» as well as a home dermabrasion kit.
Make that a microdermabrasion kit.
WHERE did you order the Lithium and derm kit from?
Thank you
» » as well as a home dermabrasion kit.
»
» Make that a microdermabrasion kit.
The “edit” function now works for up to 2 hours after posting, according to the admin! 
.
» I knew a family once that had a Iraqi father and a
» blonde European mother. Their four kids all looked differnt. One looked
» very Arab (and was slim), one looked like a farm boy from the midwest with
» medium brown hair (hefty), one of the girls looked like an middle eastern
» model (dark skin, dark hair and beautiful), and the other daughter was a
» very plain (some would say kinda homely) blonde gal with light skin (and
» blue eyes) that was prone to heaviness. It seemed to me that genetics was
» like a deck of cards and your chances of inheriting this or that came from
» those cards getting really mixed up and you drawing this one or that one.
» Two of those kids looked “very white” and the other to looked very
» Arabain. It was not a mix of the two as I’d expected. The blonde was
» very blonde—and the two that had black hair had JET-BLACK
» hair. Mystifying that such totality was “selected” and the two
» phenotypes didnt “mix” somewhat to produce brown hair like the hefty
» brother had.
What color hair did their mailman have? 
.
» » Do you know of any studies on bald vs non-bald scalp?
»
» For garlic? No I don’t. Sorry.
»
» .
Actually, I was asking about any study that compared balding vs non-balding skin in terms of skin composition i.e. which layer gets messed up the most during baldness etc.
» » Bryan,
» » The thing is man…is that androgens stimulate body
» » hair in men and women and everyone. In looking at DKK-1, I suppose I am
» » (again) looking for a piece of the puzzle in which we can “stick our
» » finger” in the MPB process and stop it.
»
» But there’s no real lack of different ways we can potentially stick our
» finger in the MPB processs and stop it. For a long time on hairloss sites
» there’s been this utter fascination with the veritable “alphabet soup” of
» substances of all kinds that show a difference in production levels between
» balding and non-balding hair follicles. Just look at all the times that
» TGF-beta-1 and TGF-beta-2 and IGF-1 and VEGF have been mentioned and
» discussed on these sites, and thought to be the final key to the
» mystery of balding! DKK-1 is just the latest addition to this list, and
» the “alphabet soup” is getting really robust and full-flavored! 
»
» Again, I feel this fascination with all the various factors that are
» different between balding and non-balding hair follicles is ok, but we’re
» really just treading water here. It’s all mainly just a smoke screen until
» we find out the fundamental REASON for the difference in production levels
» of that “alphabet soup” of substances which are different between balding
» and non-balding hair follicles. And who knows?? We may even stumble upon
» reasonably effective treatments for balding here and there by searching for
» TGF-beta inhibitors, DKK-1 inhibitors, etc. But in my humble opinion, it’s
» still basically just a waiting game until we can find out the fundamental
» REASON for those differences.
»
» » Bryan, on another note…as far as “2 different
» types
» » of hair on the head”…I just dont believe that. I reposted
» » that study showing high testosterone added to occipital scalp hairs
» caused
» » apoptosis and I seen another study (dont know if I put it up anywhere)
» that
» » showed the androgen receptors in MPB-area sebacous glands were much
» better
» » at binding male hormone than androgen-receptors from non-MPB
» » areas…leading obviously to the conclusion that more-active
» » androgen receptors or more chemically stable ones in MPB-areas are the
» » reason for the “difference” in the hairs. Ive suggested over and over
» that
» » if we could transfect someone without MPB hairs in an ex vivo
» experiment
» » with the whole hair cultured with extra androgen receptors and give them
» a
» » dose of androgens like a guy with MPB probably sees his follicles
» uptake,
» » I’d bet they’d respond negatively. I simply think Brad Pitt’s hair
» isn’t
» » seeing as much androgens as ours is via less DHT in the area, and
» androgen
» » receptors that dont function “as well” as ours do.
»
» I don’t have any doubt about that, either. But I personally have
» relatively little concern for all the various factors which get discussed
» ad nauseum on hairloss sites which have to do with different levels
» of androgenic stimulation, and the resulting different severities of
» balding from one person to another. To me, that’s a relatively trivial and
» obvious matter. What interests me far more is what accounts for the
» FUNDAMENTAL DIFFERENCE between body hair follicles and scalp hair follicles
» which makes them respond to androgens in an OPPOSITE fashion. Until we can
» figure that out, we’re mainly just spinning our wheels.
