For bryan and Foote.

[Dave001]

For your information, i have had two papers published on my theory in the journal designed for the purpose "Medical Hypotheses". I have followed all the rules in pursuing my theory, including contacting accepted experts in the field for their opinions.

I have posted the replies i have had so far as you know, and these "expert" opinions on my theory show just how sadly out of sync you are with "true" science.

What replies? The only _reply_ that I've seen was the one that everybody agreed was a standard boilerplate response to "fan mail". Have any of these scientists who allegedly share your opinion ever cited either one of your papers? No. Of course, nothing even remotely similar to your idea has been published.

Your "theory" is at least novel, I presume you will concede? So then why haven't you or another individual or pharmaceutical company applied for a patent for a method of treating alopecia that involves ameliorating what you propose as the key mediator? Altruistic motives?

 

[2tone]

Is an localised inflamation the same as a clinical edema in some important ways?

 

[2tone]

But they don't Michael, this is a myth! Show me some hard evidence?[/quote]

Oh, yes, they most certainly *are* enlarged in male pattern baldness subjects compared to nonbalding counterparts.[/quote]

isnt it that presence of the marker DHT means increases sebum production and reduced sweat gland efficiency ??

 

[S Foote.]

[quote="michael barry":9dd7e]THREE. The biggie. Sebaceous glands get BIGGER in male pattern baldness even in the front of the scalp. How can they enlarge if fluid pressure is too high to allow it?

But they don't Michael, this is a myth! Show me some hard evidence?

I believe I have previously shown you evidence for that, but not surprisingly, you just ignored it.

Bryan[/quote:9dd7e]

No Bryan, i have asked you for such evidence before, and you have yet to post any!

So if you have it post it.

S Foote.

 

[S Foote.]

Im going to quote Loren Pickart on Cyclosporin....."Cyclosporin is an immunosuppresive drug used in organ transplants to prevent the body from rejecting a new organ. It is used topically in the treatment of immune-associated severe skin conditions. In humans, cyclosporin is very effective orally (80% positive hair growth response) but only marginally effective (20%) whn used topically for aiding hair growth. It promotes hair growth in animal models and promotes human hair growth in virto.

That info was here http://www.skinbiology.com/hairregrowth ... yclosporin

That, along with the experiment of taking miniaturizing hairs from balding guys and putting them on the backs of immuno-deficient mice is why I believe the immune system attack is integral to baldness. Proctor and Pickart seem to believe this. Im guessing the makers of Tricomin and American Crew (peptides again) have invested faith in it too.

If cyclosporin is working "in another way", what do any of you think that it would be?

First let me say that i accept that many things may be effecting hair growth "directly", particularly in-vitro. Androgens may have some "direct" effect upon hair follicles and sebacous glands, but.........

My argument is that the "major" in-vivo effect of androgens that needs to be addressed, is an indirect action mediated through the normal contact inhibition of cell multiplication.

In-vivo i suggest cyclosporin and other immune suppressing drugs are reducing the tissue fluid levels. Immunology and edema are just sides to the same coin, one can cause the other and vice versa.

Immune reactions cause swelling (edema), and edema causes immune reactions (as in the lymphedema links i have posted).

In the re-growth of male pattern baldness follicles in immuno deficient mice, the lack of immunology reduces the healing fibrosis that i think is the major factor in locking follicles in the as transplanted state. I think this is why male pattern baldness follicles can re-enlarge in these mice, there is no fibrose "shell" resriticting enlargement through contact inhibition.

Stephen, have you gotten any scientists youve talked to express privately why a cure for male pattern baldness is taking so long? What do they say they are stuck on? I was assuming it was finding a topical anti-androgen that didnt break down, competed successfully for androgen receptors with DHT, and only had to be applied once a day, and was cost effective (nobody is gonna pay $200 a month for anything).

Im going to look back into the enlargening sebaceous glands. Ive read that in a few different places.



