Study: Propecia Responders and Non-Responders

[PartTimeNinja]

I was on AIM today and made sure Bryan saw this very thread. I told him "S FOOTE CALLED YOU OUT!!!" and he laughed. He'll get around to responding. After all .. he is BRYAN ... one cannot rush bryan!

HairLossTalk.com

Well, we're yelling out for him in the Proxiphen thread as well! Busy man!

 

[S Foote.]

I was on AIM today and made sure Bryan saw this very thread. I told him "S FOOTE CALLED YOU OUT!!!" and he laughed. He'll get around to responding. After all .. he is BRYAN ... one cannot rush bryan!

HairLossTalk.com

Cant wait

I would also make a polite request to Bryan when he shows up.

You know i don't mind critism of my theory Bryan, but it would help your own credibility if you would post your opinions where i have the right of reply, and not on a scientificaly censored site like HLH.

Quote:

"G-damn, there are some really eccentric theories of hairloss! First the "galea" theory, then Stephen Foote's theory, now this one!"

Go and read the scientific `rules' described here Bryan http://phyun5.ucr.edu/~wudka/Physics7/N ... node5.html

Then explain to us all what exactly is `eccentric' about my theory?

S Foote.

 

[HairlossTalk]

post your opinions where i have the right of reply, and not on a scientificaly censored site like HLH.

They delete your posts when you try to respond to Bryan?

HairLossTalk.com

 

[S Foote.]

post your opinions where i have the right of reply, and not on a scientificaly censored site like HLH.

They delete your posts when you try to respond to Bryan?

HairLossTalk.com

Farrel deletes all of my posts as Bryan and others know. So if anyone wants to take a `pop' and avoid any comment from me, they post it there. Pretty sad in my book!

The latest pathetic outburst there comes from 500 IMATT, who used to be `Frizz' at Hairsite. After i and others put this attention seeker in his place on an uncensored site, he ran to Farrels censored site and changed his handle. This is what he just posted.

>>Please stop this nonsensical talk of the hydraulic theory. S. Foote is a self promoting fool who thinks because he paid to have his article published in a crackpot journal (Med Hypotheses) that somehow it has validity. The process of publication for that journal is not double blind peer reviewed process. Further, there is no treatment protocol recommended by him. I remember his old recommendation was to apply Crinagen to the face, LOL!!!!!

I remember he emailed his "theory" to Elaine Fuchs a few times (who is one of THE leading scientists in hair biology) and she didn't even bother to reply. If she (as an expert) felt that his theory had any weight or validity she would have taken the time to reply. On the other hand, one of the most knowledgeable posters on any of these hairloss boards is UWbio. He is a real scientist and has recieved numerous replies from Elaine Fuchs via email.

Farrel, I beg you to delete this thread or delete the whole discussion of the failed hydraulic theory. <<

My response to him is a repost of my response to Farrel in the same thread, when my theory was raised by Armando. http://www.hairlosshelp.com/forums/mess ... TARTPAGE=1

My response below was deleted almost instantly!

Regards.

S Foote.

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


>>By the way I would like ask to Foote


In your theory about hair loss have a capital importance the fluid’s pressure in the pilosebaceous region. Have you considered the possible effect of sebum as integrant part of these fluids?. Sebum components change its viscosity and hydraulic properties easily when oxidised.<<

Hi Armando.

I am more than willing to discuss my views on your theory, and any critisms you may have regarding mine, in a reasonable respectful manner.

But that certainly won't happen on Farrels site!!

The last time i was engaged in a mutually respecful debate about my theory on this site, Farrel jumped in and banned me from posting here!

Farrel seems to have a problem with people who don't agree with his `personal' interpretation of the evidence for or against particular hair loss theories.

If it's a `genuine' scientific debate you want Armando, you will have to go to other sites where this is not censored.

I hope you get to read this before it gets deleted!

S Foote.


Farrel said:


>>This is bogus science, as is Footes theory.<<

You would not recognise `science' if it slapped you in the face Farrel!

