New clinical trial intended to prove the Androgenetic Alopecia theory.

[freakout]

Tell me, are you and finfighter the same person?

 

[hairhoper]

No, as an admin could easily verify.

More than 1 person has a problem with your logic, believe it or not.

Are you able to address the questions in my previous post?

 

[freakout]

Which begs the question, where is the massive leap of logic to say that any of this somehow disproves Androgenetic Alopecia theory as you claim it does?

You're just like you best friend. I never said it disproved Androgenetic Alopecia. It only indicates something is amiss in Androgenetic Alopecia.

Talk to your best friend, Mr. finasteride. Ask your flipflopper friend why he jumped from Androgenetic Alopecia to immunologic.

Furthermore, I don't have to explain myself to you. Those researchers DISCOUNTED DHT as the inhibiting factor.

PROVE THEM WRONG!! NOT ME.

Don't call me idiot unless you prove yourself to have a higher level of comprehension.

 

[hairhoper]

Furthermore, I don't have to explain myself to you. Those researchers DISCOUNTED DHT as the inhibiting factor.

No they didn't, that's my point. Nowhere do they say that. You're trying to misconstrue a study.

If you come onto a public forum mainly frequented by young men looking for advice then you do have to explain yourself when you make the statements you've been making. If you don't you will be challenged on it.

DHT has no direct effect on hair follicles - this is supported by an in vivo study few of you have heard of. Read! viewtopic.php?p=611106

A read through of the abstract and conclusions of the study clearly shows it has absolutely nothing to do with disproving that androgens directly affect hair follicles. Nowhere do they make a claim remotely like that in your signature.

I never said it disproved Androgenetic Alopecia. It only indicates something is amiss in Androgenetic Alopecia.

But you've made such statements several times, like in your signature where this study seems to be the only thing you are referencing to try and back up exactly that idea.

DHT has no direct effect on hair follicles - this is supported by an in vivo study few of you have heard of. Read! viewtopic.php?p=611106
Follicles are also immune-privileged. Androgenetics IS Junk Science

As for...

Don't call me idiot unless you prove yourself to have a higher level of comprehension.

I'm not calling you an idiot. I'm asking you to backup your points. I believe I've shown a far greater comprehension of the study you're quoting than you have.

 

[Bryan]

Oh really?? How was the link to DHT "discovered by accident"? (I can already hear other forum members beginning to laugh as I ask this question!)

Let me guess, they knew beforehand that DHT was causing this without any testing because science is based on absolute knowledge beforehand.

I don't know about "DHT" specifically, but we do know since the early studies of Hamilton in the 1940's that androgenic male hormone is definitely a requirement for male pattern baldness. To use Hamilton's own words in the title of one of his most important studies, male hormone (and DHT) is "an incitant and a prerequisite" for male pattern balding. Focus on the word "prerequisite": without sufficient male hormone, balding due to androgenetic alopecia doesn't occur.

You may laugh, but most discoveries were based on accidental discoveries because science isn't known beforehand regardless of what you may believe.

And do you suppose that that pertains to DHT, too, or things that suppress DHT?

Hell, most of the things you are using now were discovered to work against male pattern baldness(I think the male is a misnomer as it affects both sexes) by accident.

Once again: do you think that pertains to things that suppress DHT, too?

You're obviously a newbie here, because this specific issue has already been discussed over and over and over. Young boys (shortly after puberty) don't all immediately go bald for the simple reason that their hair follicles don't become sensitive to androgens until later in life. It's not just the overall level of androgens that causes balding, it's also the sensitivity to androgens in a given individual that determines whether (and how rapidly) he goes bald.

So now you are referring to epigenetics and how gene expression changes after puberty. Now the question would be what causes this change in gene expression, whether it is just DHT "maturing" the gene(could be, especially if hairloss can be defined as a secondary sex characteristics) or if it is outside factors.

I'm not sure if I'm referring to "epigenetics" or changes in "gene expression". All I know is that the sensitivity to androgens of scalp hair follicles changes over a period of time, for whatever reason(s). I can't say anything specific about exactly why that happens, just that it does.

By the way, ad hominem attacks("obviously a newbie" and so on) are no way to further actual discovery of what creates this condition in the first place or to engage in actual discourse. We are not playing King(or queen in my case) of the hill, but trying to unravel what might be causing this to begin with.

