Dispensing with old-fashioned male pattern baldness theories, and one NEW one!

[Bismarck]

(Sorry Bryan and Stephen! Carry on guys.)

I'm sure they do ... :box:

 

[Idaho X]

I’m no scientist and I haven’t read all the studies, but I’ll throw in my opinion on the subject. Maybe someone can educate me a little:

If it is proven that androgens cause male pattern baldness why is it so hard to find a cure? Why do anti-androgens not work for everybody? I know that Finasteride and Dutasteride only inhibit a certain percentage of scalp DHT, but if androgens are the problem, shouldn’t these drugs help everybody a little?

My own hair-loss feels more like an allergic reaction - it seems like my scalp is rejecting the hair. My head is constantly itchy and the areas where I am losing the most hair are red and irritated. From my personal experience, male pattern baldness appears to be an autoimmune response more than anything else.

 

[michael barry]

This is a question for two smart men, Stephen and Bryan.

In leiu of the recent discovery of the chromosome that is inherited from the mother that seems to determine the amount/potency of androgen receptors on the follicles, could male pattern baldness just be due to "too many androgen receptors" on the follicle?

My previoius little theory was that the follicle recieved androgens and male pattern baldness follicles then "sent out" information to surrounding tissue instructing it to overproduce oxides, keep sebum production high as follicle shrinks, inflame the scalp tissue and increase tissure pressure, shorten the anagen phase, lessen outer root sheet cell division, slow down keratin production, and basically "kill me".

However, now Im just beginning to think that "too many androgen receptors" allow for too much male hormone whether it be DHEAS, andro, DHT, testosterone to get in and start the process. The study says that perhaps the androgen receptors that male pattern baldness men have might be more stable and not break down as often, or that the follicle keeps making more of them, or just has more to begin with.

I'll let you guys in on why Im leaning toward this and its simply the Japanese experience of seeing Urban men on western diets balding there 4 times more often than rural Japanese. Baldness used to be almost a freak occurence in Japan 60 years ago, but now that they eat McDonalds and steroided/hormoned saturated fats from red meat and have so much more androgen and processed gunk in their arteries and capillaries..........that THEIR historically VERY good hair is hittin' the floor. This leads me to believe if we lambasted "donor" hair with androgens in experiments, they might start to miniaturize too.

Feel free to laugh out loud if ya' disagree and please tell me where you think I may be wrong. I never get mad about being corrected and love to learn. Best, M

 

[S Foote.]

I’m no scientist and I haven’t read all the studies, but I’ll throw in my opinion on the subject. Maybe someone can educate me a little:

If it is proven that androgens cause male pattern baldness why is it so hard to find a cure? Why do anti-androgens not work for everybody? I know that Finasteride and Dutasteride only inhibit a certain percentage of scalp DHT, but if androgens are the problem, shouldn’t these drugs help everybody a little?

My own hair-loss feels more like an allergic reaction - it seems like my scalp is rejecting the hair. My head is constantly itchy and the areas where I am losing the most hair are red and irritated. From my personal experience, male pattern baldness appears to be an autoimmune response more than anything else.

I think the vast majority of evidence, clearly shows that the `significant' effect of androgens in-vivo, is indirect. If it was `direct', the anti-androgen topicals would at least prevent male pattern baldness, and work a lot better than they do as a treatment.

My theory of follicle miniaturization caused by increased fluid pressure, also explains the inflammation and ultimate fibrosis. This is what happens in edemous tissue.

The immunology is something else that the `direct' theory just can't explain without making up `magic' mechanisms. If DHT is `marking' male pattern baldness follicles for an immune response, the follicles would be severly damaged or even destroyed! This is what an autoimmune response does, it destroys the cell type it is targeting. In male pattern baldness the follicles are `NOT' destroyed, they remain fully functioning. They are just miniaturised!

I think even Bryan agrees that most researchers think the inflammation is an associated, and not a causal factor in male pattern baldness.

According to my theory, the inflammation will add to the edema and so make matters worse and needs to be treated.

S Foote.

 

[S Foote.]

This is a question for two smart men, Stephen and Bryan.

In leiu of the recent discovery of the chromosome that is inherited from the mother that seems to determine the amount/potency of androgen receptors on the follicles, could male pattern baldness just be due to "too many androgen receptors" on the follicle?

