For bryan and Foote.

[Bryan]

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?

Michael, the answer is YES, and I'm a bit surprised that you don't already know all about that, because it's an issue that Stephen and I have already gone around and around over for quite a long time.

An excellent study which investigated that in a novel fashion (and since then, there's been at least one similar Japanese study which got the same results) is the much-discussed "Inhibition of Hair Growth by Testosterone in the Presence of Dermal Papilla Cells from the Frontal Bald Scalp of the Postpubertal Stumptailed Macaque", Uno et al, Endocrinology 138: 356-361. 1997. The big, important finding that came out of that study is that the hair-growth inhibition from androgens appears to be mediated through the dermal papilla. Androgens affect dermal papillae directly, and stimulate them to release either growth enhancers or growth repressors (depending on the genetic programming within a given follicle), which then migrate to the rest of the follicular structure and modify its overall growth accordingly. They showed that when dermal papillae from the balding areas of stumptailed macaques are co-cultured with epithelial cells and testosterone is added, the growth of the epithelial cells is strongly inhibited. However, testosterone added to a cell culture of those epithelial cells alone has no effect on their growth! In other words, the effect is coming by way of the dermal papilla. Furthermore, addition of testosterone to a co-culture of epithelial cells with dermal papillae from occipital follicles has no effect on the growth of the epithelial cells. I think that's a pretty damned clear indication of a key step in the balding process! :wink:

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.

Guess what, Michael, our friend Stephen Foote even has a goofy explanation for THAT study, believe it or not! After my beating him over the head with it for a period of time, he put on his thinking-cap and came up with the following marvelously ad hoc rationalization:

Ok, so maybe hair follicles are indeed directly affected by androgens to some degree (he ruefully admits) , but it's still "edema" and "contact inhibition" which actually CAUSE them to become sensitive to those androgens in the first place!

I'm not kidding! The preceding is what he actually believes!!! I think you can see now why after so many years of ad hoc excuses and rationalizations, it's hard for very many of us to take his theory seriously. No matter what evidence is cited, he just keeps trying to turn it back around on "contact inhibition".

Bryan

 

[michael barry]

Bryan,
First let me thank you on your reply. Thats a slam dunk on male pattern baldness to me. The docs (even the transplant docs) are right.....sometime during fetal development every hair on a boy's little head apparently develops genetic instructions that are apparently located in the stem cells to be mediated in the dermal papilla of the adult male. Apparently the only way to avoid the ensuing baldness is to keep androgens away from the cytoplasm's receptors on the dermal papilla, or cut androgens period, or the genetic instructions for miniaturization will be heeded.

Stephen is a nice, very educated man........but Im afraid he WANTS his theory to be true too badly. Its the only other alternative baldness theory that makes any sense though....as Ive read through quite a few of them. The latest is the galea's "downward pressure" keeping oxygen from reaching the scalp (I know....ridiculous).

Bryan, Im hoping for either stem cells re-injected, or genetic therapies that "ride" viruses to imprint their DNA on dermal papilla's (Loren Pickart mentions that on his page.......using viruses to get good hair genes to our follicles----'think' its being worked on at U. of Toronto and Michigan State). Either that.....or the Body Hair transplants that are abuzz over at Hairsite (Dr. Arvind Poswal). I can tell youve researched baldness extensively for a few years now. Do you have any prognostications to make as far as NW5+ men (Im a Norwood 3 currently.....kind of like the actor Jude Law in the hair dept.) being able to have full heads of hair in the future. I believe it WILL happen someday. I just hope its in my lifetime. M

 

[Dave001]

Guess what, Michael, our friend Stephen Foote even has a goofy explanation for THAT study, believe it or not! After my beating him over the head with it for a period of time, he put on his thinking-cap and came up with the following marvelously ad hoc rationalization:

Ok, so maybe hair follicles are indeed directly affected by androgens to some degree (he ruefully admits) , but it's still "edema" and "contact inhibition" which actually CAUSE them to become sensitive to those androgens in the first place!

I'm not kidding! The preceding is what he actually believes!!! I think you can see now why after so many years of ad hoc excuses and rationalizations, it's hard for very many of us to take his theory seriously. No matter what evidence is cited, he just keeps trying to turn it back around on "contact inhibition".

