Abstracts from the 2007 European Hair Research Society Conf

[michael barry]

Re: Abstractys from the 2007 European Hair Research Society Conf

More evidence that environmental effects can be significant in the development of male pattern baldness.

Androgenetic Alopecia: Concordance of
Hair Loss in Twin Pairs
Mirmirani, Paradi;1,2 Price, Vera;2 Ettefagh, Leila;1
1. Case Western Reserve University, Cleveland, OH, USA;
2. Universtiy of California, San Francisco, San Francisco,
CA, USA
Androgenetic alopecia is a common disorder that affects
both men and women, but its mode of inheritance has
been a contested topic. Our objective was to measure and
compare hair loss in monozygotic and dizygotic twins and
to determine concordance rates between pairs. In fraternal
twins, expected concordance is 50% for a monogenetic
simple Mendelian transmission and less than 50% for
a polygenetic trait; 100% concordance is expected for
monozygotic twins. Recruitment of twins took place at the
2004 National Twinsday Festival in Twinsburg, Ohio. Twins
filled out hair questionnaires to determine demographics
and exclusion criteria. Each participant had stereotactic
frontal/vertex/occipital scalp photographs(Canfield
Scientific). Buccal swabs were collected for zygosity
testing and were perfomed by AnaGen Technologies, Inc.
The photographs were evaluated in a blind manner by
one of the investigators(VHP) for degree of alopecia and
concordance/discordance amongst twin pairs. A total of
44 twin pairs were enrolled, 16 were excluded from the
study. Of the 28 twin pairs evaluated, 2 of the 4 dizygotic
twins were discordant(50%) and 3 of the 24 monozygotic
twins were discordant(11%). This preliminary data shows
an unexpected discordance rate of 11% amongst the
monozygotic twin pairs suggesting that environment may
have a greater influence on androgenetic alopecia than
previously recognized. Ongoing enrollment of twins in
the study will allow for larger sample size and improved
power to further evaluate the inheritance pattern of
androgenetic alopecia.

11% aint much....................why do I get the feeling one brother had a bigger sweet tooth (thus higher insulin and less globulin) than the other. I think getting insulin higher and globulin lower--------------thus increasing the activitity of type two alpha five reductase, would be a hell of alot more threatening to someones' male pattern baldness-prone hair than working in a dirty construction job, but maybe that is just me.

 

[ross007]

Re: Abstractys from the 2007 European Hair Research Society Conf

i would like to say m barry n harrold that you guys are truly dedicated to this forum and we all appreciate it! but i got lost in the science in page 1 :dunno:

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

Harold,
When I look at that above, it makes me think that several things downstream of DHT would have to be inhibited to have a "no-hormonal" intervention against alopecia. One would have to counteract all of those substances or supress at least the negative growth factors in the least in all probability as when any one gets high enough in the follicle, catagen will ensue......................and increasing the anagen inducers also would assuredly be helpful. The thing is man...............that a good 8-10 substances in all isn't it?

exactly. Its a bit dispiriting in one sense since it looks like there probably isnt a "master switch" that bridges androgens to this signalling cascade into catagen overdrive. Something we could knock out. There may be - but it probably isnt one of those listed above. PGD2 could well be it since it is not a recognised anagen inhibitor or catagen promoter. It may be responsible for turning the others on and off. But unless someone shows that one of these is much more important than the rest and something that acted on IGF-1 for instance would grow hair no matter what androgens are doing then its a bit much to try and work against all of that.

Who knows if constantly increasing one of the growth factors like wnt or beta catenin wont cause cancer down the line also, or if inhibiting a negative growth factor might not also be carcinogenic over time?

But we do know that stopping androgens via the recptor site and inhibition of DHT isn't fatal if done topically for certain (and internally with type two dht). Hence why I think its still the best "base" route to follow with other things added atop it afterwards given what we know at this point.



I sure as hell wish they could just clone our damned donor hair so we could get injected with a shitload of it and we could forget about all this stuff...................

Yeah its still the best thing we got right now. Unless Cotsarelis really has something with his PGD2 link. I would be much happier inhibiting that topically/systemically than androgens. Otherwise yeah we can just try and block androgens and then do other things like minoxidil etc that may help to thicken hair.
hh

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

More evidence that environmental effects can be significant in the development of male pattern baldness.