My previoius little theory was that the follicle recieved androgens and male pattern baldness follicles then "sent out" information to surrounding tissue instructing it to overproduce oxides, keep sebum production high as follicle shrinks, inflame the scalp tissue and increase tissure pressure, shorten the anagen phase, lessen outer root sheet cell division, slow down keratin production, and basically "kill me".

However, now Im just beginning to think that "too many androgen receptors" allow for too much male hormone whether it be DHEAS, andro, DHT, testosterone to get in and start the process. The study says that perhaps the androgen receptors that male pattern baldness men have might be more stable and not break down as often, or that the follicle keeps making more of them, or just has more to begin with.

I'll let you guys in on why Im leaning toward this and its simply the Japanese experience of seeing Urban men on western diets balding there 4 times more often than rural Japanese. Baldness used to be almost a freak occurence in Japan 60 years ago, but now that they eat McDonalds and steroided/hormoned saturated fats from red meat and have so much more androgen and processed gunk in their arteries and capillaries..........that THEIR historically VERY good hair is hittin' the floor. This leads me to believe if we lambasted "donor" hair with androgens in experiments, they might start to miniaturize too.

Feel free to laugh out loud if ya' disagree and please tell me where you think I may be wrong. I never get mad about being corrected and love to learn. Best, M

I think the fact that many different factors `can' effect hair growth, also supports an indirect effect of androgens. If it was just a case of androgens signal male pattern baldness in `pre-disposed' follicles, nothing else including Minoxidil could change things!

I think the `genetic' link is a multi- factoral effect, that determines many factors in the individual that creat male pattern baldness systematicaly.

I dont go along with the increased androgen receptor idea effecting the situation. finasteride and dutasteride creates an increase in receptors within follicle cells, but the treatment effect is still there?

Again, if the androgen receptors in follicle cells are the big issue, why dont topical receptor blockers `cure' the problem?

S Foote.

 

[Petchsky]

I think these threads are good sh*t.

Bryan and Stephen clearly have different viewpoints on male pattern baldness. I think this provides a great source of information for the reader, who, let's face it, must be interested in male pattern baldness if they are reading the Bryan v Stephen threads. You get two different educated opinions giving you a broader view without trawling through science journals and other sources that are for the really dedicated

Keep fighting the good fight! I don't know what that means, but, YEAH!!!

 

[Bryan]

If it is proven that androgens cause male pattern baldness why is it so hard to find a cure?

It's not all that easy to get a level of androgen suppression which is effective AND safe.

Why do anti-androgens not work for everybody?

I assume you're referring to TOPICAL antiandrogens (systemic ones can't really be used by men). It's quite difficult to design a topical antiandrogen that's really effective. The ones we have currently are only rather mediocre (with the _possible_ exceptions of RU58841 and fluridil).

I know that Finasteride and Dutasteride only inhibit a certain percentage of scalp DHT, but if androgens are the problem, shouldn’t these drugs help everybody a little?

I think they _do_ help everybody a little. In some cases, considerably MORE than just a little.

My own hair-loss feels more like an allergic reaction - it seems like my scalp is rejecting the hair. My head is constantly itchy and the areas where I am losing the most hair are red and irritated. From my personal experience, male pattern baldness appears to be an autoimmune response more than anything else.

It's pretty clear that there's also an immune component to balding. Probably more in the later stages.

BTW, I'm just passing through at the moment, and don't have much time. I'll have to save my replies to the others in this thread for tomorrow (including Mr. Foote's! :wink: ).

Bryan

 

[Bryan]

I'll let you guys in on why Im leaning toward this and its simply the Japanese experience of seeing Urban men on western diets balding there 4 times more often than rural Japanese. Baldness used to be almost a freak occurence in Japan 60 years ago, but now that they eat McDonalds and steroided/hormoned saturated fats from red meat and have so much more androgen and processed gunk in their arteries and capillaries..........that THEIR historically VERY good hair is hittin' the floor. This leads me to believe if we lambasted "donor" hair with androgens in experiments, they might start to miniaturize too.

Michael, I want you to think carefully about the following question, and then give me a serious answer: If we lambasted BEARD hair follicles with androgens in experiments, do you think they would start to miniaturize?

