Article I Found from the Harvard website

[Bryan]

Actually, the spelling differences between American English and English as spoken in other nations were not a result of errors at all. They were deliberate alterations that were published in the first "Webster's Dictionary of American English" in the early 1800's.

Interesting info! I didn't know that!

Thus, this is why us Americans are the only...

{GROAN}

"us Americans"???

Personally, I think that some of the American spellings make better phonetic sense

I agree.

Bryan

 

[Cassin]

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.

 

[Bryan]

I totally agree! Other people in the rest of the world make fun of us Texans for saying that, but damnit, we invented a word which OUGHT to be a standard part of the English language! It fills a need which isn't otherwise met: a unique second person plural!

Bryan

 

[S Foote.]

Getting back on track, I think I read (and I know you guys hate it when we start out that way) that minoxidil is thought to enhance hair growth by increasing... is it blood vessels in general, or just those potassium K channels... er somethin'?

Anyway, question is: Is there anything out there that supports healthy blood vessels that we might want to try using to further combat hair loss? Might even help our heart and be good for overall health as well.

Also, I made the comment before that I find it interesting that hair loss often occurs on the temples and vertex of the scalp. Do you agree that those are the "pointy" parts of the head? While the skin on the sides and back of the head are plush, the scalp is tight and thin. This does seem to correlate to the Harvard article.

You're thoughts?

My argument is that DHT increases lymphatic drainage, and this is why DHT `GROWS' hair over the larger area of the body. In particular areas that are rich in superficial lymph vessels close to hair follicles, beard, armpits, groin. The reduction in local tissue `pressure' reduces the resistence to anagen follicle enlargement, allowing larger follicles.

According to the theory, male pattern baldness developes in the individual depending upon the scalp fluid `feed and return' equation. This diagram demonstrates how the lymphatic layout in the human head, is biased towards the mid to lower (beard) area. http://137.222.110.150/calnet/DeepNeck/ ... m#section6 (Scroll down). It is interesting how the collection centres for the superficial vessels from the scalp (the Parotid, Retroauricular, Superficial Cervical and Occipital nodes), seem to match the base of the human hairline.

The lymph vessels in the male pattern baldness area lie at the ends of the `pipework' and are sparse. Any increased `pumping' created by DHT in lymph vessels, can create reduced drainage from the `ends' of the system, by known fluid dynamic principles. A simple analogy is, you are using the shower upstairs, and someone runs water `downstairs'. An increased flow lower down can reduce flow higher up at the end of the system.

If an individual has a naturaly higher fluid `feed' (blood feed pressure), such a reduced drainage of fluid from the male pattern baldness area becomes more significant, and male pattern baldness is more likely in this individual. It has been suggested that people who develope male pattern baldness, are more likely to get heart problems in later life. Is this because of a common factor of a naturaly higher blood pressure?

The `fluid' factors that would help male pattern baldness according to the theory, would reduce the build up of pressure in the male pattern baldness area. An increased blood circulation, that is flow `THOUGH' would help to `shift' fluid. This is the factor referenced in this thread. Reducing the blood `FEED', would also help to reduce scalp fluid pressure. http://www.geocities.com/bryan50001/artery_ligature.htm

Minoxidil `shifts' the fluid volume towards the central area, that is `AWAY' from the level of the hair follicles. http://www.hairsite4.com/dc/dcboard.php ... 051&page=2

Latanoprost was designed to reduce fluid pressure. http://dermatology.cdlib.org/93/comment ... /wolf.html

The common side effects of systematic 5ARI's, are reduced ejaculate, impotence, and breast tenderness and enlargement. All `HYDRAULIC' effects!!

It has been shown that where androgens increase hair growth, there is a significant reduction in sweat secretion. Conversely, where androgens reduce hair growth, there is a significant increase in sweat secretion. http://hairmillion.com/ref-hair-loss/ha ... 3.506.html

Sweat glands are not `physicaly' changed by androgens. They don't have a `pumping mechanism', and they basicaly `bleed off' tissue fluid. So, the `RATE' of sweat secretion `MUST' reflect the local tissue fluid pressure!

The recognised imunology and fibrosis that occours with time in male pattern baldness, is an already recognised feature of increased tissue fluid pressures. http://www.lymphoedema.org.au/ Click `what is lymoedema'.

