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What type of persons are more vulnerable to hairloss?

Discussion in 'Men's General Hair Loss Discussions' started by Armando Jose, May 11, 2007.

  1. docj077

    docj077 Senior Member

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    Wait Michael! That would mean that somehow the scalp somehow violates the theory of gravity. Never mind that local lymph nodes in the head are not enlarged. Nevermind that their is no external evidence for edema. Nevermind that fact that not every man has spongiosis at the histological level.

    Go to any given family physician someday. You'll probably see a handful of diatetics come in for med check-up. Not only will you learn what edema looks like, but you will learn about the extremes of edema. There is not edema in the scalp.
     
  2. docj077

    docj077 Senior Member

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    Collagen. TGF-beta increases Nf-kappaB production which in turn increases collagen locally. This combined with hyperkeratinization of the epidermis by IGF-1 decreases oxygen levels in the tissues. Collagen deposition around blood vessels and their eventual obliteration combined with decreased 02 movement across the epidermal layers more than accounts for any vascular and oxgyen deficiencies. Collagen is increased around and within vessels causing a lack of vessel flexibility and vessel obliteration. The same process can be seen with a disease such as scleroderma.

    I would argue that the opposite is true. It's TGF-beta's action that causes the hypoxia.

    Different disease with a different process. You need to do better than this.

    I would argue that there is indeed an internal difference within the follicles themselves. Androgen action encourages collagen deposition. Collagen is the contact inhibiting molecule around the follicle, but the growth restrictive molecule is TGF-beta and its downstream actions. However, the initial response is androgen dependent. Markedly reduced hair cycling only occurs after collagen deposition is increased which is well into the balding process.

    They are directly growth restricted in terms of external factors. Again, all you need is the dermal papillae cells from balding scalp (which means that they will have the defective androgen receptor) and androgens will inhibit hair growth in a dose dependent manner. The insertion of an overexpressed androgen receptor vector more than makes up for the defective androgen receptor that is lost during culturing. The response ends up being the same.

    Actually, stem cells in the hair follicle do indeed have a predisposition. They are not pluripotent. There are numerous types of stem cells and each one has a different fate. You should already be aware of this fact.

    And, Bryan is correct. Puberty is the time of increased androgen exposure and it is also the time of the most androgen action. However, you also need to understand that hair cycling and inhibition involves more than just TGF-beta. It involves acute phase reactants and whole plethora of other factors. In fact, these factors are produced in such inhibitory concentrations that follicular cycling can be altered almost immediately. TNF-alpha is an excellent example of such a molecule and is likely produced to decrease the action of TGF-beta by modulating the TGF-beta receptor response.

    Also, they've already proven there is indeed a genetic difference in terms of eventual protein production in the scalp. IGF-1, TGF-beta, TNF-alpha, Nf-kappaB, TAK1, and whole host of other inhibitory molecules have their production increased in balding scalp resulting in keratinocyte apoptosis, epithelial hyperkeratinization, increased collagen deposition, a pro-inflammatory condition, and the eventual inhibition of b-catenin and Wnt protein action which in turn prevents correct follicular cycling. That is at the gene level.
     
  3. Bryan

    Bryan Senior Member
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    Doctor, Stephen is making a different point here and asking a completely different question. He is pointing out that in Uno's stumptailed macaque study which was referenced earlier in this thread, they found that the dermal papillae of juvenile monkeys (pre-pubertal) didn't show any sensitivity to androgens (in the sense of inhibiting the growth of co-cultured keratinocytes), whereas the dermal papillae of post-pubertal monkeys _did_ show such a growth suppression in response to androgens.

    So Stephen is asking the question: what specifically is it that eventually causes the CHANGE in those dermal papillae, as we go from young to old? What causes hair follicles to go from being neutral to being sensitive to androgens? He's been attacking the standard theory of male pattern baldness relentlessly for a long time over that one specific issue.

    Uno himself doesn't have much to say about that, except for hinting vaguely that maybe a "continued exposure" to androgens is what eventually alters the response. Whiting in his article "Current Understanding of male pattern baldness" refers to the possibility of some kind of "genetic clock" within hair follicles which alters their response to androgens after puberty, but that's about it. Stephen takes great succor from the fact that this is one of the great unanswered questions within the current theory of male pattern baldness! :)
     
  4. michael barry

    michael barry Senior Member

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    Bryan,

    .......................but isn't there some cases of early alopecia in children whose hormonal levels are out of whack?


    I mean since we can only cultivate hair cells for a few weeks at a time, it would take several months or a year or two of higher androgen levels to actually see the papillas (where the action is occuring) to start putting out too much tgf-beta, pkc, thrombospondin, fgf-5, and dppk correct?


    We will probably NEVER be able to culture non-balding hairs at the precise moment they were about to begin to become sensitized to androgens, so why bother?