By the way.......on "internet scientists".......alot of people on forums are like me........just mystified that male pattern baldness is still "unsolved". When minoxidil came out in 1988, my derm told me "its just a matter of time now" and baldness would be "cured forever". This is what gives rise to alternative theories, etc. in my opinion. When computers really became advanced, I just assumed that DNA, RNA models would be run with sophisiticated software showing mathematically and chemically the effects of drugs in such an efficient way that cures for most diseases, anti-virals, vaccines, anti-biotics would ensue and old maladies would all be conquered unless new ones evolved resistances etc. Obviously it hasnt worked out that way. Stephen has stated that Dave, Bryan, (and proboably me) would disappear off forums when HM research gained more info invalidating current thought on male pattern baldness. Hey, when/if HM becomes reality and I can have my 19 year old hair back........I promise you wont see me on any forums concerning hair. I'll be enjoying it and not worrying about it like Brad Pitt proboably does.

As anyone can see from these forums, hair loss treatments todate have been dissapointing. I think this reflects the flaws in the theory they have been based on.

For example the topical anti-androgen issue. This should be the "cure" according to the current theory, and i'am sure that there is no real technical problem in getting these into the follicles where the current theory claims it matters.

I am also sure that drug companies have researched this behind closed doors given the money success would bring! So where are these treatments commercially?

I think the lack of such commercial topical's tells the real story about the validity of the current theory. Many excuses given, non scientific :wink:

I think the reasons for the delay in succesful treatments is just down to a blind alley in research, because the traditional assumptions are just plain wrong.

On the bright side HM research should highlight the way to go.

I am not against "internet scientists" and i am all for constructive, respectful debate of these issues.

But sadly some people just don't understand the principles of scientific debate, and try to decieve people about what science actually is because of a personal agenda.

S Foote.

 

[S Foote.]

For your information, i have had two papers published on my theory in the journal designed for the purpose "Medical Hypotheses". I have followed all the rules in pursuing my theory, including contacting accepted experts in the field for their opinions.

I have posted the replies i have had so far as you know, and these "expert" opinions on my theory show just how sadly out of sync you are with "true" science.

What replies? The only _reply_ that I've seen was the one that everybody agreed was a standard boilerplate response to "fan mail". Have any of these scientists who allegedly share your opinion ever cited either one of your papers? No. Of course, nothing even remotely similar to your idea has been published.

So you regard these comments by Dr Sawaya, as just a standard "fan mail" response do you?

Quote:


"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"

If you interpret that as just a fan mail response, you need some reading lessons Dave.

Your "theory" is at least novel, I presume you will concede? So then why haven't you or another individual or pharmaceutical company applied for a patent for a method of treating alopecia that involves ameliorating what you propose as the key mediator? Altruistic motives?

I'am not going to tell you what my plans are am i!

S Foote.

 

[S Foote.]

Is an localised inflamation the same as a clinical edema in some important ways?

Yes, as i say in another post, they are the two sides to the same coin. I dont think the edema has to be "clinical" as in obvious, for the increased fluid levels to effect the local immunology as in lymphedema.

S Foote.

 

[S Foote.]

But they don't Michael, this is a myth! Show me some hard evidence?

Oh, yes, they most certainly *are* enlarged in male pattern baldness subjects compared to nonbalding counterparts.[/quote]

isnt it that presence of the marker DHT means increases sebum production and reduced sweat gland efficiency ??[/quote]

Cabanac's studied the sweating capacity of the balding scalp compared to the beard area. These areas experience "opposite" effects of DHT on hair growth.

He proved that where DHT reduces growth (male pattern baldness), there is a much increased sweating capacity of the tissue. Where DHT increases hair growth (beard), there is a much reduced sweating capacity.

This is in line with DHT increasing fluid pressure in male pattern baldness, and reducing pressure in the beard area to grow hair.

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

S Foote.

 

[Dave001]

As anyone can see from these forums, hair loss treatments todate have been dissapointing. I think this reflects the flaws in the theory they have been based on.

They aren't based on theory; they are based on empirical evidence. Minoxidil was in fact "accidentally" discovered as a hair growth agent, as most here are aware.

For example the topical anti-androgen issue. This should be the "cure" according to the current theory, and i'am sure that there is no real technical problem in getting these into the follicles where the current theory claims it matters.

They do work.

 

[michael barry]

As far as fibrosis (or as the folks at Aminexil might state, collagen fibers hardening around a follicle, inhibiting it from getting larger), keeping those hard to enlarge small hairs at the front of the receeding hairline small, I can buy that.