Your unqualified remarks mean nothing, this is what a `recognised' expert had to say about my theory (Dr Sawaya). You should also note from her remarks, that i am not the only one who is thinking along these lines!!!

_________________________________________________



"Alot of good points are brought up regarding the hair follicle growth and the fact that anagen is a bit predetermined by the previous hair cycle and the "clock" that is set or how long the matrix cells can grow and divide, making a big, anagen follicle, or a smaller and smaller follicle with each hair cycle. The idea of pressure changes from localized factors is interesting as the problem with male pattern hair loss is the fibrosis/scarring that takes place so that the follicles and surrounding tissues are damaged and cannot regenerate.
Male pattern hair loss is not supposed to be a scarring, cicatricial process, but it is a mixed inflammatory process in that many people do have inflammatory changes but usually in the middle follicle, and not as much in the lower follicle, as in alopecia areata.

Overall, these are interesting arguments to stimulate anagen follicles, keeping in mind that there are many substages of anagen, each similar to the cell cycle in carrying out a specific function for a certain period of time.
Many researchers are working on similar concepts with use of growth factors to see if there is any certain one or mix of them that can effect the process.

It is a very complex process, but your thoughts are very organized and on the right path, similar to what others have been proposing, and in some ways yours are more straightforward. I think you've done a good job in thinking this through......
Hope this helps...
regards
Marty Sawaya"

 

[Bryan]

I would also make a polite request to Bryan when he shows up.

You know i don't mind critism of my theory Bryan, but it would help your own credibility if you would post your opinions where i have the right of reply, and not on a scientificaly censored site like HLH.

Stephen, for what it's worth, I regret the fact that Farrel banned you from HLH. Unless it was for something really egregious that you did that I don't know about, I don't see a justification for doing something like that except in extreme cases of people who abuse the system (a legitimate example of that might be "Common Sense" over on hairsite). I only realized myself a day or two ago that you had been banned, when Farrel mentioned it himself.

Bryan

 

[Bryan]

I think what this study shows is that some people just have more `efficient' androgen receptors than others, that more easily `take up' circulating DHT, and it is the total systematic levels of DHT that are significant in creating male pattern baldness in the individual.

The first part of your sentence about the "more efficient androgen receptors" may well be correct, but please explain the second part where you say that total CIRCULATING systemic levels of DHT are supposedly more important in creating male pattern baldness. How do you arrive at that conclusion, from this study?

I think it is the `total' systematic level of DHT in the individual that effect hair growth `indirectly'. and i think this study supports this.

Please explain how you think the study supports that notion.

An `indirect' effect of DHT on hair growth, would still have to be mediated via androgen receptors!

Probably. So what?

If it is the systematic levels of both types of enzyme produced DHT that are important, an individual with these more `efficient' receptors would require more DHT reduction for the same `effect' on male pattern baldness than others with less efficient receptors. This is the simple `odds' principle. More efficient receptors are more likely to `hook up' with the available DHT.

Yes. And wouldn't the same be true for the "Direct" theory? I don't understand your point.

I think the vast body of available evidence, supports the theory that the effect is `systematic' and not local within the follicle as is currently thought. I suggest this study is yet another nail in the coffin of the current `direct' theory.

You're dreaming.

Come on Bryan, chime in anytime!

Be careful what you ask for! :wink:

Bryan

 

[S Foote.]

Well Bryan, thank you for your response, and i accept that you were not fully aware of my inability to respond on Farrels site. Could you please therefore in future, comment on my theory on sites were i can respond? Thanks.

As you know, i am in the UK. It is getting late here now, and i will respond to the points you make tomorrow, as i want to cover your points in detail.

S Foote.

 

[gonna_win]

What is the source for this study?

 

[HairlossTalk]

Hey even Dr. Marty Sawaya said S. Foote's theory was well thought out and worthy of at least some further looking in-to!

Bryan - Im actually most interested in hearing your opinion on the study, void of others opinions. Any thoughts?

HairLossTalk.com

 

[S Foote.]