    I just have to say this: The pictures I HAVE PROVIDED of women who quickly went male pattern baldness or are balding after getting testosterone injects prove 2 things to me................................nothing during puberty causes some "change" in hair. They were destined to overproduce TGF beta and the other antigens in the first place with androgenic stimuli at normal levels. Stopping the androgens will stop the loss, and utter blockage of androgens via the receptor might show dramatic regrowth over time (like the old guy who got regrwoth with internal spironolactone over an eight year period). The immune system, like Doctor says, is probably attacking the TGF-beta presence and the collagen deposition around the follicle, but we can stop it by stopping androgen uptake at the follicle site, period. I dont think the follicles themselves have their DNA "changed" by androgen-binding.


    I'd like to remind everyone that longere ring finger lengths, are associated with androgen-related disorders like baldness, prostatitis, acne. Look at your ring fingers guys, are they longer than your index fingers? I thought so.
     
  5. Guest

    Guest Guest

    MB, can you please elaborate on this? i have heard that having a longer ring finger than index finger means that we were exposed to more testosterone in the womb. my ring fingers are maybe a quarter of an inch to a third of an inch longer than my index fingers. i have also heard that men with higher levels of testosterone(long ring fingers) are more likely to cheat:

    http://www.apa.org/monitor/dec06/testosterone.html

    but here's an article on the higher testosterone in womb thing:

    http://news.bbc.co.uk/2/hi/health/4314209.stm
     
  6. Bryan

    Bryan Senior Member
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    Yep.

    Assuming that that's the correct explanation for the change in the first place, yes. Of course, that doesn't phase Stephen Foote at all. He keeps asking, why didn't Uno see that happen just over the short length of his study? :)

    Probably not, but we still need to know what the precise mechanism is for that change in response to androgens.
     
  7. porajj

    porajj Established Member

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    My ring finger is the exact same size or shorter than my index finger on both hands. That apparently is a sign that I was exposed to a ton of estrogen in the womb.

    Benefits of that?

    Some high percentage of men (something like 80%) who make up the fields of philosophy and mathematics have this feature. Apparently the excess estrogen increases abstrat reasoning ability.

    But wait, im balding? This shouldnt be happening should it?


    Most males should have a ring finger longer than an index finger. Its a male characteristic. It doesnt have a damn thing to do with balding.
     
  8. michael barry

    michael barry Senior Member

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    Long ring fingers are indicative of higher T levels in fetal development. Women who have this often display more aggression and athletic achievement. Men who display it often display more aggression, etc.


    I'd list some studies, but you can just google-search it if youre interested.


    Ponjj, or whatever your name is, a CORRELATION has been observed. However, not every single guy with male pattern baldness is going to have this. There will be some men with ring fingers damn near as long as their middle fingers who will have full heads of hair. A mathematical trend has been observed however, so its indicative of their being an increased RISK of androgen related disorders if you have this trait. This is associated with similar genetics making the trait and the manifestations being the same.


    Over 98 percent of balding men in a German study had a particular variant of the androgen receptor gene, but only 76.1 percent of non-balding men had this gene. Researchers believed that this gene is a contributing factor to baldness (much like Doctor has expounded upon). Science is inching its way forward on drawing up the genetic profile one has to have to experience baldness, but its very complicated obviously, but it is being worked on. I always thought our secret weapon in the baldness fight would be that so many scientists seem to go bald, that one would get really interested in eradicating it, even if it was in his spare time.
     
  9. docj077

    docj077 Senior Member

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    There is obviously more than one gene involved in male pattern baldness. The insulin receptor gene, the two five alpha reductase genes, etc.


    As for the finger length thing, there was a recent study done that clearly demonstrated that people (especially men) with longer ring fingers are better at mathematics as they typically have higher math scores on the SATs. I think that a shorter ring finger was more indicative of a higher verbal, reading, and writing scores.

    http://news.yahoo.com/s/livescience/200 ... erformance
     
  10. docj077

    docj077 Senior Member

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    Bryan, I believe that you already know how this system works. All you have to do is look at bodybuilders. Resistance training increases testosterone and has been found to increase androgen receptor production in target tissues (I have a study that demonstrates this, by the way). The more androgens you put into the system, the higher the production of androgen receptors will become. You reach a physiological and signal threshold and once that occurs, the follicles are sensitized. This works faster in men with early-onset male pattern baldness, because the receptor allows you to reach that threshold faster.

    If I'm not mistaken, wasn't there recently found a link between balding men and higher androgen levels? If this is true, then SHBG levels would be decreased leading to more free androgen and more androgen-mediated action.

    We shouldn't even have to go into the insulin resistance problem and increased androgen and 5AR activity. Dammitletmin was kind enough to find that info for us.

    Michael Barry's point about length of cultivation and androgen action is likely the correct answer. male pattern baldness is a process that takes years for it to realize its full disease potential. You have to upregulate a lot of genes and deposit a lot of collagen.
     
