Alopecia in CAIS

[armandein]

Dr, Messeger is a very good scientist with a open mind and it is his recent study:

Br J Dermatol. 2010 Feb 1. [Epub ahead of print]
Female Pattern Hair Loss in Complete Androgen Insensitivity Syndrome.

Cousen P, Messenger A.

Department of Dermatology, Royal Hallamshire Hospital, Sheffield, UK.

Abstract Female pattern hair loss, also known as female androgenetic alopecia, is generally regarded as an androgen-dependent disorder representing the female counterpart of male balding. Here we describe female pattern hair loss occurring in a patient with complete androgen insensitivity syndrome suggesting that mechanisms other than direct androgen action contribute to this common form of hair loss in women.

PMID: 20128792 [PubMed - as supplied by publishet

 

[armandein]

No coments :jackit:

Armando

 

[LewdBear]

It's interesting. I'm going to check out the full text today.

I think the first, and most obvious question, would be : What is the degree of this patient's AIS? It's known that individuals (even those classified with CAIS) can have some mild amount of pubic hair, which would indicate some minimal androgen sensitivity.

If this is a case of a completely hairless individual, that makes it much more intriguing.

 

[Bryan]

I don't believe the basic premise. If it's a patient with CAIS, then her balding is obviously not from androgenetic alopecia.

 

[LewdBear]

I don't believe the basic premise. If it's a patient with CAIS, then her balding is obviously not from androgenetic alopecia.

It depends. Sometimes patients classified as "CAIS" do have some minimal degree of androgen sensitivity and might better be classified as part of the PAIS spectrum.

However, I'm also skeptical of the idea that it is "...suggesting that mechanisms other than direct androgen action contribute to this common form of hair loss in women."

Even if this were happening in a particular patient, I'm not sure how or why that would translate to female-gender hair loss, particularly given that other CAIS patients do not experience Androgenetic Alopecia.

 

[moxsom]

However, I'm also skeptical of the idea that it is "...suggesting that mechanisms other than direct androgen action contribute to this common form of hair loss in women."

It could be via INDIRECT action of androgens. I do not find that too hard to believe. In the paper I believe they allude to association with some CP450 enzyme.

Also, if it isn't androgenic hairloss, what else could it be? It's pretty easy to rule out scarring alopecia.

 

[armandein]

Hi Moxsom

It is possible read the study, have you it?

Armando

 

[moxsom]

Hi Moxsom

It is possible read the study, have you it?

Armando

http://uploading.com/files/fdd4ce73/FPHSA.pdf/

enjoy

 

[armandein]

Thank you very much

Armando

 

[moxsom]

Even if this were happening in a particular patient, I'm not sure how or why that would translate to female-gender hair loss, particularly given that other CAIS patients do not experience Androgenetic Alopecia.

Because if she is suffering from non-scarring alopecia it gives clues to possible indirect pathways that androgen may effect cells outide of the androgen receptor.

 

[Bryan]

Because if she is suffering from non-scarring alopecia it gives clues to possible indirect pathways that androgen may effect cells outide of the androgen receptor.

Please give some specific examples of that.

 

[S Foote.]

I don't believe the basic premise. If it's a patient with CAIS, then her balding is obviously not from androgenetic alopecia.

Well yes.

So given that this is also a "pattern" balding with the same follicle miniaturization and hair cycle changes seen in male pattern baldness, we should all be very interested in this study. I would encourage people to download this from the link provided by Moxon.

Quote:

"Women with female pattern hair loss (FPHL) typically present with a history of gradual thinning of scalp hair, often over a period of several years. On examination they show widening of the central parting with a diffuse reduction in hair density mainly affecting the frontal scalp and crown. The frontal hairline is usually retained. FPHL is common affecting about 5% of women by the age of 50 increasing to over 30% by age 70.1,2 The underlying change in hair follicle physiology is progressive miniaturization in a proportion of hair follicles, shortening of the growth phase of the hair cycle (anagen) and prolongation of the resting phase (telogen).3,4 FPHL has long been thought to be the female counterpart of male balding and is often referred to as female androgenetic alopecia. However, the role of androgens in FPHL is less clear-cut than in male balding.
Here we report a case of FPHL that reinforces this uncertainty and implicates androgenindependent mechanisms in the pathogenesis."

What this study supports is that it is the pattern area that is important in some way, and that androgens can initiate the same changes in this area as other factors.

How would you explain this study Bryan? What ELSE also produces the same patterns and pathology of hair loss by a "direct" action on follicles, as in the claim you make for androgens?

S Foote.

