Hair Loss - My "theory" of baldness.....................

Hair Transplant Patient Reviews

benji

08.04.2008, 20:33

My "theory" of baldness..................... (Topicals)
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For any of you who may be newbies wondering about baldness-------------you inherit a variant of the androgen receptor gene that can express itself more or less strongly depending on genetic chance. If it expresses itself strongly with CAG-repeates, the hair outside your wreaths androgen receptor's are much more adept at uptaking male hormone, especially dihydrotestosterone. Having alot of DHT in the scalp tissue (bald men have been shown to have more DHT in their scalps, but not in the blood, indicating that the alpha five reductase enzymes in the root sheaths of each and ever hair follicle on your head are probably more active than a guy with all his hair) has been shown to be able to invigorate androgen receptors even MORE. One too much androgen is uptaken..............eventually something happens to the hair follicle and a different set of genetic instructions are obeyed within it. The dermal papilla starts cranking out way too much DKK_1, which leads to the cell death of the keratincoyetes in the root sheath........................these dead cells in turn hanging around the infidulum is probably why the immune system begins attacking the hair follicle and TGF beta and excessive collagenous deposition is downstream from it. That is probably "baldness", as the immune system is going to try to eliminate dead cells and anything around the area is going to be effected by all the infllammatory subtstances the immune system will use. Baldness looks like organ rejection microscopically. Its been shown that wreath area hairs can succumb to testosterone and DHT if experiments give enough of them to the hairs.......................so I dont believe their is some magic difference in the hair's basic characteristics but a difference in the amount of DHT the hair can make via its alpha five reductase enzyme in their root sheaths and a big difference in how well the hairs androgen receptors work and how chemcially stable they are. In a way male baldness is probably because you have too-well-working-androgen-receptors and too-well-working-alpha-five-reductase-enzymes in your hair. You are "too manly" in a place you dont want to be.

Obviously, "my theory" places the blame at DKK-1's doorstep, but its all because of too-well working androgen receptors and too well working alpha five reductase enzymes. I honestly think if you could get Brad Pitts hair to uptake the amount of androgen our follicles uptake...............he'd be going bald too, by the same mechanisms we are for the most part dependent on the intesitity of his immune systems response. Its known that the variant of the androgen receptor gene is located on the x-chromosome and comes from your mother, but the other genes in baldness are autologous (or are thought to be) and aren't parent specific. Too many androgens duing fetal development may play a role. We will know if someone ever does a study on digit ratios and baldness in a large population. Im guessing at least a small correlation will be found myself.

benji is located in [NA] and he is available to meet: NO

benji

10.07.2008, 21:34

@ UWbio
My "theory" of baldness.....................
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� � But there remains the little problem of explaining why it is that
� � androgens stimulate the growth of (most) body hair, but
� � suppress the growth of scalp hair. That _does_ sound to me like
� a
� � magic difference in the hair follicles' basic characteristics! ;-)
�
� Well of course there is a difference in scalp hair follicles as opposed to
� body hair follicles. In fact there appears to be a relatively large
� difference amongst the various hair follicles on the front and top of the
� scalp compared with the sides and back!
�
� Here's one attempt to explain a couple of things:
�
� The androgen receptor has been shown to bind STAT proteins and in
� particular Stat3. Stat3 regulates growth of many stem cell populations from
� the gut to the brain and I would not be surprised if it regulated growth in
� follicular stem cells as well. When the androgen receptor is active, ie DHT
� is bound to it, and also bound to the activated Stat3 it can act as a
� repressor of many genes. This is in opposition to free Stat3, which
� typically turns on genes (hence the name Signal Transducer and Activator of
� Transcription).
�
� When EGF binds it's receptor it activates Stat proteins (by activating
� Jak2, Src, and various other proteins). So if you have a lot of active
� androgen receptors around and you have activated Stats then you get
� repression of growth. If you inhibit either pathway you get normal growth
� again, such as 5-alpha reductase inhibitors and EGFR inhibitors both of
� which have been talked about for a while now for use in hair loss.
� Activated Stats can induce many pro-inflammatory proteins as well, which
� has also been a concern in hair loss, and may be another reason why EGFR
� inhibitors might work. Maybe balding scalps express more of the EGF
� receptor than do other follicles or non-balding individuals. That said it
� seems as if Stat3 is particularly necessary for stem cells to remain stem
� cells because removal of EGF signaling can cause differentiation. Depletion
� of all stem cells via differentiation is no good either because you would
� not be able to regenerate a new follicle. So...who knows, maybe an EGFR
� inhibitor will be ok as long as it isn't too potent or maybe it won't work
� at all, but an androgen receptor inhibitor or 5-alpha reductase inhibitor
� should always be beneficial for balding scalps.
�
� The Wnt, BMP, Notch, and SHH pathways are all also implicated very
� strongly in hair loss (and it is my sneaking suspicion, for reasons I have
� gone into in the past, that the Wnt pathway is the most important pathway
� to look at for regeneration of normal sized follicles).
�
� So all in all it is extremely complicated but at least more and more
� research is coming out to help aid us in finding the right direction to
� pursue in solving the mystery of how to regenerate follicles.

