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

[abcdefg]

If the intracellular transcription and extracellular signaling pathways really play a major role in male pattern baldness follicles then the hedgehog could be very important right? The hedgehog besides being an animal, is manipulating those cellular pathways right?

 

[docj077]

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!

This statement is untrue. Not true at all. In fact, it's stupid. Cancer cells are able to invade other tissues due to their ability to produce extracellular matrix digesting proteins. Contact receptors are gained in order for them to seed other tissue sites. Contact inhibition does not apply here as contact inhibition kills cells through the FasL system or intracellular signaling.

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.

^^^^I don't recall anyone saying that. Don't be silly.

This is all basic stuff! :roll:

No, contact inhibition requires the binding of signaling molecules, whether it be a ligand or a growth receptor inhibitor. The hair shaft itself has neither. Transplantation of hair follicles requires immunosuppresion of the area of the transplant unless it's that individuals own hair.

If you think it does, prove it with an in vivo study clearly demonstrating both the molecule and its downstream effects when it comes to the molecular process of contact inhibition in the hair follicle. I want the name of the molecule or the name of the receptor and all downstream effects. I've already given you what the scientific community believes. Let's see your science.

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?

Again, you don't understand fibrosis of tissues. Fibrotic tissue is dense and the collagen that makes it up is even denser. There are numerous types of collagen. Nothing can go through collagen. That's why it's part of the extracellular matrix. Type one collagen is what makes up the majority of bone and type two makes up the majority of cartilage. I don't think you could get hair growing through collagen even if you wanted to.

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

No, it isn't. There is no hyperplasia of any cell within the follicle and the hair shaft itself is not alive to cause inhibition. This argument fails. If you believe that their is hyperplasia of any cell population in the hair follicle give me histological evidence of such.

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>No, wrong All hair follicles have the exact same genetic programming just as all cells in the human body other than gametes have the same genetic programming. Gene regulation is the only means the body has of altering the programming of individual cells. Methylation and demethylation of specific DNA sequences along with the use of silencers, enhancers, and transcription factors.

Thats the basics of the current theory, as most people understand it. Is this what you believe?
Of course this is what I believe. It's the correct theory and if you don't believe it, then email one of the people with a DOCTORATE degree and ask them yourself.

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?
I do not agree with Bryan that the mediator is TGF beta-1. It is the cellular processes that occur downstream of TGF beta-1 binding that cuases suppression of hair growth.

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. -->No, this is why I claim hair has began growing on my own head since I began taking curcumin. It's also why people who take TNF-alpha inhibitors experience hair regrowth. Both cause cellular apoptosis and fibrosis.

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.

 

[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.

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

I don't think you know how they work at all. Otherwise, you wouldn't be using words like "contact inhibition" or your belief that all that is required is DHT binding to cause hair miniaturization.

 

[michael barry]

Docj077,


Have gotta ask ya' this man. I take finasteride (and have used dutasteride in the past)...................no problems.


But green tea (this is a little embarrassing) gave me diarreaha. Straight up man, it made it rough on me in there.

I know green tea also inhibits angiogenesis (read an article on that in pubmed) even though it raises globulin levels and inhibits type one. Is there ANYTHING else that would have the positive benefit of green tea OTHER than green tea? Could one, in your opinon just use it topically?

I know soy isoflavone genistein sees a lessening in androgen receptor expression and apparently soy isoflavones do "something" to DHT in serum concentrations. I also know their are alot of phytosterols in soya. A while back I exprimented (Im nosy man) with topical flutamide while I was doing soy isoflavone pills. Propecia never effected me physically in the decade that I took it and dutasteride simply made my muscles sore a bit longer after workouts, but flutamide and soya made my sex drive plummet so far in less than two weeks that I could not lift my dick with a crowbar. I felt listless with no getup and go.

Have you felt less energized by the soy products? Still feel like yourself?

 

[michael barry]

Wookie,

Tom Hagerty noted that in adolescent males (he read this in some textbook way back) the galea thickens during and after puberty.

I suppose this could affect lymph drainage, but it also could make the T and DHT in the scalp drain away a tad more slowly too, giving it EXTRA chances to bind with receptors and MORE androgenic transcription.


The start of this entire thread was an article I posted that showed that given HIGH amounts of T and DHT, even follicles from the side of the head were shown to be able to become miniaturized.


You know Wookie, perhaps it would be interesting scientifically for some boy who has a balding lineage to have a topical receptor blocker like spironolactone applied to his head every 8 hours from ages 11-13 or so and see if it delays or affects later baldness in any way? ..........................................................................................................................couldnt' hurt.



By the way, youve managed to find some real gems and post them over the past few months.

 

[docj077]

Docj077,


Have gotta ask ya' this man. I take finasteride (and have used dutasteride in the past)...................no problems.


But green tea (this is a little embarrassing) gave me diarreaha. Straight up man, it made it rough on me in there.