That wasn't an "attack" when I called you a newbie, I was just stating a fact. We've discussed the sensitivity to androgens of hair follicles a great many times over the years, and for you to wonder why all teenagers don't automatically go bald right after puberty was a very glaring indication to me that you're a newbie here!

 

[freakout]

The study team said "the existence of an inhibitor factor other than androgens" in humans.

So tell me if DHT is an inhibiting factor, why can't castrates match full regrowth on those mice which were NOT even castrates?

Tell me why finasteride is not always effective in some cases and only delays in others and measely regrowth on others.

Is pseudohermaphroditism your only example on DHT as the inhibitor?

Your only argument on sensivity is 'genetically' programmed to shrink, why did those follicles grow like hell. What happened to donor dominance and genetic programming?

Why are you peddling Androgenetic Alopecia as a 'fact' when even Propecia scientists could not? It's a theory and open to further research.

My take: If DHT is not the inhibiting factor, it has, therefore, no direct effect on hair follicles.

 

[freakout]

Does Mercado address Alopecia Areata or Alopecia Totalis?

Nope, sorry. I know it's suspected as an auto-immune disorder. But my take on that is: the immune response could be affecting the surrounding tissues rather the the follicles themselves.

 

[squeegee]

DHT always been involved in the balding process. DHT is a stronger androgen than Testosterone. The co-factors makes the difference. Stop fighting like girls. god...

 

[hairhoper]

freakout, this statement you refer to (I've quoted the whole paragraph to put it back into its original context):

It is difficult to argue that lower systemic androgen levels in the female mouse environment (or higher in the case of the male mice) causes the rapid regeneration of vellus hair follicles from the human female. Therefore, the existence of an inhibitor factor other than androgens, particularly in women
showing diffuse/pattern alopecia,25 that is lacking in the nude mouse seems plausible. This could be some other steroid, hormone, cytokine, neuropeptide,
or an immunologically related factor.

... you're taking severely out of context and turning it into this:

DHT has no direct effect on hair follicles

and this:

Androgenetics IS Junk Science

That is, as I said before a huge leap of logic and not a claim the scientists in the study themselves are making at all.

Even out of context the statement:

the existence of an inhibitor factor other than androgens

does nothing to oppose the belief that 'androgens are an inhibiting factor'. You seem to be suggesting those statements are mutually exclusive. You're misunderstanding the meaning of 'other than' in that statement.

A implies the existence of a factor B other than C
... does not imply ...
C is not a factor

Your interpretation of that study is incorrect, whether you simply don't understand it or are intentionally misconstruing it I do not know. The fact you were cherry-picking the quotes to begin with suggests the latter.

Either way I suggest you take such misleading statements our of your signature until you can back them up with sound logic. You're spreading FUD (fear, uncertainty and doubt) on a public forum that troubled people visit for advice. That's pretty irresponsible in my book.

 

[cristi2011]

@freakout: please give us a break with your "theories"...
You have no arguments, no logic, no evidence, no studies, nothing...

 

[freakout]

Avoiding my arguments while throwing mud?? That study team was very cautious with their conclusion. I'm not.

So tell me if DHT is an inhibiting factor, why can't castrates match full regrowth on those mice which were NOT even castrates?

Tell me why finasteride is not always effective in some cases and only delays in others and measely regrowth on others.

Is pseudohermaphroditism your only example on DHT as the inhibitor?

Your only argument on sensivity is 'genetically' programmed to shrink, why did those follicles grow like hell. What happened to donor dominance and genetic programming?

Why are you peddling Androgenetic Alopecia as a 'fact' when even Propecia scientists could not?
Androgenetics is junk science because proponents like you keep insisting it's a "fact". It's a theory and open to further research.

Answer.

 

[hairhoper]

Avoiding my arguments while throwing mud?? That study team was very cautious with their conclusion. I'm not.

No kidding, you don't think they are best qualified to make their own conclusions? I'm not throwing mud, I'm answering your statements logically. I didn't avoid your arguments but was trying to keep on a single subject.

So tell me if DHT is an inhibiting factor, why can't castrates match full regrowth on those mice which were NOT even castrates?

The genetic factor in androgenetics. In the mouse study the hairs are being transplanted to mice which are not genetically predisposed to androgen sensitivity. In the castrate scenario, the castrate has a genetic predisposition to androgen-sensitivity and although the loss is halted by eliminating DHT, it does not necessarily regrow as there is no change in the genetic factor.

