DHT and Testosterone kills hair DIRECTLY........study

Bryan

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michael barry said:
Just buying the latanaprost would be cheaper.

Didn't Dr. Lee himself test latanoprost, and find the results disappointing? Isn't that why he gave up on it?

Bryan
 

docj077

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michael barry said:
Stephen will love this: http://ajpregu.physiology.org/cgi/conte ... 274/3/R790

and especially this : http://content.karger.com/ProdukteDB/pr ... elNr=68942


I'll say this in response to prostaglandin E-1 and lymphatic vaosomotion and Stephen's theory........................this is why I'd like to see Stephen get his theory tested finally and officially. So we could either pursue it or forget it. Lots of coincidences like I list earlier in the thread incredibly seeminlgy fit his idea. That prostaglandin analogues apparently slow the pumps indirectly buy f****ing with the capillaries beneath them, thus lowering upward pressure on the scalp................is 'convienient' to his idea.


Yet another coincidence. Stephen, I hope you can get your idea studied someday to give yourself personal satsfaction yea or nea. I have a very hard time thinking so many scientists who are balding themselves the world over could have all missed something one man could spot, but you still deserve that confirmation.

The problem with Stephen's idea is not the science. It's that he doesn't understand that he's merely trying to treat the symptoms of a larger disease process. The process begins far before what he considers to be veinous stasis and lymphatic stasis-induced edema secondary to lymphatic valve or lymph flow dysfunction. Androgen binding within muscle tissue and muscle hypertrophy do not explain the stasis in the scalp and face. There is no evidence of muscular hypertrophy and the lymphatics that drain the face don't run through the muscle. They run through the subcutaneous tissues very close to the skin.

By treating the symptoms, the disease remains and the disease occurs on the molecular level before it occurs on the histological or physiological level.

The process must be stopped before it has a chance to ever begin, because prolonged fibrosis of the follicle will render it useless to all treatment options.

I'm willing to work with the guy, but the approach should be one that targets both the molecular mechanisms of hair loss and the physiological outcome of the damage that occurs due to those previously mentioned mechanisms.

Lymphedema doesn't just suddenly appear anywhere unless you have an obstruction of some sort. Something has to be causing that obstruction on the molecular level. So, preventing both should be the goal of any hair loss treatment once it has moved beyond the molecular stage and into the fibrotic, collagenous, and vascular stasis stage.

This disease is multifactorial and multistep which is something that I think we all need to recognize.
 

wookster

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Bryan said:
Wookie, your posts have always struck me as being rather odd and oblique.

Bryan

:freaked: :freaked: :freaked:

http://www.medscape.com/medline/abstract/16536801

Inhibitory autocrine factors produced by the mesenchyme-derived hair follicle dermal papilla may be a key to male pattern baldness.

[...]

Although these changes are driven by androgens, most molecular mechanisms are unknown, limiting available treatments. The mesenchyme-derived dermal papilla at the base of the mainly epithelial hair follicle controls the type of hair produced and is probably the site through which androgens act on follicle cells by altering the regulatory paracrine factors produced by dermal papilla cells. During changes in hair size the relationship between the hair and dermal papilla size remains constant, with alterations in both dermal papilla volume and cell number. This suggests that alterations within the dermal papilla itself play a key role in altering hair size in response to androgens.

[...]

CONCLUSIONS:

Human balding dermal papilla cells secrete inhibitory factors which affect the growth of both human and rodent dermal papilla cells and factors which delay the onset of anagen in mice in vivo. These inhibitory factor(s) probably cause the formation of smaller dermal papillae and smaller hairs in male pattern baldness. Identification of such factor(s) could lead to novel therapeutic approaches.
 

michael barry

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Bryan,

My friend, perhaps I'll get my grubby little hands on a vial of latanaprost (or one of the two other prostaglandin analogue eye drops---there are three) and put it on a kneecap for a couple of months and see if it grows hair there.