very interesting information uwbio, thank you for posting it

benji is located in [NA] and he is available to meet: NO

UWbio

10.07.2008, 17:28

@ Bryan
My "theory" of baldness.....................
Post reply

� But there remains the little problem of explaining why it is that
� androgens stimulate the growth of (most) body hair, but
� suppress the growth of scalp hair. That _does_ sound to me like a
� magic difference in the hair follicles' basic characteristics! ;-)

Well of course there is a difference in scalp hair follicles as opposed to body hair follicles. In fact there appears to be a relatively large difference amongst the various hair follicles on the front and top of the scalp compared with the sides and back!

Here's one attempt to explain a couple of things:

The androgen receptor has been shown to bind STAT proteins and in particular Stat3. Stat3 regulates growth of many stem cell populations from the gut to the brain and I would not be surprised if it regulated growth in follicular stem cells as well. When the androgen receptor is active, ie DHT is bound to it, and also bound to the activated Stat3 it can act as a repressor of many genes. This is in opposition to free Stat3, which typically turns on genes (hence the name Signal Transducer and Activator of Transcription).

When EGF binds it's receptor it activates Stat proteins (by activating Jak2, Src, and various other proteins). So if you have a lot of active androgen receptors around and you have activated Stats then you get repression of growth. If you inhibit either pathway you get normal growth again, such as 5-alpha reductase inhibitors and EGFR inhibitors both of which have been talked about for a while now for use in hair loss. Activated Stats can induce many pro-inflammatory proteins as well, which has also been a concern in hair loss, and may be another reason why EGFR inhibitors might work. Maybe balding scalps express more of the EGF receptor than do other follicles or non-balding individuals. That said it seems as if Stat3 is particularly necessary for stem cells to remain stem cells because removal of EGF signaling can cause differentiation. Depletion of all stem cells via differentiation is no good either because you would not be able to regenerate a new follicle. So...who knows, maybe an EGFR inhibitor will be ok as long as it isn't too potent or maybe it won't work at all, but an androgen receptor inhibitor or 5-alpha reductase inhibitor should always be beneficial for balding scalps.

The Wnt, BMP, Notch, and SHH pathways are all also implicated very strongly in hair loss (and it is my sneaking suspicion, for reasons I have gone into in the past, that the Wnt pathway is the most important pathway to look at for regeneration of normal sized follicles).

So all in all it is extremely complicated but at least more and more research is coming out to help aid us in finding the right direction to pursue in solving the mystery of how to regenerate follicles.

UWbio is located in [NA] and he is available to meet: NO

Bryan

10.07.2008, 04:09

@ JamesJ
Let's focus on the FUNDAMENTALS, not the little details
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� � But that IS the reason for balding: scalp follicles are
� � damaged by androgens.
�
� Not ALL scalp follicles are damages by androgens, only some.

The best available evidence now seems to indicate that all scalp hair follicles are damaged by androgens. Some are more damaged than others. At first glance, some don't appear to be damaged by androgens, but they are if you raise the level high enough.

� And the ones that are damaged form a specific pattern. Hmm... ;-)

Correct. They don't understand the reason(s) for the pattern yet, but they're working on it.

.