I think what this study shows is that some people just have more `efficient' androgen receptors than others, that more easily `take up' circulating DHT, and it is the total systematic levels of DHT that are significant in creating male pattern baldness in the individual.

The first part of your sentence about the "more efficient androgen receptors" may well be correct, but please explain the second part where you say that total CIRCULATING systemic levels of DHT are supposedly more important in creating male pattern baldness. How do you arrive at that conclusion, from this study?

http://phyun5.ucr.edu/~wudka/Physics7/N ... node5.html[/url]

According to the scientific method the current `direct theory, isn't a theory at all, just a failed Hypothesis!

The direct `Hypothesis' was based on the interpretation of what donor dominance seemed to indicate, and was reasonable until it was dispoved by other experiments and observations. In mainstream science, such a Hypothesis would have been thrown out a long time ago!


S Foote.

 

[Bryan]

Hey even Dr. Marty Sawaya said S. Foote's theory was well thought out and worthy of at least some further looking in-to!

It had the appearance to me of a well-written "form-letter".

Bryan - Im actually most interested in hearing your opinion on the study, void of others opinions. Any thoughts?

I'll get to that presently. I wanna grill Stephen a little, first!

Bryan

 

[Bryan]

The current theory states that it is the DHT produced within follicle cells, that is important in reacting with androgen receptors within the same cells, to change the cells growth response. I think you have said this is your view in past posts Bryan, correct me if i am mis-quoting you.

Actually, you're not misquoting ME, because that's what I believe. However, I think you're mildly misquoting the "Direct Theory" in general, because doctors and researchers nowadays don't really say very much about the relative importance of serum DHT versus "local" DHT production within hair follicle cells. They acknowledge occasionally that serum DHT _can_ enter cells and have an effect, but I've never seen any discussion or theorizing of the relative importance of those two routes of access. My guess (and that's all it is) is that nowadays, most scientists would tend to agree with my position.

Well the thing about this theory is it is `VERY' direct and straight forward. In other words, there isn't much that can be `different' in individuals.

But I think there ARE various things that can be different, like those androgen receptor gene polymorphisms that apparently can make a significant difference in the "sensitivity" of androgen receptors. Furthermore, there is the all-important issue of different qualitative (as opposed to quantitative) RESPONSES to the androgenic signal, like I posted about at length a month or so ago over on HLH.

In this study, there is no reference to finasteride creating a different level of DHT reduction in people with this different receptor `code'. So the only `difference' is in the receptors. But in reality, this cannot be a `major' difference in receptor efficiency!

No reference is made to any significant differences in sexual characteristics in the individuals tested. Those with the `weaker' androgen receptors are not reported as having any `female' characteristics, nor the `stronger' receptors producing any hyper-androgenic effects.

So `BOTH' types of receptors are `working' within the normal range, producing `normal' male characteristics.

It _is_ a bit puzzling why hairloss is so strongly statistically associated with a particular AR polymorphism, for the reason you state.

How then is it possible for these individuals to demonstrate such a different `actual' treatment response to finasteride? The `direct' theory just doesn't have the `scope' to explain this given such a small difference in receptor efficiency, and the alledged `direct' action on follicle cells!

The `direct' mechanism you propose Bryan just cannot allow for the observed `difference' in this study!

On the other hand, a `systematic' action of DHT acting `indirectly' upon hair growth, has far more scope in possible mechanisms to explain the difference in treatment effect with a slight difference in receptor efficiency.

Ok, NOW we come to the part where I think you fall flat on your face, Stephen. You're simply passing the puzzle farther along! I can't completely explain why the fate of hair follicles would depend to such a degree on certain AR polymorphisms, but neither can YOU explain why those other androgen-sensitive body processes which allegedly cause balding (according to your theory) are just as sensitive to that same polymorphism. Neither one of us has a really good, complete answer to that little problem, so you can't really make any hay out of it! :wink:

BTW, did you happen to see that new Japanese study that was posted recently on HLH? It was yet another in an increasingly long line of such studies that are now looking at the differences in growth factors that are secreted by various dermal papillae (body vs. scalp), in response to androgens. Like I've told you many times, scientists are slowly but steadily working their way through these complex biochemical pathways to elucidate the differences between scalp and body hair. Have patience!

