Question for Stephen Foote, with pictures for a point

[michael barry]

Bryan,

You mentioned this :"Michael, I don't understand how you come to that conclusion about blood DHT. Did you really mean androgens in general?"

Where I picked that up exactly I cant recall. Why Im inclined to believe it is that male to female transexuals (who keep their hair usually) are advised to take flutamide and some estrogen. They still have testicles and produce testosterone, but tend to keep their hair almost always. Some hair transplant docs have to deal with middle aged men who want to be women (or women-like), and Ive seen some pictures of them before/after. Dr. Michael Beehner had a pic of one on his hairtransplant website. This got me thinkin' so I did a little research on it one night a couple of years ago (back when I didnt know androgens werent all there was to male pattern baldness). I found out that the flutamide/estrogen routine and a flutamide routine are the route alot of these people take. They generally keep their hair (or so it seems). This is why I began to believe that the DHT created in the outer root sheath/scalp binded with androgen receptors to initiate baldness much more than the microcapillaries feeding DHT in blood to the follicle. Estrogen and receptor blockers shouldnt stop baldness if DHT was signifigantly getting to the follicle via capillaries, or so it would seem (who knows for sure though man, baldness is so perplexingly complicated).


After looking around for "cyclosporine, treatment, and edema" I found this "Edema: Edema or swelling is the accumulation of fluid in the body and it may be the result of a chronic process such as hypertension, heart or liver failure, or it may be a result of an acute change such an an electrolyte imbalance. Prednisone and tacrolimus are most frequently associated with edema. Prednisone tends to cause edema in the face and legs, whereas cyclosporine an tacrolimus cause edema in the legs/ankles"
on this http://groups.msn.com/TransplantSupport ... age21.msnw website. Its pretty much claiming that cyclosporin has been known to cause edema in the legs/ankles. Im assuming Stephen would assert thats due to it moving fluid out of scalp tissue. I must admit I am fascinated with minoxidl, flutamide, dutasteride, propecia, and especially proanthocyanidins (IVE EXPERIENCED THIS MYSELF) ability to make your hands swell.

I went a little overboard with the proanthocycanidns when I got them (smell is pleasant, kinda like an apple-cologne), and the first three nights I woke up with painful swelling in my hands. They literally hurt, they were full of fluid and painful (but sort of numb too in a way.....I know that seems like a contradiction, like being both hot and cold with the flu, but there it is). Its these coincidences that lead me to keep at least an eye open on Stephen's theory. Ive stated before, his is the only idea that could have any possible chance (knowing what I do know) of being at least somewhat true. There is no other alternative baldness theory that could even be concievably true in my opinion.

 

[Bryan]

I call Bryan a fake here, because he claims to be interested in true science. True scientific debate requires some consistency in your claims, and a degree of honesty and acceptance of evidence against your personal opinions.

I suspect that everyone reading this thread is now thinking the same three words that I am:

Pot. Kettle. Black.

:lol:

Bryan

 

[Bryan]

Where I picked that up exactly I cant recall. Why Im inclined to believe it is that male to female transexuals (who keep their hair usually) are advised to take flutamide and some estrogen. They still have testicles and produce testosterone, but tend to keep their hair almost always. Some hair transplant docs have to deal with middle aged men who want to be women (or women-like), and Ive seen some pictures of them before/after. Dr. Michael Beehner had a pic of one on his hairtransplant website. This got me thinkin' so I did a little research on it one night a couple of years ago (back when I didnt know androgens werent all there was to male pattern baldness). I found out that the flutamide/estrogen routine and a flutamide routine are the route alot of these people take. They generally keep their hair (or so it seems). This is why I began to believe that the DHT created in the outer root sheath/scalp binded with androgen receptors to initiate baldness much more than the microcapillaries feeding DHT in blood to the follicle.

How does that last sentence follow from the previous sentences, Michael?

