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

[docj077]

So, if you're saying that TGF-Beta causes hair miniaturization, then why are you arguing with me. That's what I've been saying the whole time

In the human scalp, both processes are needed. TGF-beta and deposition of materials needed for fibrosis. I've given you both of those. I don't see what the problem is. Also, I don't see why you keep confusing an inflammatory response with a cellular response through fibroblast activation. They aren't the same thing.

I am arguing with you because you are just quoting observations out of context, without any details of how these changes come about!

I also believe that the expression of TGF beta-1 is a factor in male pattern baldness, but that this happens through the process of normal contact inhibition.



I do "NOT" go along with any direct influence of androgen induced TGF beta-1 in the artificial in-vitro tests. The whole in-vitro testing of follicle cell response to androgens or anything else is totaly flawed in my opinion for many reasons.

I only refered to that observation as something that many do believe, and is refuted by that mouse study.

If you want to be taken seriously here, explain the sequence of events?

How do you explain how normal terminal follicles in the male pattern baldness area, are "converted" into male pattern baldness follicles by androgens? Be specific and provide proper references.

First do that 8)

S Foote.

They aren't converted into anything by androgens. They're converted into male pattern baldness follicles by the downstream mediators that are released by androgens. I'm not posting another study to prove that to you. There's already a couple above and like I said, it's the approved scientific mechanism.

You're making the process too simplistic by simply stating that androgens do all the work. It's the intracellular transcription and extracellular signaling molecules that mediate the journey of a follicle from being normal to a male pattern baldness follicle.

 

[S Foote.]

As for you claim to have proven "hard evidence", you haven't posted anything that has discredited any of the studies I've posted. I explained to you why you're interpreting your study so poorly. It's not my fault you can't comprehend it.

Post a study that is relevant to what we're talking about. I've already told you that TGF is an immune system mediator and causes the development of fibrosis. Find me a study that proves ME wrong. Your murine study doesn't cut it and is really a piece of crap when it comes to our discussion.

I can grow a mouse kidney in another immunodeficient mouse and it'll grow just fine. Do the same thing in a immune competent mouse and there will be an immune response, TGF-beta release causing fibrosis of the vessels of the kidney, accumulation of immune complexes damaging the vessels even more and finally death of every cell in the kidney.

Find a study in humans that supports your claims. If you can't, then I win.

Bulls**t

Go and talk this rubbish to Dr Uno, who showed immunology "INCLUDING" fibrosis, was not necessary for androgen driven balding!

I don't deny that fibrosis is a factor in human male pattern baldness, in fact my own theory predicts this "LATER" event!!

But you blindly continue to insist that TGF beta-1 induced fibrosis is "REQUIRED" for male pattern baldness. :roll:

Just answer my question in my last post, about your explaination for the transformation of normal scalp follicles into male pattern baldness follicles??

If you can't do this, just stop embarrassing yourself ,and shut up :wink:

I have had enough tonight, it's late here so i'am gone!

S Foote.

 

[docj077]

As for you claim to have proven "hard evidence", you haven't posted anything that has discredited any of the studies I've posted. I explained to you why you're interpreting your study so poorly. It's not my fault you can't comprehend it.

Post a study that is relevant to what we're talking about. I've already told you that TGF is an immune system mediator and causes the development of fibrosis. Find me a study that proves ME wrong. Your murine study doesn't cut it and is really a piece of crap when it comes to our discussion.

I can grow a mouse kidney in another immunodeficient mouse and it'll grow just fine. Do the same thing in a immune competent mouse and there will be an immune response, TGF-beta release causing fibrosis of the vessels of the kidney, accumulation of immune complexes damaging the vessels even more and finally death of every cell in the kidney.

Find a study in humans that supports your claims. If you can't, then I win.

Bulls**t

Go and talk this rubbish to Dr Uno, who showed immunology "INCLUDING" fibrosis, was not necessary for androgen driven balding!

I don't deny that fibrosis is a factor in human male pattern baldness, in fact my own theory predicts this "LATER" event!!