The only hair transplant procedures that have been shown to survive long term, are those that induce either Hydraulic changes in the tissue around the follicle, or changes in the tissue resistence factor associated with the theory. http://www.hairtransplantadviser.org/fallacies.htm

Most other types of hair loss and `shedding', also demonstrate some significant increase in the local tissue fluid pressure. For example trauma, radiation effects, infections etc.

The scientific method tells us to look for common factors in trying to understand processes of change. So what is the common factor in hair loss/growth?

Regards.

S Foote.

 

[Bismarck]

Sounds interesting and intuitively correct and as if it's an excerpt from Ernie Primeau's doctoral dissertation.

 

[S Foote.]

Sounds interesting and intuitively correct and as if it's an excerpt from Ernie Primeau's doctoral dissertation.

Just curious, would you care to elaborate upon your reasoning behind this remark?

S Foote.

 

[Bismarck]

Sounds interesting and intuitively correct and as if it's an excerpt from Ernie Primeau's doctoral dissertation.

Just curious, would you care to elaborate upon your reasoning behind this remark?

S Foote.

Didn't want to make it ridiculous at all. But why do all researechers believe that DHT directly influences the follicle. And what is your conclusion, what do you suggest as a potent hair loss treatment if your theory is true?

 

[Bismarck]

S Foote. , I admit to have not fully understood your theory. It would make sense to give some facts in what way DHT influences the lymphatic system.
I typed in google "lymphatic" and "DHT" and all I found were posts from S Foote. You recommend to put antiandrogens onto the face, right? Is the intention to have a DHT vacuum on the face that soaks the DHT away from the hair follicle or what ??? What has this all to do with Ockham's Razor? Isn't that dialectics?

bis

 

[S Foote.]

>>I admit to have not fully understood your theory. It would make sense to give some facts in what way DHT influences the lymphatic system.
I typed in google "lymphatic" and "DHT" and all I found were posts from S Foote. You recommend to put antiandrogens onto the face, right? Is the intention to have a DHT vacuum on the face that soaks the DHT away from the hair follicle or what ??? What has this all to do with Ockham's Razor? Isn't that dialectics?

Didn't want to make it ridiculous at all. But why do all researechers believe that DHT directly influences the follicle. And what is your conclusion, what do you suggest as a potent hair loss treatment if your theory is true? <<

In my opinion, the problem with the observations that have lead some to conclude that DHT is acting `directly on follicle cells, have just `NOT' been properly followed up! This notion of the direct action of androgens is based upon a `percieved' donor dominance in `ONE' type of transplantation technique, and a very `dodgy' interpretation of in-vitro tests with hair cells and androgens.

For example, we are told that hair follicles in the male pattern baldness area are `different' from other follicles, and when these are exposed to rising levels of androgens, this `CAUSES' a growth restricting `CHANGE' in these particular follicle cells. So why is it that when follicle cell samples that are `KNOWN' to be susceptable to male pattern baldness, `DO NOT CHANGE' into balding `mode' when `directly' exposed to androgens in-vivo???? http://endo.endojournals.org/cgi/content/full/138/1/356

Perhaps more than anything else, the `direct' explaination just can't explain `ALL' the relevant observations, as a `true' scientific theory is required to do! Ockhams razor is a basic principle used in deciding priorities in competing scientific theories. http://phyun5.ucr.edu/~wudka/Physics7/N ... node5.html

Basicaly this prefers the theory with the least `add on mechanisms'. The current `direct' theory needs a lot of add on's to explain the observations!!

For example, the direct theory states that androgens `directly' induce a growth restriction in some follicles (male pattern baldness), and increase growth in other follicles (beard and body hair). OK, then you have to find other `add on mechanisms to explain how you get changes in the immunology and sweat secretion? Also, if it is to be argued that DHT creates an immune mediated action on follicles in the male pattern baldness area, what is the immune mediated action that increases body hair? You need yet another `mechanism' here!!!

The Hydraulic theory, is the only theory that conforms to the principles of the scientific method, and explains `ALL' the observations through `ONE' mechanism. According to this it is the `TOTAL' amount of DHT effecting the lymph vessels in the head that is the `trigger' to male pattern baldness in the individual. This is why i talked about my facial experiment, as i explained in that post.

There is a recognised lymphatic `pumping' system, that involves periodic contractions of the lymph vessels. http://www.healerwithin.com/articles/rc-lymph.htm This must involve the nervous system controlling the muscle fibre contractions. If as proposed, DHT is increasing the rate of these natural lymph vessel contractions, it must be doing this through an effect on the lymph nerve system.