Tell me why finasteride is not always effective in some cases and only delays in others and measely regrowth on others.

It stops loss in 9/10 males with male pattern baldness by eliminating 70% of DHT. It's pretty conclusive that DHT is an inhibiting factor from this fact alone. Regrowth is never assured by an antiandrogen as the damage is already done to the follicle.

Is pseudohermaphroditism your only example on DHT as the inhibitor?

I don't believe I've mentioned pseudohermaphroditism?

Your only argument on sensivity is 'genetically' programmed to shrink, why did those follicles grow like hell. What happened to donor dominance and genetic programming?

1. "genetically' programmed to shrink" - Basically, yes that is what the genetic part in androgenetics means.

2. The study says they didn't really 'grow like hell', as the thicker hairs which were also transplanted shrunk and the hairs all met at a common mean.

3. I don't think anyone has tried to suggest that the term 'donor dominance' should apply when transplanting from a human to an immunosuppressed mouse, where the donor and transplant genes differ. Donor dominance is a term used to describe what happens when transplanting from donor to transplant area in the same subject (human hair transplants).

Why are you peddling Androgenetic Alopecia as a 'fact' when even Propecia scientists could not? It's a theory and open to further research.

An observation that can be measured is a fact. The androgen factor of androgenetics can be, which seems to be the main point you are disputing. It is a fact that eliminating DHT from men suffering from male pattern baldness halts hairloss in >90% of cases. (I'm not even sure it isn't a halt in 100% of men if DHT is fully eliminated. Bryan has I believe more knowledge on castrates and transgenders where this would be the case).

The part of the theory which is still being studied is the genetic factor (see the opening post in this thread). Everybody and his dog accepts the androgen factor, except you.

 

[freakout]

It stops loss in 9/10 males with male pattern baldness by eliminating 70% of DHT. It's pretty conclusive that DHT is an inhibiting factor from this fact alone. Regrowth is never assured by an antiandrogen as the damage is already done to the follicle.

Are you twisting the words or don't you know that the Propecia study said 90% POSITIVE EFFECT. It also said 60% POSITIVE EFFECT on the placebo group. Apparently, 'delaying' hair loss was also a 'positive effect'. What kind of parameter did Merck use in that study??? It's a laugh :woot: I think I'll include this in my signature so people will know.

I don't believe I've mentioned pseudohermaphroditism?

HOW DID THEY SUSPECT DHT IN THE FIRST PLACE?? LOL!

The hairs grew like hell to me. Something finasteride nor castration couldn't match in 100% OF SUBJECT. Like hell is pretty much the only way to describe it.

I don't think anyone has tried to suggest that the term 'donor dominance' should apply when transplanting from a human to an immunosuppressed mouse, where the donor and transplant genes differ. Donor dominance is a term used to describe what happens when transplanting from donor to transplant area in the same subject (human hair transplants).

LOL Are you serious!!! Those transplant follicles are contained in biopsies. Did you take up Biology 101 yet?

The genetic factor in androgenetics. In the mouse study the hairs are being transplanted to mice which are not genetically predisposed to androgen sensitivity. In the castrate scenario, the castrate has a genetic predisposition to androgen-sensitivity and although the loss is halted by eliminating DHT, it does not necessarily regrow as there is no change in the genetic factor.

So genetics and hormones are TWO SEPARATE ISSUES IN ANDROGENETICS?? So androgens can cause hairloss even if you're not genetically predisposed??? ALL MEN HAVE ANDROGENS! How do they keep their hair? LOL!

Your thought processes and language patterns very much resembles finfighter's! I wonder why. :woot:

Let me tell you my guiding principle in complex systems: A complex biological process such as male pattern baldness cannot cannot be attributed to a simplistic equation such as 'androgenetics' specially when it associates with potentiall fatal conditions such as CVDs and prostate cancer and involves environmental factors. Period.

I have a suggestion. You should read up in the guiding principle of scientific research before you argue with me. Here
http://www.reidlyon.com/media/Scientific_principles.ppt

Good luck.

 

[hairhoper]

You seem unable to stick clearly to the points. I'm going to keep it shorter.

- What exactly is your point about Propecia? Whether you quibble over the percentages or what you class as being effective or not, the fact remains it still does cause that undeniable positive effect. You think it should cause 100% regrowth for everyone that takes it or it is somehow all a big lie?

