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

[Bryan]

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%.

Sure they raise testosterone, but the 5-AR inhibitor keeps it from converting to DHT.

Bryan

 

[Thinning]

Sure they raise testosterone, but the 5-AR inhibitor keeps it from converting to DHT.

Bryan

Right, so running dutasteride or finasteride with a test booster or AI should not produce a significant amount of hairloss since the higher test is more than offset by the 5-AR reduction.

Thats what I was getting at.

That seems to be the case for me - I am running finasteride 1.25mg daily.

Also, I am currently running a trib product ( to slightly boost test ), an AI ( to slightly lower estrogen, which also slightly raises test ), and Nettle Root Extact ( to bind to SBHG, which raises free test ). I am taking doses on the low end of the scale ( i.e. if the reccomended is 1-3 caps daily Im taking 1 ).

The results have been excellent, I have reduced the slight flab and bloat around my chest/handles/midsection with no change to my diet or training. My libido is excellent, I can handle sex with my g/f multiple times a day ( Im 35 - thats not easy - its easy to beat off twice a day but f*****g is different ). And my gains in the gym have been steady, despite stopping NO and Creatine products.

I may switch to dutasteride to further drop DHT, but Im still worried about the long half life.

 

[CCS]

I got a question for thinning, since I assume he may have researched this:

Is DHT anabolic for muscle? What about bones?

 

[Thinning]

DHT is not anabolic, but its very androgenic.

Also it acts as an AI, and can bind to SHBG.

 

[michael barry]

Docj077,

Let me quickly summarize Stephen Foote's edema theory for you and why he believes its the real cause of baldness, quickly in layman's terms.


Lymphedema is seen usually in females in the legs, but sometimes arms and extremities. Men can get it too. Where there is advanced edema, the body hair in these places is lost. Edema is, (I know you know this), when water and fluids pumped upwards toward the skin does not drain back down the one-way lymphatic pumps properly. The skin gets full of water and if you wear a snug fitting appendage over the lymhoedematic skin, it will indent it with whatever pattern the appendage is in (like your socks leaving those vertical marks that match the elastic bands on your ankles for a few minutes after taking them off). Advanced edema almost always causes hair loss in the affected area.

Men who have alot of blood feed to their scalp have to have the lymphatic pumps drain despite the higher blood pressure underneath the upward pumping (one way) lymphatic pumps. Men with thick beards, neck and chest hair who have an abundance of DHT are getting extrodinary lymph drainage in those areas as the DHT created "falls" downwards enough to supercharge the lymphatic pumps (Im assuming these pumps are somewhat androgenically stimulated). Like a tall sky scraper whose bathrooms and sinks on ALL floors drain into the one main waterline that runs down the buildings center.............................if everyone ran a bathtub full of water and drained the tub into the one central drainpipe at the same time, the main drainline would back up. Remeber Doctor, these men also have HIGH blood feed to the scalp, and thus the bigger arteries under the galea put more pressure up on the scalp from underneath. Stephen thinks the drainage issue and the pressure from underneath can slam the one-way pumps shut for periods of time, leaving lymphatic metablolic waste and gunk products up there around the follicle creating tissue fluid pressures that are slightly higher at certain depths of the scalp. Edema pathologically looks alot like an autoimmune response as far as what happens to the skin, the inflammation, the fibrotic occurences, etc. after time. Stephen believes that the reason hair is lost in the leg-edema cases as well as head cases (male pattern baldness) is that the fluid pressures around the follicle get just high enough that when the follicle is re-enlaging in one of the early EIGHT anagen sub-phases........................it cant because of contact inhibition. He believes this action to be based on the TGF-beta one pathway as their is a biological precedent for this in lung tissue and the response in that lung tissue CHANGES the tissues response to androgens (Stephen would have that link). Stephen believes that we have never been able to "CHANGE" hair's response to androgens in vitro beacause if they arent male pattern baldness hairs yet, they wont be until they are "squeezed" enough.

IN short, Stephen believes your head hair follicles "change" their response to androgens after being squeezed long enough by higher pressures. Then androgens start shrinking those follicles and as pressure rises and rises around it, the hair cant enlarge enough to make anything but a vellus hair. A map of the lymph nodes of the scalp looks strangely like a Norwood scale. Worst drainiage is in the temples and vertex bald spot, best is on the sides and over the top. Hence the typical male pattern baldness pattern.

