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Pillows, Pillows, Pillows..??..

Discussion in 'Men's General Hair Loss Discussions' started by Guest, Jul 12, 2007.

  1. michael barry

    michael barry Senior Member

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    Wook,

    Im going to go out on a limb and say she has very active androgen receptors. If you look through all my past posts, you can probably find whatever study it was I found that detailed a uptick in androgen receptors and 3 to 3.5 times the amount of DHT in balding scalp.

    Meanwhile, this is something Doctor posted a few days ago that compliments that above......................(and by the way, hair transplants survive in bald scalp, but keep in mind when they have a rest phase, the dermal papilla migrates up to the top of the dermis like any other resting hair follicle for awhile, but it can move back down when it needs too, as its not blocked by collagen streamers------I seen a post of yours that suggests that transplants work because of their depth, but male pattern baldness hairs transplanted (Nordstrom) kept on balding......why?)


    Here is what Doctor found:

    J Endocrinol. 1998 Oct;159(1):R5-8. Links
    The measurement of testosterone in hair.Wheeler MJ, Zhong YB, Kicman AT, Coutts SB.
    Department of Chemical Pathology, Guy's and St Thomas' NHS Trust, St Thomas' Hospital, London, SE1 7EH.

    Trace metals and drugs have been measured in hair for a number of years but there are no published papers on the measurement of steroids in human hair. We report here the measurement of testosterone in hair samples taken from men, women and prepubertal children. This was a preliminary investigation to see whether testosterone was detectable in hair and whether concentrations between men and women, and men and prepubertal children were different in line with concentrations of testosterone in the blood. Hair was digested in sodium hydroxide and the testosterone extracted before measurement by radioimmuno- assay. There was a clear difference between testosterone concentrations found in heir collected from men (12.9-77.7 pmol/g) and those found in hair from women (<0.9-10.8 pmol/g). There was no significant difference between the concentrations found in women and children. The authenticity of the testosterone measured was confirmed with GCMS.




    Here is another important study demonstrating the change in the external hormonal environment when you compare balding scalp to non-balding scalp.

    J Dermatol Sci. 2004 Feb;34(1):11-6. Links
    Comparative studies on level of androgens in hair and plasma with premature male-pattern baldness.Bang HJ, Yang YJ, Lho DS, Lee WY, Sim WY, Chung BC.
    Bioanalysis and Biotransformation Research Center, Korea Institute of Science and Technology, PO Box 131, Cheongryang, Seoul 130-650, South Korea.

    BACKGROUND: It is well known that male-pattern baldness (male pattern baldness) is not started from occipital, but frontal or scalp of head. We can assume that distribution of androgenic steroids is different for each region of the head. OBJECTIVE: We hypothesize that the levels of androgenic steroids are different not only between vertex hair with male pattern baldness and controls but also between occipital hair with male pattern baldness and controls. Moreover, we want to search for the biochemical indicator in plasma and hair sample (baldness: 22, non-baldness: 13) obtained from dermatology of medical center. After then, we desire to present fundamental data regarding diagnosis, medical cure, and prevention for premature male pattern baldness. METHODS: After hair and plasma were hydrolyzed, and then extracted with organic solvent. To assess androgenic steroids levels, we used gas chromatography-mass spectrometry (GC-MS) system in selected ion monitoring mode. RESULTS: The level of dihydrotestosterone (DHT) and the ratio of testosterone to epitestosterone (T/E ratio) in vertex hair from premature baldness subjects were higher than in the sample of non-baldness subjects (P<0.001, 0.001), whereas the levels of androgens in occipital hair from the same baldness group were not different. In addition, we discovered the levels of DHT, testosterone, and DHT/T ratio in plasma from premature male pattern baldness were higher than in those of control subjects (P<0.001, 0.001, 0.005). CONCLUSION: We verified that the distribution of androgenic steroids is unlike in various regions of individual subjects. Moreover, the increased DHT/T ratio in balding plasma indirectly confirms the high activity of 5alpha-reductase type II.



    Another important study demonstrating a different phenomenon; hair follicles in men and women demonstrate different responses to hormones at the gene level.

    J Investig Dermatol Symp Proc. 2005 Dec;10(3):243-6.Links
    Substantial sex-dependent differences in the response of human scalp hair follicles to estrogen stimulation in vitro advocate gender-tailored management of female versus male pattern balding.Conrad F, Ohnemus U, Bodo E, Biro T, Tychsen B, Gerstmayer B, Bosio A, Schmidt-Rose T, Altgilbers S, Bettermann A, Saathoff M, Meyer W, Paus R.
    Department of Dermatology, University Hospital Hamburg-Eppendorf, University of Hamburg, Hamburg, Germany.

