Article I Found from the Harvard website

[Bryan]

That is a very `telling' statement about your complete lack of scientific interpretation skills Bryan!

Of `COURSE' we all know there is a `time delay' in male pattern baldness!! It is however a `HUGE' speculation to conclude that this is because of some unprecidented `time delay' in `direct' hormone sensitivity!!! The whole notion is ridiculous, and goes against any known physiology! Stop avoiding the question Bryan, and cite me `ANY' recognised precident for such a `time delay in a `DIRECT' effect of hormones on a cell type????????????

I don't claim to know the exact mechanism of how cells go from being insensitive to androgens, to being sensitive to them. I don't know WHY they do, I just know THAT they do.

Have you forgotten that it is YOU who has attempted to postulate that scalp hair follicles become sensitive to androgens in vitro (in a negative way) because of their exposure to your fanciful "fluid pressure"?? Is there a precedent for THAT to occur?? :wink:

Well of course there is a precident for my theory Bryan, i have tried to explain this to you often enough, but `RECOGNISED' mechanisms of changes in cell growth seem to pass you by! You tend to prefer `magic' unfounded mechanisms!

The precident is `NORMAL' contact inhibition of cell growth, that effects `ALL' normal cell lines!! If as i propose, an increase in dermal fluid pressure is increasing resistence to anagen follicle enlargement, the premature `switching off' of anagen enlargement by normal contact inhibition, will create `FUNDAMENTAL' changes in the follicle cells! Contact inhibitions `STOPS' cells from multiplying! Therefore, contact inhibition `MUST' be inducing changes in the basic `GROWTH' reaction of these cells!!!!!!!!!!!!!

If you then culture these cells and expose them to `ANYTHING' in-vitro, `OF COURSE' they are going to show some growth restricted characteristics compared to cells that have `NOT' been `ALTERED' by contact inhibition!! It's not a hard concept to grasp, and it is based upon the most common type of `ALREADY RECOGNISED' cell growth restriction mechanism!

Nice try, but you still haven't shown me any precedent for how they become sensitive TO ANDROGENS!

Just talking about "growth restricted characteristics" in general isn't good enough. You have to demonstrate to me that they would become SENSITIVE TO ANDROGENS. You have to be specific! You can't expect ME to be specific about explaining how those hair follicles go from being insensitive to sensitive, if YOU can't even do the same! :wink:

In the early stages of male pattern baldness, before the secondary immunology and fibrosis enters the equation, anagen follicles start to miniaturise. That is, the entire follicle becomes smaller, but still functional just producing less hair.

The follicle has many different cell types, yet only the DP cells have androgen receptors. So how come `ALL' the cell types show `equal' growth restriction to `scale' down the `entire' follicle? How can your `direct' action of androgens on DP cells explain the `whole' follicle miniaturisation? It just `CAN'T'!!!!!!!!!!

Oh, Sweet Mother of Mercy!! Why are you pretending that you don't already know the answer to that??? It's all explained in that very same stumptailed macaque study that you yourself cited earlier in this thread. Go back and re-read it.

Bryan

 

[S Foote.]

S Foote. wrote:
Where a particular cell type is `directly targeted' by a hormone, the hormone attaches to a receptor within the cell, and then interacts with the genetic controls within the cell to effect the behaviour of the cell.

The Macaque study refered to, quite conclusively `PROVES' that androgens are `NOT' effecting any `CHANGE' in follicle cells by this `direct' mechanism!!

Bryan wrote:
No, it does NOT prove that! Not by a long shot! In fact, it clearly demonstrates the likely mechanism by which androgens DO affect hair follicles directly! I invite people to read the study and decide for themselves, without taking either my word for it, OR Stephen's.

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I think you have a very strange viewpoint about what is being `clearly demonstrated' in this study Bryan?? Let me make a simple analogy to what you are saying here!

According to your way of thinking, if i pour gas over the engine of my car and it doesn't start, it `WILL' do eventually! You can assure me of this because it is known that gas is needed for engines to start, right!! Yeh i believe it!!!!