I know green tea also inhibits angiogenesis (read an article on that in pubmed) even though it raises globulin levels and inhibits type one. Is there ANYTHING else that would have the positive benefit of green tea OTHER than green tea? Could one, in your opinon just use it topically?

I know soy isoflavone genistein sees a lessening in androgen receptor expression and apparently soy isoflavones do "something" to DHT in serum concentrations. I also know their are alot of phytosterols in soya. A while back I exprimented (Im nosy man) with topical flutamide while I was doing soy isoflavone pills. Propecia never effected me physically in the decade that I took it and dutasteride simply made my muscles sore a bit longer after workouts, but flutamide and soya made my sex drive plummet so far in less than two weeks that I could not lift my dick with a crowbar. I felt listless with no getup and go.

Have you felt less energized by the soy products? Still feel like yourself?

There are many antioxidants that give similar benefits as Green Tea. The simple act of taking a mutlivitamin everyday does wonders. The studies I've read have said that Green Tea is a very week androgen receptor inhibitor. In fact, I don't even consider it to be something that should be used for that purpose.

I use it for it's antioxidant purposes and the lastest issue of the Journal of the American Medical Association has simply backed up what I've been thinking all along. Using green tea significantly reduces mortality due to cardiovascular disease with very little affect on cancer outcomes.

As for the diarrhea, I've never had a problem. In fact, that's sort of odd as I've never heard of that before. You must just be really sensitive to it or something in your pills. Check the pill bottles and make sure the herbs aren't packed with something you're allergic to.

As for its angiogenesis inhibiting properties, I don't know much about that. Is that when you take it internally or as a topical? Is that in vitro test tube stuff or is that actual results measured histologically by a certified technician or pathologist? I'd like to know that, as well.

Finally, the libido issues. I don't have any problems when I use soy products. I get a little more gas than usual, but that's it. My body tolerates it very well. You might just be more sensitive to the effects of phytoestrogens and compounds that act in a similar way.

After using finasteride. for about a week, my libido returned to normal and has been fine ever since. I hate to say this, but make sure it's not just in your head and once you've done that, try some L-arginine or one of the many herbs that people recommend around here to make your little man get up and go.

Good luck.

 

[docj077]

Wookie,

Tom Hagerty noted that in adolescent males (he read this in some textbook way back) the galea thickens during and after puberty.

I suppose this could affect lymph drainage, but it also could make the T and DHT in the scalp drain away a tad more slowly too, giving it EXTRA chances to bind with receptors and MORE androgenic transcription.


The start of this entire thread was an article I posted that showed that given HIGH amounts of T and DHT, even follicles from the side of the head were shown to be able to become miniaturized.


You know Wookie, perhaps it would be interesting scientifically for some boy who has a balding lineage to have a topical receptor blocker like spironolactone applied to his head every 8 hours from ages 11-13 or so and see if it delays or affects later baldness in any way? ..........................................................................................................................couldnt' hurt.



By the way, youve managed to find some real gems and post them over the past few months.

I've always thought that the most interesting thing about hair loss on the scalp is that is pretty well correlates with the distribution of the Ophthalmic branch (V1) of the Trigeminal Nerve which is the sensory nerve for pretty much the entire face and scalp. I've always found that intriguing.

Look here for a good example.

http://en.wikipedia.org/wiki/Trigeminal_nerve

The ophthalmic branch is in green in that picture.

 

[michael barry]

Green tea study,


In vitro though.................so who knows < http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Citation

 

[docj077]

Green tea study,


In vitro though.................so who knows < http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Citation

Thanks for posting it. In vitro results are funny, because those results are usually what we base our new drugs on. Then, we go back and look for in vivo side effects. Pretty much every drug is created and tested this way. It's kind of scary, but it's true.

Again, thanks for putting that up here.

 

[wookster]

Chronic inflammation is associated with the male pattern baldness scenario...

Do the stump tailed macaques show any signs of scalp edema or inflammation... :x :? :x

http://en.wikipedia.org/wiki/Baldness_t ... _lifestyle

Diet and lifestyle

While there are a number of genetic factors which determine a person's suceptibility to androgenic alopecia including androgen receptor polymorphisms, 5-alpha-reductase levels in the scalp, androgen receptor density and distribution in the scalp, and other factors some of which may not have been discovered, the dramatic increase in baldness in the population of Japan after World War II demonstrates that hair loss can be influenced by diet and lifestyle. Increased fat or caloric intake, decrease in aerobic exercise and general "westernization" was accompanied by a dramatic increase in incidence of male pattern baldness.

Daily, vigorous aerobic exercise (as opposed to short workout periods designed to raise androgen levels and build muscle, or more sporadic exercise) and a diet which is adequate yet more moderate in terms of fat and total calorie intake have been shown to reduce baseline insulin levels as well as baseline total and free testosterone, which would significantly lower baseline DHT.

Lower insulin levels and reduced stress both result in raised levels of Sex Hormone Binding Globulin (SHBG). SHBG binds to testosterone, and prevents it from circulating free in the blood. Only free testosterone is converted to DHT. It is the level of free androgens and not total androgens which is relevant to the levels of DHT in the scalp and the progression of male pattern baldness.