Im not saying that I dont trust Dr. Richard Lee, but as you have pointed out many times, thats the same Doctor who insists Azelaic Acid is a great anti-androgen. Youve made me understand all to well that AA aint' a good anti-androgen. Perhaps Dr. Lee just likes the ease of selling high-percentage minoxidil? He doesnt have anything on his site with peptides or any other difficult topical anti-androgen for him to fool with (GLA, etc.). I believe, very much as I think you do, that a guy could just by loniten tablets and make his own minoxidil and make his own spironolactone and save a hell of a lot of money instead of buying from Lee. I also believe a guy could even mix some nizoral and some T-sal in the palm of his hand and shampoo with it, and save alot of money instead of buying Lee's new shampoo over there on Lee's site. You know Bryan, for a scientist, does not Lee strike you as a bit "lazy" in finding better solutions? All this being said, of course, Lee might be quite right and Latanaprost a big dissapointment. Dr. Kurt Stenn mentioned latanaprost before minoxidil in the last Aderans abstract however, and I'd bet he knows a hell of a lot more about hair than Lee does. I'll get off my butt and order some of it. What have we got to lose?



Wookie wrote: Inhibitory autocrine factors produced by the mesenchyme-derived hair follicle dermal papilla may be a key to male pattern baldness.

[...]

Although these changes are driven by androgens, most molecular mechanisms are unknown, limiting available treatments. The mesenchyme-derived dermal papilla at the base of the mainly epithelial hair follicle controls the type of hair produced and is probably the site through which androgens act on follicle cells by altering the regulatory paracrine factors produced by dermal papilla cells. During changes in hair size the relationship between the hair and dermal papilla size remains constant, with alterations in both dermal papilla volume and cell number. This suggests that alterations within the dermal papilla itself play a key role in altering hair size in response to androgens.

[...]

CONCLUSIONS:

Human balding dermal papilla cells secrete inhibitory factors which affect the growth of both human and rodent dermal papilla cells and factors which delay the onset of anagen in mice in vivo. These inhibitory factor(s) probably cause the formation of smaller dermal papillae and smaller hairs in male pattern baldness. Identification of such factor(s) could lead to novel therapeutic approaches"



Wookie, that sounds just like the standard theory of baldness to me. Androgens in the receptor, DP cells releasing antigens to the rest of the follicle, immuno reaction, skin damage, small follicles ensue. Is that your take on it?
 

wookster

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michael barry said:
Wookie, that sounds just like the standard theory of baldness to me. Androgens in the receptor, DP cells releasing antigens to the rest of the follicle, immuno reaction, skin damage, small follicles ensue. Is that your take on it?

Although these changes are driven by androgens, most molecular mechanisms are unknown

Contact inhibition is also associated with TGF beta 1 :freaked: :freaked: :freaked:
 

Bryan

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michael barry said:
You know Bryan, for a scientist, does not Lee strike you as a bit "lazy" in finding better solutions?

I'm not so sure I'd call him "lazy", since he does seem to work hard in trying to find more and more ways to market new topical minoxidil concoctions. I guess the way I'd characterize him is that his efforts are just so....well, maybe pedestrian is the best word for it. Topical minoxidil?? That's IT?? The best he can do is try to find ways to get higher and higher concentrations of minoxidil that will make his patients wet their pants with excitement when they hear about it?? :)

Contrast that simple approach with Dr. Proctor, who uses exotic chemicals that work in ways UNDREAMED of by Dr. Lee. What a difference.

Bryan
 

Bryan

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wookiewannabe said:
Contact inhibition is also associated with TGF beta 1

Ok, everybody say it with me all at once: SO WHAT??

That doesn't prove that every time you see a molecule of TGF beta 1, it must have been produced by the contact inhibition of some cell. Stop spending so much time at the Stephen Foote School of Shaky Medical Hypotheses.