Bryan is located in [NA] and he is available to meet: NO

JamesJ

09.07.2008, 22:47

@ Bryan
Let's focus on the FUNDAMENTALS, not the little details
Post reply

� But that IS the reason for balding: scalp follicles are damaged by
� androgens.

Not ALL scalp follicles are damages by androgens, only some. And the ones that are damaged form a specific pattern. Hmm... ;-)

JamesJ is located in [NA] and he is available to meet: NO

Bryan

05.07.2008, 19:47

@ JamesJ
Let's focus on the FUNDAMENTALS, not the little details
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� You'd think with that information, scientists would focus more on the
� genetic structure of each of the two follicles rather than trying to
� determine what causes the follicle to die off. I know that there are some
� studies that claim DHT is part of the cause, but since DHT is systemic, all
� follicles are exposed. This leads me to believe that DHT is not bad.

Well, I didn't bother to state the obvious, which is that the difference between scalp hair follicles and body hair follicles is that the former are suppressed by androgens, and the latter are stimulated by them. Scientists don't yet understand the specific biochemical reason(s) for that, but they're working on it as we speak.

But that IS the reason for balding: scalp follicles are damaged by androgens.

.

Bryan is located in [NA] and he is available to meet: NO

JamesJ

05.07.2008, 19:14

@ Bryan
Let's focus on the FUNDAMENTALS, not the little details
Post reply

� � What amazes me is that there's a follicle that ceases to produce hair
� � right next to the one that will ALWAYS produce hair. If we can identify
� the
� � differences between the two, then I'd say a cure wouldn't be too far
� away
� � from that discovery.
�
� You got THAT right! :-)
�
� � The general pattern of hair loss should be a clue (the horseshoe).
� � Why hasn't anyone figured out the reason for the pattern? Has
� � there ever been a test where a follicle on the top of the head was
� � transplanted to the side of a balding person? Did it survive?
�
� Something even better than THAT was done: in the famous Nordstrom study,
� balding hair follicles from the scalp were transplanted to a subject's arm,
� and they continued balding at the same rate as they did while they were
� still on his scalp! ;-) That pretty much settles the issue once and for
� all, and proves that there is something inherent to each individual
� hair follicle that causes balding. It disproves the various cuckoo
� theories about local "pressure" in the scalp skin causing balding, the
� old-fashioned "galea" theory, etc.

You'd think with that information, scientists would focus more on the genetic structure of each of the two follicles rather than trying to determine what causes the follicle to die off. I know that there are some studies that claim DHT is part of the cause, but since DHT is systemic, all follicles are exposed. This leads me to believe that DHT is not bad. It's probably needed in the system for something. It's like the sun and someone with a fair complexion. The person with the fair complexion will take more damage than the person with a darker complexion. It's the genetic structure of the skin that matters, not the sun.

JamesJ is located in [NA] and he is available to meet: NO

Bryan

02.07.2008, 12:29

@ JamesJ
Let's focus on the FUNDAMENTALS, not the little details
Post reply

� What amazes me is that there's a follicle that ceases to produce hair
� right next to the one that will ALWAYS produce hair. If we can identify the
� differences between the two, then I'd say a cure wouldn't be too far away
� from that discovery.

You got THAT right! :-)

� The general pattern of hair loss should be a clue (the horseshoe).
� Why hasn't anyone figured out the reason for the pattern? Has
� there ever been a test where a follicle on the top of the head was
� transplanted to the side of a balding person? Did it survive?

Something even better than THAT was done: in the famous Nordstrom study, balding hair follicles from the scalp were transplanted to a subject's arm, and they continued balding at the same rate as they did while they were still on his scalp! ;-) That pretty much settles the issue once and for all, and proves that there is something inherent to each individual hair follicle that causes balding. It disproves the various cuckoo theories about local "pressure" in the scalp skin causing balding, the old-fashioned "galea" theory, etc.

.

Bryan is located in [NA] and he is available to meet: NO

Bryan

02.07.2008, 12:18

@ Ignatius
Let's focus on the FUNDAMENTALS, not the little details
Post reply

� Maybe the problem is that scalp hair follicles in men with MBP start
� responding similarly] to body hair rather then oppositely.
�
� In men with MBP scalp hair miniaturizes under the influence of DHT, so in
� a way it becomes more like body hair.