Bryan

 

[S Foote.]

The current theory states that it is the DHT produced within follicle cells, that is important in reacting with androgen receptors within the same cells, to change the cells growth response. I think you have said this is your view in past posts Bryan, correct me if i am mis-quoting you.

Actually, you're not misquoting ME, because that's what I believe. However, I think you're mildly misquoting the "Direct Theory" in general, because doctors and researchers nowadays don't really say very much about the relative importance of serum DHT versus "local" DHT production within hair follicle cells. They acknowledge occasionally that serum DHT _can_ enter cells and have an effect, but I've never seen any discussion or theorizing of the relative importance of those two routes of access. My guess (and that's all it is) is that nowadays, most scientists would tend to agree with my position.

[quote="S Foote.":c6b6f]Well the thing about this theory is it is `VERY' direct and straight forward. In other words, there isn't much that can be `different' in individuals.

But I think there ARE various things that can be different, like those androgen receptor gene polymorphisms that apparently can make a significant difference in the "sensitivity" of androgen receptors. Furthermore, there is the all-important issue of different qualitative (as opposed to quantitative) RESPONSES to the androgenic signal, like I posted about at length a month or so ago over on HLH.

In this study, there is no reference to finasteride creating a different level of DHT reduction in people with this different receptor `code'. So the only `difference' is in the receptors. But in reality, this cannot be a `major' difference in receptor efficiency!

No reference is made to any significant differences in sexual characteristics in the individuals tested. Those with the `weaker' androgen receptors are not reported as having any `female' characteristics, nor the `stronger' receptors producing any hyper-androgenic effects.

So `BOTH' types of receptors are `working' within the normal range, producing `normal' male characteristics.

It _is_ a bit puzzling why hairloss is so strongly statistically associated with a particular AR polymorphism, for the reason you state.

How then is it possible for these individuals to demonstrate such a different `actual' treatment response to finasteride? The `direct' theory just doesn't have the `scope' to explain this given such a small difference in receptor efficiency, and the alledged `direct' action on follicle cells!

The `direct' mechanism you propose Bryan just cannot allow for the observed `difference' in this study!

On the other hand, a `systematic' action of DHT acting `indirectly' upon hair growth, has far more scope in possible mechanisms to explain the difference in treatment effect with a slight difference in receptor efficiency.

Ok, NOW we come to the part where I think you fall flat on your face, Stephen. You're simply passing the puzzle farther along! I can't completely explain why the fate of hair follicles would depend to such a degree on certain AR polymorphisms, but neither can YOU explain why those other androgen-sensitive body processes which allegedly cause balding (according to your theory) are just as sensitive to that same polymorphism. Neither one of us has a really good, complete answer to that little problem, so you can't really make any hay out of it! :wink:

BTW, did you happen to see that new Japanese study that was posted recently on HLH? It was yet another in an increasingly long line of such studies that are now looking at the differences in growth factors that are secreted by various dermal papillae (body vs. scalp), in response to androgens. Like I've told you many times, scientists are slowly but steadily working their way through these complex biochemical pathways to elucidate the differences between scalp and body hair. Have patience!

Bryan[/quote:c6b6f]

Your big critism here Bryan, is that you say i am passing the puzzle father along. But if a theory can't solve a puzzle, it `has' to be passed on!

The trouble you have Bryan, is that you can't explain this study, or most others without resorting to phrases like `there are complexities that are not yet understood' . Sure there are things about male pattern baldness that are not yet understood, but `adding' complexity to try to explain observations is a big `no no' in the established practice of science.!

I could speculate upon currently not understood complexities, to try to defend my theory against `actual' studies that didn't support it. Would you agree with me then? Of course not! Don't expect me to accept unfounded speculation in support of the current theory!

Bryan said:

"My guess (and that's all it is) is that nowadays, most scientists would tend to agree with my position."