Is it just me, or is the silence very loud? :wink:

A similar pattern of retreat can be seen whenever the issue of topical antiandrogens surfaces. For example: http://www.hairlosstalk.com/discussions ... c&start=30

The success or failure of a topical antiandrogen is always explained by Stephen as a function of percutaneous absorption; i.e, if it worked, then it must have affected those `deeper' tissues, even in the face of overwhelming evidence to the contrary. Convenience-based reasoning? :wink:

 

[2tone]

Components of Sebum

Fatty Acids (primarily Oleic Acid (highest content), Palmitoleic Acid (second highest content) and Linoleic Acid (third highest content): 5%
Glycerides: 50%
Waxes: 20%
Squalene: references 11%
Other Hydrocarbons: 4%
Cholesteryl esters: 4%
Cholesterol: references 1%
Other Sterols: 1%
Other Substances: 4%

These Substances may Enhance the Function of Sebum

Hormones

DHEA (Dehydroepiandrosterone) (administered topically via Eye Drops) stimulates the endogenous production of Sebum by the Tarsal Glands located in the Eyelids - Sebum is the constituent of Tears that prevents their evaporation. references
DHEA (administered orally or applied topically via DHEA Skin cream) also stimulates the endogenous production of Sebum by the Sebaceous Glands locatedin the Skin. references

Lipids

Dietary Fats are essential to the production of Sebum in the Sebaceous Glands: [more info]

 

[S Foote.]

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.

I fully understand Ockham, and everyone can see despite your dancing around and fancy words, that you "DONT".

If you did you would tell us all "HOW" Ockham's "SPECIFICALY" disproves my theory as you claimed?

People are just laughing at your pretence here Dave, so just answer the question if you can?

S Foote.

 

[S Foote.]

Bryan.

I want to respond to your latest posts, but my computer crashed last weekend and i have just got it back.

I need to sort some ongoing problems with my internet connection, so i won't have time to post again until these are sorted.

S Foote.

 

[Dave001]

[quote="S Foote.":59d15]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.

I fully understand Ockham, and everyone can see despite your dancing around and fancy words, that you "DONT".

If you did you would tell us all "HOW" Ockham's "SPECIFICALY" disproves my theory as you claimed?[/quote:59d15]

Ockham's razor doesn't specifically disprove anything, which is obviously the reason you've chosen to respond to this thread by demanding a formal proof of how it specifically disproves your theory, instead of responding to the evidence that does specifically disprove your harebrained theory.

The meaning of my original comment in its original context (from several *months* ago) was obvious. Ockham's razor is not a physical law, but a principle of logic that precludes the existence of your theory in the first place. I'm sorry you can't understand that, but it's time to move on.

People are just laughing at your pretence here Dave, so just answer the question if you can?

Ah, so you have Multiple Personality Disorder. That explains a lot.

 

[Bismarck]

Prolly a good idea to mention that Ockhams Razor is rather a heuristical method for generating hypotheses than a verification/falsification tool.

 

[Dave001]

Prolly a good idea to mention that Ockhams Razor is rather a heuristical method for generating hypotheses than a verification/falsification tool.

Or a tool to detract attention from the main argument of a discussion. Ockham's razor is already covered by plain old uncommon sense.

 

[S Foote.]

The meaning of my original comment in its original context (from several *months* ago) was obvious. Ockham's razor is not a physical law, but a principle of logic that precludes the existence of your theory in the first place. I'm sorry you can't understand that, but it's time to move on.

That is the point you idiot!

Ockhams razor is a principle of logic! You say above that this principle precludes my theory.

So explain your "logic" in reaching your conclusion about my theory using Ockham's razor??

But you won't explain your "opinions" in a scientific way, simply because you just cut and paste scientific terms from the net, with no understanding of what they "actually" mean!

You know if you enter a debate on this question with me, i will make you look the fool you are, so you avoid "actually" defending your statements, as everyone can see. 8)

Pretty sad in my book. :roll:

S Foote.

PS:

I will respond to Bryans latest "dancing around" the issues tommorow :wink:

 

[Dave001]

The meaning of my original comment in its original context (from several *months* ago) was obvious. Ockham's razor is not a physical law, but a principle of logic that precludes the existence of your theory in the first place. I'm sorry you can't understand that, but it's time to move on.

That is the point you idiot!

Ockhams razor is a principle of logic! You say above that this principle precludes my theory.

So explain your "logic" in reaching your conclusion about my theory using Ockham's razor??

I just did.

But you won't explain your "opinions" in a scientific way, simply because you just cut and paste scientific terms from the net, with no understanding of what they "actually" mean!