- Donor dominance is something you brought up. I was simply explaining that it is a term which is used to describe the observable effects in human hair transplants and not relevant in your mouse study. If you think it is, explain why.

As for this:

So genetics and hormones are TWO SEPARATE ISSUES IN ANDROGENETICS?? So androgens can cause hairloss even if you're not genetically predisposed??? ALL MEN HAVE ANDROGENS! How do they keep their hair? LOL!

You're just being childish and facetious. Nice capital lettered outrage there while you mock your own skewing of my words. I never suggested they were separate issues. Twice in the paragraph you posted I describe "genetic predisposition to androgen-sensitivity" so you're fully aware I understand the connection.

I'm going to ignore your nonsense statements about biology 101 and scientific reasoning. You've yet to make a single logical statement you can backup.

 

[freakout]

Good luck with your studies, Mr. finasteride!

This is the link to the study. viewtopic.php?p=611106#p611106 I suppose they will have to make their own interpretation. It should add to their knowledge whichever way they decide. Read up ppl!!

I just hope they don't begin to believe male pattern baldness is immunologically related. I still believe androgens are involved in many cases and hair follicles are immune-privileged.

 

[freakout]

I probably made the mistake of NOT stressing that the surrounding tissues of the hair follicles are NOT immune-privileged.

The studies you posted do not differenciate between those tissues and the follicles themselves. Do they? I haven't read them fully yet.

So yes, immunologically related factors are probably involved in some cases.
But my take on that is: an immune response is only a consequence of other influencing factors. That's why it's called a 'response'. Right? Wrong?

 

[Bryan]

Now, I understand that there is a difference between AA and Androgenetic Alopecia, however....the immune priviledge collapse hypothesis has been proposed as another co-factor or co-occurance to Androgenetic Alopecia. The above noted example is just a demonstration that perhaps.....and I stress perhaps.....there was another reason why those Androgenetic Alopecia hairs "grew like hell" on the immune deficient mice.

By the way, I should mention here that those transplanted hairs didn't really "grow like hell" in that study with the immune-deficient mice (freakout's favorite study). Without actually digging it out again and re-reading it for the umpteenth time, I'm pretty sure the researchers said that the back of a mouse is far from being the ideal place to grow transplanted human hair follicles, and the growth rate of such follicles is always less than what they grow when they're in their normal position on top of a human head. So everybody should keep in mind that what freakout loves to say about "growing like hell" is mainly just an exaggeration that he likes to use, to promote his own weird little agenda!

 

[freakout]

Grafting of human hairless (lesional) AA scalp to immunodeficient SCID mice results in hair regrowth similar to the results reported with nude mice.

That was particularly interesting. Lesional scalp growing hair like hell. Hell, I'd like to believe that the same will apply on hairless "Androgenetic Alopecia" scalp - growing hair like hell!

 

[freakout]

They were talking about Jahoda's experiment transplanting the bottom part of the dermal papilla on his wife's arm. The article is a third hand story so the details were already stripped but still basically what happened.

The transplanted part was also basically a dead follicle with living dermal papilla cells. It also showed that individual cells can grow into entire organs which classify them as immune-privileged stem cells.

I think Jahoda shaved off the dermal sheath knowing that it's not immune-privileged. Guy's a real hair expert.

I've been thinking about the focus on immune-responses. I think it's only a complication of the true underlying cause. I always analyse on the assumption that these are facts so I don't have to go thru the details of reading them

If it's an auto-immune response, it should be targeting tissues with the same or similar constitution. There won't be a pattern and affect any part of the scalp.

Immune-responses, otoh, are prompted by infection or dead or dying cells which are often already being consumed by bacteria. Ask the WHY again. Early cell death rather than 'early apoptosis' which could not be flushed out of the scalp?

Ask again why increased or ealy cell death? Stress and low blood supply. How are androgens implicated if the mouse study disregards them?

This goes to the root of problem solving techniques. Everyone thinks everything occurs at the biochemical level and recently at the cellular level.

 

[Rutt]

castrates don't lose hair
psuedoherms dont lose hair
people taking dutasteride in significant amounts to reduce DHT to castrade levels don't lose hair.

freakout you sound terrified of taking finasteride, you should know it's the only thing you can do until topical antiandrogens come out.