Bryan
 

Armando Jose

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A few words by Kligman MD (90 years now)

On the mechanism of sebaceous secretion.
Downing DT, Strauss JS
Arch Dermatol Res (1982) 272:343-349

During examination of the unfixed sections of scalp skin, it became apparent
that the follicular canals contained insignificant amounts of solid material that
might have originated from cellular debris, exfoliated follicular corneocytes or
bacteria. The column of sebum was a clear, transparent oil, quite unlike the mushy
follicular content that has become a familiar feature of published micrographs of
facial skin containing sebaceous follicles. Kligman noted that it was often possible
to forcefully express clear sebum from the skin of the forehead but that in some
subjects the contents of the follicles emerged as a cloudy, solid material resembling
petrolatum [8]. He concluded, and we confirm, that the pilosebaceous follicle
normally does not contain significant amounts of material other than sebum unless
this situation is affected by bacteria.

8. Kligman AM, Shelley WB (1958) An investigation into the biology of the sebaceous gland. J Invest
Dermatol 30: 99-125

In altered or healthy hair follicles? Solid material resembling petrolatum???
It could be sebum oxicided and hardened??

My idea is: Before androgen, fibrosis, inflamation, inmunologic and bacterial events, contact inhibition, etc. there was problems in sebum flow in common baldness.

Armando
 

wookster

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Bryan said:
wookiewannabe said:
Contact inhibition is also associated with TGF beta 1

Ok, everybody say it with me all at once: SO WHAT??

That doesn't prove that every time you see a molecule of TGF beta 1, it must have been produced by the contact inhibition of some cell. Stop spending so much time at the Stephen Foote School of Shaky Medical Hypotheses.

Bryan

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th_eusa_think2.gif
th_eusa_think2.gif
 

Armando Jose

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Armando why are you so obsessed with sebum? Do you not have any??

htownballa;

Because sebum can explain easily the pattern in male pattern baldness. Also Sebum is a "minor" problem, and...

The sebaceous gland needs androgens to work. Childrens have a very good hair and therefore there is androgens in the vinicity of scalp hairs in prepubertal time. Then, what's the deal with the current theory? It is neccesary remodelate it.

Armando[/quote]
 

Bryan

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Armando Jose said:
My idea is: Before androgen, fibrosis, inflamation, inmunologic and bacterial events, contact inhibition, etc. there was problems in sebum flow in common baldness....sebum can explain easily the pattern in male pattern baldness.

Oh, is that your idea that sleeping on a pillow absorbs sebum from the back and sides of the head, so balding takes place only on the TOP of the scalp that the pillow doesn't touch?? :D

Armando, you're a really funny guy...

Armando Jose said:
The sebaceous gland needs androgens to work. Childrens have a very good hair and therefore there is androgens in the vinicity of scalp hairs in prepubertal time.

Please explain to us how "having very good hair" demonstrates that there are androgens in the vicinity of scalp hair in children. As I have told you repeatedly, scalp hair grows and thrives in the TOTAL ABSENCE of androgens.

Bryan
 

docj077

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Armando Jose said:
Armando why are you so obsessed with sebum? Do you not have any??

htownballa;

Because sebum can explain easily the pattern in male pattern baldness. Also Sebum is a "minor" problem, and...

The sebaceous gland needs androgens to work. Childrens have a very good hair and therefore there is androgens in the vinicity of scalp hairs in prepubertal time. Then, what's the deal with the current theory? It is neccesary remodelate it.

Armando
[/quote]

I think you need to prove this with a study. The endocrinologists teach us quite differently in medical school.

There are three points in a male's life where there are androgen surges.

In males, I believe one is in utero and it's responsible for sexual masculinization. The second happens right after birth, peaks at levels similar to levels found during puberty and drops off to undetectable levels at around months 4 to 6 and may be responsible for brain masculinization. The third is at puberty and that surge is maintained into andropause.

Androgen levels in boys are undetectable as I said above, so I don't think that androgens have anything to do with hair growth in young boys.
 

Bryan

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Nevermind young boys...look at the THICK heads of hair on little girls!! How much androgen do THEY have??
 