The list of topicals that work for male pattern baldness are also all either acutally used to treat lymphedema or similar maladies or are strong diuretics. Stephen claims transplants work because of the fibrose scaffolds that are created around transplant sites shield the new follicles from the squeezing and make pressure between the plugs greater (although theoretically transplants deep enough to lance the galea might ameleirotate pressures).



Doctor, this is where you'll emphathize with Stephen and see why he has come to this conclusion even if you dont agree with him.

++++ Proanthocyandins are used to treat lymphedema topically. (Ive used apple poly proanthocyandins on my scalp as Im nosy......................my hands and feet swelled painfully as I used to much. Kinda a vodka headache sensation if you spray to much. You can literally feel the liquid contract on your scalp-------think about spilled apple juice on your arm and how it gets sticky and then draws inwards----
same sensation.

+++++minoxidil, a NO emulator, gets lymphatic vasomotion stimulated. Minoxidil is a diuretic. One of minoxidil's side effects (Ive experienced this also years ago when I used it) is that it moves fluid volume. My hands swelled. Some people complain of swollen faces and even some gyno with minoxidil.

+++++latanaprost. Stronger than minoxidil according to Hideo Uno's last experiments where he used .5% latanaprost on stumptailed macaques and found it grew as much hair as 5% minoxidil. Ten times as strong I guess. It also makes hair darker as it excites melanocytes. Its a prostaglandin analogue of several different prostaglandins whereas gamma linoleic acid is just a E-1 analogue and it can be counteracted by ALA in the bod. Latanaprost is a GLAUCOMA medication. Its an eye drop that docs noticed made eyebrows, lashes much darker and much thicker. However, just using Gamma linolenic acid probably would get one much of this effect if they dont use TOO much ALA (which again, somehow counteracts it)

++++++Copper peptides are sometimes used for edema. They move fluid away from the application site. I used too much prox-n one night before bed to test this. Sure enough, I had sore numb hands in the morning (painfully so in fact).


+++++++Some men experience the side effect of gynochomostia with finasteride and dutasteride. These can be considered "hydraulic"----fluid moving, effects.


+++++++++Dr. Loren Pickart mentioned that some bodybuilders he knew who took alot of saw palmetto got b**ch-tit also.

++++++++++Flutatmide, and androgen receptor blocker that really works (want to keep your hair Doctor? use flutamide), but has horrible side effects. Its given to transexuals. You grow tits on this if you stay on it. Your dick will die on you also and your skin will get soft, you'll have diarreaha all the time, no sex drive, and an upset stomach constantly. Pretty much can turn a man into a woman. Ive tried it topically hoping Bryan wasn't a 100% right about it all being absorbed. Bryan was very right and I felt like sh*t within three days. I learned not to doubt Bryan after that.

++++++++Sprionolactone is a diuretic and a potassium channel sparer.

++++++++alchohol and propylene glycol, which actually lead to higher hair counts by themselves (ask Bryan about this) are both diuretics

+++++++topical caffeine (alpecin, as mentioned in the EHRS 2006 abstract) is a diuretic.


++++++++Cyclosporin, which according to Peter Proctor, grows more hair on balding heads than anything, often sees gyno, fluid shifting to hips, etc. as a side effect.


++++++++Topical Roxythromicyn (another cytotoxic immunosuppressant thats in clinical trials for baldness right now)...............................I do not know if shifting fluid volume is a characteristic of this.


++++++++++Ice packs.....Chemo patients use ice packs on their heads to help not lose hair and it works. Ive read links on this. Its pretty damned effective. Abnormal hair growth under casts, abnormal back hair growth cited by Dr. Nasser Razack of Ice pack carriers also lend crecedence to Stephen's idea.



However, there are DIRECT effects of all of the substances listed above on hair in vitro except minoxidil. Copper peptides were proven in a korean study to help hair in test tubes resist apoptosis. Proanthocyanidins either excite epilithial cells (apple ones) or protect against TGF-beta one (barley) or excite other follicle cells in tests. Latanaprosts stirs up prostaglandin a great deal and this is what the researchers attribute its hypertrichotic ability too. We know how finas, dutas are thought to work. Caffeine has been shown in vitro to protect agains testosterone in the test tube with a hair follicle. Sprio and flutamide block receptotrs. The ice and casts just irritate body hair like rubbing it does and thus excites keratinocytes. There is an alternate explantion for why all of these things work. I trust you know all the reasons minoxidil works.