Huh? Are you implying that when scalp hair starts becoming thinner and shorter due to balding, they're becoming "more like body hair" as a result?? :-)

.

Bryan is located in [NA] and he is available to meet: NO

HanginInThere

Hair loss University,
01.07.2008, 14:32

@ benji
TAGOHL, ..... (Follica and new genetic information)
Post reply

� � Benji, thanks for the info -- very interesting. I need to ponder all
� this
� � stuff. Here's a couple more abstracts. The first one is another recent
� � genetic study which shows that a polymorphism in the ectodysplasin-A
� � receptor gene is what gives Asians thick hair. The second study shows
� that
� � ectodysplasin helps control the switch from anagen to catagen (early
� � termination of anagen -- short growth cycles -- are a feature of MPB).
� � Gene therapy for baldness would be really, really nice if it happens
� � someday.
� �
� � Hum Mol Genet. 2008 Mar 15;17(6):835-43.
� �
� � A scan for genetic determinants of human hair morphology: EDAR is
� � associated with Asian hair thickness.
� �
� � Department of Human Genetics, Graduate School of Medicine, The
� University
� � of Tokyo, Hongo, Tokyo, Japan.
� �
� � Hair morphology is one of the most differentiated traits among human
� � populations. However, genetic backgrounds of hair morphological
� � differences among populations have not been clarified yet. In addition,
� � little is known about the evolutionary forces that have acted on hair
� � morphology. To identify hair morphology-determining genes, the levels
� of
� � local genetic differentiation in 170 genes that are related to hair
� � morphogenesis were evaluated by using data from the International
� HapMap
� � project. Among highly differentiated genes, ectodysplasin A receptor
� � (EDAR) harboring an Asian-specific non-synonymous single nucleotide
� � polymorphism (1540T/C, 370Val/Ala) was identified as a strong
� candidate.
� � Association studies between genotypes and hair morphology revealed that
� � the Asian-specific 1540C allele is associated with increase in hair
� � thickness. Reporter gene assays suggested that 1540T/C affects the
� � activity of the downstream transcription factor NF-kappaB. It was
� inferred
� � from geographic distribution of 1540T/C and the long-range haplotype
� test
� � that 1540C arose after the divergence of Asians from Europeans and its
� � frequency has rapidly increased in East Asian populations. These
� findings
� � lead us to conclude that EDAR is a major genetic determinant of Asian
� hair
� � thickness and the 1540C allele spread through Asian populations due to
� � recent positive selection.
� �
� � PMID: 18065779 [PubMed - in process]
� �
� � Involvement of the Edar signaling in the control of hair follicle
� � involution (catagen).
� �
� � Department of Dermatology, Boston University School of Medicine, 609
� � Albany St., Boston, MA 02118, USA.
� �
� � Ectodysplasin (Eda) and its receptor (Edar) are required for normal
� � development of several ectodermal derivatives including hair follicles
� � (HFs). Here, we show that during the murine hair cycle the expression
� of
� � Eda A1, Edar, Edaradd, and TRAF6 transcripts are minimal in the resting
� � phase and maximal during HF transition from active growth to regression
� � (catagen). Eda A1 mRNA and Edar proteins were expressed in the hair
� matrix
� � and outer and inner root sheaths of anagen HFs. During catagen, Eda A1
� mRNA
� � and Edar protein were expressed in the outer and inner root sheaths and
� � later in the secondary hair germ. Catagen development accompanied by
� � increased apoptosis in the outer root sheath was significantly
� accelerated
� � in downless mice or after treatment of wild-type mice by a fusion
� protein
� � that inhibits Edar signaling, compared with the corresponding controls.
� � Microarray, real-time polymerase chain reaction, and
� immunohistochemical
� � analyses of skin of downless mice revealed a strong decrease of
� expression
� � of X-linked inhibitor of apoptosis protein (XIAP), compared with the
� � controls, suggesting XIAP as a target for Edar signaling. Thus, our
� data
� � demonstrate that in addition to its well-established role in HF
� � morphogenesis, Edar signaling is also involved in hair cycle control
� and
� � regulates apoptosis in HF keratinocytes during catagen.
� �
� � PMID: 17148670 [PubMed - indexed for MEDLINE]
�
�
�
�
� This is profoundly interesting information. Its the type of literal proof
� I'd always thought they'd be finding "someday" about how genetics directly
� controls hair thickness, hairlines, shapes of wreaths, etc. I noticed that
� the Edar signalling was implicated "involved in hair cycle control and
� � regulates apoptosis in HF keratinocytes during catagen". Its the
� keratinocyte cell death that is intriguing to me for the reason that I
� think it just might be dead keratinocyte cells in the infidula downstream
� of DKK1, that might get the immune system interested in the follicle. If
� men with baldness lack XIAP, the "X-linked inhibitor of apoptosis protien"
� or have much less of it genetically, perhaps its why DKK-1 is so
� detrimental to our follicles over other men.
�
� What is intriguing to me personally is
� this................what could Follica do if a way to upregulate the
� "Asian-specific non-synonymous single nucleotide
� � polymorphism (1540T/C, 370Val/Ala)" or include it in their topical or
� internal after the skin-re-epilithialization period in their process
� someday, and "give" the new hair made great hair genetics no matter where
� its made.
�
�
� Ive went on and on (Im sure youve seen it) about my "inkling" that Follica
� might be able to make very good hair back in the donor area of men
� post-FUE..............but might make hair that is just like MPB hair or
� might make thinner weaker hairs in MPB scalp due to all the genes that
� might be at play in the frontal scalp vs. donor scalp. Its a
� "defeatist"-kinda thought, but all the razzmatazz of promising treatments
� over the years have left me looking for ways things might fail vs. how they
� might succeed. ICX, for example (and Aderans), now honestly appear to be at
� least five years away in the best-case scenario to me now----if indeed
� within the next 10.
�
� I'll never forget a doctor going over baldness with me when I was 25, and
� how he said "let me show you something" and he ran his finger up the side
� of my head and told me you can "feel" where you wreath is going to start
� genetically because the hair will start feeling different (weaker) at a
� certain point. It did. This was before I got on finasteride. Now the
� "change" in feeling is much more subtle, but it was pretty obvious then.
� Ive seen Washenik discuss how the skin grows up over the top of the scalp
� in fetal development and how one's pattern seems to be determined during
� this time. It all seems so profoundly genetically hard-wired to me. Its
� amazing how genes work. 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.