Huh? What are you accusing me of having cut and pasted? I'm very careful to always properly attribute my sources. Can you point to an example where I've failed to do so?

You know if you enter a debate on this question with me, i will make you look the fool you are, so you avoid "actually" defending your statements, as everyone can see. 8)

What question? What statement have I failed to defend?

I will respond to Bryans latest "dancing around" the issues tommorow :wink:

Haha. So you've dodged the main topic for two days now -- bringing up unrelated topics in the meanwhile -- and you're now accusing Bryan of dancing around issues?

Sigh. I've really got to stop feeding trolls the attention they crave...

 

[S Foote.]

The meaning of my original comment in its original context (from several *months* ago) was obvious. Ockham's razor is not a physical law, but a principle of logic that precludes the existence of your theory in the first place. I'm sorry you can't understand that, but it's time to move on.

That is the point you idiot!

Ockhams razor is a principle of logic! You say above that this principle precludes my theory.

So explain your "logic" in reaching your conclusion about my theory using Ockham's razor??

I just did.

[quote="S Foote.":9d720]But you won't explain your "opinions" in a scientific way, simply because you just cut and paste scientific terms from the net, with no understanding of what they "actually" mean!

Huh? What are you accusing me of having cut and pasted? I'm very careful to always properly attribute my sources. Can you point to an example where I've failed to do so?

You know if you enter a debate on this question with me, i will make you look the fool you are, so you avoid "actually" defending your statements, as everyone can see. 8)

What question? What statement have I failed to defend?[/quote:9d720]

Sigh :roll:

You said that you "THINK" the logic of Ockhams razor, rules out my theory. When people make these kind of claims in science, they are required to say "HOW" a particular logic refutes something, this is how science works.

I could say that scientific principles rule out the current theory of male pattern baldness, which they do! Would you or anyone else take my statement seriously if i refused to explain my reasoning? No.

You have now had ample opportunity to justify your unqualified "remarks", and you have shown everyone here by refusing to do so that these remarks about my theory have no basis in actual science.

You are just a delusional individual.

S Foote.

 

[S Foote.]

[quote="S Foote.":62383][quote="michael barry":62383]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

No Bryan, i have asked you for such evidence before, and you have yet to post any![/quote:62383]

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.[/quote:62383]

Just point out to us all Bryan where these or "ANY" other studies, "ACTUALLY" measure the comparitive size of sebaceous glands in bald, pre-bald, and hairy tissue??

This was my point as you are well aware! There is "NO" such evidence, just assumptions based on hamster flank and other irrelevant studies.

Even the section you highlighted as it it "means" something, states sebaceous gland "enlargement" as a "hypothesis" to explain the results, "NOT" a proven fact!!

Show me a study that "ACTUALLY" proves by direct measurment, that sebaceous glands in the balding human scalp "ENLARGE" compared to pre-balding?

Never mind any changes in sebum production or anything else, my point as people can read in my post was one of sebaceous gland enlargement in the male pattern baldness scalp.

Show me some evidence of "this" Bryan?

S Foote.

 

[S Foote.]

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?

Michael, the answer is YES, and I'm a bit surprised that you don't already know all about that, because it's an issue that Stephen and I have already gone around and around over for quite a long time.

An excellent study which investigated that in a novel fashion (and since then, there's been at least one similar Japanese study which got the same results) is the much-discussed "Inhibition of Hair Growth by Testosterone in the Presence of Dermal Papilla Cells from the Frontal Bald Scalp of the Postpubertal Stumptailed Macaque", Uno et al, Endocrinology 138: 356-361. 1997. The big, important finding that came out of that study is that the hair-growth inhibition from androgens appears to be mediated through the dermal papilla. Androgens affect dermal papillae directly, and stimulate them to release either growth enhancers or growth repressors (depending on the genetic programming within a given follicle), which then migrate to the rest of the follicular structure and modify its overall growth accordingly. They showed that when dermal papillae from the balding areas of stumptailed macaques are co-cultured with epithelial cells and testosterone is added, the growth of the epithelial cells is strongly inhibited. However, testosterone added to a cell culture of those epithelial cells alone has no effect on their growth! In other words, the effect is coming by way of the dermal papilla. Furthermore, addition of testosterone to a co-culture of epithelial cells with dermal papillae from occipital follicles has no effect on the growth of the epithelial cells. I think that's a pretty damned clear indication of a key step in the balding process! :wink:

Michael, this is a perfect example of how Bryan tries to mislead people in these issues!