    In this study, it was investigated how estrogens (17-beta-estradiol, E2) affect the estrogen receptor (ER) expression and gene regulation of male versus female human scalp hair follicles in vitro. Anagen VI follicles from frontotemporal scalp skin were microdissected and organ-cultured for up to 9 d in the presence of E2 (1-100 nm). Immunohistochemistry was performed for ERbeta-expression, known to be predominant in human scalp hair follicles, and for TGF-beta2-expression (as negative key hair growth modulator), and E2-responsive genes in organ-cultured human scalp hair follicles (48 h, 10 nM) were explored by cDNA microarray, using a commercial skin focus chip (Memorec, Cologne, Germany). The distribution pattern of ERbeta and TGF-beta2-immunoreactivity differed between male and female hair follicles after 48 h culture. Of 1300 genes tested, several genes were regulated sex-dependent differently. The study reveals substantial sex-dependent differences in the response of frontotemporal human scalp hair follicles to E2. Recognition and systematic dissection of the E2-dependent gene regulation will be crucial for the development of more effective, gender-tailored management strategies for female versus male pattern balding
     
  2. wookster

    wookster Experienced Member

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    That is an interesting question. Stump tailed macaques experience miniaturization of scalp hair follicles. Do they also experience extra collagen streamers that block downward migration of the dermal papilla?
     
  3. wookster

    wookster Experienced Member

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    Also, there is a scar from 2002 on my upper right temporal recession that has many hairs growing around it.

    How does a scar cause new hair growth? :? :hairy: :?

    There is the potential for billions of dollars of revenue to be made from extended life time treatments of balding but not that much money to be made with a one time CURE for balding.
     
  4. michael barry

    michael barry Senior Member

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    Im going to bed wook, but I'll leave you with this..........and you can google these things.


    The wound-healing hair growth thing is being worked on by Costariais right now. They have found that they can wound the skin, and new hairs will form if its done right. The only problem is these "should" be more male pattern baldness hairs if they form in the same areas of the scalp as male pattern baldness hairs reside right?


    Here is the first article"..................

    News and Views
    Nature 447, 265-266 (17 May 2007) | doi:10.1038/447265a; Published online 16 May 2007

    Regenerative biology: New hair from healing wounds






    Now that this is through........................onto the macaques. I dont think Macaques were noted to have collagenous streamers under the follicles Wook, and no immunological response or inflammation. However, finasteride works much better for them than for us and RU58841 is a practical cure for them from what Ive read. I imagine transplants would also work very well on them also-----------------so what is the issue at hand on this? When they transplant a one hair follicular unit Wook.....................it shed after a week or so...............and the dermal papilla migrates upward near the surface of the skin like any other hair in a rest phase, and the stem cells from the arrector pilli and outer root sheath move to the dermal papilla and give the correct signals after a couple of weeks rest and the dermal papilla dives back downwards in the dermis and starts to build a new big anagen hair. We have seen that miniaturized hairs have the capacity to do this on immunodeficeint mouse-backs also. But it doesn't happen in humans. The authors of the mouse study opined that we have some peptide, hormore, neuropeptide, cytokine or whatever that might keep telling the hair "no".


    Keep this in mind Wook, the Nordstrom study moved bald scalp hairs (vellus) to OTHER PARTS OF THE BODY_-------and the hair didn't regrow.
    It moved donor hair to other parts of the body...................and it grew. Donor hair will grow in the frontal scalp.



    I know you Wook, you are looking for somethigng "outside". I used to be that way when I started searching for why finasteride was only slowing my hair from falling and not completely halting it. I though the scienists must be hiding something. But they are not. We just dont have a topical that blocks all DHT and blocks all receptors, and is good enough a hypertrichotic and tissue remodeller to remove all collagen fibers around the follicle, unscar the philosebaceous area, and jumpstart keratinocyte growth and start a new anagen phase well enough to get all the lost hair growing again---------------even though it will grow on an immuno deficient mouse. We transplant the "very close surround" in a transplant as some skin is moved along with the hairs themselves, so if there is anything "outside" to be found Wook, its in the very close surround. The dermal fibroblasts, the arrector pilli muscle, the stem cells of the sebaceousl gland or outer root sheath are the only other places genetic iformation about androgen response could be stored because these are the only other places that are moved with plugs.