Ive suggested that a topical diurectic or contractory substance with NO hair growth properties be placed on the scalp (petrolium jellies, alum, etc.) and see if better hair growth was achieved in a year period. Ive told Stephen this is the easiest way to test his theory. It could be done on arm hair even. Im not going to do it, its his theory. I think if he could talk a friend into doing it, he could report back with the results.

I too, believe in the standard theory of baldness by the way...........I believe TGF-beta one, PKC, and a few other antigens are released by the DP cells after androgenic transcription,...............some small inflammation results, and then the immune system's maker cells get tricked into thinking the follicle is a foreign body (or a part of the follicle) and the attack begins. But I think you can see why Stephen believes Edema might be responsible. I'd love to see him be able to get his idea scientifically tested so he could get satisfactin yea or nea.


Now you can argue with him about it.

 

[docj077]

Edema is actually caused by increased hydrostatic pressure of fluids overwhelming the oncotic pressure of blood itself, so fluid can not be pulled back into the venules after fluid has been moved into the tissues during their trip through the capillaries and interstitial fluid. Lymphatics then remove that excess fluid through an intricate maze of lymphatics and lymph nodes with it draining into two different deep areas depending on what side of the body we're talking about.

There is no defect in drainage from the scalp, because if there was you wouldn't get hair loss, you'd get something far more serious. Just look at what minimal lymphatic or venous blockage does to people with elephantiasis, hydrocephaly, or to a woman with a radical mastectomy. Such blockage would swell the head and cause pitting edema. Pitting edema is not present in individuals with hair loss as it's not present histologically. Not only that, but every single one of us would get stasis dermatitis. I don't have that, do you?

If he could show me histologically that venous stasis is occurring, contact inhibtion of hair follicles is occuring as a result of an inhibitor ligand or a growth receptor inhibitor, and then the chemical mediator responsible for the collagen deposition and fibrosis, then I'd buy his theory. He thinks that hair can grow through collagen for for goodness sakes! If he thinks that, then sure had better assume that a little venous stasis with no evident edema should grow hair just fine, as well .

Right now, there are way too many holes in it and lymphatic or venous obstruction or edema can be caused by a lot of pathologies.

If I were to say that my theory dictated that collagen deposition and fibrosis around the hair follicle caused reduced fluid movement and venous stasis with a resulting lymphatic overload, I'd be just as right and I'd have the molecular in vitro and in vivo proof for my theory. His theory assumes that lymphatics from the scalp drain into the face and area of beard growth. They don't. They drain into the cervical lymph nodes. Just like every lymph node and lymphatic in the face and scalp do. So, if we're talking about massive pressure overload in the lymphatics, the first place it should be apparent is the lateral and posterior neck, which it isn't there. I know, because I don't have it and neither does anyone else I've ever met that has hairloss.

Right now, this other guy has absolutely nothing but objective deductions. At least I have molecular evidence for my theory.

As for minoxidil, it dilates venules and veins causing a decreased afterload or just a decrease in resistence in whatever vessel it touches. That's it's mechanism of action. My theory works just as well, because venous dilation would allow for blood to move through the low resistence veins easier allowing for easier remodeling and healing of areas with collagen deposition and fibrosis of hair follicles. It does not increase NO in lymphatics as there are no smooth muscle cells in lymphatics for it to act upon. Lymphatics have only endothelial cells. That's it.

Another tidbit about Minoxidil is that people apply it to their faces to grow hair, especially thick beards. If Footes theory holds true, then they would actually decrease hair growth, because of a loss of DHT from that area as the veins dilate and any hint of stasis is removed.

As for his theory, minoxidil did not work for me at all and neither has administration of cold packs. Obviously, my pathology is not related to edema, but growth inhibition through follicular malnutrition secondary to follicular fibrosis.

The other problem is his lack of explanation for how 5AR inhibitors work in the context of edema. Lymphatics do not have androgen receptors and neither to their valves.