Androgenetic Alopecia: Concordance of
Hair Loss in Twin Pairs
Mirmirani, Paradi;1,2 Price, Vera;2 Ettefagh, Leila;1
1. Case Western Reserve University, Cleveland, OH, USA;
2. Universtiy of California, San Francisco, San Francisco,
CA, USA
Androgenetic alopecia is a common disorder that affects
both men and women, but its mode of inheritance has
been a contested topic. Our objective was to measure and
compare hair loss in monozygotic and dizygotic twins and
to determine concordance rates between pairs. In fraternal
twins, expected concordance is 50% for a monogenetic
simple Mendelian transmission and less than 50% for
a polygenetic trait; 100% concordance is expected for
monozygotic twins. Recruitment of twins took place at the
2004 National Twinsday Festival in Twinsburg, Ohio. Twins
filled out hair questionnaires to determine demographics
and exclusion criteria. Each participant had stereotactic
frontal/vertex/occipital scalp photographs(Canfield
Scientific). Buccal swabs were collected for zygosity
testing and were perfomed by AnaGen Technologies, Inc.
The photographs were evaluated in a blind manner by
one of the investigators(VHP) for degree of alopecia and
concordance/discordance amongst twin pairs. A total of
44 twin pairs were enrolled, 16 were excluded from the
study. Of the 28 twin pairs evaluated, 2 of the 4 dizygotic
twins were discordant(50%) and 3 of the 24 monozygotic
twins were discordant(11%). This preliminary data shows
an unexpected discordance rate of 11% amongst the
monozygotic twin pairs suggesting that environment may
have a greater influence on androgenetic alopecia than
previously recognized. Ongoing enrollment of twins in
the study will allow for larger sample size and improved
power to further evaluate the inheritance pattern of
androgenetic alopecia.

11% aint much....................why do I get the feeling one brother had a bigger sweet tooth (thus higher insulin and less globulin) than the other. I think getting insulin higher and globulin lower--------------thus increasing the activitity of type two alpha five reductase, would be a hell of alot more threatening to someones' male pattern baldness-prone hair than working in a dirty construction job, but maybe that is just me.

Its not much but a few times the idea has been rubbished that anything at all other than genetics determine what goes on. This doesnt give us any idea of what has such an effect or how much difference it made but it does show that something changed the outcome between the twins.
hh

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

i would like to say m barry n harrold that you guys are truly dedicated to this forum and we all appreciate it!

Thanks man

but i got lost in the science in page 1 :dunno:

Me to....but I just pretend I know what I am talking about
hh

 

[alkulk]

Re: Abstractys from the 2007 European Hair Research Society Conf

Trichodynia is hair/scalp pain. This study seems to indicate it is not a feature of male pattern baldness per se but one of chronic increased shedding.
hh

Trichodynia Is a Distinguishing Symptom of
Telogen Effluvium
Guarrera, Marcella; Baldari, Manuela; Montinari, Martina;
Rebora, Alfredo; University of Genoa, Genoa, Italy
Objectives: The prevalence of trichodynia is controversial.
Controversy may stem from the diagnostic confusion
between androgenetic alopecia (Androgenetic Alopecia), chronic telogen
effluvium (CTE) and their association (Androgenetic Alopecia+CTE).
Approach: With the aid of the modified wash test (WT)
(1), we surveyed10 men and 85 women complaining of
hair loss. After 5-day-abstention from shampooing, they
soaped and rinsed the hair in a basin and collected all hair
remaining in a gauze covering the basin bottom. Hair were
counted and divided into <3 cm hair (vellus hair) and into
>3 cm hair. Patients with <100 total hair and >10% vellus
hair were diagnosed as having Androgenetic Alopecia; those with >100 hair
and <10% vellus hair were diagnosed as having CTE; those
with >100 hair and >10% vellus hair as having Androgenetic Alopecia+Telogen Effluvium
and patients with >100 hair and <10% vellus hair as having
CTE in remission.
Results: Trichodynia was reported by 22 patients: 17 had
CTE, 2 Androgenetic Alopecia and 3 CTE+Androgenetic Alopecia. None has CTE in remission.
The prevalence (51%) of trichodynia in patients with
CTE and CTE+Androgenetic Alopecia was statistically highly significant
(c2 = 20.077, p <0.001).
Conclusion: Trichodynia is almost exclusive of patients with
CTE as it affects about one half of the them and may be a
marker of activity of an inflammatory peripilar process.

Wow, that is really interesting. But how did they diagnose CTE? What are its symptoms, what is the hair loss pattern of Telogen Effluvium and what can be done about it?

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

Wow, that is really interesting. But how did they diagnose CTE? What are its symptoms, what is the hair loss pattern of Telogen Effluvium and what can be done about it?

They used a rough and ready classification they describe here
"After 5-day-abstention from shampooing, they
soaped and rinsed the hair in a basin and collected all hair
remaining in a gauze covering the basin bottom. Hair were
counted and divided into <3 cm hair (vellus hair) and into
>3 cm hair. Patients with <100 total hair and >10% vellus
hair were diagnosed as having Androgenetic Alopecia; those with >100 hair
and <10% vellus hair were diagnosed as having CTE; those
with >100 hair and >10% vellus hair as having Androgenetic Alopecia+Telogen Effluvium
and patients with >100 hair and <10% vellus hair as having
CTE in remission."