Estrogen and receptor blockers shouldnt stop baldness if DHT was signifigantly getting to the follicle via capillaries, or so it would seem

Why do you think that antiandrogens wouldn't be able to stop blood-borne androgens from causing balding? What difference do you think it makes what the source of the androgens is?

Bryan

 

[michael barry]

Now that you put it that way, I see what you mean. Even blood-borne androgens must bind with receptor sites to affect the follicle. I keep thinking of follicles as mini organs....................apparently blood androgens dont just "flow into" the follicle like blood pumping into your arm. Sorry about that. Never really have thought of it that way before.



Stephen, did you note what I posted about cyclosporin's (and my own experience with proanthocyanidins) fluid shifting results? Have woken up with swollen hands. Its described in my earlier post. This suprised me, as I didn't expect that.

 

[Bryan]

Now that you put it that way, I see what you mean. Even blood-borne androgens must bind with receptor sites to affect the follicle.

I actually AGREE with what you said earlier about blood DHT having less of an effect on hair follicles than the DHT that's naturally produced within hair follicles cells; it's just that I couldn't make any sense out of WHY you thought that was true.

DHT in the bloodstream is eliminated fairly rapidly; according to the Gisloskog et al studies on finasteride and dutasteride, it has a half-life in the bloostream of only an hour or two. Therefore, I seriously doubt that any DHT molecules that leak out of cells into the blood have much of an endocrine effect on other tissues. They're simply eliminated too quickly! There's no doubt in my mind that if you could somehow take a "snap-shot" of a hair follicle dermal papilla cell at any given instant and trace the original source of each DHT molecule that you find inside it, the great majority of them will be ones that were originally generated right their within that same cell.

Bryan

 

[wookster]

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

It has also been shown that sebaceous and sweat gland efficiency is related to the action of DHT (5), (6). Where DHT increases hair growth there is a corresponding increase in sebum production, and reduced sweating efficiency. Where DHT reduces hair growth, there is a reduction in sebum production and increased sweating efficiency. There is therefore a known link between the action of DHT, and the activity of the main dermal structures.

This appears to be true, in my case. For several years my "balding area", forehead and face, would sweat profusely, after any extended physical exertion. In recent times the balding region has not sweated much after vellus hair began to increase. Now, after starting minoxidil, the less balding area along with the entire top of scalp does not have any detectible sweating when running two miles. The ol' forehead was really pumping out some sweat though. :freaked: :hairy: :freaked:

Been buzzing the scalp with a zero guard, so it is easy to detect the presence or absense of sweating on the noggin

 

[Bryan]

What I find highly questionable is the following claim:

Where DHT reduces hair growth, there is a reduction in sebum production...

I don't know where Stephen got THAT idea, but it's probably false.

Bryan

 

[wookster]

What I find highly questionable is the following claim:

Where DHT reduces hair growth, there is a reduction in sebum production...

I don't know where Stephen got THAT idea, but it's probably false.

Bryan

If sebum production and dandruff are related, and most bald heads are free of dandruff, then it could be true. :hairy:

 

[Armando Jose]

Bryan wrote:
"I actually AGREE with what you said earlier about blood DHT having less of an effect on hair follicles than the DHT that's naturally produced within hair follicles cells".

Yes, this is a important key. The DHT inside the follicle.I bet that in scalp hairs there is androgens also in prepubertal, DHT in special, but not circulating DHT, only in its neighboring cells. This is the base of the human scalp asynchronocity, and part of intracrinology issue( U. Laval)

It is clear the androgent relation and dependence of sebacecous gland, also there is a lot of balding people with problems with sebum (excess or defect), sebum soak the pilosebaceous unit where are the stem cells neccesaries to renew the hair follicle (miniaturization), sebum is a important part of the hydraulics in the skin, sebum is a part of the antioxidant system (vit E), and.etc etc,..., and then, why it is nutter think that problems with sebum are implicated in the multifactorial events of common alopecia?

Armando

 

[S Foote.]

I call Bryan a fake here, because he claims to be interested in true science. True scientific debate requires some consistency in your claims, and a degree of honesty and acceptance of evidence against your personal opinions.