  11. Armando Jose

    Armando Jose Senior Member My Regimen

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    Well, friends, this is a very interesting post but, let us sum up, the current androgenetic theory don’t explain the dynamic model of common hair loss and growth of alopecia area, and it is necessary introduce a type of gradient on the supposed “sensibleâ€￾ hairs. My theory explains it easily because hairs in the crown are less in contact themselves because orientation and angle continuously are changing. The same with hairs in front of head where they are located in the frontier zone of forehead without hairs.

    On the other hand, my theory explain the miniaturisation of hairs in common baldness because the sebum flow is interrupted or altered in its travel and interfere with the transport of stem cells from bulge to dermal papilla and don’t arrive all of them. What is the explanation with the current theory? I don’t know really because the impact of androgens with DNA would affect as a switch and don’t as a class of potentiometer modulating the robustness of scalp hair. The biological signals of androgens with the current theory is or grow or don’t grow the hair. Any ideas?

    Docj007 wrote: “The alternative is that the transportation machinery of the cell is somehow disrupted.â€￾ and
    Foote wrote: “The authors of that study said the transplantation effects could be because of an effect very close to the follicle.â€￾

    Anyone more?

    Docj007 pointed out: “androgens will inhibit hair growth in a dose dependent manner. The insertion of an overexpressed androgen receptor vector more than makes up for the defective androgen receptor that is lost during culturing.â€￾
    Is the dose dependent manner of androgens the explanation of hair miniaturisation?
    I don’t know.


    By the way,
    Docj007 wrote: “Can you prove that the follicle itself is hypoxic and not just the surrounding tissue? Personally, I think that if there is hypoxia, it is due to collagen deposition and it is a process that is accompanied by prolonged male pattern baldness conditions within the scalp.â€￾
    I think that stem cells can be transformed in any type of specialised cells, then if they don’t arrive to its target, they are surrounding with collagen cells and it is possible that this will be its destiny = collagen deposition by prolonged male pattern baldness conditions.

    Docj007 wrote: “Actually, stem cells in the hair follicle do indeed have a predisposition. They are not pluripotent.â€￾
    Is it the reality? I don’t know, it is necessary corroborate this issue.

    Docj007 wrote: “Also, they've already proven there is indeed a genetic difference in terms of eventual protein production in the scalp. IGF-1, TGF-beta, TNF-alpha, Nf-kappaB, TAK1, and whole host of other inhibitory molecules have their production increased in balding scalp resulting in keratinocyte apoptosis, epithelial hyperkeratinization, increased collagen deposition, a pro-inflammatory condition, and the eventual inhibition of b-catenin and Wnt protein action which in turn prevents correct follicular cycling. That is at the gene level.â€￾
    And Bryan wrote: “So Stephen is asking the question: what specifically is it that eventually causes the CHANGE in those dermal papillae, as we go from young to old? What causes hair follicles to go from being neutral to being sensitive to androgens? He's been attacking the standard theory of male pattern baldness relentlessly for a long time over that one specific issue.
    Uno himself doesn't have much to say about that, except for hinting vaguely that maybe a "continued exposure" to androgens is what eventually alters the response. Whiting in his article "Current Understanding of male pattern baldness" refers to the possibility of some kind of "genetic clock" within hair follicles which alters their response to androgens after puberty, but that's about it.â€￾

    What would William of Ockam have said was the most likely explanation for that?
    My theory explains that the first and triggering event is problems in sebum flow, and it is the slowest and lasting process of all them, and reversible. A simple explanation for the “time vectorâ€￾ in common baldness,


    Armando
     
  12. docj077

    docj077 Senior Member

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    So, you think that the stem cells either become collagen itself or they become collagen producing cells, right? The first is impossible. Stem cells do not become collagen. The second doesn't matter. The collagen producing cells or dermal fibroblasts have androgen receptors, so they are under the influence of androgens. The abundance of collagen deposition is not necessarily due to increased collagen production (which does happen, by the way), but more due a decrease in collagenase production.

    Yes, those stem cells are multipotent. They are not pluripotent or totipotent. They are already programmed enough so they are only capable of becoming particular tissue subtypes. As far as I know, there are no pluripotent stem cells in the adult body except for the following:

    Hematopoietic stem cells may differentiate into: three major types of brain cells (neurons, oligodendrocytes, and astrocytes); skeletal muscle cells; cardiac muscle cells; and liver cells.

    Bone marrow stromal cells may differentiate into: cardiac muscle cells and skeletal muscle cells.

    Brain stem cells may differentiate into: blood cells and skeletal muscle cells.

    Here is a breakdown for you to study:

    Totipotent cells. In mammals, totipotent cells have the potential to become
    any type in the adult body;
    any cell of the extraembryonic membranes (e.g., placenta).
    The only totipotent cells are the fertilized egg and the first 4 or so cells produced by its cleavage (as shown by the ability of mammals to produce identical twins, triplets, etc.).

    In mammals, the expression totipotent stem cells is a misnomer — totipotent cells cannot make more of themselves.