    Remember, with plugs, you have to have re-vascularization after the not only the cutting, but the first quick shed phase in shock of the surgery that happens in just a couple of weeks------------------the rest phase at the surface, the new dive down deep. I really really really dont think its just oxygen in the scalp or any of that. Lack of hair will lead to lack of capillaries feeding the hair in bald scalp, hence the lack of hemoglobin carrying oxygen. It makes perfect sense. As you can tell-------------I pretty much accept the standard theory of baldness after looking into it these past few years.
    Cheng-Ming Chuong1

    AbstractIn mammals, most wounds heal by repair, not regeneration. It now seems that, as they heal, open skin wounds in adult mice form new hair follicles that follow similar developmental paths to those of embryos.

    A person whose leg is amputated is left with a stump, whereas some amphibians have the awe-inspiring ability to regenerate new limbs after amputation. Overall, adult mammals have very limited regenerative ability; this could be due to a lack of stem cells or the absence of proper environmental signals. On page 316 of this issue, Ito et al.1 report an unexpected finding that could change our current understanding of repair and regeneration in adult mammals. They show that the outermost skin layer — the epidermis — of wounded adult mice can regenerate new hair follicles during healing, and that this ability depends on the characteristics of the wound.

    Observations some 50 years ago had indicated that, in mice, rabbits and humans2, 3, 4, 5, some hair follicles develop anew after wounding. But because of a lack of definitive evidence, these findings had generally been discounted. Now, using advanced cellular and molecular techniques to study normal adult mice, Ito et al. have rediscovered these forgotten phenomena. The authors made large wounds (1–2.25 cm2) on the animals' backs, to the full depth of the skin. They found that if, following wound closure, the healed wound was larger than around 0.5 cm in diameter, new hairs formed at the centre of the wound. An examination of the sections of the healed skin revealed changes that resembled various stages of embryonic hair-follicle development. The new hair follicles grew, passed through the hair cycle, and eventually became indistinguishable from neighbouring hair (Fig. 1).

    Figure 1: Formation of new hair in a healed wound.
    a, Ito and colleagues1 found that when a large open wound is generated in the skin of adult mice, re-epithelialization occurs. b, If the healed skin is larger than around 0.5 cm in diameter, new hair follicles originating from the epidermis form in the centre of the wound.

    High resolution image and legend (60K)

    Why has this phenomenon previously been missed? The reason might be that large wounds in humans are treated with sutures and dressings. Although such procedures help wound closure, they might not be ideal for the generation of new hair follicles. Similarly, it is not common practice to leave wounds open in mice. The authors did this here because they wanted to trace the fate of hair-follicle stem cells, which normally reside in the bulge in the hair follicle (Fig. 1), during wound healing. Thus, a combination of altered experimental design and careful observation led to these exciting findings, which verify the preliminary observations from the 1950s and help to explain the controversy.

    What is the origin of the cells that make up these new hair follicles? Are they derived from existing hair follicles located at the wound edge, or from inter-follicular epidermis? Under normal conditions, the epidermis and the hair follicles maintain separate stem-cell compartments6, 7, 8, 9. Following wounding, however, cells derived from the hair bulge contribute to re-epithelialization — a process of new epidermis formation to cover the denuded dermis layer. This indicates that hair-bulge stem cells can turn into wound epidermis, although their contribution seems to be transient; with the exception of some cells from the upper part of the follicles, most of the hair-bulge-derived cells later disappear from the wounded epidermis6, 7, 8, 9.

    To determine the origin of the hair follicles that develop following wound repair, Ito et al.1 used a mouse model in which the bulge cells or inter-follicular epidermal cells were genetically labelled before wounding, so that they could be traced afterwards. The authors found that cells constituting the newly formed hair follicles are derived from inter-follicular epidermis, and not from existing hair bulges. Whether the new hair follicles themselves are generated from epidermal stem cells or through de-differentiation of existing epidermal cells is unknown.