Bryan

 

[michael barry]

Bryan,
Im supposing the beard hair would grow more rapidly and more of it would enter the anagen phase because DHT makes body and beard hair grow, opposite its effect on head hair, making for some real cave-man beard growth I would imagine. I wonder if the urban japanese have more facial hair now than they used to? That would be a good question to pursue.
Ive seen that body hair moved to the scalp grows longer and thicker much like head hair and we suppose its hormonal influences in the skin that has this effect on keratin production.

Castration proves to me that androgens are the trigger of male pattern baldness. I see that you and Stephen disagree on where the trigger is tripped. You believe its in the follicle proper, proboably the dermal papilla. Stephen believes its in the very close surrounding skin and tissue fluid pressure increases as a result and chokes the follicle's expansion in one of the earlier of 8 total anagen phases.

If you are right and the trigger is in the follicle proper, it would seem to be in the part of the follicle that remains in telogen phase when detatched from the papilla, because this part is always there and never leaving. Im guessing you think that after hair cycle number X in genetically predisposed follicles, the DNA instructions from the follicle to surrounding tissues, root sheeth, keratinocytes, sebum gland, etc.....become different and say "start miniaturization now"

I personally am waiting on cloning like everyone else, but Im not optomistic about it, and therefore and looking for ways to keep what Ive got as long as possible........Have a great weekend everybody, M

 

[Bryan]

Michael, I asked you that question because I want people to focus more on the qualitative differences among hair follicles, not just the quantitative differences. Many people seem to think that the main difference between balding and non-balding scalps is just a difference in the AMOUNT of response: all scalps have pretty much the same propensity to go bald in response to androgens (so they assume), but some guys are lucky enough to have fewer androgen receptors, less 5a-reductase, less testosterone or whatever, so they retain most or all of their hair.

I want people to consider the possibility of a different qualitative response from one follicle to another. The fact that androgens make beard follicles grow nice and big and fat while at the same time causing balding scalp follicles to miniaturize obviously has nothing to do with a difference in the number of androgen receptors (or whatever). It has to do with a fundamentally different RESPONSE that's progarammed into those two different types of follicles. I also suggest that the difference between balding and non-balding scalp follicles has more to do with that fundamentally different RESPONSE to androgens, not just a difference in the levels of androgens themselves.

I can cite you some evidence that seems to support that idea: there was an in vitro study with human scalp follicles which found that in addition to all the follicles whose growth was stunted when testosterone was added to the culture medium (exactly what you'd expect in androgenetic alopecia), there were also the occasional oddball follicles which did NOT seem to be affected one way or the other by testosterone. Those "immune" follicles were just randomly dispersed among the normal balding ones, with no apparent pattern. In other words, there could be neighboring follicles with different responses to testosterone: one which miniaturizes from male pattern baldness, and another one only 1 mm away which grows normally. Some guys have in fact noticed normally-growing hairs right in the middle of thinning/balding areas.

BTW, that's another difficult phenomenon for Stephen to explain with his theory: I wonder why individual hair follicles here and there in an area of generalized edema would be spared from that alleged "contact inhibition", while the others all around it succumb to the "pressure" and go bald! :wink:

Bryan

 

[michael barry]

Bryan,
I have noticed some unusual frontal baldness and "wild hairs" on balding men myself and wondered why some hairs were "die-hard" when I see this. Ive wondered also whether the DNA in some follicles (or very close surround) is just different and when it recieves androgen and reads it, then tells surrounding glands, tissues, and parts of the follicle to begin male pattern baldness when other follicles either dont or wait so much longer to give out the suicidal instructions.

Brian and Steve, Have you ever observed that the hippocratic wreaths of bald men thin? The wreath stays the same size, but its definintely not as thick as it once was. Ive seen almost "see-though" wreath hair before. I wondered if 2 or 3 out of 10 wreath hairs are male pattern baldness to an extent. This is one reason that Im dubioius about transplantation. A guy may get a 2500 graft transplant and look "fair" from the front, but 20 years from now that "gee its kinda thin when you run your fingers through it" hair on the back and sides might turn into "I hope its not wet out or everyone will be looking at how unusually much scalp I have visible on the back of my head". *Note: I seen a 60'ish guy at a Pierre Amelotte Transplant office once with a full frontal hairline who turned around and had bangs-thin hair on the back of his head that he grew into a small mullet to hide the fact it had receeded upwards from the bottom to an extent. Needless to say, this didnt look natural and his side/ear recession made it look even more so.