I know my theory works, because hair is filling in all along my hairline now. Granted it's vellus, but just within the last month it's already grown to be about an 1/8 of an inch by simply inhibiting every step of the hair loss pathway that I know. If I could take a picture of it, I would to prove my point, but it's too thin to show. My results are even with my forced lowering of the dosage of finasteride I take everyday.

I'm glad you believe in my theory somewhat. You have a good head on your shoulders.

 

[docj077]

And Michael Barry,

It's not that I don't see the logic in his theory. It's just that I don't trust the physiology that he's trying to use to explain his theory. He's taking processes that would clearly be visually presentable and turning them into microscopic pathologies. It doesn't work that way when it comes to lymphatics. It doesn't work that way at all.

Not only that, but the application of cold packs will worsen the stasis and not prevent it. There is no inflammatory response to prevent, so we're not trying to stop vasodilation so macrophages can move into a specific area. Application of cold packs contricts vessels and shifts blood back to the core. It would cause stasis of veins and lymphatics like he claims and worsen hair lose. Not help it.

Heat, on the other hand, is a different story.

Also, the response in an autoimmune response and the response to edema are two very different processes. With an autoimmune response, you're talking about lymphocytic infiltrates and complete tissue destruction. With edema, all that is seen is failure of veins with dilated lumens. Continued dilations can cause lumenal remodeling, but not with lymphocytic infiltrates or really any hint of an immune response.

Also, be aware that with venous stasis not only hair loss occurs, but ulcerations are quite common and so are discolorations.

 

[michael barry]

Docj077,

Tom Hagerty highly praises circumin (tumeric extract) .

There is a supplement that has curcumin, green tea extract, milk thistle extract, bacopa, and ashwagandha extract all in it called Protandim. I have a bottle left over. Took it for a while (its pricey). Im going to take that while I get some more Tumeric.

Some of the things youre doing remind me of some literature on hairloss-research.org in reference to PKC down-regulation, etc.


Have you ever considered a receptor blocker like topical spironolactone or fluridil? Do you think that they may not be active 24 hours a day and the few hours they are not would ruin the effect? I keep going back to receptor blockage or using an estrogen mimicker because if we could seemingly do this, none of the other bad downstream Dermal Papilla mediated antigens would seemingly get released.


Look at this picture of a woman who injected herself with testosterone. She wanted to be a man http://www.oprah.com/tows/slide/200509/ ... _107.jhtml. She went NW4 bald. Her twin sister here http://www.oprah.com/tows/slide/200509/ ... _106.jhtml still has her hair.

Here are two other female TWINS together. One takes testosterone to be like a man (no sex change in this photo yet either, still female genitalia). Look at how much her face and hair have aged compared to her twin sister http://www.oprah.com/tows/slide/200509/ ... _102.jhtml. Now, have a close look at her neck and face and aged appearance of her hair (and beard) http://www.oprah.com/tows/slide/200509/ ... _103.jhtml


Those pics said it ALL to me. If you go to alpecin.com, they explain that testosterone and its metabolite are the biggest ageing hormones effecting skin. Testosterone is hard on dermal tissues. Thats why so many of us got so high on RU58841 a few years back because it was a receptor blocker with seeminlgy no side effects. Could have been applied topically every day and zap!.....no more balding. One could have used regrowth and anti-fibrotic agents with it like Prox-N (I have a very positive impression of this) and aminexil and really made a stab at getting back a great deal of hair. Besides opening potassium channels, upping VEGF, and speeding up DNA activity in hair cells, minoxidil supposedly resisted the cross linking of collagen in the connective tissue sheath. It also is a weak prostaglandin up regulator. Used in conjunction with a reallly effective topical receptor blocker, a man seemingly would have a good chance at really converting some vellus hairs to terminal ones (my opinion).

Tell me what you think of those pics........................reminds me of the Hamilton castrates whos supposedly balded within a year or so of recieving testosterone injections (although some here think that whole study may be something of a myth). However, those pics pretty much show that women have baldness genes but are protected from baldness by estrogens and low T levels.

 

[Armando Jose]

Look at this picture of a woman who injected herself with testosterone. She wanted to be a man http://www.oprah.com/tows/slide/200509/ ... _107.jhtml. She went NW4 bald. Her twin sister here http://www.oprah.com/tows/slide/200509/ ... _106.jhtml still has her hair.