But you blindly continue to insist that TGF beta-1 induced fibrosis is "REQUIRED" for male pattern baldness. :roll:

Just answer my question in my last post, about your explaination for the transformation of normal scalp follicles into male pattern baldness follicles??

If you can't do this, just stop embarrassing yourself ,and shut up :wink:

I have had enough tonight, it's late here so i'am gone!

S Foote.

Fine, then here's a model in vivo in a mouse, since you adore them so much.

Transforming growth factor type beta: rapid induction of fibrosis and angiogenesis in vivo and stimulation of collagen formation in vitro.Roberts AB, Sporn MB, Assoian RK, Smith JM, Roche NS, Wakefield LM, Heine UI, Liotta LA, Falanga V, Kehrl JH, et al.
Transforming growth factor type beta (TGF-beta), when injected subcutaneously in newborn mice, causes formation of granulation tissue (induction of angiogenesis and activation of fibroblasts to produce collagen) at the site of injection. These effects occur within 2-3 days at dose levels than 1 microgram. Parallel in vitro studies show that TGF-beta causes marked increase of either proline or leucine incorporation into collagen in either an NRK rat fibroblast cell line or early passage human dermal fibroblasts. Epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) do not cause these same in vivo and in vitro effects; in both rat and human fibroblast cultures, EGF antagonizes the effects of TGF-beta on collagen formation. We have obtained further data to support a role for TGF-beta as an intrinsic mediator of collagen formation: conditioned media obtained from activated human tonsillar T lymphocytes contain greatly elevated levels of TGF-beta compared to media obtained from unactivated lymphocytes. These activated media markedly stimulate proline incorporation into collagen in NRK cells; this effect is blocked by a specific antibody to TGF-beta. The data are all compatible with the hypothesis that TGF-beta is an important mediator of tissue repair.

 

[S Foote.]

So, if you're saying that TGF-Beta causes hair miniaturization, then why are you arguing with me. That's what I've been saying the whole time

In the human scalp, both processes are needed. TGF-beta and deposition of materials needed for fibrosis. I've given you both of those. I don't see what the problem is. Also, I don't see why you keep confusing an inflammatory response with a cellular response through fibroblast activation. They aren't the same thing.

I am arguing with you because you are just quoting observations out of context, without any details of how these changes come about!

I also believe that the expression of TGF beta-1 is a factor in male pattern baldness, but that this happens through the process of normal contact inhibition.



I do "NOT" go along with any direct influence of androgen induced TGF beta-1 in the artificial in-vitro tests. The whole in-vitro testing of follicle cell response to androgens or anything else is totaly flawed in my opinion for many reasons.

I only refered to that observation as something that many do believe, and is refuted by that mouse study.

If you want to be taken seriously here, explain the sequence of events?

How do you explain how normal terminal follicles in the male pattern baldness area, are "converted" into male pattern baldness follicles by androgens? Be specific and provide proper references.

First do that 8)

S Foote.

They aren't converted into anything by androgens. They're converted into male pattern baldness follicles by the downstream mediators that are released by androgens. I'm not posting another study to prove that to you. There's already a couple above and like I said, it's the approved scientific mechanism.

You're making the process too simplistic by simply stating that androgens do all the work. It's the intracellular transcription and extracellular signaling molecules that mediate the journey of a follicle from being normal to a male pattern baldness follicle.

Jesus Christ! :roll:

So why do only certain follicles respond in this way?????

Explain what it is about follicles that makes them respond differently to androgens?

THIS is what i want you to explain with proper scientific support!!!

S Foote.

 

[docj077]

As for you claim to have proven "hard evidence", you haven't posted anything that has discredited any of the studies I've posted. I explained to you why you're interpreting your study so poorly. It's not my fault you can't comprehend it.

Post a study that is relevant to what we're talking about. I've already told you that TGF is an immune system mediator and causes the development of fibrosis. Find me a study that proves ME wrong. Your murine study doesn't cut it and is really a piece of crap when it comes to our discussion.