As far as contact inhibition/ anti-inflammation is concerned, I wonder if an icepack at night on the head or just a good anti-inflammatory cream that lasts 24 hours would show benefit. In a couple of years, photographic evidence should show yea or nay it would seem. I'd like to see male pattern baldness hairs INDIVIDUALLY moved from the temple up to the widows peak or further up the temple and see their response in 2-3 years as far as diameter is concerned. It proboably wouldnt take 10 hairs total to get a good idea about fibrosis scaffolds and whether they provide protection from androgens and/or allow for early angagen enlargement.


On an unrelated note that did intrigue me a little about Armondo Jose and his idea. I washed my pillowcases (I do this about monthly) recently and really took a look at the pillow beneath. Sure enough, their is a faint dark yellow film on them which has to be sebum secretions. I know that the sebum glands on each hair keep pumping out sebum at pre male pattern baldness levels even as hair miniaturizes. The DHT in the gunk can be reabsorbed. You know, just from a "treatment" perspective, he may be right about a bit of joboba oil in the shampoo or whatnot. The male pattern baldness affected areas make too much of this gunk and it cant be good for us fightin' it. Have a great weekend guys and enjoy your very informative debates, even if you two are awfully hard on each other, M

 

[Armando Jose]

Bryan,
I have noticed some unusual frontal baldness and "wild hairs" on balding men myself and wondered why some hairs were "die-hard" when I see this. Ive wondered also whether the DNA in some follicles (or very close surround) is just different and when it recieves androgen and reads it, then tells surrounding glands, tissues, and parts of the follicle to begin male pattern baldness when other follicles either dont or wait so much longer to give out the suicidal instructions.

Brian and Steve, Have you ever observed that the hippocratic wreaths of bald men thin? The wreath stays the same size, but its definintely not as thick as it once was. Ive seen almost "see-though" wreath hair before. I wondered if 2 or 3 out of 10 wreath hairs are male pattern baldness to an extent. This is one reason that Im dubioius about transplantation. A guy may get a 2500 graft transplant and look "fair" from the front, but 20 years from now that "gee its kinda thin when you run your fingers through it" hair on the back and sides might turn into "I hope its not wet out or everyone will be looking at how unusually much scalp I have visible on the back of my head". *Note: I seen a 60'ish guy at a Pierre Amelotte Transplant office once with a full frontal hairline who turned around and had bangs-thin hair on the back of his head that he grew into a small mullet to hide the fact it had receeded upwards from the bottom to an extent. Needless to say, this didnt look natural and his side/ear recession made it look even more so.

As far as contact inhibition/ anti-inflammation is concerned, I wonder if an icepack at night on the head or just a good anti-inflammatory cream that lasts 24 hours would show benefit. In a couple of years, photographic evidence should show yea or nay it would seem. I'd like to see male pattern baldness hairs INDIVIDUALLY moved from the temple up to the widows peak or further up the temple and see their response in 2-3 years as far as diameter is concerned. It proboably wouldnt take 10 hairs total to get a good idea about fibrosis scaffolds and whether they provide protection from androgens and/or allow for early angagen enlargement.


On an unrelated note that did intrigue me a little about Armondo Jose and his idea. I washed my pillowcases (I do this about monthly) recently and really took a look at the pillow beneath. Sure enough, their is a faint dark yellow film on them which has to be sebum secretions. I know that the sebum glands on each hair keep pumping out sebum at pre male pattern baldness levels even as hair miniaturizes. The DHT in the gunk can be reabsorbed. You know, just from a "treatment" perspective, he may be right about a bit of joboba oil in the shampoo or whatnot. The male pattern baldness affected areas make too much of this gunk and it cant be good for us fightin' it. Have a great weekend guys and enjoy your very informative debates, even if you two are awfully hard on each other, M

Yes Michael, this is my idea but, IMO sebum inward flow it is the crucial point in common baldness, not only outward flow of sebum.
Sebum is easily oxidiced, and then the problems arrive.

Armando

 

[S Foote.]