Basically if you are shedding lots and lots of long hairs you were CTE. If you were shedding less hair and some were vellus hairs then you had Androgenetic Alopecia. If you were shedding lots and some were vellus you were both. Telogen Effluvium has no hair loss pattern - it is hair loss from everywhere. As to what can be done about it depends on the cause.
hh

 

[harold]

Re: Abstractys from the 2007 European Hair Research Society Conf

This finding is mentioned in the Cotsarelis prostaglandin patent from last year. Thats the one that doesnt deal with Follica stuff and therefore isnt as interesting to most people. Anyway it seems that although stem cells that produce hair follicles are not lost even in slick bald scalp they are smaller, less active and a certain subset that expresses a marker telling the immune system not to attack them does disapper.
The talk about exression profiling revealing an upregulation of inflammation related genes with this loss makes me wonder if this talk includes the whole PGD2 thing which seemed to be the big finding in that patent. Though perhaps that is being saved for a different publication.
hh

Adult Stem Cell Compartment Changes
in Androgenetic Alopecia Demonstrate
Maintenance of Progenitor Stem Cells With
Loss of Descendant CD200 High A6 Integrin
High Expressing Cells
Garza, Luis A.; Lee, Michelle; Liu, Yaping; David, Stanton;
Lee, Carrasco; Tobias, John; Costsarelis; George, University of
Pennsylvania, Philadelpiha, PA, USA
The status of adult stem cell compartments in tissue specific
disease has not been thoroughly addressed. We tested the
hypothesis that hair follicle stem cells might be depleted
in androgenetic alopecia (Androgenetic Alopecia), which is characterized by
drastic miniaturization of the hair follicle. To compare hair
follicle stem cell numbers between paired haired and bald
scalp samples from the same individuals, we used flow
cytometry to quantitate cell cycle, cell size, and expression
of CYTOKERATIN 15 (KRT15), FOLLISTATIN (FST), CD200
and alpha-6 integrin. We found a gradient of stem cell
characteristics, as defined by a high degree of KRT15 and
FST expression, cellular quiescence and small cell size.
This gradient is not grossly altered between haired and
bald scalp, and stem cells are maintained in bald scalp.
However, a specific CD200 high alpha-6-integrin high
population, which has characteristics of early stem cell
progeny, is lost in bald scalp. Consistent with the loss
of the immunosuppressive CD200 protein, array based
expression profiling demonstrates significant increases in
inflammation associated genes in androgenetic alopecia.
Previous reports of CD200 loss leading to alopecia in mouse
models suggest that Androgenetic Alopecia may be exacerbated or caused by
CD200 downregulation in the human hair follicle stem cell
compartment.

 

[ross007]

so harrold, what did you make of reading all that information? sound like its going to work? thanks

 

[mpower]

Re: Abstractys from the 2007 European Hair Research Society Conf

Another reason is this...........................I put Revivogen on my right wrist for three months THREE YEARS AGO. Guess what, my right wrist still has obviously weaker, thinner, wavier hair than my left wrist.

so actually what you are saying is that revivogen killed your wrist hair ?

 

[harold]

so harrold, what did you make of reading all that information? sound like its going to work? thanks

Which particular information are you referring to?
hh

 

[harold]

One more since I'm getting into the EGF side of things.

"EGF and FGF Signalling Have a Role in Mouse
Hair Follicle Morphogenesis and Patterning
Richardson, Gavin D.;1 Bazzi, Hisham;2 Jahoda, Colin;1 Waters,
James;1 Christiano, Angela M.;3 Fantauzzo, Katherine;2
Crawford, Heather;1 Hynd, Phil;4
1. Department of Biological Sciences, University of Durham,
Durham, UK; 2. Departments of Development and Dermatology,
Columbia University, New York, NY, USA; 3. Departments
of Genetics & Development and Dermatology, Columbia
University,, New York, NY, USA; 4. School of Agriculture, Food
& Wine, The University of Adelaide, Adelaide, SA, Australia
Epidermal growth factor (EGF) has previously been shown
to block hair follicle (HF) morphogenesis. However, the
mechanism underpinning this phenomenon has not been
investigated in detail, perhaps because EGF ligand is not
endogeneously expressed in skin during early HF initiation
and patterning. Keratinocyte growth factor (KGF) has also
been shown to block follicle formation in organ culture in a
manner not yet understood. In this study, we revisited the
roles of the EGF and KGF signalling pathways in normal HF
morphogenesis in mice.
first, semi-quantitive PCR was used to profile the
expression of EGF and KGF ligands and receptors within
separated epidermis and dermis of E12.5-15.5 mouse
dorso-lateral skin. This analysis discovered endogenous
expression of EGFR ligands, Heparin binding EGF and
Amphiregulin, as well as the KGFR ligand KGF. Intriguingly,
immunohistochemistry revealed a marked reduction in both
EGFR and KGFR expression in developing placodes and
subsequent hair germs. Functional studies using embryonic
skin organ cultures identified that EGFR or KGFR activation
within E13.5 skin (before placode formation) inhibited
HF development in a dose dependent manner. This was
confirmed by in situ hybridisation and immunological
detection of molecular markers specific to developing HFs.
Activation of either receptor within E14.5 skin (post placode
formation) had no effect on hair follicle development.
We propose a role for EGF and KGF signalling in which
receptor downregulation may be required for epidermal
cells to escape ligand stimulation, thus permitting placodal
cells to follow a follicular rather than an interfollicular
differentiation pathway."

Translation: EGF (and KGF) signalling has to stop during normal hair follicle development to allow cells to become hair follicles rather than skin cells. Once cells had chosen their fate (placode formation) EGF siganlling had no further effect.
hh