Understanding Androgenetic Alopecia

[Swoop]

What people really need to understand is that the assumptions made about transplantation, have never been properly tested!

The early studies accepted two possibilities. The survival of large follicles transplanted into the bald area, is either because of internal differences, or external effects caused by the procedure itself.

This is a very important point because the supporters of the traditional direct androgen action idea, quote transplantation as proving this. But the lack of confirmation testing, leaves this question open.

There is certainly no incentive for the proper testing of this question, within the industry itself. Think about this. Transplants have always been sold on the basis that the transplanted hair is different, and resistent to balding. If it was demonstrated that these hairs are not different, and it is the procedure that makes the difference what would happen?

Everone who has ever had a bad transplant procedure, would have have a legal case for misrepresentation. Think about the implications of that?

From the early transplantation studies using large grafts, and the much later experience of repairing these we get some insight.

The early large grafts suffered central hair loss, that looks just like the male pattern baldness process effecting alledged resistent follicles. These large grafts also suffered from a central swelling refered to as cobblestoning. There are so called explainations for these effects, but the time scale of the early studies is against these explainations.

The overall data suggests that the only follicles to survive long term in the male pattern baldness area, are those within scar tissue. This would indicate it is the procedure that makes the difference, and not internal follicle differences. This is also in line with the evolution of procedures towards small grafts.

Whatever any one's opinions, proper testing of this question is possible. Untill this is actually done, people should not just assume the answer here as is often the case in these debates.

Stop being drunk Foote. You sure make my day every time you post though. You think this for over 20 years now and are so convinced of your theory. You know what's the most funny thing about it all? That you are incompetent besides being ignorant too.

What stops you from buying a punch yourself for a few bucks and test this out yourself? It's easy as you know. Show to the world that a hair miniaturized hair follicle reverses to it's previous healthy state when transplanted to a other area. You will gain worldwide recognition and basically become a legend.

What stops you from doing this?

 

[Armando Jose]

This is a very important point because the supporters of the traditional direct androgen action idea, quote transplantation as proving this. But the lack of confirmation testing, leaves this question open.

There is certainly no incentive for the proper testing of this question, within the industry itself. Think about this. Transplants have always been sold on the basis that the transplanted hair is different, and resistent to balding. If it was demonstrated that these hairs are not different, and it is the procedure that makes the difference what would happen?

what would happen???
A big step in order understanding the process.......?

 

[Ventures]

- Why do hair follicles stay resistant when transplanted from the occipital scalp to the balding area?

So reasons why hair follicle transplanted from donor region doesn't miniaturise (and fall out) is:

• it is less genetically predisposed to DHT miniaturisation, because it contains less androgen receptors
• it produces less follicular DHT (inside Dermal papilla); http://www.ncbi.nlm.nih.gov/pubmed/9284093
  

Do you agree that both factors contribute to its resistance and permanent life cycle, and which factor is more important ? Another question, how many times is donor hair "more resistant" to DHT level than balding hair in the same individual. What I wanted to ask you, if a threshold for miniaturisation of balding hair is, lets say, 5 pmol/g, than what level of DHT concentration inside follicles can harm donor hair in the same person. Is this level two or three times greater than 5 pmol/g ? Apparently it seems that people with aggressive hair loss often tend to have thinning donor zone which means even 10-20% or even more of hair in that donor zone also miniaturise latter in life.

 

[brunobald]

"'Cept if he read page 2 he would have seen the link to the peer reviewed paper in Cell that demonstrated mice repopulate dpc's and the sheath with with viable cells and regrow follicles"

Is this for real, where is the study? If the cells are sensence/unviable then the mouse cells need to clear them before repopulating dpc's. Isn't this the crux of our problem. The mouse must be breaking the "sensence lock" to make space for new cells

 

[Fbalding84]

I am too fascinated by trying to implant a miniturized hair else where. I might work!