The results of follicle cell samples from the male pattern baldness and hairy areas, only "differ" when exposed to androgens in-vivo, "IF" the samples were "already" different!

Bryan claims quote:

" Androgens affect dermal papillae directly, and stimulate them to release either growth enhancers or growth repressors (depending on the genetic programming within a given follicle), which then migrate to the rest of the follicular structure and modify its overall growth accordingly. "

Which is completely wrong, and proven to be so by the very studies he is quoting!

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

The pre-balding, "normal" follicles in macaques, that are known to bald in response to androgens, do "NOT" change into balding mode when directly exposed to androgens in-vitro!!

So future balding follicles are no different in their direct response to androgens than any other scalp follicle from outside the male pattern baldness area.

This is what disproves the current theory of a direct action of androgens on follicles, and is something Bryan always conveniently forgets to mention :wink:

There are other more logical explainations for the in-vitro results, that don't need "anti science magic mechanisms" to make results "fit"!!

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.

Guess what, Michael, our friend Stephen Foote even has a goofy explanation for THAT study, believe it or not! After my beating him over the head with it for a period of time, he put on his thinking-cap and came up with the following marvelously ad hoc rationalization:

Ok, so maybe hair follicles are indeed directly affected by androgens to some degree (he ruefully admits) , but it's still "edema" and "contact inhibition" which actually CAUSE them to become sensitive to those androgens in the first place!

I'm not kidding! The preceding is what he actually believes!!! I think you can see now why after so many years of ad hoc excuses and rationalizations, it's hard for very many of us to take his theory seriously. No matter what evidence is cited, he just keeps trying to turn it back around on "contact inhibition".

Bryan

Yea right Bryan.

Just because you can't grasp the science of my arguments doesn't mean you are fooling people about the validity of them. :wink:

It's all in the studies, work it out for yourself 8)

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

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

I really don't care what you think about my theory Bryan, because your "opinions" are not based on science. I have posted the responses to my theory by real scientists, and if you don't like that reality thats tough :wink:

S Foote.

 

[michael barry]

Stephen, the scientists that conducted those studies all stated in their conclusion/discussion segements at the end of those articles (except the short third PubMed one) conclude "more or less" exactly what Bryan states. That the dermal papilla reacts to androgens by mediating the growth of the rest of the follicle to summarize it without using precise verbiage. Its apparently dependent on whether the follicle is in the balding area or not as androgens added to occipital follicles dont seem to do anything to THOSE hairs in co-culture.

If you are arguing that the dermal papilla "CHANGE THEIR REACTION TO ANDROGENS" after the skin fluids put the "SQUEEZE" on them, that would take some reaction heretrofore UNKNOWN in biology. Think about it dermal papilla recieves androgens in puberty......releases growth enhancers. But at 25, tissue fluid pressures rise and the very same dermal papilla recieves androgens through an androgen receptor and releases growth inhibitors instead, due to the genetic instructions "changing" in response to fluid pressures. Thats akin to saying my eyeballs start to "hear noises" if Im in a room with no light isnt it?

The RU58841, androgen receptor blocker, increased some vellus hairs to terminal status. It only blocks dermal papilla androgen receptors.....thats it. No effect on DHT. If its acting "further down", it must be doing so to the shock and suprise of the scientists who designed the drug, because its not made to do that and they (designers) would no doubt deny it could (because prospective users dont want the feminizing effects that would bring).

In conclusion, the scientists in the studies all seem to support the direct theory. Look, Ive NO ideological ax to grind. Just wanna find out about baldness and ways to effectively treat it. Think the accepted medical theory is right in this case after viewing all the info presented.


A note on RU58841, Will Brink, writer for bodybuilding mags and life-extension writer, has wrote articles over the years (he's a fan of Dr. Proctor and Dr. Pickart as his writings attest and indicates propecia, nizoral, minoxidil, and folligen as the most cost efficient hairloss "stack" or regimine in Bodybuilder terminology), has stated that he knows several wealthy trainee clients who have paid to have private formulations of RU58841 for their own personal use. These are the type of men who've tried the most expensive (Proxiphen, etc.) treatments. Brink reported that the users say its the best thing they've ever used as far as real regrowth.

Bryan, do you think Im way off base in my interpretation of those studies conclusions? Dave? thoughts?

 

[S Foote.]