Not the up to date scientists Bryan! If you are right, why did Dr Sawaya state in her response i posted above, that others are proposing similar ideas as me? If the professional scientists were content with the current theory, why the re-think?

I haven't read the Japanese study you mention, and i am pushed for time now. Please post a link, and over the weekend i will read it and point out where you are wrong in your interpretation.

S Foote.

 

[Bryan]

The trouble you have Bryan, is that you can't explain this study, or most others without resorting to phrases like `there are complexities that are not yet understood' . Sure there are things about male pattern baldness that are not yet understood, but `adding' complexity to try to explain observations is a big `no no' in the established practice of science.!

Once again I'll give my favorite Einstein quote: "Physics should be made as simple as possible, but not simpler." Think about that! :wink: It's the same with physiology and biochemistry: when it's complex, it's complex. I don't "add" complexity except when it's necessary.

Bryan said:

"My guess (and that's all it is) is that nowadays, most scientists would tend to agree with my position."

Not the up to date scientists Bryan! If you are right, why did Dr Sawaya state in her response i posted above, that others are proposing similar ideas as me? If the professional scientists were content with the current theory, why the re-think?

HUH?? What does what Sawaya (or "up to date" scientists) said have to do with what _I_ said about serum DHT versus "local" DHT? You've lost me.

I haven't read the Japanese study you mention, and i am pushed for time now. Please post a link, and over the weekend i will read it and point out where you are wrong in your interpretation.

I'll try to find the abstract again tomorrow and post it in this thread.

Bryan

 

[Bryan]

Here's that study I was talking about. I've put in bold text a couple of the relevant statements for you:


"Pathomechanism of androgenetic alopecia and new treatment"

[Article in Japanese]

Itami S.

Department of Dermatology, Course of Molecular Medicine, Graduate School of Medicine, Osaka University.

Hair follicles are composed primarily of epithelial and dermal components that develop from embryonic ectoderm and mesoderm respectively. The hair growth cycle is coordinated with complex processes that are dependent on the interactions of epithelial and dermal components. Beard and frontal scalp dermal papilla cells (DPCs) show the characteristics of androgen target cells. These DPCs expressed androgen receptor and type II 5alpha-reductase mRNA. To understand the mode of androgen action in human hair follicles, we developed an in vitro co-culture system using DPCs and follicular keratinocytes. Androgen significantly stimulated the proliferation of keratinocytes co-cultured with beard DPCs, suggesting that these DPCs produce androgen-dependent diffusible growth factors. Insulin-like growth factor-I (IGF-I) was identified as one of the androgen dependent paracrine growth factors from beard DPCs. On the other hand, we identified inhibitory roles of androgen on the growth of keratinocytes co-cultured with DPCs from human balding frontal scalp, when DPCs were transfected with the AR expression vector. This inhibitory effect was mediated by TGF-beta1 from the DPCs. Minoxidil and Finasteride were recently introduced for the treatment of androgenetic alopecia in Japan, and TGF-beta1 is the next target for innovative treatment.

 

[kevinme]

so an increase in IGF-I (found in colostrum) is positive?

 

[S Foote.]

S Foote. wrote:
The trouble you have Bryan, is that you can't explain this study, or most others without resorting to phrases like `there are complexities that are not yet understood' . Sure there are things about male pattern baldness that are not yet understood, but `adding' complexity to try to explain observations is a big `no no' in the established practice of science.!


>>Once again I'll give my favorite Einstein quote: "Physics should be made as simple as possible, but not simpler." Think about that! It's the same with physiology and biochemistry: when it's complex, it's complex. I don't "add" complexity except when it's necessary. <<

I don't need to "think about that" as you put it Bryan, it is a principle i have been trying to teach you for a long time!

You say above: " I don't "add" complexity except when it's necessary. "

But thats `EXACTLY' what you and other supporters of the current direct theory `have to do' to try to justify it!!

Lets be sure about the issue we are discussing here Bryan.

The current direct theory of DHT related hair growth/loss, relies upon a `built in' difference in hair follicles. It is this built in difference that is `supposed' to dictate the different changes in growth of various follicles, when `directly' exposed to rising levels of androgens.