What if DHT causes enlarged sebum gland only causing the hair follicle to fight for space. I might be a possibility

 

[S Foote.]

Stop being drunk Foote. You sure make my day every time you post though. You think this for over 20 years now and are so convinced of your theory. You know what's the most funny thing about it all? That you are incompetent besides being ignorant too.

What stops you from buying a punch yourself for a few bucks and test this out yourself? It's easy as you know. Show to the world that a hair miniaturized hair follicle reverses to it's previous healthy state when transplanted to a other area. You will gain worldwide recognition and basically become a legend.

What stops you from doing this?

So that's your idea of a scientific argument then?

All you ever do is show people that when you are put on the spot, you just have nothing to say.

 

[Swoop]

So that's your idea of a scientific argument then?

All you ever do is show people that when you are put on the spot, you just have nothing to say.

I'm really not going to even argue with someone like you as I said before. You have been stomped into oblivion by several members in the past seeing from you post history. Now please stay out of this topic unless you have relevant questions to ask, not based on your fantasy hypothesis which is total nonsense. Do you want the world to prove otherwise, which has already been proven? Go for it, till then shut up !

- - - Updated - - -

So reasons why hair follicle transplanted from donor region doesn't miniaturise (and fall out) is:

• it is less genetically predisposed to DHT miniaturisation, because it contains less androgen receptors
• it produces less follicular DHT (inside Dermal papilla); http://www.ncbi.nlm.nih.gov/pubmed/9284093
  

Do you agree that both factors contribute to its resistance and permanent life cycle, and which factor is more important ? Another question, how many times is donor hair "more resistant" to DHT level than balding hair in the same individual. What I wanted to ask you, if a threshold for miniaturisation of balding hair is, lets say, 5 pmol/g, than what level of DHT concentration inside follicles can harm donor hair in the same person. Is this level two or three times greater than 5 pmol/g ? Apparently it seems that people with aggressive hair loss often tend to have thinning donor zone which means even 10-20% or even more of hair in that donor zone also miniaturise latter in life.

Hey ventures, I’ll explain it this way; DHT needs to bind to androgen receptors as you know. If there are no androgen receptors present DHT wouldn’t be able to exert any effect on the dermal papilla cells. The dermal papilla cells posses the androgen receptors of the hair follicle. The more DHT will attach to the androgen receptor the stronger the androgen receptor will be “activated”. As we see there is much evidence occurring of the androgen receptor having to play a role in this on a genetic basis in androgenetic alopecia. Let’s call this just “stress” in this one.

Every hair is really a mini-organ composed of many types of cells, stem cells, transit amplifying cells and progenitor cells. They are the building blocks of the hair follicle. In fact as you know cells are the building blocks of life.
I can’t answer all your questions herein, because we are all programmed differently, so are your cells within the hair follicle.

Androgenetic Alopecia is a polygenic inheritance too. In that sense, yes probably some people inherit strong genes that even their donor hair may be affected to some extent. To answer your question generally though, do I believe that there is a “threshold” for everyone when miniaturizing occurs?

Let me go further to explain this. The dermal papilla of the hair follicle is composed of around 3000 dermal papilla cells. They are seen as a extremely important master regulator of the hair follicle as you have read in my story. There is more literature on this too. Every cell of those 3000 is really a individual little machine, like all cells are.

You know sometimes people only start showing temple recession when they are older. That’s strange because testosterone levels decline when you get older and subsequently your DHT.

The dermal papilla cells, all 3000 of them will individually decide their cell fate under this stress and that really depends on the dosage and duration of exposure to the stress in Androgenetic Alopecia. This will differ in every individual. It’s not like all 3000 of them will say in synchronizing state we are going to senescent now! If that would happen you would lose your hair immediately and not even have a miniaturized hair shaft.