I can grow a mouse kidney in another immunodeficient mouse and it'll grow just fine. Do the same thing in a immune competent mouse and there will be an immune response, TGF-beta release causing fibrosis of the vessels of the kidney, accumulation of immune complexes damaging the vessels even more and finally death of every cell in the kidney.

Find a study in humans that supports your claims. If you can't, then I win.

Bulls**t

Go and talk this rubbish to Dr Uno, who showed immunology "INCLUDING" fibrosis, was not necessary for androgen driven balding!

I don't deny that fibrosis is a factor in human male pattern baldness, in fact my own theory predicts this "LATER" event!!

But you blindly continue to insist that TGF beta-1 induced fibrosis is "REQUIRED" for male pattern baldness. :roll:

Just answer my question in my last post, about your explaination for the transformation of normal scalp follicles into male pattern baldness follicles??

If you can't do this, just stop embarrassing yourself ,and shut up :wink:

I have had enough tonight, it's late here so i'am gone!

S Foote.

*more of my stupid ramblings*

 

[docj077]

[quote="S Foote.":f475a]

So, if you're saying that TGF-Beta causes hair miniaturization, then why are you arguing with me. That's what I've been saying the whole time

In the human scalp, both processes are needed. TGF-beta and deposition of materials needed for fibrosis. I've given you both of those. I don't see what the problem is. Also, I don't see why you keep confusing an inflammatory response with a cellular response through fibroblast activation. They aren't the same thing.

I am arguing with you because you are just quoting observations out of context, without any details of how these changes come about!

I also believe that the expression of TGF beta-1 is a factor in male pattern baldness, but that this happens through the process of normal contact inhibition.



I do "NOT" go along with any direct influence of androgen induced TGF beta-1 in the artificial in-vitro tests. The whole in-vitro testing of follicle cell response to androgens or anything else is totaly flawed in my opinion for many reasons.

I only refered to that observation as something that many do believe, and is refuted by that mouse study.

If you want to be taken seriously here, explain the sequence of events?

How do you explain how normal terminal follicles in the male pattern baldness area, are "converted" into male pattern baldness follicles by androgens? Be specific and provide proper references.

First do that 8)

S Foote.

They aren't converted into anything by androgens. They're converted into male pattern baldness follicles by the downstream mediators that are released by androgens. I'm not posting another study to prove that to you. There's already a couple above and like I said, it's the approved scientific mechanism.

You're making the process too simplistic by simply stating that androgens do all the work. It's the intracellular transcription and extracellular signaling molecules that mediate the journey of a follicle from being normal to a male pattern baldness follicle.

Jesus Christ! :roll:

So why do only certain follicles respond in this way?????

Explain what it is about follicles that makes them respond differently to androgens?

THIS is what i want you to explain with proper scientific support!!!

S Foote.[/quote:f475a]

In the scalp, the downstream mediator is TGF-beta. Believe me on this one, I know it's right. Fibrosis and increased collagen synthesis have been observed in MOST cases of male pattern baldness.

Now, I say most. Some cases aren't so easily explainable and maybe you could help me out with that.

In the face, the downstream mediator is IGF-1. I posted an abstract from a paper that demonstrated that in vivo earlier. It causes hair growth and has been shown to be upregulated in vivo in the scalp hair follicles of people who take propecia.

I don't understand what you're trying to figure out. I can't show the receptor conformation change, because I don't have a crystalline structure. I just can't show you that.

I don't know what else you want.

 

[S Foote.]

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

This was my first crude explaination, and since then more supporting evidence can be added.

Now i really have had enough for tonight!

S Foote.

 

[Dave001]

There's already a couple above and like I said, it's the approved scientific mechanism.

Is there a committee that oversees the approval of hair follicle transformation mechanisms?

 

[docj077]

Foote, when you read this again, there is something that you need to understand. There is no such thing as contact inhibition in the hair follicle. I've seen those studies and it doesn't exist. When you talk about contact inhibition, you're talking about cancer. Sure, a hair follicle that is surrounded with no place to go will cease to grow. But, it's not contact inhibition of the hair itself, because the hair isn't alive.