I suspect that everyone reading this thread is now thinking the same three words that I am:

Pot. Kettle. Black.

:lol:

Bryan

Can you back that up with any evidence that "I" post different opinions in different threads, or ignore proper scientific evidence???

Talk is cheap :wink:

S Foote.

 

[S Foote.]

Now that you put it that way, I see what you mean. Even blood-borne androgens must bind with receptor sites to affect the follicle. I keep thinking of follicles as mini organs....................apparently blood androgens dont just "flow into" the follicle like blood pumping into your arm. Sorry about that. Never really have thought of it that way before.



Stephen, did you note what I posted about cyclosporin's (and my own experience with proanthocyanidins) fluid shifting results? Have woken up with swollen hands. Its described in my earlier post. This suprised me, as I didn't expect that.

I think the effect of changing local tissue fluid levels is the common factor Michael.

Minoxidil shifts fluid volume to lower levels of tissue.

http://www.hairsite4.com/dc/dcboard.php ... 051&page=2

Quote:


"Treatment of normotensive or hypertensive humans or rats with arterial vasodilators such as hydralazine or minoxidil results in marked haemodynamic changes, which can be described as a 'hyperdynamic circulation'. Acutely, these changes are a consequence of vagal withdrawal, reflex-mediated increases in sympathetic activity and renin release and a shift of blood to the central blood volume."

Even Latanoprost that was intended to reduce fluid pressure, was shown to increase hair growth.

http://dermatology.cdlib.org/93/comment ... /wolf.html

We should also remember that the reported cases of lipedematous scalp, and lipedematous alopecia show how it is possible for different levels of fluid to exist in different levels of tissue.

http://alopecia.researchtoday.net/archive/1/2/66.htm

S Foote.

 

[S Foote.]

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

It has also been shown that sebaceous and sweat gland efficiency is related to the action of DHT (5), (6). Where DHT increases hair growth there is a corresponding increase in sebum production, and reduced sweating efficiency. Where DHT reduces hair growth, there is a reduction in sebum production and increased sweating efficiency. There is therefore a known link between the action of DHT, and the activity of the main dermal structures.

This appears to be true, in my case. For several years my "balding area", forehead and face, would sweat profusely, after any extended physical exertion. In recent times the balding region has not sweated much after vellus hair began to increase. Now, after starting minoxidil, the less balding area along with the entire top of scalp does not have any detectible sweating when running two miles. The ol' forehead was really pumping out some sweat though. :freaked: :hairy: :freaked:

Been buzzing the scalp with a zero guard, so it is easy to detect the presence or absense of sweating on the noggin

I don't know if you saw this study, i referenced it in my paper. Here's the abstract.

http://hairmillion.com/ref-hair-loss/ha ... 3.506.html

I have the full paper, and it proves a direct relationship with the ability of tissue to sweat, and the presense of DHT related hair growth or loss.

This is perfectly in line with DHT induced changes in local tissue fluid pressures (sweat is tissue fluid).

S Foote.

 

[Bryan]

What I find highly questionable is the following claim:

Where DHT reduces hair growth, there is a reduction in sebum production...

I don't know where Stephen got THAT idea, but it's probably false.

Bryan

If sebum production and dandruff are related, and most bald heads are free of dandruff, then it could be true. :hairy:

But ARE bald heads less associated with dandruff? Not to my knowledge...

Bryan

 

[Bryan]

It is clear the androgent relation and dependence of sebacecous gland, also there is a lot of balding people with problems with sebum (excess or defect), sebum soak the pilosebaceous unit where are the stem cells neccesaries to renew the hair follicle (miniaturization), sebum is a important part of the hydraulics in the skin, sebum is a part of the antioxidant system (vit E), and.etc etc,..., and then, why it is nutter think that problems with sebum are implicated in the multifactorial events of common alopecia?

