he also has a new hypothetical Androgenetic Alopecia pathogenesis model paper - http://www.medical-hypotheses.com/article/S0306-9877(17)31041-1/fulltext
the following is NOT the paper, but some musing form him.....
..... I’m not here to undermine any of Cotsarelis’ work (because I think it’s incredibly important). After all, he and his team are responsible for the discovery that at hair follicle sites, PGD2 prevents stem cells from converting into progenitor cells (though I think there are several other factors at play than just PGD2).
When it comes to the current thinkings of hair loss pathology, there are essentially two lines of thought: 1) Androgenetic Alopecia is genetically predetermined and the problem lies within the hair follicle itself; or 2) Androgenetic Alopecia is a symptom of tissue remodeling. I tend to believe the latter — because the data overwhelmingly supports that Androgenetic Alopecia is simply just a symptom of scarring (perifollicular fibrosis and dermal sheath thickening).
People who fall within that first camp tend to adamantly oppose the idea that Androgenetic Alopecia is symptomatic of scarring, and use evidence of rhesus macaques’ hair transplantation success and the infamous “donor dominance” study as their counterpoints. But a deeper look into all of those studies reveals a series of misinterpretations from these opposers — and in study design flaws — and a lot of challenges surrounding “strip transplantation” and the fact that surrounding tissue sites were transferred alongside the hairs.
The “donor dominance” paper is also often mischaracterized as clear-cut evidence that “transplanted hairs will never thin” — but anyone who actually reads beyond the abstract would realize this is just a gross mischaracterization of the study’s actual findings.
Finally, there’s more recent evidence that when a single human Androgenetic Alopecia-thinning hair follicle is transplanted into the back of a mouse, it regrows as well (and sometimes even better) than a non-Androgenetic Alopecia hair from a human scalp. This, alongside the fact that DHT tends to increase hair growth everywhere else in the body, seems to suggest that the DHT-genetic sensitivity argument to hair loss has significant flaws — and deserves reevaluation. Furthermore, no one has yet to explain PGD2’s arrival to balding scalp sites — or its exact role in hair thinning.
I’ve recently refined my opinions of Androgenetic Alopecia pathology, and I published a paper for a new hypothetical Androgenetic Alopecia pathogenesis model, if you’re interested:
http://www.medical-hypotheses.com/article/S0306-9877(17)31041-1/fulltext
the following is NOT the paper, but some musing form him.....
..... I’m not here to undermine any of Cotsarelis’ work (because I think it’s incredibly important). After all, he and his team are responsible for the discovery that at hair follicle sites, PGD2 prevents stem cells from converting into progenitor cells (though I think there are several other factors at play than just PGD2).
When it comes to the current thinkings of hair loss pathology, there are essentially two lines of thought: 1) Androgenetic Alopecia is genetically predetermined and the problem lies within the hair follicle itself; or 2) Androgenetic Alopecia is a symptom of tissue remodeling. I tend to believe the latter — because the data overwhelmingly supports that Androgenetic Alopecia is simply just a symptom of scarring (perifollicular fibrosis and dermal sheath thickening).
People who fall within that first camp tend to adamantly oppose the idea that Androgenetic Alopecia is symptomatic of scarring, and use evidence of rhesus macaques’ hair transplantation success and the infamous “donor dominance” study as their counterpoints. But a deeper look into all of those studies reveals a series of misinterpretations from these opposers — and in study design flaws — and a lot of challenges surrounding “strip transplantation” and the fact that surrounding tissue sites were transferred alongside the hairs.
The “donor dominance” paper is also often mischaracterized as clear-cut evidence that “transplanted hairs will never thin” — but anyone who actually reads beyond the abstract would realize this is just a gross mischaracterization of the study’s actual findings.
Finally, there’s more recent evidence that when a single human Androgenetic Alopecia-thinning hair follicle is transplanted into the back of a mouse, it regrows as well (and sometimes even better) than a non-Androgenetic Alopecia hair from a human scalp. This, alongside the fact that DHT tends to increase hair growth everywhere else in the body, seems to suggest that the DHT-genetic sensitivity argument to hair loss has significant flaws — and deserves reevaluation. Furthermore, no one has yet to explain PGD2’s arrival to balding scalp sites — or its exact role in hair thinning.
I’ve recently refined my opinions of Androgenetic Alopecia pathology, and I published a paper for a new hypothetical Androgenetic Alopecia pathogenesis model, if you’re interested:
http://www.medical-hypotheses.com/article/S0306-9877(17)31041-1/fulltext