There is evidence for an effect of DHT on the nervous system. People have made reports on this when using systematic 5ARI's.

I think it is important when trying to understand any physiological process, to always consider the big picture! The studies often quoted on hair loss sites, have to be placed in the context of a `PROPER' scientific theory! If not they are meaningless! You will notice that people often post these studies and put a `personal spin' on these that the `ACTUAL' authors just don't do!!

All living things evolved in a `fluid' environment. We are `Hydraulic' systems! The Hydraulic theory of androgen related hair growth/loss, explains `ALL' the observations, it's as simple as that! No other theory can do this!

I do not recommend `ANY' particular treatments to people. Any treatments based on the Hydraulic theory would require proper testing by those in a position to do this, i am not in this position.

Regards.

S Foote.

 

[Guest]

Bryan and The Gardener don't make me b**ch slap (â„¢UK 1993) the pairs' of you, trying to intelleculise yo' mistakes is just macking yu luck stuppid.


Ty

 

[Bryan]

For example, we are told that hair follicles in the male pattern baldness area are `different' from other follicles, and when these are exposed to rising levels of androgens, this `CAUSES' a growth restricting `CHANGE' in these particular follicle cells. So why is it that when follicle cell samples that are `KNOWN' to be susceptable to male pattern baldness, `DO NOT CHANGE' into balding `mode' when `directly' exposed to androgens in-vivo???? http://endo.endojournals.org/cgi/content/full/138/1/356

It doesn't happen overnight while sitting in a petri dish, it occurs very gradually during puberty.

Bryan

 

[S Foote.]

For example, we are told that hair follicles in the male pattern baldness area are `different' from other follicles, and when these are exposed to rising levels of androgens, this `CAUSES' a growth restricting `CHANGE' in these particular follicle cells. So why is it that when follicle cell samples that are `KNOWN' to be susceptable to male pattern baldness, `DO NOT CHANGE' into balding `mode' when `directly' exposed to androgens in-vivo???? http://endo.endojournals.org/cgi/content/full/138/1/356

It doesn't happen overnight while sitting in a petri dish, it occurs very gradually during puberty.

Bryan

Oh yeh!

You have `proof' of that do you Bryan? Show me one of your `studies' that proves that statement!

The simple truth is, that this is a pretty pathetic excuse for observations that just don't suit your personal opinion!

Where is the biological precident for this `assumption' Bryan??? Cells are either responsive to certain hormones or they are not! There is `ABSOLUTELY NO' precident for cells to `LEARN' hormone sensitivity by a prolonged exposure to them!!

The in-vitro experiments `PROVE' beyond question that androgens `DO NOT DIRECTLY CHANGE HAIR GROWTH CHARACTERISTICS!!!!!' Therefore, the mechanism of follicle growth `CHANGE', has to be an in-vivo `INDIRECT' action of androgens!!!

S Foote.

 

[Bismarck]

So if DHT doesn't induce follicle miniaturisations directly - why are there androgen receptors locatad at the follicle?

 

[Bryan]

It doesn't happen overnight while sitting in a petri dish, it occurs very gradually during puberty.

Oh yeh!

You have `proof' of that do you Bryan? Show me one of your `studies' that proves that statement!

HUH?? Is that a joke, Stephen? The "proof" is the simple observation that ALL of us have made, which is that balding develops over a period of years once puberty has been reached. In fact, it doesn't even have to start DURING puberty...it frequently starts well AFTER puberty, as it did in my own case (in my early 40's). Don't "play dumb" with me! :wink:

Where is the biological precident for this `assumption' Bryan??? Cells are either responsive to certain hormones or they are not! There is `ABSOLUTELY NO' precident for cells to `LEARN' hormone sensitivity by a prolonged exposure to them!!

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:

Bryan

 

[S Foote.]

So if DHT doesn't induce follicle miniaturisations directly - why are there androgen receptors locatad at the follicle?

As far as i am aware, and i think Bryan agree's here, there are androgen receptors in `ALL' scalp hair! Yet there is no `CHANGE' induced by androgens in scalp hair `outside' of the male pattern baldness area!

I think it important to emphasise that the important thing here is to try to understand the mechanisms of `CHANGE' in androgen related hair growth! This is the key to preventing or reversing male pattern baldness.