Anybody can come up with half-way plausible theories of what might be contributing to hair loss. The really tricky part is finding EVIDENCE in support of those theories. I don't see any EVIDENCE from you that supports your theory, Armando.

Bryan

 

[Bryan]

I think the effect of changing local tissue fluid levels is the common factor Michael.

Minoxidil shifts fluid volume to lower levels of tissue.

http://www.hairsite4.com/dc/dcboard.php ... 051&page=2

Quote:

"Treatment of normotensive or hypertensive humans or rats with arterial vasodilators such as hydralazine or minoxidil results in marked haemodynamic changes, which can be described as a 'hyperdynamic circulation'. Acutely, these changes are a consequence of vagal withdrawal, reflex-mediated increases in sympathetic activity and renin release and a shift of blood to the central blood volume."

And yet there have been complaints from topical minoxidil users of facial "puffiness". So do you think all that alleged "edema" merely dropped two or three inches from their scalp to their face? Do you think that they experienced less BEARD growth as a result? How does that jive with the often-reported complaints from minoxidil users of excessive BODY HAIR growth? :wink:

Even Latanoprost that was intended to reduce fluid pressure, was shown to increase hair growth.

http://dermatology.cdlib.org/93/comment ... /wolf.html

Wow. So even eyelids supposedly have edema, which suppresses the growth of eyelashes. Right, Stephen? Well, you're nothing if not persistent! :wink:

Bryan

 

[S Foote.]

I think the effect of changing local tissue fluid levels is the common factor Michael.

Minoxidil shifts fluid volume to lower levels of tissue.

http://www.hairsite4.com/dc/dcboard.php ... 051&page=2

Quote:

"Treatment of normotensive or hypertensive humans or rats with arterial vasodilators such as hydralazine or minoxidil results in marked haemodynamic changes, which can be described as a 'hyperdynamic circulation'. Acutely, these changes are a consequence of vagal withdrawal, reflex-mediated increases in sympathetic activity and renin release and a shift of blood to the central blood volume."

And yet there have been complaints from topical minoxidil users of facial "puffiness". So do you think all that alleged "edema" merely dropped two or three inches from their scalp to their face? Do you think that they experienced less BEARD growth as a result? How does that jive with the often-reported complaints from minoxidil users of excessive BODY HAIR growth? :wink:

It's very clear that you cannot even grasp the facts reported in your own links Bryan :roll:

"YOU" posted that Minoxidil link for God's sake, did you bother to read it?

That and the lipedematous scalp/alopecia links i posted, should have educated even you in how different fluid levels can exist in different layers of tissue. :freaked:

So you can have a swelling of the face "and" increased hair growth!

It just means the body of fluid has shifted from around the follicles to the deeper tissue.

Or are you once again trying to deny something made clear in one of your own posts? :wink:

Even Latanoprost that was intended to reduce fluid pressure, was shown to increase hair growth.

http://dermatology.cdlib.org/93/comment ... /wolf.html

Wow. So even eyelids supposedly have edema, which suppresses the growth of eyelashes. Right, Stephen? Well, you're nothing if not persistent! :wink:

Bryan

This is really pathetic Bryan :roll:

You know damm well my theory is about changes in tissue fluid levels, and "NOT" just the extremes of edematous tissue. :roll:

Or are you just stupid enough to think there is "NO" tissue fluid "at all" in hairy tissue, and pure edema in hairless tissue?

Instead of your usual distractions after i have asked "you" a question, just answer my question about that mouse study?

How do you explain those results according to the theory you support?

While your at it, you can tell us all how Latanoprost increases hair growth, if not by the mechanism i suggest??

People get sick of your constant dodging of the important issues 8)

S Foote.

 

[wookster]

But ARE bald heads less associated with dandruff? Not to my knowledge...

Bryan

:wink:

That is a good question. I don't ever recall seeing a slick bald head with flakes of dandruff on it. :hairy:

 

[Bryan]

It's very clear that you cannot even grasp the facts reported in your own links Bryan :roll:

"YOU" posted that Minoxidil link for God's sake, did you bother to read it?