    That the epidermis can turn into skin appendages (hairs, glands, feathers) is not entirely surprising. Previous studies have shown that, by combining cells from different tissue components under appropriate experimental conditions, scales can turn into feathers, oral mucosa (the membrane covering structures inside the mouth) can turn into tooth-like appendages, and even the corneal epithelium can become hair follicles10. Some of these changes can be achieved by altering the balance of relevant molecules in the cell. For example, -catenin is a component of a signalling pathway mediated by Wnt proteins that is involved in regulating development. Increasing the activity of -catenin can trigger the formation of new hair follicles in the interfollicular epidermis of adult mice without the use of hair-bulge stem cells11. However, such cellular processes are occurring under experimental conditions. What is remarkable about the findings of Ito and colleagues is that skin wounds stimulate the formation of hair spontaneously, as part of the normal healing process.

    Ito et al.1 went on to show that wounding activates the Wnt-mediated signalling pathway, which is essential for normal hair development and cycling12. Inhibiting this pathway in the skin during wounding led to a substantial decrease in the number of new hairs. By contrast, when mice with increased Wnt activity in their epidermal layer were wounded, there was a significant increase in new hair follicles compared with mice with normal Wnt activity. As these cellular events seem to recapitulate those seen in embryonic development, it is possible that hair formation during embryogenesis and following wounding share several signalling pathways, including Wnt.

    What are the essential criteria for triggering the formation of new hair follicles in a patch of adult skin? The size of the healed wound seems to be critical. This implies that an 'embryonic skin-like field' must be established first. Self-organization of hair follicles then progresses, and periodically arranged primordia (aggregates of embryonic cells that indicate the first traces of a structure) emerge. As new hair patterns after wounding are not predetermined, it is possible to manipulate the number and size of the follicles through positive- and negative-feedback regulation of inhibitors and activators of signalling pathways such as Wnt10, 13.

    Adult organisms contain several types of cells with remarkable regenerative potential12, 14, 15 — if we could only provide the appropriate chemical and physical environment. The best teacher for this is nature. Indeed, an event that parallels the work of Ito and colleagues is the regeneration of deer antlers. After an antler is cast, the large open wound that forms is followed by re-epithelialization and the development of new hair follicles, as well as budding of the new antler16. Further studies on animal models should reveal other unexpected and ingenious ways of awakening stem cells with appropriate environmental cues when regeneration is needed10.

    Repair and regeneration seem to be competing processes. As closing wounds fast is essential for survival, repair often dominates. Regenerative medicine promises to identify natural healing power and a shift from repair to regeneration. Thus, by simply altering the environment of stem cells10 during wound healing, future wounds might heal with appendages reformed. As human and mouse skin heals differently, the results of Ito et al.1 are yet to be verified in humans. However, these findings will undoubtedly inspire new thinking in the management of alopecia, in tissue engineering and in the regeneration of other organs
     
  5. wookster

    wookster Experienced Member

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    Like you, I am looking for real answers :wink:

    So finasteride, or just about any of the current hairloss treatments is essentially a "cure" for the stump tailed macaque because the stump tailed macaques must go bald by a slightly different mechanism than humans do?

    Thinning, or elastosis/tightening of the underlying scalp tissues in human baldness is an observation that many have made. You say it is caused by the inevitable lack of circulation due to the effect of androgens causing the follicles to send out negative growth factors due to the statistical distribution of genetic reaction in hair follicles to androgen exposure.

    That really doesn't explain why an isolated hair island exists in the front of many balding scalps.

    But points of mechanical stress explain isolated hair islands quite well.
     
  6. wookster

    wookster Experienced Member

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    http://joe.endocrinology-journals.org/c ... t/156/1/59

     
  7. wookster

    wookster Experienced Member

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    http://www.morphollica.com/research/how ... r_grow.php

    [​IMG]

    The deeper rooted transplants probably wouldn't suffer from a buildup of collagen/streamers/stellae. :hairy:

    http://www.ehrs.org/conferenceabstracts ... hiting.htm

     
  8. wookster

    wookster Experienced Member

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    Not necessarily. The hairs growing on the periphery of my scalp scar tissue appear to be very "robust" :D :hairy: :D
     
  9. Bryan

    Bryan Senior Member
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    That may or may not be true, but again, that's a separate issue from this important point that Stephen and I have been discussing for a long time. We want to know what causes a follicle to change over the years in its inherent sensitivity to androgens (it has nothing to do with numbers of androgen receptors, and nothing to do with levels of androgens). That phenomenon was clearly demonstrated in both Uno's macaque study, and the Japanese study whose link I posted. If you think about that for just a bit, it's a PROFOUNDLY important question. It desperately needs to be answered.

    Sure they do!