However, look at this photo at the bottom of this page for the drug Eucapil http://eucapil.com/xhtml_en/hair.shtml

Eucapil is just an androgen-receptor blocker (or pre-emptive binder for Dave : ), and it obviously regrew a good amount of hair on this man. Tests on rats and rabbits, that have skin that is up to six times as "penetrateable" as humans show no systemic absorption of the drug took place. Twelve month tests on people show no absorption took place, no libido drops, no endrocine level changes.

Dave said current treatments DO work. I agree with him if you catch hair that hasnt been gone very long (and especially if youre young) as this guy here http://hairlosstalk.com/photogallery/pgmartin.htm who was on "the big 3" alone. Just think if he had access to a Eucapil and a copper peptide and he ate a good vitamin-rich, low fat diet........He'd have proboably had terrific success.

But my temples have been receeded for about five years now......doesnt look like anything's gonna regrow those. Rest of my hairs really thick though : )

 

[Bryan]

[quote="S Foote.":76f86][quote="michael barry":76f86]THREE. The biggie. Sebaceous glands get BIGGER in male pattern baldness even in the front of the scalp. How can they enlarge if fluid pressure is too high to allow it?

But they don't Michael, this is a myth! Show me some hard evidence?

I believe I have previously shown you evidence for that, but not surprisingly, you just ignored it.

Bryan[/quote:76f86]

No Bryan, i have asked you for such evidence before, and you have yet to post any![/quote:76f86]

Oh, bullshit! So now you're suffering from AMNESIA, Stephen?? We've discussed this in the past, and I'm not going to spend hours going back through all my notes and studies just to refresh your faltering memory. However, here's a couple of relevant studies which I found in just a couple of minutes (I've highlighted in bold certain important statements):

---------------------------------------------
J Invest Dermatol. 1987 Jul;89(1):87-92

"Is increased 5 alpha-reductase activity a primary phenomenon in androgen-dependent skin disorders?"

Dijkstra AC, Goos CM, Cunliffe WJ, Sultan C, Vermorken AJ.

Testosterone metabolism was investigated in fractions of human skin, enriched in epidermis, dermis, sebaceous glands, and sweat glands, by histologic sectioning of skin punch biopsies, and the results were compared with two culturable skin cells, i.e., keratinocytes and fibroblasts. Since sebocytes could not be brought in culture, metabolism was also investigated in the hamster flank model. In the epidermal tissue of the skin biopsies the predominant metabolite was androstenedione, formed by the enzyme 17 beta-hydroxysteroid dehydrogenase. The same was true for cultured hair follicle keratinocytes. In the deeper skin layers the formation of androstenedione was markedly reduced, whereas the formation of 5 alpha-reduced metabolites was highly increased, with a maximum in the skin fractions containing large sebaceous glands. Cultured shoulder skin fibroblasts showed a markedly different testosterone metabolism compared with the sectioned skin biopsies, suggesting that dermal fibroblasts play a less important role in the overall skin testosterone metabolism. The present approach, allowing the comparison of testosterone metabolism in different substructures of the same skin biopsy provides new evidence that the high 5 alpha-reductase activity in the specific skin fractions must be mainly ascribed to the sebaceous glands. These results render a previous hypothesis, stating that the elevated level of 5 alpha-reductase and subsequent formation of dihydrotestosterone in androgenetic alopecia and acne (usually accompanied by seborrhea) could therefore simply be the consequence of sebaceous gland enlargement, much stronger. This hypothesis is further evaluated by quantitative correlation of sebaceous gland size with enzyme activity in the hamster flank model.

---------------------------------------------
J Invest Dermatol. 1989 Jan;92(1):91-5.

"Increased androgen binding capacity in sebaceous glands in scalp of male-pattern baldness"

Sawaya ME, Honig LS, Hsia SL.