Here are two other female TWINS together. One takes testosterone to be like a man (no sex change in this photo yet either, still female genitalia). Look at how much her face and hair have aged compared to her twin sister http://www.oprah.com/tows/slide/200509/ ... _102.jhtml. Now, have a close look at her neck and face and aged appearance of her hair (and beard) http://www.oprah.com/tows/slide/200509/ ... _103.jhtml

It is easy look the different lenght of scalp hairs in the "new" men. Curiously the bald have a short hair, and the other one have a sufficient lenght of hair to avoid problems in sebum flow and he preserve his hair.
Coincidence or causality?

Bryan
Trasplanted hair also can suffer again this process, but it is slow and normally trasplanted hairs is allowed to grow long. Also the trasplanted hairs are given more attention. And, naturally not all trasplanted hairs survive for ever and ever.

Armando

 

[still_trying]

[quote="still_trying":b28f2]for us non-scientists without the time to read 16 pages of arguments (!) could someone summarise anything important that has arisen from all this please?

Sure, I'll take care of that for you. Here's the most important summary of all that you need:

Stephen Foote should confine his efforts to the specific endeavor for which he has demonstrated a clear and obvious talent (DESIGNING AUTOMOBILE ENGINES)!

Bryan

So you still have nothing scientific to counter my arguments with Bryan, just your usual sarcasm?

Well thats going to convince people you know something about science isn't it (not!) 8)

PS:

Have you managed to come up with any scientific justification yet for your regular posts calling my theory "ridiculous"?

You've had enough time since i last called you out on this, but still you can't back up your arogant claim!

People will reach their own conclusions Bryan :wink:

S Foote.[/quote:b28f2]

thanks for clearing that up for us guys....all is clear.

l :hairy: :-x

 

[docj077]

Look at this picture of a woman who injected herself with testosterone. She wanted to be a man http://www.oprah.com/tows/slide/200509/ ... _107.jhtml. She went NW4 bald. Her twin sister here http://www.oprah.com/tows/slide/200509/ ... _106.jhtml still has her hair.

Here are two other female TWINS together. One takes testosterone to be like a man (no sex change in this photo yet either, still female genitalia). Look at how much her face and hair have aged compared to her twin sister http://www.oprah.com/tows/slide/200509/ ... _102.jhtml. Now, have a close look at her neck and face and aged appearance of her hair (and beard) http://www.oprah.com/tows/slide/200509/ ... _103.jhtml

It is easy look the different lenght of scalp hairs in the "new" men. Curiously the bald have a short hair, and the other one have a sufficient lenght of hair to avoid problems in sebum flow and he preserve his hair.
Coincidence or causality?

Bryan
Trasplanted hair also can suffer again this process, but it is slow and normally trasplanted hairs is allowed to grow long. Also the trasplanted hairs are given more attention. And, naturally not all trasplanted hairs survive for ever and ever.

Armando

Sebum flow does not cause hair loss. If it did, the first reaction would be folliculitis. Not miniaturization. You would have pimples everywhere on your scalp.

 

[docj077]

Michael Barry,

Those pics are quite fascinating. Women have lower testosterone levels, because the only place they get it from is their adrenal glands. Congenital adrenal hyperplasia is an excellent reason for an XX female to be born a man (because the clitoris is enlarged to look like a penis) and later become a woman due to personal and psychological issues.

Women have androgen receptors just like men, but the high circulating estrogens are very protective.

You know they're protective, because once a woman goes through menopause, if she inherited a faulty x chromosome and it's active, she'll begin to have thinning of her hair. You see it all the time in the older ladies. A lot of them are wearing wigs.

 

[Bryan]

The other problem is his lack of explanation for how 5AR inhibitors work in the context of edema. Lymphatics do not have androgen receptors and neither to their valves.

AHA!!! Thanks for clearing that up! I've asked Stephen about that on at least one occasion in the past, but I've never gotten a clear response from him. I even wasted some time myself in an effort to find out about the presence of androgen receptors in the lymphatics and how reducing DHT _might_ be useful for increasing drainage, but I came up empty. It does look like another large hole (among others) in his "edema" theory of hairloss.

Bryan

 

[S Foote.]

The other problem is his lack of explanation for how 5AR inhibitors work in the context of edema. Lymphatics do not have androgen receptors and neither to their valves.