CCS

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bryan,

you keep asking us how much androgen little girls have have, but you never tell us. what makes you so sure they have zero? I'd like to know the average extrogen, DHT, and testosterone levels of men and women at verious ages, and at pregnancy, so we can note some trends.

i've seen plenty of women with hair that has very little volume to it. I've also noticed that women have a lot of variation to how high there hair lines are, but 75% have hair lines that are lower than the hair lines of 75% of mens. little girls tend to have much higher hair lines than adult women.
 

Bryan

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collegechemistrystudent said:
bryan,

you keep asking us how much androgen little girls have have, but you never tell us. what makes you so sure they have zero? I'd like to know the average extrogen, DHT, and testosterone levels of men and women at verious ages, and at pregnancy, so we can note some trends.

Good heavens, I've never ever said that they have ZERO androgen; the obvious implication is that they have VERY LITTLE androgen, even less than boys of the same age. I like to point that out mainly for the benefit of kooks like Ernie, who are convinced that ALL hair (even scalp hair) requires androgens to grow. A somewhat less egregious kook like Armando needs to keep that in mind, too. God knows I have to remind of him of that often enough, like when he routinely states that sebum is necessary for hair growth.

Bryan
 

Widows_Peak

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I will again ask, as I did 3 pages ago, that....

1. If high levels of testosterone killed your hair, you would go bald when you hit puberty.
How many bald 13 year olds have you seen?

2. For most men, baldness starts around 30, which is when testosterone levels start to seriously decline.


3. If it's NOT androgens, then why is it that eunuchs don't go bald?
(BTW, Eunuchs also don't regrow hair that fell out, prior to castration.)

4. If testosterone kills hair, then why does it increase acetylcholine, which in turn increases Nitric Oxide production, which initiates and maintains hair growth.

5. If testosterone kills hair, why is my regimen, which includes taking beta-sitoaterol, which blocks the binding of 5ar to testosterone to make DHT, thereby increasing the amount of free testosterone in my body, in addition to abstaining from sex, which gives my body a 145% in serum testosterone levels, working for me?

6. What about relaxin, the hormone produced by the body that inhibits DHT, that is depleted in the body when one ejaculates, in addition to acetylcholine and the testosterone lost when one ejaculates?

Anyone wanna tackle these questions?

I've got the photos to prove that my regimen works, BTW.
http://hairregrowth.blogspot.com
 

Dave001

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Bryan said:
michael barry said:
You know Bryan, for a scientist, does not Lee strike you as a bit "lazy" in finding better solutions?

I'm not so sure I'd call him "lazy", since he does seem to work hard in trying to find more and more ways to market new topical minoxidil concoctions. I guess the way I'd characterize him is that his efforts are just so....well, maybe pedestrian is the best word for it. Topical minoxidil?? That's IT?? The best he can do is try to find ways to get higher and higher concentrations of minoxidil that will make his patients wet their pants with excitement when they hear about it?? :)

You forget that he sells custom formulations of minoxidil that contain reduced concentrations of propylene glycol (which may not even work as well as the standard, or cause untoward systemic absorption). There's no denying the ingenuity in that.

When I read the text that you quoted from Michael, what stood out in my mind was the bit about Dr. Lee being a scientist. Now that is an outrageous proposition. ;)
 

Dave001

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Widows_Peak said:
2. For most men, baldness starts around 30, which is when testosterone levels start to seriously decline. [/b]

Neither part of this statement is correct. For one thing, testosterone levels do not begin to "seriously decline" at age 30; there is a very slow and gradual decline beginning once peak levels are reached.
 

Bryan

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Widows_Peak said:
I will again ask, as I did 3 pages ago, that....

1. If high levels of testosterone killed your hair, you would go bald when you hit puberty.
How many bald 13 year olds have you seen?

2. For most men, baldness starts around 30, which is when testosterone levels start to seriously decline.

That's been discussed in detail on all these hairloss sites. The damage to hair follicles is usually slow and progressive. It usually happens over the course of many years, not weeks or months. Maybe even more importantly, hair follicles probably only become sensitive to androgens in the first place in a slow and progressive manner, too.

Bryan
 
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