    Pluripotent stem cells. These are true stem cells, with the potential to make any differentiated cell in the body (but probably not all those of the extraembryonic membranes, which are derived from the trophoblast).
    Three types of pluripotent stem cells have been found

    Embryonic Stem (ES) Cells. These can be isolated from the inner cell mass (ICM) of the blastocyst — the stage of embryonic development when implantation occurs. For humans, excess embryos produced during in vitro fertilization (IVF) procedures are used. Harvesting ES cells from human blastocysts is controversial because it destroys the embryo, which could have been implanted to produce another baby (but often was simply going to be discarded).
    Embryonic Germ (EG) Cells. These can be isolated from the precursor to the gonads in aborted fetuses.
    Embryonic Carcinoma (EC) Cells. These can be isolated from teratocarcinomas, a tumor that occasionally occurs in a gonad of a fetus. Unlike the other two, they are usually aneuploid.
    All three of these types of pluripotent stem cells

    can only be isolated from embryonic or fetal tissue;
    can be grown in culture, but only with special methods to prevent them from differentiating.


    Multipotent stem cells. These are true stem cells but can only differentiate into a limited number of types. For example, the bone marrow contains multipotent stem cells that give rise to all the cells of the blood but not to other types of cells. [Discussion]
    Multipotent stem cells are found in adult animals; perhaps most organs in the body (e.g., brain, liver) contain them where they can replace dead or damaged cells. These adult stem cells may also be the cells that — when one accumulates sufficient mutations — produce a clone of cancer cells.


    Ockham would have been confused, because the current direct theory is actually the simplest theory. It takes what we currently know about hair loss science and directly applies it. There are no hypotheticals or unknown external factors mediating the process.


    I enjoy your resolve Armando, but I really don't think you're right.
     
  13. michael barry

    michael barry Senior Member

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    I dont enjoy your resolve Armando.

    WRONG baldness theories simply hurt young men trying to treat it.


    Finasteride has a 277 hair increase per square inch over place at year FIVE Armando. Finasteride DOES NOTHING to sebum secretion. This was tested with over 1500 men in a large Merk Trial.

    Hair transplants, and plugs that have been up front on men's heads for DECADES but dont fall out disprove that sebum is effecting them in anyway. Dr. Gary Hitzig's old transplant was done IN 1974,
    http://www.nyhairloss.com/aboutdr.htm
    and was 'pluggy". He has since had the hairs RE-DISTRIBUTED in a more natural way. They have yet to fall out 34 YEARS LATER. Look at the pictures. He wears his hair SHORT. His frontal hair is ALL THERE.


    MK386, an alpha five type one inhibitor dramatically reduces sebum secretions...............................but has hardly any effect on hair AT ALL, while finasteride has a great effect on hair.




    Those three points alone disprove your idea. Sebum isn't causing baldness in ANY WAY.

    All hairs dont need sebum either. Nose hairs dont need it, finger hairs dont need it, toe hairs dont need it. Eyebrow hairs dont need it (or androgens either). Androgens aren't necessary for scalp hair growth AT ALL as people with androgen-insensitivity syndrome prove.



    Youre idea is not only wrong, but easily disprovable, and a big waste of newbies time. Its also, quite frankly, childish. The hallmark of most (except Stephen's) baldness theories that we see are their "silly simplicity". The "oh its just tension in one area of the scalp" or its " just lack of blood flow in the temples" or its "just big pillows, robbing the hair of nutrition" or its "just too much body hair stealing all the nutrients away from head hair" or "its just the galea thickening, starving the hairs for oxygen". All of them are bullshit.

    These two fluridil photos ALONE (with short hair) disprove you idea:


    Joined: 28 Aug 2006
    Posts: 168

    Posted: Fri Jun 01, 2007 8:37 pm Post subject:

    --------------------------------------------------------------------------------

    yeah you could argue about above pictures but you can't argue about other two
     
  14. Armando Jose

    Armando Jose Senior Member My Regimen

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    Thank you Doctor for your assert, but I did read a study where stem cells of bulge area were transformed in neurons. These cells (Which colud be its denomination?) can be transformed in keratinocytes, dermal papilla cells, and sebaceous gland cells, is it so?

    You write: “Ockham would have been confused, because the current direct theory is actually the simplest theory. It takes what we currently know about hair loss science and directly applies it. There are no hypotheticals or unknown external factors mediating the process.â€￾
    I’ll write Ockham forever, thanks.
    My first problem with the current theory is that I have not a real evidence of the genetic different in HEALTHY scalp hairs. Have you anyone?. This acceptance is, in my opinion, only an hypothesis.


    To Michael Barry:
    I would like to see a photo of Dr. Hitzig before transplant. His actual hair is not so short and it is combed backwards, a manner to increase contact among hairs to avoid problems with sebum. There is not problem with my theory.

    You write: “All hairs dont need sebum eitherâ€￾.
    Then why all hairs have a sebaceous gland attached? Another waste of time and energy from the squanderer Mother Nature?