AHA!!! Thanks for clearing that up! I've asked Stephen about that on at least one occasion in the past, but I've never gotten a clear response from him. I even wasted some time myself in an effort to find out about the presence of androgen receptors in the lymphatics and how reducing DHT _might_ be useful for increasing drainage, but I came up empty. It does look like another large hole (among others) in his "edema" theory of hairloss.

Bryan

Before i become involved any further in this, have you got a proper reference for your claim that there are "NO" androgen receptors in any part of lymphatic vessels Doctor?

Be specific instead of "i once read" OK!

S Foote.

 

[Thinning]

Sebum flow does not cause hair loss. If it did, the first reaction would be folliculitis. Not miniaturization. You would have pimples everywhere on your scalp.

Actually thats how my hairloss started. I was even put on antibiotics to stop the folliculitis.

 

[docj077]

The other problem is his lack of explanation for how 5AR inhibitors work in the context of edema. Lymphatics do not have androgen receptors and neither to their valves.

AHA!!! Thanks for clearing that up! I've asked Stephen about that on at least one occasion in the past, but I've never gotten a clear response from him. I even wasted some time myself in an effort to find out about the presence of androgen receptors in the lymphatics and how reducing DHT _might_ be useful for increasing drainage, but I came up empty. It does look like another large hole (among others) in his "edema" theory of hairloss.

Bryan

Before i become involved any further in this, have you got a proper reference for your claim that there are "NO" androgen receptors in any part of lymphatic vessels Doctor?

Be specific instead of "i once read" OK!

S Foote.

I'm not going to be specific for receptors as I don't have time. The clue to what I say is the fact that metastatic prostate cancer is identified with immunohistochemical staining for the androgen receptor in both the lymph node and even in the lymphatics themselves as carcinomas typically move through lymphatics while sarcomas move through the blood stream. Only the cancer with androgen receptors will show up microscopically with no evident staining of androgen receptors in either lymph node or lymph vessels.

That's the best I can give you right now. Sorry, but I'll look for more later.

 

[docj077]

Sebum flow does not cause hair loss. If it did, the first reaction would be folliculitis. Not miniaturization. You would have pimples everywhere on your scalp.

Actually thats how my hairloss started. I was even put on antibiotics to stop the folliculitis.

You're a different case. Hairloss has numerous causes. Unfortunately, mine isn't as easy as scalp inflammation. I wish it was.

 

[S Foote.]

The other problem is his lack of explanation for how 5AR inhibitors work in the context of edema. Lymphatics do not have androgen receptors and neither to their valves.

AHA!!! Thanks for clearing that up! I've asked Stephen about that on at least one occasion in the past, but I've never gotten a clear response from him. I even wasted some time myself in an effort to find out about the presence of androgen receptors in the lymphatics and how reducing DHT _might_ be useful for increasing drainage, but I came up empty. It does look like another large hole (among others) in his "edema" theory of hairloss.

Bryan

Before i become involved any further in this, have you got a proper reference for your claim that there are "NO" androgen receptors in any part of lymphatic vessels Doctor?

Be specific instead of "i once read" OK!

S Foote.

I'm not going to be specific for receptors as I don't have time. The clue to what I say is the fact that metastatic prostate cancer is identified with immunohistochemical staining for the androgen receptor in both the lymph node and even in the lymphatics themselves as carcinomas typically move through lymphatics while sarcomas move through the blood stream. Only the cancer with androgen receptors will show up microscopically with no evident staining of androgen receptors in either lymph node or lymph vessels.

That's the best I can give you right now. Sorry, but I'll look for more later.

But that is just your un-referenced speculation, as is most of your arguments so far! :roll:

My theory clearly argues that androgens are increasing the already known contraction rate of lymphatic vessels.

These contractions are "powered" by muscle fibers in the lymph vessel walls.

This study has "specificaly" looked for androgen receptors in muscle related cell lines.

http://jcem.endojournals.org/cgi/conten ... 89/10/5245

Quote:

"Many myonuclei in muscle fibers also demonstrated AR immunostaining".

AND!

"AR expression was also observed in vascular endothelial and smooth muscle cells."

So there "ARE" androgen receptors in the muscle fibers and other cells known to power lymphatic vessel contractions 8)

This is called providing "genuine" evidence for an argument Doctor :wink:

In your reply to my last post, you once again made statements not supported by "specific" links or references, and again demonstrated that you don't understand the mechanics of my theory or normal contact inhibition.