OK just wrote and lost a large reply but basically - those various factors you are talking about are in themselves the fundamental difference that you are looking for. One may prove to be upstream of the others or more important but there is no reason for scalp hairs to behave differently to body hairs beyond the fact that they are different cell types and thus express different genes just as skin cells and muscle cells do. On the other hand all may be equally important or some may only play a part in balding white men, others in Asian men etc. But at the end of the day theres no reason behind it other than the reality of which genes get transcribed when the androgen binds to the androgen receptor and travels into the nucleus.
hh
» OK just wrote and lost a large reply…
Sounds like you took so long that the “posting timer” timed-out on you, and you lost everythign you had written! That’s a PISSER when that happens, isn’t it?? 
David (hairsite admin)!! Get this problem fixed once and for all!!!
» …but basically - those various factors
» you are talking about are in themselves the fundamental difference that you
» are looking for. One may prove to be upstream of the others or more
» important but there is no reason for scalp hairs to behave differently to
» body hairs beyond the fact that they are different cell types and thus
» express different genes just as skin cells and muscle cells do. On the
» other hand all may be equally important or some may only play a part in
» balding white men, others in Asian men etc. But at the end of the day
» theres no reason behind it other than the reality of which genes get
» transcribed when the androgen binds to the androgen receptor and travels
» into the nucleus.
I’m not entirely sure what your overall point is. I don’t really disagree with anything you said.
.
» » OK just wrote and lost a large reply…
»
» Sounds like you took so long that the “posting timer” timed-out on you,
» and you lost everythign you had written! That’s a PISSER when that
» happens, isn’t it??
Oh man I thought that must have been what happened - it asked me to login again. Yeah that was super annoying.
» David (hairsite admin)!! Get this problem fixed once and for all!!!
»
» » …but basically - those various factors
» » you are talking about are in themselves the fundamental difference that
» you
» » are looking for. One may prove to be upstream of the others or more
» » important but there is no reason for scalp hairs to behave differently
» to
» » body hairs beyond the fact that they are different cell types and thus
» » express different genes just as skin cells and muscle cells do. On the
» » other hand all may be equally important or some may only play a part in
» » balding white men, others in Asian men etc. But at the end of the day
» » theres no reason behind it other than the reality of which genes get
» » transcribed when the androgen binds to the androgen receptor and
» travels
» » into the nucleus.
»
» I’m not entirely sure what your overall point is. I don’t really disagree
» with anything you said.
I guess from your earlier post it seemed like you felt the study of and worrying about stuff like TGF-Beta etc was not important because there was a fundamental difference that would explain WHY scalp hairs produced growth inhibitors when exposed to DHT and why beard hairs produced growth promoters. Whereas I was trying to say that there is no reason behind the difference - it just is. Maybe I misunderstood you in that you were saying that it is a waste of our time now to worry about it when we still dont know exactly how much of a role each of these new factors plays in the balding process and what needs to be done to stop them but it sounded like you wanted to know why they were produced at all.
At any rate I do think that whole alphabet soup stuff is really important and exciting and that is where any breakthrough in understanding and treatment effectiveness is going to come from in this whole thing. If every study since the first TGF-Beta/IGF had reported the same central importance of TGF-Beta 1 I would be betting the hair on trying to find some topical to inhibit TGF-Beta 1 activity right now.
hh
» » I’m not entirely sure what your overall point is. I don’t
» » really disagree with anything you said.
»
» I guess from your earlier post it seemed like you felt the study of and
» worrying about stuff like TGF-Beta etc was not important because there was
» a fundamental difference that would explain WHY scalp hairs produced growth
» inhibitors when exposed to DHT and why beard hairs produced growth
» promoters.
I think the study of and worrying about stuff like TGF-beta IS important (at least for the time being), because it’s things like that that are the only ways we currently have of fighting MPB. These “downstream” methods like TGF-beta inhibitors, antiandrogens, etc., are still relatively crude, but we don’t yet have anything more “upstream”.
And there IS a fundamental difference that will explain why scalp hairs and body hairs respond in opposite fashion to androgens. We just don’t know what it is yet.