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!!

One thing i think people who read these debates really should consider, is the validity of what is being argued in the context of the scientific method. The scientific method was developed over time by eminent scientists to give a framework for valid proposals, and a means of sorting what is valid and what is not!! http://phyun5.ucr.edu/~wudka/Physics7/N ... node5.html

I strongly recommend that anyone who is `TRULY' interested in scientific debate, make themselves aware of the correct ground rules! It is easy to put a `personal spin' on a particular study, and throw in a bit of scientific terminology!

S Foote.

 

[Bryan]

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!!

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.

Bryan

 

[MidnightFlyer]

Yeah, yeah, yeah. We got one going, ladies and gentlemen.

2 formidable adversarys. Who shall get the last word?

Go Bryan, go!

 

[S Foote.]

It doesn't happen overnight while sitting in a petri dish, it occurs very gradually during puberty.

Oh yeh!

You have `proof' of that do you Bryan? Show me one of your `studies' that proves that statement!

HUH?? Is that a joke, Stephen? The "proof" is the simple observation that ALL of us have made, which is that balding develops over a period of years once puberty has been reached. In fact, it doesn't even have to start DURING puberty...it frequently starts well AFTER puberty, as it did in my own case (in my early 40's). Don't "play dumb" with me! :wink:

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????????????

Where is the biological precident for this `assumption' Bryan??? Cells are either responsive to certain hormones or they are not! There is `ABSOLUTELY NO' precident for cells to `LEARN' hormone sensitivity by a prolonged exposure to them!!

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:

Bryan

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!

Here's something to think about Bryan?

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'!!!!!!!!!!

The only `RECOGNISED' mechanism that is `KNOWN' to create a growth restriction in `ALL' cell types is contact inhibition!!! No `MAGIC' required!!!

S Foote.

 

[Armando Jose]

MINIATURIZATION OF HAIR

Thank you for your statements, are very interesting and useful.

M. 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'!!!!!!!!!!

The only `RECOGNISED' mechanism that is `KNOWN' to create a growth restriction in `ALL' cell types is contact inhibition!!! No `MAGIC' required!!! "

In my opinion DHT' theory of AAG can not explain easily the miniaturization of hair. DHT acts as a disruptor of biological mechanism, and there is only two possibilities, to grow hair or don't grow hair. Hair miniaturization is observed before the hair is lost completely. Mr. Foote indicates contact inhibition as the mechanism of miniaturization, but in my opinion there is another possibility, a lower number of stem cells that arrive to the dermal papilla.

In this and the following slide http://www.hairlosstalk.com/newsletter/ ... le&sid=268 can be observed that stem or TA's cells must arrive to the dermal papila in order to form a healthy hair. Stem cells are formed in the bulge area and travel along hair till arrive dermal papilla, the same travel that sebum makes. If sebum consolidated and don't flow then are problems because stem cells don't arrive to the target. Only a fraction of these cell arrive to the lower area of the hair producing miniaturization process.

In my opinion problems of sebum flow is the initial and triggering factor of AAG or common alopecia.

Best regards
Armando

 

[Bismarck]

Just found this, might be interesting (unfortuanetely, fulltext is not available):

_____________________________________________________________
Is androgenic alopecia a result of endocrine effects on the vasculature?

Hernandez BA.

College of Osteopathic Medicine, The University of Health Sciences, 1750 Independence Avenue, Kansas City, MO 64106, USA. chernandez.edu
Androgenic alopecia is a condition of concern for many patients. Though much has been learned about this condition, the exact pathophysiological mechanism is yet to be established. Currently most study concerning androgenic alopecia has focused on the effects of androgens on the pilosebaceous unit itself. An area of study that has received considerably less attention is that of androgens inducing baldness by indirect effects, that is, effects on tissues other than the pilosebaceous unit. In this paper, the author offers a novel hypothesis in which androgenic hair loss is mediated via the effects of androgens on the vasculature supplying the scalp. In this new hypothesis androgens effect anatomical changes in the vasculature of susceptible individuals, resulting in an environment in which hair growth is hindered and eventually ceases. The author discusses past studies demonstrating the effects of androgens on vessels and how these effects may relate to anatomical changes in the vasculature leading to hair loss. Also included is a discussion on future experimentation to test this new hypothesis.

PMID: 14975518 [PubMed - in process]
_____________________________________________________________