Michael, I asked you that question because I want people to focus more on the qualitative differences among hair follicles, not just the quantitative differences. Many people seem to think that the main difference between balding and non-balding scalps is just a difference in the AMOUNT of response: all scalps have pretty much the same propensity to go bald in response to androgens (so they assume), but some guys are lucky enough to have fewer androgen receptors, less 5a-reductase, less testosterone or whatever, so they retain most or all of their hair.

I want people to consider the possibility of a different qualitative response from one follicle to another. The fact that androgens make beard follicles grow nice and big and fat while at the same time causing balding scalp follicles to miniaturize obviously has nothing to do with a difference in the number of androgen receptors (or whatever). It has to do with a fundamentally different RESPONSE that's progarammed into those two different types of follicles. I also suggest that the difference between balding and non-balding scalp follicles has more to do with that fundamentally different RESPONSE to androgens, not just a difference in the levels of androgens themselves.

The problem with your suggestion here Bryan, is that this `different pre-programing' idea has been tested and found to be wrong!

You say above quote:
"I also suggest that the difference between balding and non-balding scalp follicles has more to do with that fundamentally different RESPONSE to androgens"

But you `KNOW' thats just plain wrong Bryan :roll:

When normal terminal hair producing follicles that are known to be `future' male pattern baldness follicles are exposed to androgens in-vitro, nothing happens! These future male pattern baldness follicles are `NOT' converted into male pattern baldness follicles by androgens `directly'. So there can be no `pre-program' waiting in these follicles that is any `different' than other scalp terminal follicles.

The in-vitro studies are very clear in that androgens do not directly `CHANGE' the pre-existing growth characteristics of `ANY' hair follicle!

http://endo.endojournals.org/cgi/content/full/138/1/356

http://www.fasebj.org/cgi/content/full/16/14/1967

In order to try to `excuse' these testing results, the supporters of the direct theory have `made up' a mechanism to try to explain this. This piece of guesswork `ASSUMES' that given enough time a direct exposure to androgens `would' change the way that follicles respond to them?

This is despite the fact that there is no known precedent in biology for such a `magic' mechanism, and in my opinion this demonstrates the poor science that has held back hair loss research for many years.

I can cite you some evidence that seems to support that idea: there was an in vitro study with human scalp follicles which found that in addition to all the follicles whose growth was stunted when testosterone was added to the culture medium (exactly what you'd expect in androgenetic alopecia), there were also the occasional oddball follicles which did NOT seem to be affected one way or the other by testosterone. Those "immune" follicles were just randomly dispersed among the normal balding ones, with no apparent pattern. In other words, there could be neighboring follicles with different responses to testosterone: one which miniaturizes from male pattern baldness, and another one only 1 mm away which grows normally. Some guys have in fact noticed normally-growing hairs right in the middle of thinning/balding areas.

BTW, that's another difficult phenomenon for Stephen to explain with his theory: I wonder why individual hair follicles here and there in an area of generalized edema would be spared from that alleged "contact inhibition", while the others all around it succumb to the "pressure" and go bald! :wink:

Bryan

Well if we assume that the researchers didn't make a mistake Bryan, `ALL' the samples in the culture would have come from in-vivo male pattern baldness follicles correct?

So if they then got the odd sample that grew normally in-vito in the presence of androgens, that `screws' the direct theory you support Bryan!

If the follicle samples were a `mixed' bunch from the male pattern baldness area, and some of these were not `yet' miniaturised, this study just confirms what i said above! The samples are `NOT' directly `CHANGED' by androgens! Your direct theory is still `screwed' Bryan 8)

The long term survival of some follicles in the male pattern baldness area `IN-VIVO', can be easily explained through my theory using recognised follicle biology!

I have emphasized before that the increased pressure only effects follicles entering the anagen enlargement phase, and resists their enlargement through normal contact inhibition. Those follicles `ALREADY' enlarged at the time of increased pressure, will not be effected until they go through telogen and enter anagen `AGAIN'!!

The anagen phase can last for up to 12 years, maybe even longer in scalp hair! So you will get long term `survivors' depending on the point in the hair cycle they were in at the time of increased pressure.

The pressure increase itself can also take time to build and extend through the male pattern baldness area!

These factors combined explain the pattern of loss in male pattern baldness, the time frame difference in loss, and the `thinning' and long term survival of some follicles.

