important.





One more thing for you Stephen before I go..................Intercytex has released a couple of photos of phase one. Better hair growth is apparent in them. They show success. If phase two is very successful Stephen.......................and they go directly to phase three and get a release date and their product really is good and a good amount of new hair can be "made" from donor-area cells and stem cells--------------I think alot of research into hair may be put into other things. I mean hell, baldness will be 'solved' for almost all then right? Bryan once said "I'll believe it when I see it" in reference to Hair Multiplication. Well, we have seen a small example of it. I think this is the real "cure" for most any of us who'd like to get a little hair back. This includes you and my damned temples.


I still hope you can get your theory tested in some fashion for your own personal curiousity. I keep thinking there should be some sort of medical instrument that can be stuck in the dermis that would measure fluid pressure in different places to test for a difference. However, Im out of any reasonable ideas as far as potential testing. It must be frustrating for you. I know you must have developed your ideas before 2001. However time does not make them correct, and they could be every bit as wrong as I think (and Bryan and Doctor and Dave) think Armando's alternative theory is.