The problem you have Bryan is that the relevant in-vitro studies `DISPROVE' this theory!!

Here's the sections of that Japanese study you think in some way support the `direct' theory.


>>Androgen significantly stimulated the proliferation of keratinocytes co-cultured with beard DPCs, suggesting that these DPCs produce androgen-dependent diffusible growth factors. Insulin-like growth factor-I (IGF-I) was identified as one of the androgen dependent paracrine growth factors from beard DPCs.<<

>> On the other hand, we identified inhibitory roles of androgen on the growth of keratinocytes co-cultured with DPCs from human balding frontal scalp,<<

So what! The evidence you need to support the current theory is `missing' from this study as i think you know Bryan!

This study is essentialy the same as the Macaque study we discussed before. The `big' difference is that in the Macaque study, they `directly' exposed known `pre-balding' samples to androgens as well. As you know Bryan, direct exposure to androgens did `NOT' change healthy pre-balding follicle cells `INTO' balding follicle cells! http://endo.endojournals.org/cgi/content/full/138/1/356

The current `direct' theory says that androgens SHOULD directly `switch' these cells into balding mode. The Macaque study clearly `DISPROVES' this, and i'am willing to bet any similar human study would also show that this doesn't happen.

The in-vitro observations you are so fond of quoting in support of your arguments Bryan, are `AFTER' the fact. The samples you quote have `ALREADY' had their `particular' growth characteristics `CHANGED' by some kind of in-vivo process. Further exposure to any number of substances in-vitro, including androgens, could just be magnifying the `particular' existing growth characteristics of the samples. Cream cheese could have the same effect as androgens on these `ALREADY' growth transformed cells. Do we then say male pattern baldness is `CAUSED' by cream cheese!! Thats the reasoning you are using here Bryan!

The all important cause of the `CHANGE' in hair growth characteristics is what we want to know about!! The studies show this is `NOT' done through direct exposure to androgens, so the `direct' theory is disproved, simple!

This is where you and others have to add `unnecessary' complexity to try to keep your direct theory going. Not only this, but you have to make up un-precidented speculative mechanisms that go against existing knowledge in physiology!

This is your claim that given enough time, direct exposure of follicle cells to androgens `converts' these via a genetic `clock', into `directly' androgen responsive cells. Cells are either directly responsive to hormones or their not! There is no possible precident for such a `transformation through exposure' Bryan, and every time i ask you to quote a precident, you don't reply!

>>Once again I'll give my favorite Einstein quote: "Physics should be made as simple as possible, but not simpler<<

Exactly Bryan! This means as simple as `KNOWN' mechanisms allow!

The Hydraulic theory does precisely this.

All the observations in DHT related hair growth/loss, can be explained through `recognised' physiological mechanisms, by `ONE' primary action of DHT. This is an increase in the regular contractions of lymph vessels induced by DHT.

The only unresolved question this leaves is how my proposed influence of normal contact inhibition relates to the hair transplantation issue. Further resrearch by those in a position to do this would resolve this question.

But at least the Hydraulic theory doesn't have to `make up' fantasy biology to make it work, like the current theory does!

S Foote.

 

[Old Baldy]

S. Foote: Let's take your hydraulic theory to a more simple level.

Those areas of the body that are horizontal to gravity are the top of the scalp, shoulders and feet. Why do I still have hair on my shoulders and feet?

Also. I don't understand how these areas of many mens' bodies still have hair unless there is a "direct" action of DHT on certain (I'd say mutated) follicles?

Maybe if we could discover why these top of the scalp follicles "mutated" we'd be alot closer to a remedy. It has to do with the genetic makeup of these follicles IMHO. Mechanical mechanisms may aggravate the condition but they don't seem to trigger the "death knell" of minaturization?

I've read many times (Dr. Proctor is one example) that the minaturized follicle resembles an organ that is being rejected by the body. This has nothing to do with mechanical aggravations does it? What am I missing?

 

[S Foote.]