In contrast, the direct theory not only `needs' a magic genetic clock in male pattern baldness follicles, it needs a `different' setting for this genetic clock in `EACH' follicle!

This is just another of many un-precedented `band aid' fixes required to patch up the crumbling `direct' theory. :wink:

S Foote.

 

[S Foote.]

Bryan,
I have noticed some unusual frontal baldness and "wild hairs" on balding men myself and wondered why some hairs were "die-hard" when I see this. Ive wondered also whether the DNA in some follicles (or very close surround) is just different and when it recieves androgen and reads it, then tells surrounding glands, tissues, and parts of the follicle to begin male pattern baldness when other follicles either dont or wait so much longer to give out the suicidal instructions.

Brian and Steve, Have you ever observed that the hippocratic wreaths of bald men thin? The wreath stays the same size, but its definintely not as thick as it once was. Ive seen almost "see-though" wreath hair before. I wondered if 2 or 3 out of 10 wreath hairs are male pattern baldness to an extent. This is one reason that Im dubioius about transplantation. A guy may get a 2500 graft transplant and look "fair" from the front, but 20 years from now that "gee its kinda thin when you run your fingers through it" hair on the back and sides might turn into "I hope its not wet out or everyone will be looking at how unusually much scalp I have visible on the back of my head". *Note: I seen a 60'ish guy at a Pierre Amelotte Transplant office once with a full frontal hairline who turned around and had bangs-thin hair on the back of his head that he grew into a small mullet to hide the fact it had receeded upwards from the bottom to an extent. Needless to say, this didnt look natural and his side/ear recession made it look even more so.

I agree that there is some thinning of the side/back hair in male pattern baldness, and certainly an upwards recession at the back over time as you describe.

I think there is a wider effect than is currently recognised, and lets not forget the hair that starts sprouting from the nose and ears in old folks like Bryan and me!

I think these `secondary' effects over a long time period are just the result of the slow building fluid level changes induced by androgens in various places.

lAs far as contact inhibition/ anti-inflammation is concerned, I wonder if an icepack at night on the head or just a good anti-inflammatory cream that lasts 24 hours would show benefit. In a couple of years, photographic evidence should show yea or nay it would seem. I'd like to see male pattern baldness hairs INDIVIDUALLY moved from the temple up to the widows peak or further up the temple and see their response in 2-3 years as far as diameter is concerned. It proboably wouldnt take 10 hairs total to get a good idea about fibrosis scaffolds and whether they provide protection from androgens and/or allow for early angagen enlargement.

I think ice packs used regularly `will' make a noticable improvement. The problem is just one of convenience. If you can do this for 15-20 mins twice a day it should help.

I did this when i was having out patient chemotheropy for cancer, and it saved a lot of my hair compared to others on the same course at the same time. Chemotheropy causes massive edema.

I think it would be interesting to study the results of topical coumarin and other benzo-pyrones in male pattern baldness. These are effective in treating edema in lymphedema, but are prescription only drugs.

http://www.lymphoedema.org.au/ (Click on treatments)



Yes there are a range of transplantation tests that could be done to resolve the questions. The trouble is the current research is mainly done by people in the industry who have a vested interest!

S Foote.

 

[Greg1]

Oh my gosh, you guys are at it again?! Let it rest guys! Please!

 

[S Foote.]

Oh my gosh, you guys are at it again?! Let it rest guys! Please!

Greg, don't you think that these debates at least get people thinking for themselves, rather than just going along with someone else's opinion?

Science is all about the argument of different opinions, and the scientific method evolved to `test' the various opinions.

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

The trouble on these hair loss forums is that people are emotionally involved, and often just want to `believe' that a particular thing offers `hope'.

This is why it is often easy for real science to be overlooked in male pattern baldness, but in the long term it is only `real' science that will provide the answers!

S Foote.

 

[WiseJoeyD]

Okay, sorry if anyone's mentioned this, but the mentions made of follicles in laborartaries bombarded with androgens to no effct; due maybe since they do 'do' something that highlights the follicles to the immune system, but since therse aren't in these 'in vitro' (correct usage?!) might mean it looks like nothing happens. Mind you it technically would show DHT doens't actually miniature them it'd be the turn of the immune system. Of course what both of yous have been saying variously about tissue pressure and the like as well as immune response issues has been very illuminating.