A other example is for instance when someone takes finasteride and if they are lucky they might turn their miniaturized hair follicle into a terminal hair follicle again. Again from a cell perspective it’s easy to explain this. You remove the threshold of stress from the cells and DNA repair genes can repair the cells if they didn’t create a lock yet. Sometimes it also happens that people take finasteride and see those small vellus – half terminal hair follicles. Yet they don’t want to grow any longer to the previous state. In that specific situation some cells already decided to not repair themselves and stay into a senescent state while some didn’t adopt this cell fate “lock” yet.

Every individual will differ in this. Hope that helps a bit.

 

[IDW2BB]

Perhaps we need to change the skin on the scalp as well as the hair that grows on it.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057739/



Full free text

 

[S Foote.]

I'm really not going to even argue with someone like you as I said before. You have been stomped into oblivion by several members in the past seeing from you post history. Now please stay out of this topic unless you have relevant questions to ask, not based on your fantasy hypothesis which is total nonsense. Do you want the world to prove otherwise, which has already been proven? Go for it, till then shut up !

You cannot answer my original question, so you think just flaming me will distract from it. You don't fool people with this. We hear all the same vague meaningless science jargon from you, that we have heard from many others over the years.

We all get sick of these after the fact pointless threads, that people like you post just to try to impress. I will ask my question again.

You claim in this thread that all these changes start with a direct androgen action upon follicle DP cells. So explain to us all how this happens, when it goes against everything that is recognised about direct hormone actions?

Why does this take many years to happen? Why is the action not a constant, in that it increases every hair cycle once it does start to happen? And why if you remove androgens almost completely, does the effect not change?

We know that all this is just not true, in cells that are known to be directly targeted by steroid hormones.

Scientists cannot explain all this, but your sure about it. So impress us all and just answer the question.

 

[Swoop]

You cannot answer my original question, so you think just flaming me will distract from it. You don't fool people with this. We hear all the same vague meaningless science jargon from you, that we have heard from many others over the years.

We all get sick of these after the fact pointless threads, that people like you post just to try to impress. I will ask my question again.

You claim in this thread that all these changes start with a direct androgen action upon follicle DP cells. So explain to us all how this happens, when it goes against everything that is recognised about direct hormone actions?

Why does this take many years to happen? Why is the action not a constant, in that it increases every hair cycle once it does start to happen? And why if you remove androgens almost completely, does the effect not change?

We know that all this is just not true, in cells that are known to be directly targeted by steroid hormones.

Scientists cannot explain all this, but your sure about it. So impress us all and just answer the question.

S. Foote I'm not going to respond to those dumb questions you troll, it's all described in this topic. Now hush back again. You are getting boring. One more time that you will ask dumb meaningless questions I'm going to PM a moderator. Ignorant old man .

 

[S Foote.]

S. Foote I'm not going to respond to those dumb questions you troll, it's all described in this topic. Now hush back again. You are getting boring. One more time that you will ask dumb meaningless questions I'm going to PM a moderator. Ignorant old man .

Everything you claim in this thread is based upon a direct action of androgens on follicle DP cells. I ask you how this works and you claim my question is not relevant, and say your going to report me to a moderator. I could post the PM you just sent me, and let people judge your sanity for themselves.

I think a moderator should explain to you what scientific debate is all about!

 

[maher]

Everything you claim in this thread is based upon a direct action of androgens on follicle DP cells. I ask you how this works and you claim my question is not relevant, and say your going to report me to a moderator. I could post the PM you just sent me, and let people judge your sanity for themselves.

I think a moderator should explain to you what scientific debate is all about!

Post it.

 

[Swoop]

Everything you claim in this thread is based upon a direct action of androgens on follicle DP cells. I ask you how this works and you claim my question is not relevant, and say your going to report me to a moderator. I could post the PM you just sent me, and let people judge your sanity for themselves.

I think a moderator should explain to you what scientific debate is all about!

That's the point you are really getting old or you are just trolling. I redirect here to TONS of literature which explain your question and there are literally going billions into this research. Your post history says it all troll. To answer your question read this paper in full;

http://link.springer.com/content/pdf/10.1007%2Fs00018-014-1691-3.pdf

If you have troubles with definitions or context of this paper you can ask.