you need to take a class on genetics
then you will understand more the intricacies of gene mixing

HanginInThere is located in HAIR LOSS UNIVERSITY and he is available to meet: NO
---
Hangin Regimen...........

Maxi Hair by Country Life 2/day
Kal Amino Max ..Chelated Multi Mineral..2/day

DHT blockers (daily intake)
Saw Palmetto, 320mg Standardized
Pygeum 500mg
Nettles 500mg
Beta Sitosterol 125mg

Ignatius

01.07.2008, 05:03

@ JamesJ
Let's focus on the FUNDAMENTALS, not the little details
Post reply

� Bryan:
� 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.

Maybe the problem is that scalp hair follicles in men with MBP start responding similarly] to body hair rather then oppositely.

In men with MBP scalp hair miniaturizes under the influence of DHT, so in a way it becomes more like body hair.The pattern in which this occurs is then related to genetics, just like expression of hair on the rest of your body.

Ignatius is located in [NA] and he is available to meet: NO

JamesJ

03.06.2008, 00:13

@ Bryan
Let's focus on the FUNDAMENTALS, not the little details
Post reply

Bryan:
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.

I'm a bit more interested in the fundamental differences in the scalp hair follicles that are more susceptible to hair loss and the scalp hair follicles that are not. Meaning, the sides and back of the head. Body hair seems further apart in relationship to scalp hair (i.e. the characteristics are different).

What amazes me is that there's a follicle that ceases to produce hair right next to the one that will ALWAYS produce hair. If we can identify the differences between the two, then I'd say a cure wouldn't be too far away from that discovery. The general pattern of hair loss should be a clue (the horseshoe). Why hasn't anyone figured out the reason for the pattern? Has there ever been a test where a follicle on the top of the head was transplanted to the side of a balding person? Did it survive?

JamesJ is located in [NA] and he is available to meet: NO

haroldo

21.04.2008, 02:19

@ Bryan
Let's focus on the FUNDAMENTALS, not the little details
Post reply

� � 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...