Steriod hormones must move intracellularly in order to function correctly. They are lipid soluble, thus their effect is within the nucleus of their target cell. Hormones that are not lipid soluble bind a receptor and activate a second messenger system. Epinephrine is one such hormone. In this case, androgens are internalized by the androgen receptor much like a simple process as receptor-mediated endocytosis. Once the androgen binds the receptor, it induces a confirmation change and moves to the nucleus to directly transcribe the TGF-beta gene. TGF-beta release causes it to bind its ligand on another cell, which in turn activates the Smad signaling pathway. A nuclear transcription factor then binds with Smad3/Smad4 to activate downstream genes within the nucleus of the cell that TGF-beta has bound to. In the case of the hair follicle cell, it activates the caspase cascade which cause apoptosis of hair follicle epidermal cells. No product form these cells = no hair growth. TGF-beta also causes the activation of the cellular machinery necessary for fibroblasts to produce massive amounts of collagen, which causes the fibrosis and collagen accumulation that is seen with histological examination.

The end result is that hair follicle appears weak, the hair sheath appears unhealthy, there is a general lack of hair follicle epidermal cells, and collagen and fibrosis surround the follicle.

All pathways are taken from Lodish, et. al. Molecular Cell Biology. Fifth Edition.

Now, that's my side of things. I'm interested to hear your side. This is taken from a molecular biology textbook and the latest studies back up my claim.

 

[Dave001]

My argument is that androgens act "indirectly" in-vivo to effect follicle growth through normal contact inhibition of growth.

Yet the susceptibility (or lack thereof) of individual follicles is maintained after transplanation to different sites.

 

[michael barry]

Doccj077,

You seem to believe that if we could just keep TGF-beta 1 from activating in the cells of predisposed follicles, we'd not "start the process" of miniaturization in those follicles. If that's the case, would you think that the B-3 proanthocyandins would pretty much stop further baldness if applied daily to the scalp (or twice daily if the essential compounds therein break down in less than 24 hours) based on this http://www.ncbi.nlm.nih.gov/entrez/quer ... query_hl=7

I thought the relevant content in that study of the B-3 proanthocyandins was this: "
For the purpose of examining the hair-growing mechanisms of procyanidin B-3, we examined its relationship to the TGF-beta signal pathway, which is known to be a regulator of catagen induction. Addition of TGF-beta1 to hair epithelial cell cultures dose-dependently decreased the cell growth, and addition of procyanidin B-3 to the culture neutralized the growth-inhibiting effect of TGF-beta1. From these results, it is concluded that procyanidin B-3 can directly promote hair epithelial cell growth in vitro, has the potential to counteract the growth-inhibiting effect caused by TGF-beta1 in vitro, and has potential to stimulate anagen induction in vivo."


The fact that TGF-beta one DOSE DEPENDENTLY decreases cell growth of hair cells proves that it needs no immunology to shrink a follicle (or to me anyway). Whatever B-3 proanthocyandins do, they seemingly counteract this negative effect and stimulate anagen induction in vivo. It would seem that topically this would be very effective in the baldness fight.




By the way...........................Ive long felt that if we could find compounds that mimick estrogen in the scalp, perhaps we could "positively" block the androgen receptors by making them uptake lots of estrogen instead of androgens. Receptor "blockers" supposedly see the receptors mutate over time and be able to host other things like insulin AS AN ANDROGEN. I read that in a EHRS abstract a while back on an article about the receptor blocker, fluridil.

This is why Ive been recently tinkering with a topical substance I think might mimick estrogen (ant there is a Japanese patent out for its topical use in androgenic alopecia), beta sitosterol. Im putting pine oil on one of my hands and small finger. Have only been doing it a week. I want to see if it causes weaker growth in about 3 months. It would be especially impressive if it would because there ARE proanthocyandins in pine bark, and no doubt some in this oil. Ive been meaning to buy some beta sis tablets and crush them up and mix with an alchohol/water solution and try it topically on another patch of body hair too in case the pine oil doesnt absorb that well.