 

[S Foote.]

That's the point you are really getting old or you are just trolling. I redirect here to TONS of literature which explain your question and there are literally going billions into this research. Your post history says it all troll. To answer your question read this paper in full;

http://link.springer.com/content/pdf/10.1007%2Fs00018-014-1691-3.pdf

If you have troubles with definitions or context of this paper you can ask.

Your unbelievable!

You post a thread titled "Understanding Androgenetic Alopecia " I ask you to explain the details of the androgen action that causes alopecia, and you claim the question is irrelevant!

Then finally you post a study about the consequences of cell senescence, that has nothing at all to do with the question of how androgens cause this in the first place!

I really don't know what its going to take, to make you understand a simple point?

You make a claim in this thread that androgens acting directly upon follicle cells, cause cell senescence and male pattern baldness. Your claim, so your responsibility to describe the process involved. This is how science works by the way!

You have yet to post any study here that explains what we can all see for ourselves. Why does the androgen action in male pattern baldness, take years before it happens? Direct hormone actions do not take years to happen!

- - - Updated - - -

Post it.

"S. Foote old man I think it's time to retire for you. If you ain't got relevant questions please stay out of my topic ok? If not I will be forced to PM a moderator. Thanks for your understanding. Swooping.

ps. I sure do a better job at "impressing" people than you LOL"

 

[Swoop]

Your unbelievable!

You post a thread titled "Understanding Androgenetic Alopecia " I ask you to explain the details of the androgen action that causes alopecia, and you claim the question is irrelevant!

Then finally you post a study about the consequences of cell senescence, that has nothing at all to do with the question of how androgens cause this in the first place!

I really don't know what its going to take, to make you understand a simple point?

You make a claim in this thread that androgens acting directly upon follicle cells, cause cell senescence and male pattern baldness. Your claim, so your responsibility to describe the process involved. This is how science works by the way!

You have yet to post any study here that explains what we can all see for ourselves. Why does the androgen action in male pattern baldness, take years before it happens? Direct hormone actions do not take years to happen!

- - - Updated - - -



"S. Foote old man I think it's time to retire for you. If you ain't got relevant questions please stay out of my topic ok? If not I will be forced to PM a moderator. Thanks for your understanding. Swooping.

ps. I sure do a better job at "impressing" people than you LOL"

Your unbelievable!

You post a thread titled "Understanding Androgenetic Alopecia " I ask you to explain the details of the androgen action that causes alopecia, and you claim the question is irrelevant!

Then finally you post a study about the consequences of cell senescence, that has nothing at all to do with the question of how androgens cause this in the first place!

I really don't know what its going to take, to make you understand a simple point?

You make a claim in this thread that androgens acting directly upon follicle cells, cause cell senescence and male pattern baldness. Your claim, so your responsibility to describe the process involved. This is how science works by the way!

You have yet to post any study here that explains what we can all see for ourselves. Why does the androgen action in male pattern baldness, take years before it happens? Direct hormone actions do not take years to happen!

- - - Updated - - -



"S. Foote old man I think it's time to retire for you. If you ain't got relevant questions please stay out of my topic ok? If not I will be forced to PM a moderator. Thanks for your understanding. Swooping.

ps. I sure do a better job at "impressing" people than you LOL"

In the study named “Premature Senescence of Balding Dermal Papilla Cells In Vitro Is Associated with p16INK4a Expression”(3). They confirmed as other studies already did(4) that balding dermal papilla cells grow way slower in vitro when compared to non-balding dermal papilla cells. Not only that they found out that balding dermal papilla cells undergo premature senescence. This was associated with the following in the balding dermal papilla cells;

- Increased Expression of p16ink4a
- Increased Expression of pRb
- Expression of senescence-associated β-galactosidase
- Loss of expression of bmi-1
- Increased expression of oxidative stress and dna damage markers like HSP-27, ATM and ATR

Now a study published in November 2014 called “ Androgen Receptor Accelerates Premature Senescence of Human Dermal Papilla Cells in Association with DNA Damage” (5) found ;

- Also a increase of p16ink4a in balding dermal papilla cells and not in non-balding in vitro
- DNA damage accompanied with senescence in the balding dermal papilla cells
- Most importantly when you remove the androgen receptor from the balding dermal papilla cells DNA damage does NOT occur and senescence does NOT occur.
- The dermal papilla cells changed in morphology, they enlarged.