Sebaceous glands were isolated by manual dissection under a microscope from surgical specimens of scalp skin with male pattern baldness and skin specimens of hairy and bald scalp obtained at autopsy. The 800 X g pellet (nuclear fraction) and the 164,000 X g supernatant fraction (cytosol) of homogenates of the sebaceous glands were used for measurements of androgen binding characteristics, using dextran-coated charcoal and sucrose gradient methods. Scatchard plots showed high affinity binding for [3H]dihydrotestosterone (DHT) and [3H]methyltrienolone (R1881). Nuclei prepared from bald scalp contained greater total androgen binding capacity than nuclei of hairy scalp, although Kd values of type I binding were similar (0.68 vs 0.56 nM, respectively). On sucrose gradient, the binding protein from cytosol was found in the 7 to 8S density range. Androgen binding by cytosol of sebaceous glands of hairy scalp had Kd of 1.89 +/- .79 and 2.05 +/- .56 nM for DHT and R1881, respectively, and Bmax of 18.7 +/- 4.4 and 20.0 +/- 4.6 fmol/mg protein for DHT and R1881, respectively. Cytosol from sebaceous glands of bald scalp had Kd values approximately half those of hairy scalp, and Bmax values 50%-100% higher. The bound 3H labeled DHT and R1881 could be partially displaced by testosterone (40-50%), moxestrol (28-32%), promegestone (19-26%), and delta 4-androstenedione (6-12%), but not by dehydroepiandrosterone. These data demonstrate the presence of specific androgen binding protein in sebaceous glands, and that sebaceous glands of bald scalp have greater binding affinity and capacity for androgens than those in hairy scalp. This difference may explain the greater androgenic response in androgenic alopecia.

 

[Dave001]

However, look at this photo at the bottom of this page for the drug Eucapil http://eucapil.com/xhtml_en/hair.shtml

Eucapil is just an androgen-receptor blocker (or pre-emptive binder for Dave : ), and it obviously regrew a good amount of hair on this man. Tests on rats and rabbits, that have skin that is up to six times as "penetrateable" as humans show no systemic absorption of the drug took place. Twelve month tests on people show no absorption took place, no libido drops, no endrocine level changes.

Dave said current treatments DO work. I agree with him if you catch hair that hasnt been gone very long (and especially if youre young) as this guy here http://hairlosstalk.com/photogallery/pgmartin.htm who was on "the big 3" alone.

Yes, topical antiandrogens are still only antiandrogens. One must set his expectations accordingly.

I'd caution against giving credibility to Eucapil (fluridil). There is nothing yet to suggest that it has any activity at all.

 

[michael barry]

Dave,
Im aware that Eucapil hasn't been submitted for peer review. Why, since Dr. Sawaya is involved with it, do you think this is so? Perhaps it doesnt work as well as the maker had hoped, etc? You have an opinion on it?



I dont know how you feel about skin changes over time making it hard for vellus hair to "re-enlarge", Im guessing that the hardening of collagen around the follicle may be why hair thats been lost for a few years is hard to regain even if one is on dutasteride and takes minoxidil, proanthrocyanidrins etc.......the skin is just "too far gone" to support a hair follicle renewal at that point. Transplant would be the only way..

 

[Bryan]

Dave,
Im aware that Eucapil hasn't been submitted for peer review. Why, since Dr. Sawaya is involved with it, do you think this is so?

Where'd you get the idea that Sawaya was involved with fluridil? She isn't, as far as I know.

Bryan

 

[Bryan]

First let me say that i accept that many things may be effecting hair growth "directly", particularly in-vitro. Androgens may have some "direct" effect upon hair follicles and sebacous glands...

No sh*t??

As anyone can see from these forums, hair loss treatments todate have been dissapointing.

And have YOUR treatments done any better? :wink:

For example the topical anti-androgen issue. This should be the "cure" according to the current theory...

As I've been pointing out for years on hairloss sites, even complete androgen ablation doesn't cause a full regrowth of hair, so it's completely inappropriate to use the word "cure" in this context. However, I think one could reasonably expect to see at least a halt to further balding, if one could obtain an effective antiandrogenic program.

...and i'am sure that there is no real technical problem in getting these into the follicles where the current theory claims it matters.

There sure as hell IS a technical problem with that! Truly effective topical antiandrogens are few and far between. It's high time for you to stop using that as an excuse to Propecia-up your eccentric theory.

Bryan

 

[michael barry]

Bryan,
On Sawaya and Eucapil Tom Hagerty wrote "what does 'cosmetic' agent mean to you? Perhaps the company is just being cautious, or perhaps the company does not want any lawsuits. I know many people from the Czech Republic. It's a litigious society. By the way, both women, Virginia Price and Marty Sawaya, who the article quotes are from Czech. (I think Sawaya was born in the US though. She's had some credibility problems lately with her professional credentials.)