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S Foote. wrote:
That is a very `telling' statement about your complete lack of scientific interpretation skills Bryan!

Of `COURSE' we all know there is a `time delay' in male pattern baldness!! It is however a `HUGE' speculation to conclude that this is because of some unprecidented `time delay' in `direct' hormone sensitivity!!! The whole notion is ridiculous, and goes against any known physiology! Stop avoiding the question Bryan, and cite me `ANY' recognised precident for such a `time delay in a `DIRECT' effect of hormones on a cell type????????????

Bryan wrote:
I don't claim to know the exact mechanism of how cells go from being insensitive to androgens, to being sensitive to them. I don't know WHY they do, I just know THAT they do.

---------------------------------------------------


Don't you see just how scientificaly naive you are being here Bryan? The `BIG' question here is `HOW' are androgens creating growth `CHANGES' in follicle cells!!! The macaque study clearly shows that it is `NOT' by a `direct' action! `ALL' the samples in the study are behaving in the same way in-vitro, as they did in-vivo!! The all important `CHANGE' in follicle cell characteristics therefore `MUST' be induced by some kind of in-vivo `INDIRECT' effect of androgens!

----------------------------------------------------


Bryan wrote:
Have you forgotten that it is YOU who has attempted to postulate that scalp hair follicles become sensitive to androgens in vitro (in a negative way) because of their exposure to your fanciful "fluid pressure"?? Is there a precedent for THAT to occur??


S Foote. wrote:
Well of course there is a precident for my theory Bryan, i have tried to explain this to you often enough, but `RECOGNISED' mechanisms of changes in cell growth seem to pass you by! You tend to prefer `magic' unfounded mechanisms!

The precident is `NORMAL' contact inhibition of cell growth, that effects `ALL' normal cell lines!! If as i propose, an increase in dermal fluid pressure is increasing resistence to anagen follicle enlargement, the premature `switching off' of anagen enlargement by normal contact inhibition, will create `FUNDAMENTAL' changes in the follicle cells! Contact inhibitions `STOPS' cells from multiplying! Therefore, contact inhibition `MUST' be inducing changes in the basic `GROWTH' reaction of these cells!!!!!!!!!!!!!

If you then culture these cells and expose them to `ANYTHING' in-vitro, `OF COURSE' they are going to show some growth restricted characteristics compared to cells that have `NOT' been `ALTERED' by contact inhibition!! It's not a hard concept to grasp, and it is based upon the most common type of `ALREADY RECOGNISED' cell growth restriction mechanism!

Bryan wrote:
Nice try, but you still haven't shown me any precedent for how they become sensitive TO ANDROGENS!

Just talking about "growth restricted characteristics" in general isn't good enough. You have to demonstrate to me that they would become SENSITIVE TO ANDROGENS. You have to be specific! You can't expect ME to be specific about explaining how those hair follicles go from being insensitive to sensitive, if YOU can't even do the same!

--------------------------------------------------------

You want specific Bryan? i'll give you specific!!

The macaque study `PROVES' that hair follicle cells are `NOT DIRECTLY SENSITIVE' to androgens!! The term `sensitive to', means an exposure of follicle cells to androgens `SHOULD' induce a `CHANGE', but no `CHANGE' is being induced!!!! The `DIRECT' exposure of follicle cells to androgens, is `NOT CHANGING' the `PRE-EXISTING' cell characteristics!! Follicle cells `CANNOT' therefore be `DIRECTLY SENSITIVE' to androgens!

-------------------------------------------------------

S Foote. wrote:
In the early stages of male pattern baldness, before the secondary immunology and fibrosis enters the equation, anagen follicles start to miniaturise. That is, the entire follicle becomes smaller, but still functional just producing less hair.

The follicle has many different cell types, yet only the DP cells have androgen receptors. So how come `ALL' the cell types show `equal' growth restriction to `scale' down the `entire' follicle? How can your `direct' action of androgens on DP cells explain the `whole' follicle miniaturisation? It just `CAN'T'!!!!!!!!!!