>>S. Foote: Let's take your hydraulic theory to a more simple level.

Those areas of the body that are horizontal to gravity are the top of the scalp, shoulders and feet. Why do I still have hair on my shoulders and feet?

Also. I don't understand how these areas of many mens' bodies still have hair unless there is a "direct" action of DHT on certain (I'd say mutated) follicles? <<

I don't think that gravity has any influence here. I think it is the local fluid `feed and return' equation that are important.

I suggest that DHT significantly increases lymphatic drainage efficiency, and that this is it's primary evolutionary function as a male hormone.

Increased lymphatic drainage reduces the amount of fluid and it's pressure in tissues. This reduces the `resistence' to anagen follicle enlargement, and allows a larger follicle before normal contact inhibition of follicle cell growth `kicks' in.

If there are a greater number of lymph vessels close to hair follicles, the reduction in the local fluid pressure will be greater, and the follicles here should be larger (according to the theory), producing more hair growth.

This would account for the increased hair growth of the pubic, armpit, and beard areas. These same areas have increased amounts of superficial lymph vessels.

The `Hydraulic' feed and return system of the human head is very complex, with a high pressure fluid `feed', scalp wounds bleed a lot!

In contrast the lymph vessels of the scalp are sparse, and any induced restriction in their fluid drainage, would increase fluid build up in the scalp. The higher the blood presure feeding the scalp in an individual, the more likely fluid build up would happen with any reduction in drainage efficiency. This fits with the link with male pattern baldness and heart disease studies ( a higher blood pressure effects both conditions).

This is a good diagram of the lymph vessel layout of the head. http://137.222.110.150/calnet/DeepNeck/ ... m#section6

The male pattern baldness area lies at the end of the drainage system, and fluid from this area has to pass through the more complex system of lower vessels. If DHT is increasing the contraction rate of lymph vessels, this is `slaming' the one way valves in the vessels shut against flow from the end of the `pipe work' (the male pattern baldness area). There would be a certain level of DHT in the individual that would create this back pressure effect. A crude analogy would be you are running the water upstairs and someone turns on the water downstairs. The `change' in flow effects the flow at the end of the system (upstairs).

>>Maybe if we could discover why these top of the scalp follicles "mutated" we'd be alot closer to a remedy. It has to do with the genetic makeup of these follicles IMHO. Mechanical mechanisms may aggravate the condition but they don't seem to trigger the "death knell" of minaturization? <<

I think that the `whole' miniaturization of follicles is an important point. We only have androgen receptors in the DP cells. So how come the `whole' follicle becomes miniaturized? The only KNOWN mechanism in physiology that can explain `whole organ' miniaturization, is contact inhibition!

>>I've read many times (Dr. Proctor is one example) that the minaturized follicle resembles an organ that is being rejected by the body. This has nothing to do with mechanical aggravations does it? What am I missing? <<

I dont think many scientists would propose miniaturization is mediated by some kind of immunology. The immune infiltrate is a factor that tends to occour after the miniaturization. I think it is now rightly regarded by most as an associated factor in male pattern baldness.

The Hydraulic theory explains the immunology in male pattern baldness by `known' physiology. This kind of immunology, fibrosis, and sensitivity to inflamation is already recognised in lymphedema. http://www.lymphoedema.org.au/index.htm

Good Luck.

S Foote.

 

[Old Baldy]

Interesting, how do we relieve this "pressure" on the "valve(s)"?

Note: I have to reread, then reread what you have written and what is stated in the links you provided. These types of things take time for me to learn and digest.

I firmly believe in the "shotgun" approach to fighting male pattern baldness. What I believe should be taken with a grain of salt because I'm so new at this game, but why not attack male pattern baldness from all known angles.

You see, pressure on blood vessels, etc., have always caused calamity in our bodies but I do admit I'm having a hard time digesting why this "male pattern baldness" scenario would only occur in the scalp area. I hear what you are saying but for the top of the scalp to have this type of "unique" structure, making it vulnerable to "pressure" still is questionable to this layman.

Like I said, I have to reread and reread. LOL