Re: Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells.

ninjishal Tue Feb 23, 2016 4:05 am

Thank you, CF. I guess it really doesn't say anything about CD34

On the other hand, from what I could read in the same table, it raises PGD2 receptors and decreases PGE2 receptor 3, right?

PTGDR was increased (1.4 fold change) - bad
PTGER3 was decreased (-4.3 fold change) - bad

So, it's probably not good for hair IMO

CausticSymmetry Tue Feb 23, 2016 7:03 am

Because palm oil isn't the most tasty oil, I just take Toco-Sorb
for this.

CF Tue Feb 23, 2016 11:22 am

ninjishal wrote:Thank you, CF. I guess it really doesn't say anything about CD34

On the other hand, from what I could read in the same table, it raises PGD2 receptors and decreases PGE2 receptor 3, right?

PTGDR was increased (1.4 fold change) - bad
PTGER3 was decreased (-4.3 fold change) - bad

So, it's probably not good for hair IMO

Thank you ninjishal, good find.

CausticSymmetry Tue Feb 23, 2016 2:41 pm

To the point on the the tocotrienols

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3819075/

lutz Fri Feb 26, 2016 2:55 am

tonyj wrote:The study brings up more questions than answers, although, we're getting closer to a solution. The study points out in Alopecia Areata the progenitors cells are attacked by inflammation and spares the follicle stems cells but in Androgenic Alopecia, there is a defect in the follicle stem cell itself that stops producing progenitor cells. From what I gather, it is critical that there are progenitors cells along with follicle hair stem cells in order to grow hair. So is the defect a result of inflammation attack or mechanical interference like poor circulation? And still that pesky question, why a common balding pattern, if follicle stem cells can have a defect on any of the hair follicle stem cells then why are vertex and temples usually the first to go? Why not the sides?

And what is the connection to Testosterone - DHT- _______________ -Diminished progenitor cells.

Lately, I've been working with kids all day long. And I'm surprised I've never read about the correlation between how human hair grows in and how we lose it. Working with 3-14 year olds it is amazing to see so many younger kids with an NW2-4 that fill in to an NW0 by the time they are 12 or 13. A lot of kids have sparse temples and super thin crowns until puberty is in full swing. Maybe you and I don't understand the physiology completely. Maybe no one does. But it doesn't seem to be that much of a mystery why the crown and temples are the first to go. So many babies are born basically bald, but they fill in in the same pattern that people go bald. Temples and crowns fill in last and they are also the first to go. These areas must be the most difficult or require the greatest energy levels for the body to be able to grow.

Xenon Sat Feb 27, 2016 12:27 pm

tonyj wrote:The study brings up more questions than answers, although, we're getting closer to a solution. The study points out in Alopecia Areata the progenitors cells are attacked by inflammation and spares the follicle stems cells but in Androgenic Alopecia, there is a defect in the follicle stem cell itself that stops producing progenitor cells. From what I gather, it is critical that there are progenitors cells along with follicle hair stem cells in order to grow hair. So is the defect a result of inflammation attack or mechanical interference like poor circulation? And still that pesky question, why a common balding pattern, if follicle stem cells can have a defect on any of the hair follicle stem cells then why are vertex and temples usually the first to go? Why not the sides?

And what is the connection to Testosterone - DHT- _______________ -Diminished progenitor cells.

I'd say a baldness gene is responsible for diminished progenitors. At the risk of repeating myself, you only have to look at transsexuals on T therapy: some go bald, some retain their hair. My reckoning is, T / DHT triggers a baldness gene (apparently inherited by mother), which then causes follicles to inflame, and progenitors to diminish. I think this is the most plausible explanation. There are other factors which worsen this condition, but I think genetics is the root cause.

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