» Whereas I was trying to say that there is no reason behind
» the difference - it just is.
HUH?? What do you mean, “there is no reason”? Do you think they respond in opposite fashion to androgens just because God (or the Devil) tells them to?? 
» Maybe I misunderstood you in that you were saying
» that it is a waste of our time now to worry about it when we still dont
» know exactly how much of a role each of these new factors plays in the
» balding process and what needs to be done to stop them but it sounded
» like you wanted to know why they were produced at all.
Oh, I guarantee you that I most definitely do want to know why scalp hair follicles and body hair follicles produce growth suppressors and growth promoters (respectively). Understanding that difference would obviously be required for us to attack the problem at the most UPSTREAM point in the process, which almost certainly would be more desirable.
» At any rate I do think that whole alphabet soup stuff is really important
» and exciting and that is where any breakthrough in understanding and
» treatment effectiveness is going to come from in this whole thing.
It’s a relative thing. Finding out more and more about each member of the alphabet soup that’s involved in balding SEEMS important, but that’s only because we don’t understand the initial steps in the process. We need to know the FUNDAMENTAL REASON(S) why scalp follicles and body follicles respond in opposite ways to androgens before we can really get to the heart of the matter with the most direct treatments, as opposed to the indirect treatments that we have today, and probably the forseeable future.
.
» » » I’m not entirely sure what your overall point is. I don’t
» » » really disagree with anything you said.
» »
» » I guess from your earlier post it seemed like you felt the study of and
» » worrying about stuff like TGF-Beta etc was not important because there
» was
» » a fundamental difference that would explain WHY scalp hairs produced
» growth
» » inhibitors when exposed to DHT and why beard hairs produced growth
» » promoters.
»
» I think the study of and worrying about stuff like TGF-beta IS important
» (at least for the time being), because it’s things like that that are the
» only ways we currently have of fighting MPB. These “downstream” methods
» like TGF-beta inhibitors, antiandrogens, etc., are still relatively crude,
» but we don’t yet have anything more “upstream”.
Well I would tend to think of antiandrogens as acting upstream relative to something like a TGF-Beta inhibitor which is more downstream in that it is expressed in response to androgens.
»
» And there IS a fundamental difference that will explain why scalp hairs
» and body hairs respond in opposite fashion to androgens. We just don’t
» know what it is yet.
»
» » Whereas I was trying to say that there is no reason behind
» » the difference - it just is.
»
» HUH?? What do you mean, “there is no reason”? Do you think they respond
» in opposite fashion to androgens just because God (or the Devil) tells them
» to??
No. They respond in opposite fashions because they express proteins that have opposite effect on keratinocytes. Thats it. There is no deeper reason than that and we already know this and no many of the proteins in question. Thats what I am saying in terms of there is no reason beyond the genetic reality
» » Maybe I misunderstood you in that you were saying
» » that it is a waste of our time now to worry about it when we still dont
» » know exactly how much of a role each of these new factors plays in the
» » balding process and what needs to be done to stop them but it sounded
» » like you wanted to know why they were produced at all.
»
» Oh, I guarantee you that I most definitely do want to know why scalp
» hair follicles and body hair follicles produce growth suppressors and
» growth promoters (respectively). Understanding that difference would
» obviously be required for us to attack the problem at the most UPSTREAM
» point in the process, which almost certainly would be more desirable.
Well I think androgens are the most upstream part of the pathway. And that is a step that is, at least for many people, somewhat undesirable to attack. A local intervention on something downstream of that seems preferrable to my mind.
» » At any rate I do think that whole alphabet soup stuff is really
» important
» » and exciting and that is where any breakthrough in understanding and
» » treatment effectiveness is going to come from in this whole thing.
»
» It’s a relative thing. Finding out more and more about each member
» of the alphabet soup that’s involved in balding SEEMS important, but that’s
» only because we don’t understand the initial steps in the process. We need
» to know the FUNDAMENTAL REASON(S) why scalp follicles and body follicles
» respond in opposite ways to androgens before we can really get to the heart
» of the matter with the most direct treatments, as opposed to the
» indirect treatments that we have today, and probably the forseeable
» future.