    Well, if you are a champion of the current theory and the FDA approved meds, why are more cases nowadays in common baldness? Why labs continue searching in male pattern baldness? You seem to say that is all OK.

    By the way, where are photos of fluridil?


    Armando
     
  15. michael barry

    michael barry Senior Member

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    Before I delve into you Armando, why in the phuck cant you ever answer what it is about finasteride that allows it to grow 277 more hairs per square inch at year five than placebo, depsite no effect on sebum? Why didnt Merks MK386, drastically reducing sebum, not have any effect on hair?


    Armando wrote:

    "To Michael Barry:
    I would like to see a photo of Dr. Hitzig before transplant. His actual hair is not so short and it is combed backwards, a manner to increase contact among hairs to avoid problems with sebum. There is not problem with my theory.

    ARMANDO, ARE YOU TRYING TO TELL ME THAT BY COMBING HIS SHORT HAIR BACK, HITZIG HAS NOT WENT BALD AND THE TRANSPLANTS HE HAD 34 YEARS AGO WOULD HAVE FELL OUT IF HE'D WORN THEM COMBED FORWARD ?!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! look again at Hitzig Armando, http://www.nyhairloss.com/aboutdr.htm

    http://www.hairtransplantinfo.org/custo ... HitwBk.jpg

    http://images.google.com/imgres?imgurl= ... 16,GGLR:en



    You write: “All hairs dont need sebum eitherâ€￾.
    Then why all hairs have a sebaceous gland attached? Another waste of time and energy from the squanderer Mother Nature?

    NOSE HAIRS DO NOT HAVE SEBUM GLANDS ATTATCHED. DO TOE HAIRS EXCRETE SEBUM? WHAT ABOUT FINGER HAIRS? EYELASHES? EYEBROWS? Is sebum why eyebrows thin with age Armando? To quote Ernie Primeau, 'crazier and crazier'.






    Well, if you are a champion of the current theory and the FDA approved meds, why are more cases nowadays in common baldness? Why labs continue searching in male pattern baldness? You seem to say that is all OK.


    COMMON BALDNESS IS SPEEDING UP THESE DAYS FOR MANY OF THE SAME REASONS IT HAS SPED UP IN JAPAN. INSULIN-RESISTANCE CAUSES MORE ACTIVITY OF THE ALPHA FIVE REDUCTASE ENZYMES LOCATED IN HAIR FOLLICLES, IT ALSO CAUSES A RISE IN THE AMOUNT OF TESTOSTERONE MADE IN THE ADRENAL GLAND AND LESS GLOBULIN (SEX HORMONE BINDING GLOBULIN) TO BE RELEASED INTO THE BLOOD STREAM, THEREFORE MEN HAVE MORE FREE TESTOSTERONE IN THEIR BLOOD THAN WHAT THEY DID BEFORE WW2 AND THE CHANGE IN DIETS THERE, THEREFORE MORE ANDROGENS ARE IN THE SKIN AND MORE ARE BINDING TO RECEPTOR SITES, THUS INITIATING THE BALDESS PROCESS SOONER THAT WHAT IT USED TO BE INITIATED. Everybody on these forums knows this, as they have been discussed ad nauseaum here. Men in Japan before WW2 didnt wear their hair LONG, nor did men in America before 1900 or so when baldness was a little less common than it is now. We are almost getting into the "shampoo causes baldness' territory.

    Why, Armando, do men who have no alpha five reductase type two enzyme genetically never go bald.

    By the way, where are photos of fluridil?



    HERE ARE THREE PICTURES OF FLURIDIL, A TOPICAL ANDROGEN RECPTOR BLOCKER, REGROWING HAIR ON MEN,
    http://www.menspharma.com/results.htm








    I consider you to be either a real nutter (like the shampoo people who insist that shampoo causes baldness) or someone attempting to sell a baldness product by telling men what they want to hear (that their own genetics are not at fault) and that they can get some hair back with that product you sell on your website, or even perhaps a paid shill from the transplant or wig business, here to attempt to get men to delay using the sccessful treatments we have (finasteride, dutasteride, minoxidil, ketoconazole, pirictone olamine) long enough for them to really experience some loss, so that they will be more likely to get a wig or get a transplant. You cant be a rational human being and honestly believe the bullshiit that you spout about sebum backing up initiating the baldness process. There is no way. Ive been able to disprove that in several different ways, yet you go on and on. I took a look at your website the other day, hardly anyone posts in your discussion forum at all, thats because nobody believes your idea. I can think of one doctor who has ever mentioned anything similar about baldness. Its plain wrong, and if it delays a few men from perusing things that really work, it hurts their chances of hanging onto their hair until a real cure (cloning, genetic manipulation) actually comes out. What a waste.
     
  16. docj077

    docj077 Senior Member

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    A study is one thing, Armando. The human body is quite another. It is possible to take stem cells and make them regress into early stem cell types (ie change a multipotent stem cell into a pluripotent stem cell), but that requires special chemicals and conditions not supplied by the human body. The stem cells are multipotent and capable of transforming into the various cell types that make up the follicular unit.