You also suggested i contact "experts", quote:

"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."

I have already done just that, as you should have known if you had read this thread properly. :wink:

For your benefit i will again post the response to my theory of the well known hair loss expert Dr Marty Sawaya:

"It is a very complex process, but your thoughts are very organized and on the right path, similar to what others have been proposing, and in some ways yours are more straightforward. I think you've done a good job in thinking this through......
Hope this helps...
regards
Marty Sawaya"

The most notable thing here, is Dr Sawaya's confirmation that others are thinking along the same lines! Real scientists that is!

So what exactly is YOUR "expert" qualification?

S Foote.

 

[docj077]

[quote="S Foote.":505fd]

The other problem is his lack of explanation for how 5AR inhibitors work in the context of edema. Lymphatics do not have androgen receptors and neither to their valves.

AHA!!! Thanks for clearing that up! I've asked Stephen about that on at least one occasion in the past, but I've never gotten a clear response from him. I even wasted some time myself in an effort to find out about the presence of androgen receptors in the lymphatics and how reducing DHT _might_ be useful for increasing drainage, but I came up empty. It does look like another large hole (among others) in his "edema" theory of hairloss.

Bryan

Before i become involved any further in this, have you got a proper reference for your claim that there are "NO" androgen receptors in any part of lymphatic vessels Doctor?

Be specific instead of "i once read" OK!

S Foote.

I'm not going to be specific for receptors as I don't have time. The clue to what I say is the fact that metastatic prostate cancer is identified with immunohistochemical staining for the androgen receptor in both the lymph node and even in the lymphatics themselves as carcinomas typically move through lymphatics while sarcomas move through the blood stream. Only the cancer with androgen receptors will show up microscopically with no evident staining of androgen receptors in either lymph node or lymph vessels.

That's the best I can give you right now. Sorry, but I'll look for more later.

Gibberish.

Brought to everyone by,

S Foote.

[/quote:505fd]

This is your theory, so the burden of proof is on you. You were arguing for AR on lymphatic endothelial cells and valves. I don't see your proof of that. That study is for endothelial cells lining capillaries within muscle. Not lymphatic capillaries. You can say there is a direct relationship, but the relationship is circumstantial if your theory dictates that lymphatic congestion is the basis of hair loss. Prove that it's venous or lymphatic.

The second burden of proof for you is you must show that lympathic drainage is either slowed or increased (whatever your theory says) due to AR stimulation of either muscle fibers or lymphatics. If you can not do that, then your theory does not work. Simply demonstrating muscle changes, does not mean that lymphatics undergo the same physiology. If so, then post the article proving that AR receptor binding in muscle decreases lympthatic return. Besides, the article that you posted sort of discredits your whole argument. If AR receptors exist on muscle and binding of androgen causes hypertrophy of said muscle cells, then why would lymphatic congestion occur in the face in the first place. The lymphatics that drain the face and scalp are within the fatty tissue that overlays the muscles of the face. Skeletal muscle hypertrophy has no effect. If you don't believe me, get a Netter Anatomy atlas and see for your self.

Also, if you think it's venous, then you must demonstrate with histological evidence that venous stasis occurs in a male pattern baldness follicle.

The third item that you must prove is that contact inhibition even occurs in the hair follice. What is the mechanism? What are the inhibitors on the molecular level? What is the ligand that the hair shaft binds to so as to inhibit either proliferation or production from hair follicle cells?

The last item of proof is what I said about minoxidil earlier. Why does it work on the face and cause the growth of thick, course beards? Your theory needs poor lymphatic drainage to be the cause and minoxidil does quite the opposite in the face for some people. It even causes incredibly dry skin with dermatitis. Can you prove that DHT is even found in lymph?

Those are my questions. Answer all of them.

 

[S Foote.]

http://www.lymphoedema.org.au/lymphoed.html[/url]

Click on "what is lymphedema"

Quote:

"The excess protein also acts as a stimulus for chronic inflammation. One of the results of this is the formation of much excess fibrous tissue."

If you "really" had any medical knowledge, you would have known this!

Sorry, but your pretence of being a medical expert has been blown.

If anyone still takes this person seriously they do so at their own risk :wink:

I'am gone 8)

S Foote.