OK. Its the whole fundamental reasons thing that I dont understand/dont think exists. androgen + receptor -> production of hair promoters/inhibitors.Thats it really. Trying to understand why beyond that is like wanting to understand the fundamental reason why someone has blonde hair rather than black beyond understanding that they have genes that encode for different hair pigments. IMO the why was explained a few years ago in that first study on beard vs balding scalp dermal papillae.
» Well I would tend to think of antiandrogens as acting upstream relative to
» something like a TGF-Beta inhibitor which is more downstream in that it is
» expressed in response to androgens.
Sure, it’s more upstream than a TGF-beta inhibitor would be, but I want to go ALL the way upstream where that first little creek starts to form!
» » HUH?? What do you mean, “there is no reason”? Do you think they
» » respond in opposite fashion to androgens just because God (or the
» » Devil) tells then to??
»
» No. They respond in opposite fashions because they express proteins
» that have opposite effect on keratinocytes. Thats it.
Ok. Now tell me WHY they do that!
» There is no deeper reason than that and
» we already know this and no many of the proteins in question.
» Thats what I am saying in terms of there is no reason beyond
» the genetic reality
You’ve gotta do a LOT better than that. No burying your head in the sand and saying that it happens because it happens! 
» Well I think androgens are the most upstream part of the pathway.
Nope, that’s not the most upstream part. The most upstream part is the reason for the paradoxical nature of the response to androgens.
» OK. Its the whole fundamental reasons thing that I dont understand/dont
» think exists. androgen + receptor -> production of hair
» promoters/inhibitors.Thats it really.
Harold, come on, man. Pull your head out of the sand.
.
Bryan,
You seem to be suggesting we can “turn off” certain genes within the papilla or supress their expression, so that when androgen is uptaken and brought to the nucleus of the papilla–the “bad” instructions are not followed.
Hey man…I’d be all for it, and it would be the most elegant solution to male baldness -ever- and would probably see even vellus hairs eventually regenerate with other growth factors over time. But is it actually do-able in the near-to-mid-term future? I’d be quite suprised (happily though:clap: 
) if it was.
I don’t know if it’s doable in the near-future, either, but it’s obviously the ULTIMATE goal in the search for a solution to balding. All this other crap involving long and tedious searches for all the members of the Alphabet Soup and attempting to find substances which alter the production of those elements, together with trying to find the best possible 5a-reductase inhibitors and the best possible antiandrogens, yada-yada-yada, all those are just stop-gap measures. We’re just biding our time until we can finally learn how to “switch-off” the harmful response that our scalp hair follicles have to androgens.
.
» » Well I would tend to think of antiandrogens as acting upstream relative
» to
» » something like a TGF-Beta inhibitor which is more downstream in that it
» is
» » expressed in response to androgens.
»
» Sure, it’s more upstream than a TGF-beta inhibitor would be, but I want to
» go ALL the way upstream where that first little creek starts to form!
I think I know what you mean by upstream now. Its not what people mean when they talk about upstream or downstream in terms of signal transduction but I think you are talking about the developmental stage as in “why does a skin cell become a skin cell? why does a hair cell become a hair cell? why does a scalp hair become a scalp hair etc” If thats so then…I dont really think that stuff is going to be of much use to us. They might be useful for engineering people without hairloss or hair multiplication but otherwise i dont see how it helps so much as the horse as already bolted so to speak.
» » » HUH?? What do you mean, “there is no reason”? Do you think they
» » » respond in opposite fashion to androgens just because God (or the
» » » Devil) tells then to??
» »
» » No. They respond in opposite fashions because they express proteins
» » that have opposite effect on keratinocytes. Thats it.
»
» Ok. Now tell me WHY they do that!
They do that for the same reason that skin cells transcribe whatever proteins they do in response to androgens just as cells of the prostate do. Because those are the genes that will be expressed in response to androgens in those cell types.
» » There is no deeper reason than that and
» » we already know this and no many of the proteins in question.
» » Thats what I am saying in terms of there is no reason beyond
» » the genetic reality
»
» You’ve gotta do a LOT better than that. No burying your head in the sand
» and saying that it happens because it happens!
