Because Cotsarelis seems to agree with me;
http://edition.cnn.com/2014/06/20/health/baldness-cure-alopecia/
Nah joke, that would be a bad reason.
I have several reasons but the following would be probably the most important one. When you go to this study;
http://advances.sciencemag.org/content/1/9/e1500973.full
They probably refer with that to this study;
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4362521/
Which says;
It's likely that they refer to the AA mice model in this case.. Because in this case indeed, a topical formulation showed superiority over systemic treatment in AA mice model. As we can indeed also read from the supplemental material;
It wasn't much slower btw..
But let's assume they actually refer to actual humans that have tried oral formulations (actually published) and topical formulations (not published anywhere) of a JAK inhibitor for AA, from which they found that the oral resulted in more "robust" hair growth.
Well have you looked at actual case reports of people that found success for AA with a JAK inhibitor like tofactinib? Or even the ruxolitinib case reports in the last link?
Look at one example here which I posted recently on this link;
https://www.instagram.com/thealopeciaexperiment/
Or at the case report of that guy in the first link where Cotsarelis talks. How can hair growth be more "robust" than that? In both cases it's pretty much rapid complete reversal lol.... So that wouldn't make sense would it. Besides let's assume that indeed they have seen more rapid hair growth in AA on humans with a topical formulation. Then what does it matter? At best it would maybe be a tiny bit faster, but eventually it's about the end result. Complete reversal of in this case AA, as displayed in these case reports.
Now the thing is that drugs have biological activity towards a target right? Finasteride primarily has activity towards the 5ar2 enzyme, and also towards 5ar1 at higher dosages. Just like JAK inhibitors have biological activity towards the JAK enzymes.
Now let's take a look at AA;
To simplify it in AA, "killer" T cells attack the epithelial compartment of the hair follicle. They hang around the bulb of the hair follicle. So what do JAK inhibitors do? Well they disrupt this process by latching onto these enzymes (which you can see in the above picture). By doing this they disrupt this process which leads to a decrease in these T cells and now the hair follicle is freed to produce a hair shaft again.
The funny thing is.... These killer T cells are around the close proximity of the hair follicle bulb right? So explain to me how these JAK inhibitors can overthrow these JAK enzymes in these T cells in AA (as evidenced by oral AA test subjects) but wouldn't for example on any other cell type in the hair follicle itself? That would be a laughable thing to assume.. And indeed as evidenced in the picture above you see that the picture illustrates that the compound latches towards the enzymes in the follicular ephitelial cells. The same could be said for every cell pretty much of the hair follicle...
Also remember oral JAK inhibitors do not work for Androgenetic Alopecia at the same dosages, period.
All in all there is really no evidence to believe this will do much at all. I'll eat my shoe if this will work and I obviously hope that it will work. But I'll believe it when I'll see it. Not going to get excited from a useless sh*t mice model. Even when you look at that mice model, SAG initiated hair growth just as about as fast as tofactinib so... There would be more, but I'll leave it at this if you don't mind :mrgreen:.