A other study in 2009 called “Proliferation, DNA repair and apoptosis in androgenetic alopecia (6)” found out that in comparison with occipital scalp and frontal balding scalp;

- P53 was overexpressed frontal balding scalp
- P53 showed a inverse correlation with APE-1 (dna damage repair marker)

Another study called "Analysis of microRNA expression profile in 5α -dihydrotestosterone-treated normal human dermal papilla cells" (http://www.papersearch.net/view/deta...l_key=27731029)


Background: Clinical evidence shows that accumulation of 5 α-dihydrotestosterone(DHT) in dermal papilla cells(DPCs) is implicated in androgenetic alopecia. Objectives: To determine whether DHT affects cell growth, cell cycle arrest, cell death, senescence, and induction of reactive oxygen species(ROS), and whether these effects aremediated by microRNA(miRNA)-dependent mechanisms. Methods: We measured cell viability and cell cycle, detected ROS, and performed senescence-associated β-galactosidase assays in normal human DPCs(nHDPCs). Further, we performed miRNA expression profiling using miRNA microarray to determine whether changes in miRNA expression were associated with the cellular effects of DHT. Results: We found that DHT decreased cell growth by inducing cell death and G2 cell cycle arrest and by increasing ROS production and senescence in nHDPCs. 55 miRNAs were up-regulated and 6 miRNAs were down-regulated in DHT-treated nHDPCs. Bioinformatic analysis showed that putative target genes of these up- and down-regulated miRNAs were involved in cell growth, cell cycle arrest, cell death, senescence, and ROS production.

Conclusion: These results demonstrate that miRNA expression is altered in DHT-treated nHDPCs and suggest a potential mechanism of DHTinduced cell growth repression, cell cycle arrest, cell death, senescence, and ROS induction.

6 studies specifically related to Androgenetic Alopecia and senescence. Do you need more? I'll dig them up this week. Funny that you say this was known for ages because we couldn't even identify senescent cells till a few years ago because we didn't have the proper biological markers.

I never said I know the exact pathway which converge and set in the senescent pathways after AR transcription did I? But the evidence of senescence is clearly here simple as that. Therefore schematically;

DHT > AR > ROS/DNA DAMAGE? (pathways unknown, although I refer to literature here which could be possible, not saying that it is) > senescence regulators (p53,p16ink4a,pRB etc) > downstream signalling

What is so hard to understand Foote? Did I conduct those studies and show these senescent markers are over expressed in bald scalp? Did I show that balding DP cells in vitro undergo senescence where non balding DP don't show this? Did I show that balding DP upon receiving DHT suffer from dna damage.. etc etc? No I did not, several researchers did and this is very new and known only since like 5 years.

You can disagree/agree I honestly don't give a ****, but this is 100x more likely than your drunk hypothesis based on 0 facts and your old man fantasy from the 1990's. Simple as that. Well at least you got your answer now. If you furthermore think that these researchers are all lying, that's cool man. But they actually conducted research with biological marker screening both in vivo and in vitro while your hypothesis is based on N O T H I N G and quite impossible. You keep screaming for 20+ years now , but proved nothing till date :doh:. Those researchers actually do prove something.