Well…it does. But I now see more what you are getting at with I think. That you are interested in why some hairs express growth factors etc. But with the evidence that androgens can destroy even occipital hairs in high enough concentration I think theres a fair chance that all scalp hairs are set up in such a way and that the differences in balding between different areas of the scalp and different people could pretty much be explained in terms of androgen receptor expression/sensitivity and local androgen levels as is already the case. At any rate since dermal papillae wherein the bad response originates are not replaced fromm cycle to cycle I dont think there is that much that could be done to fundamentally change a “bad one” to a “good one” them even if there are such things.
» » Well I think androgens are the most upstream part of the pathway.
»
» Nope, that’s not the most upstream part. The most upstream part is the
» reason for the paradoxical nature of the response to androgens.
»
» » OK. Its the whole fundamental reasons thing that I dont understand/dont
» » think exists. androgen + receptor -> production of hair
» » promoters/inhibitors.Thats it really.
»
» Harold, come on, man. Pull your head out of the sand.
I think I understand what you are saying now. At the same time, unless you are planning to replace most of your existing follicles with new ones a la Follica then I think you have to look at all that alphabet soup stuff. Cos once that follicle has developed in such a way that it is going to produce those genes in response to androgen you either have to keep it away from androgens, interfere with the resulting production of those genes or introduce a growth factor or other third party that is powerful enough to overcome those negative signals.
hh
» » Sure, it’s more upstream than a TGF-beta inhibitor would be,
» » but I want to go ALL the way upstream where that first little
» » creek starts to form!
»
» I think I know what you mean by upstream now.
You weren’t completely sure what I meant by “upstream” until now??
» Its not what people mean
» when they talk about upstream or downstream in terms of signal transduction
» but I think you are talking about the developmental stage as in “why does a
» skin cell become a skin cell? why does a hair cell become a hair cell? why
» does a scalp hair become a scalp hair etc”
Ummm…once again, I’m talking about the SPECIFIC genetic and biochemical reasons that cause a hair follicle to become either STIMULATED by androgens, or SUPPRESSED by them. How can there be any confusion about what I mean??
» If thats so then…I dont really think
» that stuff is going to be of much use to us. They might be
» useful for engineering people without hairloss or hair multiplication
» but otherwise i dont see how it helps so much as the horse as already
» bolted so to speak.
Before you make any predictions about how un-useful it’s going to turn out to be, let’s actually FIND OUT what the reasons are. It may or may not be all that amenable to treatment once we find out, but let’s cross that bridge when we come to it.
» » » No. They respond in opposite fashions because they express
» » » proteins that have opposite effect on keratinocytes. Thats it.
» »
» » Ok. Now tell me WHY they do that!
»
» They do that for the same reason that skin cells transcribe whatever
» proteins they do in response to androgens just as cells of the prostate do.
» Because those are the genes that will be expressed in response to androgens
» in those cell types.
And WHY are those the genes that will be expressed in response to androgens in those cell types??? I’m trying to get you to understand that we have to find out the SPECIFIC BIOCHEMICAL REASONS for those responses, Harold, and all you’re doing is saying in effect, “that’s just the way they are”. You’ve got to do a LOT better than that!!
What if they had said in 1963, “Look, we just CAN’T go to the moon, it’s impossible, and that’s just the way it is”??
» But I now see more what you are getting at with I think.
I don’t know any different ways to say it. I’ve been making this same point throughout this thread, and also on all the hairloss sites for years. I don’t know why you’ve had trouble understanding what I’m saying.
» That you are interested in why some hairs express growth factors etc. But
» with the evidence that androgens can destroy even occipital hairs in high
» enough concentration I think theres a fair chance that all scalp hairs are
» set up in such a way and that the differences in balding between different
» areas of the scalp and different people could pretty much be explained in
» terms of androgen receptor expression/sensitivity and local androgen levels
» as is already the case.
Exactly. But as I’ve said before, that doesn’t particularly interest me because it’s obvious and trivial. I want to know what accounts for the completely OPPOSITE response to androgens from one hair follicle to another, depending on body location.
» At any rate since dermal papillae wherein the bad
» response originates are not replaced fromm cycle to cycle I dont think
» there is that much that could be done to fundamentally change a “bad one”
» to a “good one” them even if there are such things.
Again, that’s just speculation. Let’s actually FIND OUT what accounts for the difference, before we go and declare that there’s no way to change a hair follicle from one kind to another.
» » Harold, come on, man. Pull your head out of the sand.