In short, aerobic exercise is capable of significantly lowering DHT.

Androgenic alopecia has been shown to correlate with metabolic syndrome. Medically increasing androgen levels does not worsen this condition, demonstrating that androgens do not cause metabolic syndrome. Instead, high insulin levels (and possibly chronic inflammation) seem the likely link in the demonstrated correlation between baldness and metabolic syndrome. This reinforces the notion that behaviors which help to keep insulin levels low and reduce chronic inflammation might also help to preserve hair.

 

[Armando Jose]

The key in male pattern baldness is the special Pattern of hair loss.

Mr. Foote wrote:
So why do only certain follicles respond in this way?????
Explain what it is about follicles that makes them respond differently to androgens?

Docj077 wrote:
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.

And:
I've always thought that the most interesting thing about hair loss on the scalp is that is pretty well correlates with the distribution of the Ophthalmic branch (V1) of the Trigeminal Nerve which is the sensory nerve for pretty much the entire face and scalp. I've always found that intriguing.


It is very interesting thought, more than the chicken theory, but what is the deal with the loss of hair in the crown area?
I suppose that all agreed about the equality of all scalp healthy hairs. My bet is very simple: areas without problems to remove sebum are protected to develop common baldness. The hairs that have not problems in sebum flow are located in the lateral area of scalp due they are in contact with a absorbent surface while we sleep.
In my opinion this could be the initial trigger in the multifactorial process of common baldness. This first event is a slow process, but the other ones are more irreversible.

OTOH this post is very enlightened.

Armando

 

[CCS]

If scalp angle is the problem, wash your hair more, and swim more. But I don't think the viscoscity of sebum allows it to drip down even if it is on the sides of yorur head. And this does not explain the NW7's, or why after all the sebum drips to the wreath, that does not kill the hairs there.

 

[Armando Jose]

The real problem with sebum is inside the follicle.

Armando

 

[docj077]

The key in male pattern baldness is the special Pattern of hair loss.



Docj077 wrote:
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.

And:
I've always thought that the most interesting thing about hair loss on the scalp is that is pretty well correlates with the distribution of the Ophthalmic branch (V1) of the Trigeminal Nerve which is the sensory nerve for pretty much the entire face and scalp. I've always found that intriguing.


It is very interesting thought, more than the chicken theory, but what is the deal with the loss of hair in the crown area?
I suppose that all agreed about the equality of all scalp healthy hairs. My bet is very simple: areas without problems to remove sebum are protected to develop common baldness. The hairs that have not problems in sebum flow are located in the lateral area of scalp due they are in contact with a absorbent surface while we sleep.
In my opinion this could be the initial trigger in the multifactorial process of common baldness. This first event is a slow process, but the other ones are more irreversible.

OTOH this post is very enlightened.

Armando

Armando, that's what I'm trying to get this guy to see. It's the androgen binding, the receptor/androgen complex acting as a transcription factor transcribing TGF-beta, and TGF-beta's effects around the hair follicle to cause collagen deposition and fibrosis causing follicle malnutrition.

I've been trying to convince him of this for most of this week, but he's one stubborn guy.

As for the trigeminal nerve distribution thing, I've thought about that for a while and that's why I posted it. It's actually really interesting.

 

[CCS]

can fibrisis be reversed? I think that is the million dollar question right now.

 

[docj077]

can fibrisis be reversed? I think that is the million dollar question right now.

Check my story in the Tell your story thread or whatevery that's called. I'm thinking so, just based on my results. They aren't great, but it looks like an improvement.

I read a study that once the hair follicle has begins to become fibrosed, that hair will survive so many years or something like that and then normal methods of regrowth cease to work. Perhaps, we need to find something that will reverse the process.

I really don't know, to be honest.

 

[amibald]

does that mean, over masturbating causes hair loss?

 

[docj077]

does that mean, over masturbating causes hair loss?

No. It means that men get screwed when it comes to one of the two hormones that makes them so manly in the first place.

 

[Thinning]

A general question that's related to this thread: Would a testosterone-raising herbal compound such as Biotest's Tribex possibly lead to more scalp hair loss in those with male pattern baldness?

I doubt it - likely those only raise your test levels by 15-20%, 30% is max, and your hair is MUCH more sensitve to DHT than to T.

Well, you seem to be overlooking one other point, which is that DHT levels are obviously determined to a considerable extent by the level of available testosterone.

Bryan

But if you are on a 5-AR inhibitor, is that also the case? Because 5-AR inhibitors themselves raise test 5-10%.

 

[Bryan]

My bet is very simple: areas without problems to remove sebum are protected to develop common baldness. The hairs that have not problems in sebum flow are located in the lateral area of scalp due they are in contact with a absorbent surface while we sleep.

So hair follicles transplanted to the top of the scalp continue to grow just fine because....?