    So anyway, what's your response to Stephen Foote, when he claims that there is no biological precedent for constant exposure to a hormone causing a fundamental change in the way that a tissue responds to that hormone (as in going from essentially a neutral response to a very negative one)? Can anybody refute his objection? :)
     
  10. wookster

    wookster Experienced Member

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    http://www.abstracts2view.com/endo/view ... 395&terms=


    :? :? :?

     
  11. wookster

    wookster Experienced Member

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  12. michael barry

    michael barry Senior Member

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    Bryan,

    My response to Foote is the same as its been..............we can only keep hairs alive ex vivo for about 2 weeks, and its just not long enough to catch hairs at the right time that they are about to get "sensitive" to androgens for the experiments for whatever reason.

    I would postulate that there is something in the "very close surround" that is giving signalling that is necessary for the negative response to begin, but the cultured occipital hair cells becoming weakened by high androgen stimulis would invalidate that thought.


    I simply think, like Washenik, that when the skin grows over the top of the head in fetal development in bald men, something different goes on there genetically, and a predetermined later response to androgens in specific areas of hair is determined there.




    Wook, you asked about why is there an area of hair (the tuft) that is left for a long while in baldness.................................in my opinion its not much different that occipital hair. It simply either has less receptor expression, less DHT, less sensitivity to androgens INDIVIDUALLY, or all three. Probably all three. If you transplanted them, they'd probably grow for several years "until there time came", but if you transplanted the balding temporal hairs........................they'd stay balding and would be lost pretty soon.




    Wook, the large hairs you have near a scar are interesting. Perhaps when hair results from wounding the skin---------whatever genes encode baldness dont participate in this, resulting in "good" hair. That would be great wouldn't it. I suppose someone could test this.......merely boil a needle in water to sterilize it, pluck your temples three or four times, and let them bleed normally and a blood scab to form over them (heal naturally). I dont know the depth of the wound necessary to try this though. If you had a whack hair growing at four months..................you could report back on here that you found a way to grow new hair. I remember a while back some dude was claiming success with something like that with minoxidil on one of these sites.

    Wook, the reason I think the determination rests in the hairs themselves (or the very close surround that is also moved with a transplant located in the arrector pilli, sebaceous gland, or the root sheath or little sliver of skin that is moved along with a transplant) is this.....................................................Nordstrom. Thinning hairs miniatruized pretty quickly when he moved them to other parts of the body. Donor-wreath hairs stay big wherever they are moved. Body hairs can grow on the scalp, but retain their characteristics other than longer lengths---their curl, diameter, etc.

    Dr. John Cole, a transplant surgeon, moves nape of the neck hairs in transplants to the hairline becuase they look more natural up front because they are smaller in diameter than heart of the donor area follicles are. They then retain their characteristics in this way. Bading hairs are still going to bald if they are moved to another area of the scalp or body. Therefore, I think the genetics are located within the hairs themselves and must be determined when the scalp is formed back in fetal development as skin grows over the top of the cranium. This is the standard thought on this by the way. Its what the researchers believe also.

    However Wook, if Cosarialis is right (and Stenn too, because they have been researching this together), and skin can be wounded in a certain way, and hairs will form up there..........................being on finasteride might have the androgen stimulis in the new hairs be low enough from inception (they are NEW hairs, formed out of the dermis, not regenerated old ones) that they might not get responsive to testosterone. It might be a second chance to keep the hairs. Ive seen Bryan postulate on here that if a guy got on finasteride back before he was balding at all, the androgenic stimulation of the hairs might not ever get high enough to "kick off" the baldness genetics therein. We are seeing loss of hair mass before we ever even notice that hair is growing a little more weakly in response to androgens. I was thinning in a NW3 pattern back before I ever got on finas...............................



    A little news for you two on Aderans I got from hairtech. IN mice, cloned dermal papilla/stem cells put back in the mice have a problem in that they go through a rest phase in exactly 21 days. This is before they have a chance to grow a hair long enough to break through the skin, so you have a dead hair that is shed sitting there in the dermis, causing inflammation while a new hair is attempting to grow behind it. Its causing problems and Aderans is lookng for a way around it (biodegradable tissue scaffolds, growing hair outside the body and re-implanting, etc.). Interctyex must be doing things differently because they are facing no inflammation and grew hair in their phase one human trial (pictures of that have now been shown and were on hairsite-----there was some new hair indeed). Phase 2 at intercytex (results expected before years end) should tell us where we are with that. I still think this is the most logical route-------more donor hair "made" by cloning. [/quote]
     
  13. wookster

    wookster Experienced Member

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    Why did "natural selection" leave a tuft of hair if the androgen receptor/sensitivity model is the correct one?