»
» I think I understand what you are saying now.
Thank God!
» At the same time, unless you
» are planning to replace most of your existing follicles with new ones a la
» Follica then I think you have to look at all that alphabet soup stuff. Cos
» once that follicle has developed in such a way that it is going to produce
» those genes in response to androgen you either have to keep it away from
» androgens, interfere with the resulting production of those genes or
» introduce a growth factor or other third party that is powerful enough to
» overcome those negative signals.
Time will tell. Until then, I’m certainly not going to assume that there’s no way to make one little alteration in the response of a hair follicle to a specific hormone.
.
.
Time will tell. Until then, I’m certainly not going to assume that there’s no way to make one little alteration in the response of a hair follicle to a specific hormone.
you do that Bryan, and they will erect a statue to you in Houston Texas as the man who made men’s hair grow better with more testosterone. I’d look like “Cousin It” on the Munsters if it were so.
Gene therapy, and that is what we are talking about here, seems so far off to the point that it almost sounds like science fiction, but you are quite right…someday they may be able to make a compound that makes your head hair grow better via androgens like body hair does. I dont think it will be in the next decade however and that sucks for me
I think I hate this forum. Thats the 2nd long reply I have lost in a couple of days. This one seemed to go through. Anyway…
» » » Sure, it’s more upstream than a TGF-beta inhibitor would be,
» » » but I want to go ALL the way upstream where that first little
» » » creek starts to form!
» »
» » I think I know what you mean by upstream now.
»
» You weren’t completely sure what I meant by “upstream” until now??
Well technically the androgen is the most upstream signal in this process. There is nothing upstream of that as the term upstream and downstream is used in terms of signal transduction. But now I know that you meant a developmental stage that occured before the hair follicle cells had committed to becoming hair follicle cells.
» » Its not what people mean
» » when they talk about upstream or downstream in terms of signal
» transduction
» » but I think you are talking about the developmental stage as in “why
» does a
» » skin cell become a skin cell? why does a hair cell become a hair cell?
» why
» » does a scalp hair become a scalp hair etc”
»
» Ummm…once again, I’m talking about the SPECIFIC genetic and biochemical
» reasons that cause a hair follicle to become either STIMULATED by
» androgens, or SUPPRESSED by them. How can there be any confusion about
» what I mean??
Because what causes keratinocytes to be either stimulated or inhibited is the alphabet soup of cytokines etc released by the dermal papilla when it makes contact with DHT etc. But what causes a dermal papilla to become the type that reacts in one way rather than the other is another question.
» » If thats so then…I dont really think
» » that stuff is going to be of much use to us. They might be
» » useful for engineering people without hairloss or hair multiplication
» » but otherwise i dont see how it helps so much as the horse as already
» » bolted so to speak.
»
» Before you make any predictions about how un-useful it’s going to turn out
» to be, let’s actually FIND OUT what the reasons are. It may or may not be
» all that amenable to treatment once we find out, but let’s cross that
» bridge when we come to it.
OK. But what causes one type to become one or the other has already been and gone by the time we are here to worry about it. Causing one hair follicle to change into another type of hair follicle once they have diffferentiated is like getting a skin cell to change into a muscle cell. Possible in the test tube perhaps but very tricky at the least in vivo.
» » » » No. They respond in opposite fashions because they express
» » » » proteins that have opposite effect on keratinocytes. Thats it.
» » »
» » » Ok. Now tell me WHY they do that!
» »
» » They do that for the same reason that skin cells transcribe whatever
» » proteins they do in response to androgens just as cells of the prostate
» do.
» » Because those are the genes that will be expressed in response to
» androgens
» » in those cell types.
»
» And WHY are those the genes that will be expressed in response to
» androgens in those cell types??? I’m trying to get you to understand that
» we have to find out the SPECIFIC BIOCHEMICAL REASONS for those responses,
» Harold, and all you’re doing is saying in effect, “that’s just the way they
» are”. You’ve got to do a LOT better than that!!
»
» What if they had said in 1963, “Look, we just CAN’T go to the moon, it’s
» impossible, and that’s just the way it is”??