    For this very reason, the only cells that actually need to be transplanted are the dermal papillae cells. They will reorganize and produce functional follicular units.



    Armando, I hate to do this to you, but you need to read the following article. Hopefully, you'll be able to find the appropriate research article to go with it.

    http://www.sciencedaily.com/releases/20 ... 080932.htm

    You'll be able to see that the stem cells involved in sebaceous gland creation are different from follicular stem cells. The stem cells for the sebaceous gland exist outside the follicle and are not part of the stem cell population that renews the follicle. What is more important is to notice the following:

    "Valerie Horsley, a postdoc in the Fuchs lab and first author of the paper, had been interested in Blimp1's role in hair follicle development, and had engineered mice that were missing the Blimp1 gene in their skin. "When the mice were born, they formed normal hair follicles, which was quite disappointing," says Horsley. "But when they were around one month of age I noticed that the mice started getting very oily skin."

    The sebaceous glands in mice missing Blimp1 were much larger than in normal skin."



    When sebaceous gland ducts become plugged, there is back pressure that leads to sebaceous infiltrates into the dermis. As far as I know, this is not a common occurance in male pattern baldness, but perhaps you have a study that demonstrates this phenomenon in male pattern baldness. The plugging and infiltration should lead to a massive immune response. Especially, if bacteria in the area breaking down the the sebum into pro-inflammatory fatty acids.

    Also, be aware of the following. There are two different types of hair growth. When there is terminal hair growth, the medullated hair becomes the prominant structure. When there is vellus hair growth or sebaceous follicle growth, the sebaceous gland is the prominant structure. So, if sebum is required, then why is less of it present in terminal hair when compared to a sebaceous follicle with vellous hair growth? You also need to remember that the follicle and the sebaceous unit DO NOT develop together. The follicle develops first and then signals the sebaceous unit to develop. Also, the sebaceous unit-follicle communication is required for proper formation of the pilosebaceous unit. However, once the unit is formed, sebum is not required for growth. It's the signaling between the two that is required.

    I think that you need to read up on follicular cycling and development. The following article will assist you:

    http://edrv.endojournals.org/cgi/content/full/21/4/363


    As for the genetics, yes there is a genetic difference between non-balding and balding hair follicles. Balding hair follicles with have cells with abnormal follicular cycling due to inhibition of the Wnt and B-catenin genes. Normal follicles do not have this inhibition. The inhibition is brought about by TGF-beta and the increased action of the sebaceous glands and follicular metaplasia is likely due to Smad-7s inhibition of TGF-beta action.

    As for a genetic difference between scalp and body hair follicles, I don't have an answer. I can tell you that there is an intrinsic difference in growth rate and growth duration in scalp hair vs. body hair. I can also tell you that there is a difference in androgen dosage requirements between beard hair and other hair. So, obviously, there are intrinsic genetic differences, because the hair requires different doses of extrinsic signals. The answer either lies in the production of androgen receptors or the external production of androgens. The local tissue response to androgens appears to be tissue specific and location specific meaning that there has to be a regulatory genetic difference.
     
  17. S Foote.

    S Foote. Experienced Member

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    Yes Michael, my theory states that DHT is increasing lymphatic vessel pumping all over the body. The main areas of increased growth, armpits, groin, and particularly the beard areas have a greater number of superficial lymphatic vessels, hence the greater effect on hair growth.

    The base of the human hair bearing scalp is the point at which the surface lymph vessels start to go deep.

    http://137.222.110.150/calnet/DeepNeck/ ... m#section6

    The other factor i have clearly pointed out before, is the natural tissue resilience in the area. If the tissue is not as rigid, it offers less "natural" resistence to follicle enlargement and you will get larger follicles.

    The eyebrows are one example of this, the tissue is known to be weak beneath the eyebrows just ask boxers? You can feel this for yourself.

    S Foote.
     
  18. S Foote.

    S Foote. Experienced Member

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    Ok i am not an unreasonable person, if you want to continue to call yourself "Doctor" for sentimental reasons, go ahead.

    But put a disclaimer in your posts like many other people do, so that vunerable newbies are not given the wrong idea you seem to want them to have :roll:

    I personaly think you are a dangerous misleading individual on these forums. You read your medical textbooks, then shout about them like you are preaching from a pulpit!

    You read all this information, but you haven't got a clue on how to put together a scientific argument from it!

    Even Bryan has pointed out to you my argument on pre-didposition about three times, but still you just don't understand it!

    When i first told you in this thread about the problems with the in-vitro tests and androgen seeding, you said yourself that such testing would be completely misleading. But now you try to use these "SAME" in-vitro tests as proof of your androgen inducable TGF beta-1 "cause" of male pattern baldness! :roll:

    You clearly claim in this thread that androgens are creating male pattern baldness by increasing TGF beta-1 from DP cells in a dose dependent manner.