Cool.

� � 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. A tricky area but yeah this is a problem/question the Follica guys are going to run into and examine before too long so I think the chances are good that we might have the beginnings of an answer and possibly an idea of how it might be controlled within a couple of years. Which is pretty good.

� � 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.

True.

� � 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! :-)

Indeed. It would be nice if the Gods of Hairlosss Research smiled upon us true believers for once
As I mentioned one of the biggest questions around the Follica technique will be are the new hair follicles as DHT sensitive as the previous follicles in the area. If they are then I suspect they will at least begin trying to figure out why they are and if that can be changed (they seemed to figure out the pigmented/unpigmented hair thing pretty quickly). If not they may not worry about it too much. So the good news is that people should be looking into this very question. Fingers crossed.
hh

haroldo is located in [NA] and he is available to meet: NO

Bryan

19.04.2008, 17:39

@ haroldo
Let's focus on the FUNDAMENTALS, not the little details
Post reply

� 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! :-)

.

Bryan is located in [NA] and he is available to meet: NO

Bryan

19.04.2008, 16:36
(edited by Bryan, 19.04.2008, 17:25)

@ haroldo
Let's focus on the FUNDAMENTALS, not the little details
Post reply

.

Bryan is located in [NA] and he is available to meet: NO

haroldo

18.04.2008, 10:32

@ Bryan
Let's focus on the FUNDAMENTALS, not the little details
Post reply

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!! :-D
�
� 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"?? :-P

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

haroldo is located in [NA] and he is available to meet: NO

benji

18.04.2008, 01:07

@ Bryan
Let's focus on the FUNDAMENTALS, not the little details
Post reply

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

benji is located in [NA] and he is available to meet: NO

Bryan

17.04.2008, 23:02
(edited by Bryan, 17.04.2008, 23:09)

@ Bryan
Let's focus on the FUNDAMENTALS, not the little details
Post reply

.

Bryan is located in [NA] and he is available to meet: NO

Bryan

17.04.2008, 22:46
(edited by Bryan, 17.04.2008, 23:05)

@ haroldo
Let's focus on the FUNDAMENTALS, not the little details
Post reply

� � 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!! :-D

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"?? :-P

� 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.

.

Bryan is located in [NA] and he is available to meet: NO

haroldo

17.04.2008, 05:37

@ Bryan
Let's focus on the FUNDAMENTALS, not the little details
Post reply

� � 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?? :-P
� �
� � 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! :confused:

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

haroldo is located in [NA] and he is available to meet: NO

Bryan

16.04.2008, 23:16

@ benji
Let's focus on the FUNDAMENTALS, not the little details
Post reply

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.

.

Bryan is located in [NA] and he is available to meet: NO

benji

16.04.2008, 22:56

@ Bryan
Let's focus on the FUNDAMENTALS, not the little details
Post reply

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: :ok: ) if it was.

benji is located in [NA] and he is available to meet: NO

Bryan

16.04.2008, 22:25

@ haroldo
Let's focus on the FUNDAMENTALS, not the little details
Post reply

� 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?? :-P
�
� 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! :confused:

� 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 is located in [NA] and he is available to meet: NO

haroldo

16.04.2008, 14:42

@ Bryan
Let's focus on the FUNDAMENTALS, not the little details
Post reply

� � � 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?? :-P

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.

haroldo is located in [NA] and he is available to meet: NO

Bryan

16.04.2008, 05:44
(edited by Bryan, 16.04.2008, 06:01)

@ haroldo
Let's focus on the FUNDAMENTALS, not the little details
Post reply

� � 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?? :-P

� 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.

.

Bryan is located in [NA] and he is available to meet: NO

haroldo

16.04.2008, 03:59

@ Bryan
Let's focus on the FUNDAMENTALS, not the little details
Post reply

� � 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?? :angry:

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

haroldo is located in [NA] and he is available to meet: NO

Bryan

15.04.2008, 15:35

@ haroldo
Let's focus on the FUNDAMENTALS, not the little details
Post reply

� 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?? :angry:

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.

.

Bryan is located in [NA] and he is available to meet: NO

haroldo

15.04.2008, 01:45

@ Bryan
Let's focus on the FUNDAMENTALS, not the little details