Stephen, the scientists that conducted those studies all stated in their conclusion/discussion segements at the end of those articles (except the short third PubMed one) conclude "more or less" exactly what Bryan states. That the dermal papilla reacts to androgens by mediating the growth of the rest of the follicle to summarize it without using precise verbiage. Its apparently dependent on whether the follicle is in the balding area or not as androgens added to occipital follicles dont seem to do anything to THOSE hairs in co-culture.

If you are arguing that the dermal papilla "CHANGE THEIR REACTION TO ANDROGENS" after the skin fluids put the "SQUEEZE" on them, that would take some reaction heretrofore UNKNOWN in biology. Think about it dermal papilla recieves androgens in puberty......releases growth enhancers. But at 25, tissue fluid pressures rise and the very same dermal papilla recieves androgens through an androgen receptor and releases growth inhibitors instead, due to the genetic instructions "changing" in response to fluid pressures. Thats akin to saying my eyeballs start to "hear noises" if Im in a room with no light isnt it?

Michael, you touch on the central issue when you say quote:

" If you are arguing that the dermal papilla "CHANGE THEIR REACTION TO ANDROGENS" after the skin fluids put the "SQUEEZE" on them, that would take some reaction heretrofore UNKNOWN in biology. "

This is exactly what i am saying happens.

The "squeeze" as you put it, induces contact inhibition of growth in an early stage of follicle enlargement in anagen. So the result is miniaturised follicles.

Whilst we don't yet know all the details of the pathways involved in contact inhibition, we do know that contact inhibition effects the same molecullar pathways involved in the action of TGF Beta-1.

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

TGF Beta-1 is recognised as the growth factor that androgens induce to restrict male pattern baldness follicle cell growth in-vitro.

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

Now we know from the in-vitro studies that follicles pre-male pattern baldness are not growth effected by androgens in-vitro. So something must be happening in-vivo that is altering the TGF Beta-1 expression in male pattern baldness follicles that subsequently allows androgens to "directly" effect follicle samples in-vitro.

I am saying that if contact inhibition is restricting follicle cell growth in-vivo, this is going to "change" the genetic growth pathways in these cells. The fact that we know contact inhibition effects the expression of TGF Beta-1 in the study above, shows how prior contact inhibition fits in with the TGF Beta-1 expression we see in the in-vitro studies.

So we "DO" have a recognised pathway where by an in-vivo "squeeze" can change the in-vitro growth of cells when exposed to androgens, or other substances!

So what is important here? The important thing is understanding the in-vivo male pattern baldness process! The only candidate for this using accepted science is normal contact inhibition.

Your interest in the true science of the male pattern baldness issues, and the respectfull way you discuss these questions, is a fine example to people truly interested in progress in this field Michael.

Regards.

S Foote.

 

[Dave001]

Just point out to us all Bryan where these or "ANY" other studies, "ACTUALLY" measure the comparitive size of sebaceous glands in bald, pre-bald, and hairy tissue??

This was my point as you are well aware! There is "NO" such evidence, just assumptions based on hamster flank and other irrelevant studies.

Even the section you highlighted as it it "means" something, states sebaceous gland "enlargement" as a "hypothesis" to explain the results, "NOT" a proven fact!!?

No, that is absurd as anyone can see from reading the abstracts. The hypotheses had nothing to do with whether or not sebaceous glands are enlarged in balding scalps, which is something that can and has been measured.

The stated correlation is not based on obscure observations, but is well documented in the literature. Show us the queries and corresponding database name(s) that you used to try to locate the relevant information.

Show me a study that "ACTUALLY" proves by direct measurment, that sebaceous glands in the balding human scalp "ENLARGE" compared to pre-balding?

Can't you read? Does it have to include an interactive slide-show or something?

 

[Dave001]

Stephen, the scientists that conducted those studies all stated in their conclusion/discussion segements at the end of those articles (except the short third PubMed one) conclude "more or less" exactly what Bryan states. That the dermal papilla reacts to androgens by mediating the growth of the rest of the follicle to summarize it without using precise verbiage. Its apparently dependent on whether the follicle is in the balding area or not as androgens added to occipital follicles dont seem to do anything to THOSE hairs in co-culture.

If you are arguing that the dermal papilla "CHANGE THEIR REACTION TO ANDROGENS" after the skin fluids put the "SQUEEZE" on them, that would take some reaction heretrofore UNKNOWN in biology. Think about it dermal papilla recieves androgens in puberty......releases growth enhancers. But at 25, tissue fluid pressures rise and the very same dermal papilla recieves androgens through an androgen receptor and releases growth inhibitors instead, due to the genetic instructions "changing" in response to fluid pressures. Thats akin to saying my eyeballs start to "hear noises" if Im in a room with no light isnt it?