    Your whole argument about androgen inducable TGF beta-1 from DP cells "causing" male pattern baldness, is completely refuted by The immuno deficient mice study.

    http://www.hairlosshelp.com/forums/mess ... &forumid=1

    In this study, there was no maintained effect of androgen inducable TGF beta-1 in a dose dependant, or any other manner! The results were the same in both male and female mice.

    Your whole argument falls down with that one study :wink:

    Of course you wiil come up with your usual tirade of disjointed medical textbook phrases, but the reality is right there for all to see.

    Bryan also tried a quick U turn regarding this study when he realised it supported my arguments! But if people take the time to read his original posts in that link, yet again they will see how the rules of evidence get "changed" when it doesn't suit! Just like the donor dominance argument! :roll: :roll:

    I got involved in this thread because people were having a go at Armando. I also do not agree with Armando for reasons i have explained before.

    But there has been a lot of "pot calling kettle black" here. If you are going to demand other people conform to the rules of scientific evidence, you have to stick to these yourself!

    Both you and Bryan regularly show everyone that you both don't mind breaking these rules when it suits your personal arguments. So there is really no point going on with yet another boring repetitive thread, where people just ignore true science :roll:


    S Foote.
     
  19. docj077

    docj077 Senior Member

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    I appreciate your willingness to allow me to keep my name. As I said, I may not be a "Doctor", but Doctor is still my nickname and it really was given to me by my grandfather before he passed away due to complications from glioblastoma multiforme.

    I typically strive to only post relevant articles and interpretations. I find that I have a little more insight into the world of research than most people as I've worked in a lab and done the experiments that everyone seems to argue about. It's rather frustrating to see someone like you post that androgen receptors were added during cellular culturing when my biochemistry and research training tells me that it's simply an impossibility. That's why I was very grateful that michael barry posted the article that demonstrated how they used a vector with the androgen receptor gene. They not only used it, but they upregulated it. So, any andrognen response in that study was quite likely equal to the response in balding scalp.

    So, when you post your interpretations and I come along and tear you down, I'm not doing it, because those are my interpretations. I'm doing it, because I know what needs to be done for it to be done right. I worked with vectors, vector cloning, and PCR for a long time. I hope that you can understand that.

    You're right, Mr. Foote, I did say that. That's why I came up with a logical explanation of why exogenous androgen receptor can not be added to cellular culture. Michael simply proved my point when he posted the study, I read the methods section, and it clearly pointed out that they used a vector system. That's how I would have done it, but I either misinterpreted what you said or you simply didn't explain it correctly.

    Now, seeing you post what you just posted above really hurts my eyes. I know that you're better than this and I know that you understand how to read studies. Nowhere in that study do they mention TGF-beta, so one can not assume anything regarding that molecule as they did not measure it. There are rules that need to followed here, Mr. Foote. You're breaking them with your interpretations.

    The way I understand this article is probably quite different from you. They are taking balding and non-balding hair follicles and putting them into immunodeficient mice. In both cases, the hair follicles demonstrate very similar growth characteristics at 22 weeks. Now, by taking balding follicles out of their balding environment and putting them into a immunodeficient and "normal" environment, you do two things. You remove one of the very characteristics of molecules like Il-1, TNF-alpha, and TGF-beta in that you remove their pro-inflammatory and chemotactic capabilities, because the mice are immune deficient. Not only is this true, but you remove the balding follicles from their normal inhibitory environment. Remember, the action of TGF-beta is inhibitory and it also causes increased collagen deposition to the point of growth and contact inhibition. This inhibition is no longer surrounding the follicle, so obviously, it is going to resume normal growth characteristics. You know and I know that no study demonstrates follicular inhibition at 22 weeks. Do this same study for a year and then you can come and talk to me about interpretations. male pattern baldness is a prolonged, aggressive, and gradually worsening disease. As far as I'm concerned, this study is inappropriate. Not because of their interpretations, but because there is no possible way that such a study would demonstrate anything other than growth. It should demonstrate such findings, because that is exactly what it is set up to do. The mechanism takes time to set up. I know, Bryan knows, and you should know it, as well.


    I'm glad and you and I agree when it comes to Armando. You have to agree that science and evidence are funny things on these forums. For the most part, they seem to be up to personal interpretation when I don't even know if any of us are truly qualified. I've worked in a lab and I'm two years away from my M.D. I have no idea what sort of training that you, Bryan, Michael, or Armando have, so I rarely play the education card. I simply post what I think is right, because that is my interpretation based upon a two years studying medical biochemistry, medical physiology, and medical pathology. I have a 3.6 GPA in medical school, so obviously I've learned something along the way and I frequently score in the top 85% of medical students in this country on board examinations. So, when you think that my opinion is worthless, don't be surprised when I think you're wrong. I've earned my opinion and my current top 15 ranking in my medical school class.

    There are no rules to conform to here, but when somebody posts a study that refutes your argument, you should be just as willing to go out and find the right scientific evidence to back your claims. You do that, but I think that sometimes you use your own interpretation of the study instead of the actual authors to come to a conclusion that backs your opinion.