 

[Ventures]

Swoop,

Thank you for your brief explanation and I appreciate your contribution on this thread as well as other members. Yes, indeed, androgen stimulus on genetically marked scalp hair follicles is certainly dominant reason for premature balding. And when I say premature I mean in 20s, 30s, 40s and even later in life. But in old age contact inhibition on dermal papilla might also play certain role since galea region is very tight. It might cause pure or low oxygen circulation even though yo mentioned DP cells enjoy low oxygen environment. Which actually is a bit of unexpected to me. Since some medications like minoxidil act as vasolidators of potassium channels and thus increase blood supply. How, else would you explain mechanism of minoxidil as hair loss medication, is it minoxidil act as vasolidator or, as some other members propose, it balances PGE2 levels ?


Another thing, is there any reason why only top of the head is affected by androgens ? I mean, we all agree, unless you have DUPA, androgens don't miniaturize donor hair ? Is there some reason why hair follicles oversensitive to androgens are located only on top of the head, but not in occipital region ? Is this just coincidence, or there must be some unexpected relation with galea region? On the other hand, it is interesting to note if you look at baby hair in early formation. The areas on a baby's head that are filled in last with hair are the ones that are hit by Androgenetic Alopecia/male pattern baldness first?

- is donor hair also susceptible to balding due to androgen stimulus. If you expose non-balding hair follicles to extra levels of T and DHT, would it start to miniaturize. Do you think that people who don't have male pattern baldness, have even donor hair more resistant to DHT, then people with male pattern baldness. Thus, people with standard male pattern baldness even have donor hair more susceptible to androgens.

- Do all affected hair follicles in male pattern baldness sufferer are equally susceptible/sensitive to balding, e.g. contan same number of AR in DP ? How do you explain pattern of male pattern baldness, which usually starts with temporal recession ? Why even some woman form mature hairline? Is this because Caucasians have more receptive front hair follicles, and that is why temples are first gone ?

- Why some men develop diffuse hair loss and some start recession, is that due to genetics or ?

- Is DHT only culprit, or all androgens exhibit negative effect on scalp hair ? I mean DHT has highest affinity towards AR located in prostate cells and hair follicles, right? But, T alone can also damage hair follciles ?

 

[S Foote.]

6 studies specifically related to Androgenetic Alopecia and senescence. Do you need more? I'll dig them up this week. Funny that you say this was known for ages because we couldn't even identify senescent cells till a few years ago because we didn't have the proper biological markers.

I never said I know the exact pathway which converge and set in the senescent pathways after AR transcription did I? But the evidence of senescence is clearly here simple as that. Therefore schematically;

DHT > AR > ROS/DNA DAMAGE? (pathways unknown, although I refer to literature here which could be possible, not saying that it is) > senescence regulators (p53,p16ink4a,pRB etc) > downstream signalling

What is so hard to understand Foote? Did I conduct those studies and show these senescent markers are over expressed in bald scalp? Did I show that balding DP cells in vitro undergo senescence where non balding DP don't show this? Did I show that balding DP upon receiving DHT suffer from dna damage.. etc etc? No I did not, several researchers did and this is very new and known only since like 5 years.

You can disagree/agree I honestly don't give a ****, but this is 100x more likely than your drunk hypothesis based on 0 facts and your old man fantasy from the 1990's. Simple as that. Well at least you got your answer now. If you furthermore think that these researchers are all lying, that's cool man. But they actually conducted research with biological marker screening both in vivo and in vitro while your hypothesis is based on N O T H I N G and quite impossible. You keep screaming for 20+ years now , but proved nothing till date :doh:. Those researchers actually do prove something.

I knew you just would not get the point here, as it requires some original thinking!

As I have said many times, I have no problem with the validity of any of the studies you post. The big problem is they all look at follicle cells after the change. These studies tell us nothing about how we get from point A to point B.

Androgens and perhaps tomato sauce could show direct effects on senescence in male pattern baldness cell samples. This tells us nothing about how these first got to be male pattern baldness cells!!

Even professional scientists make a big assumption here. Just because androgens are known to be involved, the assumption is that the actual change from healthy large follicles to male pattern baldness follicles is a direct action of androgens.