 

[moxsom]

Because if she is suffering from non-scarring alopecia it gives clues to possible indirect pathways that androgen may effect cells outide of the androgen receptor.

Please give some specific examples of that.

Did you read the paper? they dicuss a few.

 

[Bryan]

I don't believe the basic premise. If it's a patient with CAIS, then her balding is obviously not from androgenetic alopecia.

Well yes.

So given that this is also a "pattern" balding with the same follicle miniaturization and hair cycle changes seen in male pattern baldness, we should all be very interested in this study.

I think it's a bit of a stretch to refer to it as "pattern" balding. The diffuseness of her balding appears to me to be spread pretty much across the whole top of her scalp. However, I'll admit that I wish they had provided photos of the back and sides of her head, too.

What this study supports is that it is the pattern area that is important in some way, and that androgens can initiate the same changes in this area as other factors.

How would you explain this study Bryan? What ELSE also produces the same patterns and pathology of hair loss by a "direct" action on follicles, as in the claim you make for androgens?

I have no idea, Stephen. It certainly does seem to demonstrate something else going on with that woman that has nothing to do with androgens; maybe a heretofore undiagnosed nutritional deficiency of some sort? Roger Williams did a lot of good work in his career emphasizing individual variability for nutritional elements, and maybe that woman has a really exceptional requirement for one of them that isn't being met.

I know you're simply hinting (not so subtly) about your own thoroughly discredited theory, but all that really does is just beg the question. You haven't explained (and cannot explain) why the total lack of androgenic stimulus in that woman isn't sufficient to stop thinning even from your silly theory, as it is in men.

 

[Bryan]

Because if she is suffering from non-scarring alopecia it gives clues to possible indirect pathways that androgen may effect cells outide of the androgen receptor.

Please give some specific examples of that.

Did you read the paper? they dicuss a few.

After about half a dozen attempts, I was finally able to get it downloaded, and I just now read it!

They list only ONE possibility for that; it's just the corny old idea that testosterone is converted to estrogen, which adversely affects hair growth in animals, and they (amusingly) assume that it may adversely affect human scalp hair, too; they seem to be unaware of recent studies discrediting that old idea.

So we're back to Square One: how could androgens affect scalp hair follicle cells outside of the androgen receptor? :dunno:

 

[armandein]

In the study:

Secondly, androgens may be acting through non-androgen
receptor mechanisms. For example, androgens may be aromatised to oestrogens in the hair follicle by the cytochrome P450 enzyme complex.13 Oestrogens inhibit hair growth in animal models 14 and oestrogen receptor-beta (ER?) is expressed in human scalp hair follicles.15

13 Thornton MJ, Nelson LD, Taylor AH et al. The modulation of aromatase and
estrogen receptor alpha in cultured human dermal papilla cells by dexamethasone: a novel mechanism for selective action of estrogen via estrogen receptor beta? J Invest Dermatol 2006; 126: 2010-8.
14 Ebling FJ. Hair. J Invest Dermatol 1976; 67: 98-105.
15 Thornton MJ, Taylor AH, Mulligan K et al. Oestrogen receptor beta is the
predominant oestrogen receptor in human scalp skin. Exp Dermatol 2003; 12:
181-90.

 

[Bryan]

What's your point, Armando? I've already addressed that.

 

[S Foote.]

What this study supports is that it is the pattern area that is important in some way, and that androgens can initiate the same changes in this area as other factors.

How would you explain this study Bryan? What ELSE also produces the same patterns and pathology of hair loss by a "direct" action on follicles, as in the claim you make for androgens?

I have no idea, Stephen. It certainly does seem to demonstrate something else going on with that woman that has nothing to do with androgens; maybe a heretofore undiagnosed nutritional deficiency of some sort? Roger Williams did a lot of good work in his career emphasizing individual variability for nutritional elements, and maybe that woman has a really exceptional requirement for one of them that isn't being met.

I know you're simply hinting (not so subtly) about your own thoroughly discredited theory, but all that really does is just beg the question. You haven't explained (and cannot explain) why the total lack of androgenic stimulus in that woman isn't sufficient to stop thinning even from your silly theory, as it is in men.

You say quote:

"You haven't explained (and cannot explain) why the total lack of androgenic stimulus in that woman isn't sufficient to stop thinning "

It is the ideas you support that requires a direct action of androgens, not my theory. According to my theory, there are many factors that can trigger the mechanism of hair loss i propose. This particular study challenges your opinions Bryan not mine!


I think you understood the point of my post Bryan, and you just wish to skirt around it by making your usual unsubstanciated claims about my particular theory.