Bryan wrote:
Oh, Sweet Mother of Mercy!! Why are you pretending that you don't already know the answer to that??? It's all explained in that very same stumptailed macaque study that you yourself cited earlier in this thread. Go back and re-read it.

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The `ANSWER' Bryan! you know an answer here???

I have read that study very carefully, and i suggest other people do the same! Here's a quote from it:

" Together our data indicate that the inhibitory effect of testosterone on proliferation of epithelial cells is age dependent, and androgen may play an essential role in hair growth either by inducing repressor(s) from dermal papilla cells, which may then inhibit the growth of epithelial cells of the hair follicle,"

Note the use by the author of the word `MAY'!!! The `ACTUAL' scientist who did the study, `SPECULATES' about `THEORETICAL' cell interactions that `MAY' be happening here! But you claim to know for certain Bryan?

The direct theory `SPECULATES' about `THEORETICAL' cell signaling mechanisms that `MAY' explain follicle miniaturisation? Normal contact inhibition is `ALREADY' known to induce growth restriction in `ALL' normal cell types! No `SPECULATIVE MAGIC' required!

Where the direct theory you support Bryan `REALLY' falls down, is in peoples theroputic experiences! We would at least be able to `PREVENT' male pattern baldness by a simple topical anti-androgen! The drug companies would have made fortunes by developing this kind of preventitive treatment! The advertising would go like this, "Does male pattern baldness run in your family?, use our preventitive anti-androgen spray" Do you think they haven't researched this Bryan? So where is it, and `WHY' is it that the systematic 5ARI's and anti-androgens work better in male pattern baldness than the equivelent `topicals', if the effect is `DIRECT'????????????

Let's hear your usual excuses!

S Foote.

 

[Bryan]

Of `COURSE' we all know there is a `time delay' in male pattern baldness!! It is however a `HUGE' speculation to conclude that this is because of some unprecidented `time delay' in `direct' hormone sensitivity!!! The whole notion is ridiculous, and goes against any known physiology! Stop avoiding the question Bryan, and cite me `ANY' recognised precident for such a `time delay in a `DIRECT' effect of hormones on a cell type????????????

I can't do that, any more than YOU can cite a precedent for contact inhibition causing a sensitivity to androgens.

Bryan wrote:
I don't claim to know the exact mechanism of how cells go from being insensitive to androgens, to being sensitive to them. I don't know WHY they do, I just know THAT they do.

Don't you see just how scientificaly naive you are being here Bryan? The `BIG' question here is `HOW' are androgens creating growth `CHANGES' in follicle cells!!! The macaque study clearly shows that it is `NOT' by a `direct' action!

No it doesn't. Read the study. It explains how androgens affect the production of growth factors (or possibly growth inhibitors, for that matter) in the dermal papilla, which then affects the growth of the rest of the follicle in a paracrine fashion.

The precident is `NORMAL' contact inhibition of cell growth, that effects `ALL' normal cell lines!! If as i propose, an increase in dermal fluid pressure is increasing resistence to anagen follicle enlargement, the premature `switching off' of anagen enlargement by normal contact inhibition, will create `FUNDAMENTAL' changes in the follicle cells! Contact inhibitions `STOPS' cells from multiplying! Therefore, contact inhibition `MUST' be inducing changes in the basic `GROWTH' reaction of these cells!!!!!!!!!!!!!

LOL! That still doesn't prove that contact inhibition is what causes balding! :wink:

If you then culture these cells and expose them to `ANYTHING' in-vitro, `OF COURSE' they are going to show some growth restricted characteristics compared to cells that have `NOT' been `ALTERED' by contact inhibition!! It's not a hard concept to grasp, and it is based upon the most common type of `ALREADY RECOGNISED' cell growth restriction mechanism!

So that PROVES that contact inhibition causes androgen sensitivity, right, Stephen?