    You claim contact inhibition is the cause. I claim androgen induced production of TGF-beta is the cause. I have studies that clearly show that TGF-beta is upregulated as a result of androgen action. I also have studies that show that TGF-beta is associated with increased collagen deposition as a result of increased procollagen expression and decreased collagenase production. Plus, I have studies that demonstrate that TGF-beta upregulates the necessary inhibitor molecules to cause the arrest of proper follicular cycling. Lastly, I have studies that demonstate that collagen is a molecule that promotes contact inhibition.

    As far as hair cycling and differences in follicular capabilities go, I have proof of that, as well. The study that I posted early for Armando demonstrates that different hair from different areas of the body including the scalp and the beard require differing concentrations of androgens to achieve the type of hair growth that is readily observed. The only answer for that is an initial different in the intrinsic growth response.

    Not only that, but in the total absence of androgen action (like in AIS), scalp hair grows at a different rate from all other hair of the human body including axillary and pubic hair which will still grow in the absence of androgens, but WILL ONLY GROW once puberty begins.


    Mr. Foote, you bring a lot of good thoughts to this forum and I appreciate your willingness to step out and say that there is vascular insufficiency and contact inhibition. Unfortunately, the action of TGF-beta and subsequent increase in collagen deposition around the follicle and in vessels resulting in contact inhibition and a lack of vessel flexibility combined with increased vessel obliteration more than makes up for what you currently believe in.

    So, believe what you want, but I can explain the whole process from the time the androgen binds to the mutated receptor all the way up to the formation of a vellus hair follicle with an increased sebaceous unit/follicle ratio with ease using what I know about biochemistry and the studies that I've read.

    Believe what you want, but that doesn't mean that I'm going to believe it along with you. Sorry, but the journey and the interpretations that I believe in are very different from yours.


    Also, I apologize that I responded to you in such a way with multiple responses like this. I get annoyed when people do it to me, but I really have no choice as I had a lot to say. Only reply to what you want to reply to.
     
  20. michael barry

    michael barry Senior Member

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    Doctor wrote this paragraph:


    "The way I understand this article is probably quite different from you. They are taking balding and non-balding hair follicles and putting them into immunodeficient mice. In both cases, the hair follicles demonstrate very similar growth characteristics at 22 weeks. Now, by taking balding follicles out of their balding environment and putting them into a immunodeficient and "normal" environment, you do two things. You remove one of the very characteristics of molecules like Il-1, TNF-alpha, and TGF-beta in that you remove their pro-inflammatory and chemotactic capabilities, because the mice are immune deficient. Not only is this true, but you remove the balding follicles from their normal inhibitory environment. Remember, the action of TGF-beta is inhibitory and it also causes increased collagen deposition to the point of growth and contact inhibition. This inhibition is no longer surrounding the follicle, so obviously, it is going to resume normal growth characteristics. You know and I know that no study demonstrates follicular inhibition at 22 weeks. Do this same study for a year and then you can come and talk to me about interpretations. male pattern baldness is a prolonged, aggressive, and gradually worsening disease. As far as I'm concerned, this study is inappropriate. Not because of their interpretations, but because there is no possible way that such a study would demonstrate anything other than growth. It should demonstrate such findings, because that is exactly what it is set up to do. The mechanism takes time to set up. I know, Bryan knows, and you should know it, as well. "


    That above is a very legitamate, honest interpretation of that study from Doctor in my opinion. Anyone is free to disagree with it, but privately Ive wondered things along similar lines. 22 weeks isn't very long. Follicles, now in the back of a mouse and not a bald scalp that has been subject to an immuno response for years that is a hardened rubberized callous of skin, probably much lower androgen levels, no cytokines or superoxides to fight, the increased WNT wound healing around the transplant site.......................only 22 weeks. Perfectly reasonable for them to grow much better. A year and some androgen shots for the mouse might be an eye opener, just like Doctor says.


    Stephen's theory must be frustrating to Stephen because it would be so difficult to really test-------------------------however, I thought the RU58841 study where miniaturizing hairs were moved to mouse backs, and 28 percent of the RU groups hairs re-enlarged for a second phase, while only 2 hairs in the placebo groups re-enlarged, was about as close to a test for it as we could see. Tissue scaffolds of scar tissue should have been formed at the transplant sites, so why didn't the hairs grow for a second phase? It would seem that androgens shut them down to me anyway.


    Im attempting to see if cold will make hair grow better however, and have only missed a few days in the past three weeks or so of putting an ice pack on above my right knee. If I have a little extra hair on that leg within four months or so...............I'll let everybody know something. I read the net about every day for at least half an hour, so its not much trouble.


    THere used to be some evidence about green tea and TGF beta, but I cant find it when googling it. That would seem to be a super topical for male pattern baldness------------stops the TGF beta and is, at least on flank organs, very anti-androgenic topically.
     

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