The Japanese patent for topical usage of beta sis got me interested in it. The fact that bronze and iron age celt mummies in Ireland were found to use pine oil in their hair furthered my interest. However, this post by Hairy Wookie at HLR really got my attention about it possibly "tricking" a receptor into thinking it was an estrogen:

http://www.medscape.com/medline/abstrac ... 3?prt=true



--------------------------------------------------------------------------------
quote:
Separation and identification of phytoestrogenic compounds isolated from bourbon.
Alcohol Alcohol Suppl. 1987; 1:551-5 (ISSN: 1358-6173)Rosenblum ER ; Van Thiel DH ; Campbell IM ; Eagon PK ; Gavaler JS
University of Pittsburgh School of Medicine, PA.

There is considerable evidence that several plant metabolites have estrogenic properties. Given that many alcoholic beverages are made from plants which have been shown to possess estrogenic activity, we considered the possibility that alcoholic beverages may contain estrogenically active substances. To evaluate this hypothesis we first extracted and then used gas chromatography/mass spectrometry to identify two phytoestrogens, biochanin A and beta-sitosterol in the bourbon extracts. Based on these findings we suggest that the feminization observed in chronic male alcoholics with liver disease may reflect, at least in part, the presence of biologically active phytoestrogens in the alcoholic beverages they consume.

PreMedline Identifier: 3426733


;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;


Doccj077,

This is Mike again,...........have you ever noticed how old street drunks seemingly mysteriously have good hair in many cases? Lousy nutrition, dont bathe........................but 60 f*****g years old with not only hair, but in many cases pretty damn good wavy hair. That salient fact had even led a few poor souls to conclude that shampoo might be the cause of hairloss and a website was created to that end and achieved some popularity a few years back. I knew it was ridiculous, but DID agree that old drunks seem to have unusually good hair.

Tom Hagerty noted a news article about a man who drank a PINT of Jack Daniels a day being admitted to a local hospital. The guy had hardly ANY body hair, hardly any pubic hair, gynochomostia, musclar atrophy, feminine characteristics, a class3+edema on his legs.........................................and probably a pretty good head of hair. Ive noted in the past that guys (Dr. Loren PIckart mentioned this on his forum, he's the inventor of Tricomin and Folligen) that he knew some bodybuilders who get side effects like gyno with very large doses of saw palmetto (like a thousand mgs). Beta sitorsterol is the one common component in saw palmetto, african pygeum, stinging nettles, and pumkin seeds. All are associated with BPH and baldness alternative remedies. We know they dont lessen DHT. I had hopes they slightly interefered with receptors and this might be how they'd work.


Anyhoo.................................I guess in about 3 months I'll be able to report if Ive had anti-androgenic success with the body hair on the back of my hand or not. If not, I'd like to mix up some beta sis tablets with alchohol and water and try it in one other spot. We will see.


Those are my own to little guesses of a couple of substances that might help men topically. Blueberries, now associated with reducing prostate cancer (they have anthocyanidns also) might be another thing to try at some point if I get the time.

 

[docj077]

Foote,

I finally got my other textbook back. This isn't to prove my point anymore. I just wanted to tell you how the androgen receptor works, because you were asking about it. Sorry if I offended you at any point during our discussion.

"The androgen receptor functions as a homodimer (AR/AR) and is a member of the family of nuclear receptors. The AR/AR receptor complex is a transcription factor that binds to hormone response elements on DNA located 5' from the genes that the androgens control. Interaction between the receptor-steriod complex and the nuclear chromatin causes increased transcription of structural genes, the appearance of mRNA, and the subseqent translation and production of new proteins."

Nuclear receptors are defined in the context of the following (all sex hormones work this way)...