The macaque study `PROVES' that hair follicle cells are `NOT DIRECTLY SENSITIVE' to androgens!! The term `sensitive to', means an exposure of follicle cells to androgens `SHOULD' induce a `CHANGE', but no `CHANGE' is being induced!!!! The `DIRECT' exposure of follicle cells to androgens, is `NOT CHANGING' the `PRE-EXISTING' cell characteristics!! Follicle cells `CANNOT' therefore be `DIRECTLY SENSITIVE' to androgens!

Once again, the study provided POWERFUL evidence that androgens affect the secretion of growth factors (or growth inhibitors) from the dermal papilla, which then affects the rest of the follicle. I also provided you in the past with another study by Randall which argued in favor of the same mechanism to explain the effect of androgns on hair growth. Why are you being so obstinate about all this??

In the early stages of male pattern baldness, before the secondary immunology and fibrosis enters the equation, anagen follicles start to miniaturise. That is, the entire follicle becomes smaller, but still functional just producing less hair.

The follicle has many different cell types, yet only the DP cells have androgen receptors. So how come `ALL' the cell types show `equal' growth restriction to `scale' down the `entire' follicle? How can your `direct' action of androgens on DP cells explain the `whole' follicle miniaturisation? It just `CAN'T'!!!!!!!!!!

I've now explained that SEVERAL TIMES. Pay attention.

I have read that study very carefully, and i suggest other people do the same! Here's a quote from it:

" Together our data indicate that the inhibitory effect of testosterone on proliferation of epithelial cells is age dependent, and androgen may play an essential role in hair growth either by inducing repressor(s) from dermal papilla cells, which may then inhibit the growth of epithelial cells of the hair follicle,"

Hey, now we're getting somewhere! You actually READ THE STUDY!!

Note the use by the author of the word `MAY'!!! The `ACTUAL' scientist who did the study, `SPECULATES' about `THEORETICAL' cell interactions that `MAY' be happening here! But you claim to know for certain Bryan?

LOL!! You're really scraping the bottom of the barrel now, Stephen! Scientists ALWAYS speak very cautiously like that. And YOU have the unmitigated gall to cite that as a possible uncertainty in what they're saying, in a desperate attempt to bolster your own eccentric theory. You should be ashamed of yourself for stooping that low!

The direct theory `SPECULATES' about `THEORETICAL' cell signaling mechanisms that `MAY' explain follicle miniaturisation? Normal contact inhibition is `ALREADY' known to induce growth restriction in `ALL' normal cell types! No `SPECULATIVE MAGIC' required!

Such desperation as what you just said is painful to witness...

Where the direct theory you support Bryan `REALLY' falls down, is in peoples theroputic experiences! We would at least be able to `PREVENT' male pattern baldness by a simple topical anti-androgen!

I think we CAN do that, with a good one.

The drug companies would have made fortunes by developing this kind of preventitive treatment!

Extremely unlikely. Merck hasn't come anywhere NEAR making a fortune, even with an easy-to-take pill for hairloss.

The advertising would go like this, "Does male pattern baldness run in your family?, use our preventitive anti-androgen spray" Do you think they haven't researched this Bryan? So where is it, and `WHY' is it that the systematic 5ARI's and anti-androgens work better in male pattern baldness than the equivelent `topicals', if the effect is `DIRECT'????????????

That is PURE SPECULATION on your part. I think a decent topical antiandrogen WOULD be just as effective. It certainly was in stumptailed macaques, as I've pointed out to you repeatedly! :wink:

Bryan

 

[S Foote.]

Well Bryan, you may be missing the point here. (or avoiding it!!), but the issue is very simple. Let's get down to the basics. These long posts just get repetitive and boring!

S Foote wrote:
Of `COURSE' we all know there is a `time delay' in male pattern baldness!! It is however a `HUGE' speculation to conclude that this is because of some unprecidented `time delay' in `direct' hormone sensitivity!!! The whole notion is ridiculous, and goes against any known physiology! Stop avoiding the question Bryan, and cite me `ANY' recognised precident for such a `time delay in a `DIRECT' effect of hormones on a cell type????????????


Bryan wrote:
I can't do that, any more than YOU can cite a precedent for contact inhibition causing a sensitivity to androgens.