Yes. Now answer the questions I asked you.

So you can have a swelling of the face "and" increased hair growth!

It just means the body of fluid has shifted from around the follicles to the deeper tissue.

I'll leave it up to the individual reader to decide for himself how credible that answer is. Now answer these other two questions which you conveniently ignored before:

Do you think that they experienced less BEARD growth as a result? How does that jive with the often-reported complaints from minoxidil users of excessive BODY HAIR growth?

Instead of your usual distractions after i have asked "you" a question, just answer my question about that mouse study?

I already have. Several times.

While your at it, you can tell us all how Latanoprost increases hair growth, if not by the mechanism i suggest??

Some as-yet unknown mechanism, apparently. BTW, latanoprost appears to have fizzled-out as a hairgrowth stimulant.

Bryan

 

[michael barry]

Stephen,
Your theory is fascinating in alot of ways. Even if it were proven to be wrong on head hair growth........Im inclined to believe it still might have relevance in body hair growth as Ive contemplated the "cast-hair growth phenomena" and the effects of carrying ice on the ice pack carriers growing a good bit of back hair (dont want it there though man : ).

The Latanoprost's article's authors did have a guess on why it might work that didn't have to do with fluid volume though.........(although they may be very wrong----hell the stuff is for your eyes (wonder if Proctor will ever slip this in Proxihphen as he's found a way to stuff every growth stimulant known to man in there-----a pharmacological genius that man must be).
Anyhoo......here was "their" explanation again for those following the thread:
:.............................................. "demonstrated that minoxidil is indeed a potent activator of purified PGHS-1, by assaying oxygen consumption and prostaglandin (PG)E2 production.[21] This activation was also evidenced by increased PGE2 production by BALB/c 3T3 fibroblasts and by human dermal papilla fibroblasts in culture. These findings suggest that the mechanism behind the hair-growth-stimulating effect of minoxidil is stimulation of PGE2 synthesis. If this conclusion were the case, it would stand to reason that other, more specific, PG activators (PG analogs) might show even better results."

So, in cultures, activating prostaglandin HS-1, increases in PGE2 production increased fibroblasts and human dermal papilla fibroblasts. They are stating that minoxidil might work because it stimulates PGE2 synthesis, and therefore PG activators like Latanoprost "might show even better results". Thats there explanation for one way latanoprost might work anyway. I dont know if Bryan would agree with their suggestion.

Yet again however, you have shown a fluid-shifting subsance to increase hair growth. The list from SOD's, proanthocyanidins, minoxidil. has another member.......latanoprost. It must be frustrating not to be able to get this tested.


Stephen, I dont know if youve forgotten an earlier experimental suggestion that I had. Simply talking someone who didnt plan to do anything about his hairloss to put a strong diuretic on his scalp a couple of times a day. Like petroleum jelly and ice packs for 6-12 months. Know any balding friends at work that you could pay a little money to try this for a little monetary incentive? Just a thought. I know that putting a cast or ice on an arm increases body hair growth......It would have to be head hair. Coal tar shampoos proboably wouldnt be enough.......but that could be the shampoo to be used. Ice packs too?

Perhaps we could get one of those specially bred "androgenic" mice? Dr. Uno or even better Waseda over at hairsite might be able to swing something like that. Waseda actually responds to emails over there? ......

 

[wookster]

I have a question about androgen receptors and the hydraulic theory of baldness:

http://www.ehrs.org/conferenceabstracts ... sawaya.htm

All scalp biopsies from patients obtained 6 months after finasteride treatment revealed intense upregulation of AR expression in comparison to pre-treatment biopsies of the same patient, whereas ERs were not affected, indicating that AR is very sensitive to the affects of 5a-R type II suppression of DHT.

:freaked: :freaked: :freaked:

How does the hydraulic theory of baldness explain this upregulation of androgen receptors due to finasteride and what part do androgen receptors play in the hydraulic/androgenic balding scenario.