"OK, here's what I don't understand. "Fluridil is also designed to degrade in an aqueous environment in order to prevent systemic side effects."

......."The receptor sites for androgens are not on the cell membrane. They are in the cytoplasm of the cell. To reach the cytoplasm of the cell the Fluridil molecules would have to negotiate their way through many water molecules since the body is roughly two-thirds water (this includes the cells). Fluridil is supposed to be "hydrolytically degradeable" so as not to have systemic side effect. But to be effective at "rendering the androgen receptors inactive," it evidently has to dance its way through alot of the H20 molecules."


That post was about a year or so back........Marty, Czechoslovakia, Eucapil, and Fluridil must have stuck in my mind and I associated that drug with her. Re-lookin' at the Eucapil website I didnt see Marty's name and googled her+Fluridil to see where I associated it......led me back to good ol' Tom (a truly nice gentlemen in Hairloss that gives honest advice on his website and helps guys just learnin' avoid gettin' scammed into B.S. products and surgery if they are bad candidates for it). I believe Ive read "somewhere" that Sawaya gave Fluridil a positive evaluation and being a Czech praising a Czech drug gave rise to questions about her credibility (but there was a rumor about Christiano telling folks that some concoction called HairGenisis {or some such product} was good news also and I have no idea if thats true either......but Ive read it somewhere as it sticks in my mind, and guys on alt.baldspot had doubts about her because of it. (Its hard to remember all this information.....I should write it all down).

By the way, what do you think about Fluridil topically? Ive noticed they havent posted any new "proof" pics on their website, no peer-reviewed trials. That troubles me as propecia and minoxidil have good clinical pics of a few of the guys who have had success.

 

[Bryan]

I have an agnostic attitude toward fluridil: I don't know if it works, or not. I'm waiting for independent testing.

Bryan

 

[Dave001]

Bryan,
On Sawaya and Eucapil Tom Hagerty wrote "what does 'cosmetic' agent mean to you? Perhaps the company is just being cautious, or perhaps the company does not want any lawsuits. I know many people from the Czech Republic. It's a litigious society. By the way, both women, Virginia Price and Marty Sawaya, who the article quotes are from Czech. (I think Sawaya was born in the US though. She's had some credibility problems lately with her professional credentials.)

"OK, here's what I don't understand. "Fluridil is also designed to degrade in an aqueous environment in order to prevent systemic side effects."

......."The receptor sites for androgens are not on the cell membrane. They are in the cytoplasm of the cell. To reach the cytoplasm of the cell the Fluridil molecules would have to negotiate their way through many water molecules since the body is roughly two-thirds water (this includes the cells). Fluridil is supposed to be "hydrolytically degradeable" so as not to have systemic side effect. But to be effective at "rendering the androgen receptors inactive," it evidently has to dance its way through alot of the H20 molecules."

I can't discern whom those quotations are attributed to. The last two paragraphs mirror what I've said many times.

Fluridil sounds more like an irrationally designed antiandrogen than a rationally designed one (regarding the logic behind its alleged systemic "shield").

 

[Dave001]

You have claimed that the scientific tool of Ockham's razor proves my theory to be wrong. Yet every time i have asked you to explain how Ockhams razor does this, you have refused to respond!

I know that you just came across the scientific term "Ockhams razor" on the net, and thought that if you refered to this on these forums people would think you had some scientific knowledge.

Hahaha! You're a piece of work. Does principle of parsimony parse?

We'll try Laplace since you don't understand Ockham: Je n'ai pas besoin de cette hypothèse (roughly, I have no need for that hypothesis). He was referring to your cuckoo theory in that well known quotation.

 

[michael barry]

Dave,
Tom Hagerty was the source for all the paragraphs in that post.



Bryan,
This is a question for you and it should clear everything up for me, (cant believe Ive never thought to ask this of you). When androgens are added to hair cells experimentally from the Male Pattern Bald area in experiments, do the results differ from androgens added to hair cells culled from the hippocratic wreath area?

If the results are different in these experiments (i.e. slowing of the cell division of root sheath, keratinocytes, epithileal, etc....) that pretty much proves beyond any doubt that some innate genetic difference between these hairs exists (other than extra androgen receptors on the male pattern baldness hairs and being located in parts of the scalp that produce more alpha 5).


That, if affirmative, would end all alternative explanations other than the direct theory.