The quoted study `clearly' demonstrates that follicle cells are `NOT DIRECTLY SENSITIVE' to androgens in the `TRUE' sense of the term! A sensitivity to something, means some kind of induced `change'. The pre-balding sample cells are `NOT CHANGED'into growth restricted cells by `direct' exposure to androgens! This shows the `induced' change in growth characteristics, `must' be some kind of in-vivo `indirect' effect of androgens!


Even when these now `different' cell samples are exposed to androgens in-vitro, they are `NOT' demonstrating any `CHANGE' in their growth response! When exposed to substances in an artificial in-vitro `soup', any number of different substances could `enable' the `particular' growth potential of the various cell samples, including androgens! Cream cheese could `enable' the `in built' growth potential of follicle cells in-vitro! Do we then conclude that cream cheese `DIRECTLY CAUSES' male pattern baldness? Of course not!!


You give yourself away Bryan, in the way you quote `studies' to try to give `authority' to your personal opinions! For example:


S Foote wrote:
Don't you see just how scientificaly naive you are being here Bryan? The `BIG' question here is `HOW' are androgens creating growth `CHANGES' in follicle cells!!! The macaque study clearly shows that it is `NOT' by a `direct' action!


Bryan wrote:
No it doesn't. Read the study. It explains how androgens affect the production of growth factors (or possibly growth inhibitors, for that matter) in the dermal papilla, which then affects the growth of the rest of the follicle in a paracrine fashion.


But that's `NOT' what the author says is it Bryan? The professional scientist uses the word `MAY' because they work within the framework of the scientific method. Something you consistently avoid, just to try to justify your `personal' opinion!


You can quote all the studies you like about the `theoretical' efficacy of topical anti-androgens. Everyone here knows the `ACTUAL' reality!!



S Foote wrote:
The precident is `NORMAL' contact inhibition of cell growth, that effects `ALL' normal cell lines!! If as i propose, an increase in dermal fluid pressure is increasing resistence to anagen follicle enlargement, the premature `switching off' of anagen enlargement by normal contact inhibition, will create `FUNDAMENTAL' changes in the follicle cells! Contact inhibitions `STOPS' cells from multiplying! Therefore, contact inhibition `MUST' be inducing changes in the basic `GROWTH' reaction of these cells!!!!!!!!!!!!!


Bryan wrote:
LOL! That still doesn't prove that contact inhibition is what causes balding!


I find it curious Bryan that you have avoided the regular threads on hair loss sites, about the profound effect of the Wnt's beta-catenin, E-cadherin pathways on hair follicle growth? These pathways are known to be linked to the process of contact inhibition, and it has been shown that manipulation here creates major changes in hair follicle developement!!!!

http://www.blackwell-synergy.com/links/ ... x/full/#h8 http://www.ucalgary.ca/UofC/eduweb/virt ... ancer.html http://kinase.uhnres.utoronto.ca/Wnt_Rest/Bcat.html http://www.stormingmedia.us/68/6898/A689814.html http://www.hhmi.org/news/fuchs2.html http://www.healthsystem.virginia.edu/in ... ideintro=1

Ever heard the saying "There are non so blind as those who will not see" ?

S Foote.

 

[MidnightFlyer]

CHECKMATE! :shock:

 

[The Gardener]

I think ya'll should be considered the proper description for a group of people as it is much less cumbersome than........

You guys , You all, All of you.......etc.......

I hear it all of the time of course in Texas, and in the proper context, it makes much more sense to me.

I agree, I tend to like the use of "y'all" as a second person plural pronoun. Much more politically correct than the "you guys" used here in California. But, if y'all is second person plural, then what exactly is "all y'all"?

It is interesting how the second person plural pronoun differs so much regionally. Here are a few examples:

Traditional: You
Emphatic: You all
Southern US: Y'all
Western US: You guys
Boston US: You assholes

 

[Bryan]

Well, don't forget the classic one:

New York: Youz

For example, "Get out of here, all of youz!!"

Bryan