Indeed. But what if they had said “Lets not go to the moon with a crappy rocket - lets work on teleportation”
I really think understanding the alphabet soup stuff is the best, most versatile and most powerful way to approach it. And its something thats achievable in the not too distant future. we are pretty close now. And if you can manipulate those proliferative/inhibitory signals then you can make any hairs grow or not grow as thick or thin as you like. Whereas you might end up with androgen dependent scalp hairs if you tried to flip that genetic switch before the cells had made up there mind what they wanted to be. Engineering an individual to have scalp hairs that did not express androgen receptors would be the most elegant solution but this is not feasible at this point. It might be interesting to people at follica who are creating new follicles (a place where the alphabet soup and the developmental stage go hand in hand) but otherwise I think the idea of a honest to goodness “super-minox” is much more feasible.
» » But I now see more what you are getting at with I think.
»
» I don’t know any different ways to say it. I’ve been making this same
» point throughout this thread, and also on all the hairloss sites for years.
» I don’t know why you’ve had trouble understanding what I’m saying.
»
» » That you are interested in why some hairs express growth factors etc.
» But
» » with the evidence that androgens can destroy even occipital hairs in
» high
» » enough concentration I think theres a fair chance that all scalp hairs
» are
» » set up in such a way and that the differences in balding between
» different
» » areas of the scalp and different people could pretty much be explained
» in
» » terms of androgen receptor expression/sensitivity and local androgen
» levels
» » as is already the case.
»
» Exactly. But as I’ve said before, that doesn’t particularly interest me
» because it’s obvious and trivial. I want to know what accounts for the
» completely OPPOSITE response to androgens from one hair follicle to
» another, depending on body location.
OK. I suspect the answer wont be particularly profound though. Its always good to understand more about the process though and I am interested in the question of whether all scalp hair reacts in the same way as balding mens if it expresses androgen receptors that are sufficiently stimulated. A question I hadnt really considered before.
» » At any rate since dermal papillae wherein the bad
» » response originates are not replaced fromm cycle to cycle I dont think
» » there is that much that could be done to fundamentally change a “bad
» one”
» » to a “good one” them even if there are such things.
»
» Again, that’s just speculation. Let’s actually FIND OUT what accounts for
» the difference, before we go and declare that there’s no way to change a
» hair follicle from one kind to another.
Fair enough.
» » » Harold, come on, man. Pull your head out of the sand.
» »
» » I think I understand what you are saying now.
»
» Thank God!
It may have taken me a while but I am glad I got there in the end
» » At the same time, unless you
» » are planning to replace most of your existing follicles with new ones a
» la
» » Follica then I think you have to look at all that alphabet soup stuff.
» Cos
» » once that follicle has developed in such a way that it is going to
» produce
» » those genes in response to androgen you either have to keep it away
» from
» » androgens, interfere with the resulting production of those genes or
» » introduce a growth factor or other third party that is powerful enough
» to
» » overcome those negative signals.
»
» Time will tell. Until then, I’m certainly not going to assume that
» there’s no way to make one little alteration in the response of a hair
» follicle to a specific hormone.
In the meantime we will convert you to the way of the alphabet soup and have you digging through all those studies on TGF-Beta/wnt/EDAR etc
hh
.
» I think I hate this forum. Thats the 2nd long reply I have lost in a couple
» of days. This one seemed to go through. Anyway…
David thought he had a fix for the problem, but I just emailed him a while ago to let him know that it’s still not working…
» Well technically the androgen is the most upstream signal in this process.
» There is nothing upstream of that as the term upstream and downstream is
» used in terms of signal transduction. But now I know that you meant a
» developmental stage that occured before the hair follicle cells had
» committed to becoming hair follicle cells.
I’m using that term more generally than just in the context of “signal transduction”. I’m using it to describe a whole sequence of events, starting with the initial reason(s) for why hair follicles first become either suppressed, stimulated, or stay neutral to androgens.
» OK. But what causes one type to become one or the other has already been
» and gone by the time we are here to worry about it. Causing one hair
» follicle to change into another type of hair follicle once they have
» diffferentiated is like getting a skin cell to change into a muscle cell.
» Possible in the test tube perhaps but very tricky at the least in vivo.
I’m not so sure about all that. Time will tell.
» OK. I suspect the answer wont be particularly profound though.
Hey, I’m counting on that!
I suspect that the simpler the explanation is, the more likely it is that we’ll be able to formulate the Ultimate Treatment for MPB!
.