Recently my scalp has begun tingling again! Not quite itchyness. Would Nizoral 2%, which I've been using, be enough to qwell this response? Coud be it's just dried out my scalp an dit's not the aforementioned immuno-response

 

[S Foote.]

Okay, sorry if anyone's mentioned this, but the mentions made of follicles in laborartaries bombarded with androgens to no effct; due maybe since they do 'do' something that highlights the follicles to the immune system, but since therse aren't in these 'in vitro' (correct usage?!) might mean it looks like nothing happens. Mind you it technically would show DHT doens't actually miniature them it'd be the turn of the immune system. Of course what both of yous have been saying variously about tissue pressure and the like as well as immune response issues has been very illuminating.

Recently my scalp has begun tingling again! Not quite itchyness. Would Nizoral 2%, which I've been using, be enough to qwell this response? Coud be it's just dried out my scalp an dit's not the aforementioned immuno-response

I certainly think that it is an in-vivo effect of androgens that is creating the all important `change', and the in-vitro results confirm this in my opinion. I dont think the immunology in male pattern baldness is the `cause' of male pattern baldness, just an associated factor. The increased inflammation and ultimate fibrosis will make the situation worse, and make it harder to reverse follicle miniaturisation, so it does need to be addressed.

What has to be remembered from the scientific perspective is this.

If you are going to propose that the immunology is `causing' DHT related hair loss, you have to also explain how the immunology `causes' DHT related hair `GROWTH'!

DHT grows hair over the larger part of the body, but there is no evidence for any immune involvement?

I think it is the DHT induced changes in tissue fluid pressures, that change anagen follicle size via normal contact inhibition. Where DHT increases fluid pressure to create follicle miniaturization (the male pattern baldness area), the increased fluid level `ALSO' changes the local immunology. Increased fluid levels (edema), are known to produce the kind of immunology and fibrosis we see in male pattern baldness.

http://www.lymphoedema.org.au/ (Click `what is lymphoedema').

I think you should search the forums for others experiences with Nizorall, or anything else related to treating the inflammatory aspect.

Good luck.

S Foote.

 

[WiseJoeyD]

Thanks for the info!

PS What is contact inhibition?! Anything to do with swelling (edema...wait, that IS the right term?!) causing the hair follicle to find it hard to grow back thick?

 

[S Foote.]

Thanks for the info!

PS What is contact inhibition?! Anything to do with swelling (edema...wait, that IS the right term?!) causing the hair follicle to find it hard to grow back thick?

Contact inhibition is a `force' that all `normal' cell growth is subject to. Basicaly, this is an inbuilt mechanism that controls cell multiplication in multi-cellular biology. Whatever signals cells in an organ may get to grow, say to repair that organ after injury, this cell multiplication can only happen if there is `room' for this. When there is a certain level of resistence from the tissues around this cell growth and expansion, the `contact force' turns off this cell growth.

The only cell types that dont respond to this contact inhibition of cell growth, are cancer cells. This is why cancer cells can `invade' other tissues causing damage.

The hair follicle is the only organ that regularly goes through a natural shrinkage and enlargement process (the normal hair cycle). When the follicle enters the anagen growth phase, it has to `grow' (expand) within the dermal tissue. If the dermal tissue has a high resistence to movement, normal contact inhibition will happen earlier in the follicles growth. The follicle growth will be swiched off earlier creating miniaturized follicles.

In understanding how increased fluid pressure in the dermal tissue can increase the `resistence' of dermal tissue to follicle growth, i suggest the `balloon' analogy.

If you take an ordinary party balloon and try to push a finger into it, how hard it is to push your finger in depends on the `pressure' within the balloon!

The growing anagen follicle is trying to make a hollow space in the dermal tissue, like your finger is in the balloon. The harder it is to do this, the earlier the normal contact inhibition level is reached, the sooner follicle enlargement is switched off! The result is miniaturized anagen follicles as seen in male pattern baldness.

I suggest that hair follicles and the hair cycle evolved to `read' tissue resistence in this way, to adjust hair growth in line with mammals `Hydraulic' temperature controls. I describe this in my paper here.

http://www.hairsite2.com/library/abst-167.htm

I suggest in my arguments that androgen related changes in hair growth are via similar androgen induced `Hydraulic' changes in the tissue around the follicles.

S Foote.