"A number of important signalling molecules produce their effects not by binding to receptors on the cell membrane, but by binding to intracellular receptors (also called nuclear receptors) that are transcription factors....once inside the cell, these substances bind to intracellular receptors. The ligand-bound receptors are activated transcription factors that regulate the expression of target genes by binding specific DNA sequences."

Taken from Boron and Boulpaep. Medical Physiology. Updated Edition. Copyright 2005.


As for testosterone and DHT having different effects on the conformational effects of said androgen receptor, I have that in my endocrinology notes, but I can ask my endocrinology professor for the reference if you need me to. For now, I'm going to stick with my theory of TGF-beta causing hair loss and IGF-1 causing hair growth. Like you said, it's taken out of context, but for now, that's the best we have.

So, I can take you up to the binding of the DNA with medical textbooks and signaling pathways. I can not give you a study that clearly demonstrates that the receptor/androgen complex binds to the DNA and transcribes the TGF-beta gene. That's taken from the studies I've listed and that material is in vitro, as far as I know. However, in vivio, decreased androgen receptor binding corresponds with decreased TGF-beta. Somehow, the androgen complex regulates the production of TGF-beta. We'll just have to figure this one out.

Once TGF-beta is produced, scientists believe that is causes fibroblasts to produce more collagen with the end result being parafollicular fibrosis. I can only show you high TGF-beta in tissues with a corresponding fibrosis of anything it touches using basic histological methods. Apparently, but I can't find it, scientists have seen high TGF-beta levels in follicles that have fibrosed, as well.

I do believe that I'm mistaken if I ever said that it's an immune response. I don't believe that and I think I made the mistake of repeating that over and over for some reason. TGF-beta is an immune system modulator in the right tissues, but I think in the hair follicle its merely responsible for the increased collagen and fibrosis with no infiltration of lymphocytes or macrophages.

So, if you have the time to read all this come up with some questions or some thoughts. I'm interested to see what you have to say. The best I can give you on the textbook stuff is that it seems to be proven material.

 

[docj077]

There's already a couple above and like I said, it's the approved scientific mechanism.

Is there a committee that oversees the approval of hair follicle transformation mechanisms?

Yes, I'm head of the committee. Shhh...don't tell anyone. :freaked2:

 

[docj077]

Michael Barry,

Your heart is in the right place when it comes to the studies I'm looking for. I just need more in vivo evidence. All I have is upregulated TGF-beta staining and the fibrotic effects it has on hair follicles. What needs to be found out is if this is the only compound causing this effect, if so, how can we stop it, and which herbs or drugs will be of benefit with proven in vivo results.

Curcumin is promising and so are some other herbs that have been listed.

For now, I'll keep being my own person science experiment. I will keep everyone posted when I see terminal hair growth.

Thanks for your help and that alcoholic article was very interesting.

 

[CCS]

can these supplements put our hair into perpetual anagen, and if so, would that be good or bad? Even if they are in anagen, does that mean shaft diameter will not shrink?

 

[wookster]

But from the mechanistic viewpoint, we know androgens can miniaturise follicles in the male pattern baldness area without any inflammatory component. The macaque studies prove that.

http://www.hairsite4.com/dc/dcboard.php ... ting_type=

Also according to the rules of scientific theories, if someone argues DHT causes male pattern baldness via immunology, they also have to explain how DHT grows body hair via immunology?

Good points. The argument appears to be that the balding scalp hair follicles[which coincidentally grow over the galea aponeurosis regions of scalp] respond to androgens by miniaturizing, which is opposite to what happens to body and beard hair follicles - which grow larger in response to androgens.

http://www.medscape.com/viewarticle/470297_print[/url]

The effect of minoxidil on hair growth has been studied extensively in the stump-tailed macaque, a primate that develops postadolescent scalp hair loss closely resembling human androgenetic alopecia. Topical minoxidil prevents the development of scalp hair loss in periadolescent macaques and promotes regrowth of hair in balding animals.

There appears to be an androgen independent mechanism of hair growth that is related to fluid balance/differential?

How long did those macaques maintain their hair regrowth after minoxidil treatments?