You say "maybe this maybe that", but why are only "some" follicles effected by "whatever", in the same way as in male pattern baldness?

Your claim in male pattern baldness is that certain follicles are vunerable to a growth restricting direct action of androgens, and it can take years of androgen exposure for these follicles to respond to androgens.

Are you making the same claim about whatever factor is at work in this study? Please keep to my point.

While we are on the subject of your claim about a direct exposure of androgens being necessary for "years", before any effect is seen in the alledged directly effected cells. I will ask you the same question you asked Moxon in this thread.

"Please give me some specific examples of that?"

S Foote.

 

[Bryan]

It is the ideas you support that requires a direct action of androgens, not my theory. According to my theory, there are many factors that can trigger the mechanism of hair loss i propose. This particular study challenges your opinions Bryan not mine

Not at all. As I said in plain English early in this thread, I don't believe the woman has androgenetic alopecia.

I think you understood the point of my post Bryan, and you just wish to skirt around it by making your usual unsubstanciated claims about my particular theory.

The things I've said about your theory are not "unsubstantiated". They are DEVASTATING to it, and you know it as well as I do.

You say "maybe this maybe that", but why are only "some" follicles effected by "whatever", in the same way as in male pattern baldness?

Your claim in male pattern baldness is that certain follicles are vunerable to a growth restricting direct action of androgens, and it can take years of androgen exposure for these follicles to respond to androgens.

As I've already told you over and over and over and over, it's just a hypothesis that it takes years of androgen exposure for scalp hair follicles to go from "neutral" to "sensitive" to androgens. I don't really claim to know the REAL reason why that happens. Someday doctors and scientists will work that out with certainty.

Are you making the same claim about whatever factor is at work in this study? Please keep to my point.

I've already told you (you don't listen very well, do you?) that I don't KNOW what's going on with the woman in this study. I speculated about one vague possibility.

While we are on the subject of your claim about a direct exposure of androgens being necessary for "years", before any effect is seen in the alledged directly effected cells. I will ask you the same question you asked Moxon in this thread.

"Please give me some specific examples of that?"

Hey, let ME ask YOU a question: you laughably claimed that contact inhibition could change the way that a cell responds to androgens. Please give me some specific examples of that?

 

[S Foote.]

You say "maybe this maybe that", but why are only "some" follicles effected by "whatever", in the same way as in male pattern baldness?

Your claim in male pattern baldness is that certain follicles are vunerable to a growth restricting direct action of androgens, and it can take years of androgen exposure for these follicles to respond to androgens.

As I've already told you over and over and over and over, it's just a hypothesis that it takes years of androgen exposure for scalp hair follicles to go from "neutral" to "sensitive" to androgens. I don't really claim to know the REAL reason why that happens. Someday doctors and scientists will work that out with certainty.

So you cannot explain, let alone prove the mechanism that you often use to claim other people are wrong. :whistle:

The simple bottom line is this Bryan. You try to put down other ideas about male pattern baldness, based on the claim that the evidence for a direct effect of androgens on certain follicles is overwhelming and irrefutable. You always try to skirt around any evidence that would cast doubt upon your claim. Female pattern hair loss has been quoted as supporting this "direct androgen effect", because of the pattern and the "alledged" involvement of androgens.

This study and it's references clearly do not go along with that claim, and demomstrate that FPHH cannot be used to support the "direct androgen action" idea in male pattern baldness.


People can read this study and see this for themselves.

While we are on the subject of your claim about a direct exposure of androgens being necessary for "years", before any effect is seen in the alledged directly effected cells. I will ask you the same question you asked Moxon in this thread.

"Please give me some specific examples of that?"

Hey, let ME ask YOU a question: you laughably claimed that contact inhibition could change the way that a cell responds to androgens. Please give me some specific examples of that?

Yet again you cannot support your arguments in a proper scientific manner, and just answer my question with a question. :thumbdown2:

OK Bryan i will give you an example of my claim (unlike your avoidence of my questions).

When follicle cells are tested in culture, it has been claimed (and i dont argue with this in-vitro observation), that pre-existing male pattern baldness cells are continued to be growth resticted by androgen inducable TGF-beta1.

Contact inhibition study:
http://ajplung.physiology.org/cgi/conte ... 270/5/L879

Quote:

"Thus suppression of p45, cyclin D2/Cdk-4, and cyclin B1/Cdc-2 expression and/or activities is targeted both by contact inhibition and by TGF-beta 1 and may define common mechanisms through which these negative growth signals are integrated. "


This is called scientific reasoning Bryan, you should try it sometime.


S Foote.