The reality is that non of the follicle samples of various growth types, are "changed" from one growth type to another by direct androgen exposure. Full growth scalp follicles known to be future male pattern baldness follicles, are not changed into male pattern baldness follicles by direct androgen action in-vitro.

This has to be explained, as such a delayed direct action is not recognised in cells that are known to be directly hormone responsive to "CHANGE".

Anyway you don't understand the issue OK have a nice thread.

 

[maher]

Swoop,

Thank you for your brief explanation and I appreciate your contribution on this thread as well as other members. Yes, indeed, androgen stimulus on genetically marked scalp hair follicles is certainly dominant reason for premature balding. And when I say premature I mean in 20s, 30s, 40s and even later in life. But in old age contact inhibition on dermal papilla might also play certain role since galea region is very tight. It might cause pure or low oxygen circulation even though yo mentioned DP cells enjoy low oxygen environment. Which actually is a bit of unexpected to me. Since some medications like minoxidil act as vasolidators of potassium channels and thus increase blood supply. How, else would you explain mechanism of minoxidil as hair loss medication, is it minoxidil act as vasolidator or, as some other members propose, it balances PGE2 levels ?


Another thing, is there any reason why only top of the head is affected by androgens ? I mean, we all agree, unless you have DUPA, androgens don't miniaturize donor hair ? Is there some reason why hair follicles oversensitive to androgens are located only on top of the head, but not in occipital region ? Is this just coincidence, or there must be some unexpected relation with galea region? On the other hand, it is interesting to note if you look at baby hair in early formation. The areas on a baby's head that are filled in last with hair are the ones that are hit by Androgenetic Alopecia/male pattern baldness first?

- is donor hair also susceptible to balding due to androgen stimulus. If you expose non-balding hair follicles to extra levels of T and DHT, would it start to miniaturize. Do you think that people who don't have male pattern baldness, have even donor hair more resistant to DHT, then people with male pattern baldness. Thus, people with standard male pattern baldness even have donor hair more susceptible to androgens.

- Do all affected hair follicles in male pattern baldness sufferer are equally susceptible/sensitive to balding, e.g. contan same number of AR in DP ? How do you explain pattern of male pattern baldness, which usually starts with temporal recession ? Why even some woman form mature hairline? Is this because Caucasians have more receptive front hair follicles, and that is why temples are first gone ?

- Why some men develop diffuse hair loss and some start recession, is that due to genetics or ?

- Is DHT only culprit, or all androgens exhibit negative effect on scalp hair ? I mean DHT has highest affinity towards AR located in prostate cells and hair follicles, right? But, T alone can also damage hair follciles ?

Actually,. his "explanation" was anything but brief. This study answers many of your questions:

A PGD synthase-positive mast cell gradient characterizes scalp patterning


A PGD synthase-positive mast cell gradient characterizes scalp patterning:

"We found significantly more dermal mast cells immunoreactive for prostaglandin d-synthase in the vertex compared to the lateral aspects of the scalp, with a decrement that spatially approximated the pattern of androgenetic alopecia. This difference was present in both balding and non-balding scalps and was independent of gender. Dual labeling established dermal cells expressing prostaglandin d-synthase as mast cells"

CONCLUSIONS:These data indicate that scalp is spatially programmed via mast cell prostaglandin d-synthase distribution in a manner reminiscent of the pattern seen in androgenetic alopecia.

http://www.ncbi.nlm.nih.gov/pubmed/24438498

 

[Armando Jose]

Interesting study, but even Hamilton used more subjects


I am wondering if they tested it in childrens with healthy scalp and hair? differebces between sexes?

More investigation .....

 

[Nadester]

Would anyone look into LOSARTAN?? Its a blood pressure pill.It down regulated the TGFB receptor something in the kidneys of mice.I don't know how good or even relevant it is but we are talking about inhibition and all sciency here right?