 

[S Foote.]

Foote, when you read this again, there is something that you need to understand. There is no such thing as contact inhibition in the hair follicle. I've seen those studies and it doesn't exist. When you talk about contact inhibition, you're talking about cancer. Sure, a hair follicle that is surrounded with no place to go will cease to grow. But, it's not contact inhibition of the hair itself, because the hair isn't alive.

:freaked: If thats the extent of your knowledge of basic physiology, i have to say you are a total fraud.

Listen very carefully, "ALL" normal cells respond to the contact inhibition of cell multiplication. Cancer cells have "LOST" their response to contact inhibition, and thats "WHY" they can invade other tissues!

Growing anagen follicle cells are not "dead" and they will stop growing if there is a certain degree of resistence to this from surrounding tissues, though normal contact inhibition. Anagen follicle size determines the amount of hair produced by that follicle.

This is all basic stuff! :roll:

You "yourself" are claiming that fibrosis forming around follicles is preventing them from enlarging. So how do you think that could happen? Why don't the growing follicles just "force" their way through this tough fibrose tissue?

It's called normal contact inhibition of cell multiplication :wink:

If your ill informed statement above is based on a "genuine" doctors training (which i now doubt very much), God help your patients :roll:

>>snip<<Now, that's my side of things. I'm interested to hear your side. This is taken from a molecular biology textbook and the latest studies back up my claim.

Let's just get down to the very basics here.

We are already familiar with the studies and the fact that levels of TGF beta and other growth factors effect tissue growth.

But so far your collection of studies doesn't justify your opinion of how all this information "fits" together in androgen related hair loss (male pattern baldness), and so far a few of your comments have been clearly contradictory!

So lets be clear about the evidence here, and stick to the basics. Please answer my points below in a clear and concise way.

I presume you go along with the current theory of a "direct" effect of DHT within hair follicle cells where testosterone is converted to DHT?

This states that the DHT produced in these cells reacts through the androgen receptor then the genes to alter the expression of growth/suppression substances within these cells. The difference in the expression of these growth altering substances in different follicles, is because of a difference in the follicles genetic "programing"

Thats the basics of the current theory, as most people understand it. Is this what you believe?

In my debates with Bryan Shelton about the in-vitro studies (at least one of which you have referenced), i argued that any conclusions reached were unsafe for a number of reasons.

Bryan is on the record as insisting that these in-vitro studies prove the direct growth suppresion of male pattern baldness cells through TGF beta-1.

But it seems you don't agree with Bryan?

You claimed that it was necessary for an immunue system presence for TGF beta-1 to inhibit follicle growth, and you claimed this was why male pattern baldness follicles re-grew in that mouse study.

There is also no immune presence in the in-vitro studies where TGF beta-1 apparenty "directly" suppressed male pattern baldness cell growth. So are you saying the in-vitro tests are not a true test of the androgen effect on follicles as Bryan tries to claim?

It is important that you make your position "VERY" clear on this!

S Foote.

 

[S Foote.]

My argument is that androgens act "indirectly" in-vivo to effect follicle growth through normal contact inhibition of growth.

Yet the susceptibility (or lack thereof) of individual follicles is maintained after transplanation to different sites.

No it's not Dave!

Do try to keep up with modern transplantation research :roll:

I am sure Michael will enlighten you if you are to lazy to do your own research.

 

[S Foote.]

Foote,

I finally got my other textbook back. This isn't to prove my point anymore. I just wanted to tell you how the androgen receptor works, because you were asking about it. Sorry if I offended you at any point during our discussion.

I have just seen this post after i posted above.

I know how androgen receptors work, my contention is that the androgen effect in other tissues results in "indirect" effects on follicles, that are more significant on hair growth in-vivo.

Please respond to my questions in my other post.

S Foote.

 

[vegeguy]

okay...some updated questions

Let's summarize this abstract...
Testosterone and DHT enter follicle cells and caused apoptosis (programmed cell death). Is that the take home message here?