The RU58841, androgen receptor blocker, increased some vellus hairs to terminal status. It only blocks dermal papilla androgen receptors.....thats it. No effect on DHT. If its acting "further down", it must be doing so to the shock and suprise of the scientists who designed the drug, because its not made to do that and they (designers) would no doubt deny it could (because prospective users dont want the feminizing effects that would bring).

In conclusion, the scientists in the studies all seem to support the direct theory. Look, Ive NO ideological ax to grind. Just wanna find out about baldness and ways to effectively treat it. Think the accepted medical theory is right in this case after viewing all the info presented.


A note on RU58841, Will Brink, writer for bodybuilding mags and life-extension writer, has wrote articles over the years (he's a fan of Dr. Proctor and Dr. Pickart as his writings attest and indicates propecia, nizoral, minoxidil, and folligen as the most cost efficient hairloss "stack" or regimine in Bodybuilder terminology), has stated that he knows several wealthy trainee clients who have paid to have private formulations of RU58841 for their own personal use. These are the type of men who've tried the most expensive (Proxiphen, etc.) treatments. Brink reported that the users say its the best thing they've ever used as far as real regrowth.

Bryan, do you think Im way off base in my interpretation of those studies conclusions? Dave? thoughts?

You've got the basic idea.

BTW, are you aware of the human clinical trial results of RU58841? They haven't been published in any scholarly journals or the like yet, but they are described in brief on the present license holder's Web site. In view of RU58841's known mechanism of action and earlier studies -- particularly those in the stump-tailed macaques -- the results sound quite plausible. It fared a bit better than oral finasteride. I hope the trial gets formally published.

 

[Bryan]

Michael, this is a perfect example of how Bryan tries to mislead people in these issues!

The results of follicle cell samples from the male pattern baldness and hairy areas, only "differ" when exposed to androgens in-vivo, "IF" the samples were "already" different!

The pre-balding, "normal" follicles in macaques, that are known to bald in response to androgens, do "NOT" change into balding mode when directly exposed to androgens in-vitro!!

So future balding follicles are no different in their direct response to androgens than any other scalp follicle from outside the male pattern baldness area.

This is what disproves the current theory of a direct action of androgens on follicles, and is something Bryan always conveniently forgets to mention :wink:

ROTFLMFAO!!! You seem to hang your hat on the simple fact that nobody knows yet what causes pre-pubertal hair follicles eventually to become sensitive to androgens (in the male pattern baldness sense). But guess what, Stephen: it's a House of Cards. Do you think that one missing piece of information is going to convince any serious scientist that YOUR nutso theory is correct? Wake up and smell the coffee, my friend.

Bryan

 

[Bryan]

[quote="michael barry":dd906]If you are arguing that the dermal papilla "CHANGE THEIR REACTION TO ANDROGENS" after the skin fluids put the "SQUEEZE" on them, that would take some reaction heretrofore UNKNOWN in biology. Think about it dermal papilla recieves androgens in puberty......releases growth enhancers. But at 25, tissue fluid pressures rise and the very same dermal papilla recieves androgens through an androgen receptor and releases growth inhibitors instead, due to the genetic instructions "changing" in response to fluid pressures. Thats akin to saying my eyeballs start to "hear noises" if Im in a room with no light isnt it?

Michael, you touch on the central issue when you say quote:

"If you are arguing that the dermal papilla "CHANGE THEIR REACTION TO ANDROGENS" after the skin fluids put the "SQUEEZE" on them, that would take some reaction heretrofore UNKNOWN in biology. "

This is exactly what i am saying happens.

The "squeeze" as you put it, induces contact inhibition of growth in an early stage of follicle enlargement in anagen. So the result is miniaturised follicles.

Whilst we don't yet know all the details of the pathways involved in contact inhibition, we do know that contact inhibition effects the same molecullar pathways involved in the action of TGF Beta-1.[/quote:dd906]

LOL!!! That's not good enough, Stephen! You have to find another example in biology where contact inhibition caused a CHANGE IN THE RESPONSE OF SOME BODY TISSUE TO ANDROGENS WHICH CONSISTED OF THE UPREGULATION OF TGF BETA-1. We're not going to let you get away with a form of "guilt by association"! It's "Put-Up or Shut-Up Time" for you: either find an example of that happening somewhere else, or get your butt back to the drawing-board.

Bryan