    Stephen Foote's contact inhibition idea explains much :hairy:

    The David Hatch engineering theory might not be 100% correct but it is interesting. Pressure from mechanical stress provides the required contact inhibition :hairy:

    http://www.malepatternbaldness.net/

    [​IMG]
     
  14. S Foote.

    S Foote. Experienced Member

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    Your mechanism could only be validated if the controls i suggested were also tested in the same way. They weren't!

    The studies i quoted used such alledged "opposite" samples, so have "some" scientific validity.

    That study i posted "specificaly" tested your claim about androgen receptors.

    They proved that there was no difference in the receptors in male pattern baldness cells and pre-male pattern baldness cells. They tested this because of the lack of "direct" androgen response in the pre-male pattern baldness cells that you claim are directly "causing" male pattern baldness!

    So your "mutant" receptor idea is plainly wrong.

    S Foote.
     
  15. michael barry

    michael barry Senior Member

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    Wook,


    Its Wnt signalling that Costarialis and Stenn were working with. Minxoidil supposeldy ups Wnt signalling. I wonder if one could use a derma-roller while doing finas and minoxidil and see if some new haris could literally be "created" near the front of the hairline. Perhaps this would be interesting if the derma-roller was going at the right depth?


    you mentioned:
    "Why did "natural selection" leave a tuft of hair if the androgen receptor/sensitivity model is the correct one? "

    Maybe natural selection is trying to make us look "mature" then? Or hell, maybe its just making us look old so that we will grow up...........It certainly isn't because we want to look that way, I can tell you that.
     
  16. wookster

    wookster Experienced Member

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    :D :hairy: :D

    http://www.pubmedcentral.nih.gov/botren ... tid=110627

     
  17. Bryan

    Bryan Senior Member
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    So you're still going along with the general idea that it's the constant exposure to androgens which eventually causes them to change their response to those androgens, but you can't give any other example of such a change elsewhere in biology, as Stephen requests?

    The issue of even those occipital hair cells being sensitive to high levels of androgens doesn't interest me all that much. It could quite reasonably turn out that ALL scalp hairs, occipital ones included, are actually sensitive to androgens, it's just that some are far more sensitive than others. That possibility doesn't really interest me as much as what causes a specific hair follicle to CHANGE in its sensitivity over a period of time, as Uno and the Japanese researchers demonstrated.

    Now you're suggesting that it's not JUST the constant exposure to androgens, but maybe something else, too? The phrase "predetermined later response to androgens" does have a distinct smell that's similar to "genetic clock"! :)
     
  18. michael barry

    michael barry Senior Member

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    Bryan, you used this verbiage:

    "So you're still going along with the general idea that it's the constant exposure to androgens which eventually causes them to change their response to those androgens, but you can't give any other example of such a change elsewhere in biology, as Stephen requests? "



    Let me clear it up for you------------I think that once androgens reach a certain point in transcription within a hairs papilla, THEN the hairs become sensitive to them. But I believe the --level-- at which this happens should vary (of course) in different parts of the scalp, and from person to person also.

    You could very well be right about a "genetic clock", but would it not make more biological horse-sense to say that when a hair is entertaining a factor of 100---DHT, that its "too much" and most non-wreath hairs will start to miniaturize at that level, and perhaps it takes a factor of 200---DHT to make wreath hairs susceptible to androgen than to postulate that on "hair cycle 13----you will begin to be poisioned by hormone"----says the DNA to the hair follicle?



    But, of course, this is all conjecture..................and the hair cycle clock could really be just the thing.
     
  19. docj077

    docj077 Senior Member

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    Actually, the mutation is a proven phenomenon and involves a single nucleotide. I don't know where you get your information from.
     
  20. Bryan

    Bryan Senior Member
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    I'm not sure what you mean. What do you think determines that "certain point of transcription"? The length of time that they're exposed to androgens? Isn't that basically the same thing as what you said before?

    Sure, that would make sense if we simply postulate from the beginning that exposure to androgens DOES IN FACT cause tissues to become more sensitive to them over time. But we haven't been able to provide any initial support for that idea yet, in the way of scientific evidence.
     

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