First of all, DKK-1 sounds like a rapper to me…
Now, to get serious, here is a definition of DKK-1:
Boston Baldy said that DKK-1 (which, as stated above, is a gene) is turning out to be a “bigger culprit” than DHT in male pattern baldness.
I think the answer to this mystery is that the presence of DHT, and cell receptor sensitivity to DHT, triggers a cascade reaction which leads to the switching on of the DKK-1 gene.
So, the two are intimately related. Without DHT and DHT-receptor sensitivity (present in people who have the MPB genotype), then DKK-1 wouldn’t matter. It’s just a gene that is involved in the pathway of shutting down hair growth, and this pathway can be traced backward to (1) the presence of DHT; and (2) genetically-mediated cell receptor sensitivity to DHT.
But the point is, DHT receptor sensitivity starts the whole cascade, and short of GENE THERAPY, there is nothing we can do to remove the genetic phenotype of DHT receptor sensitivity in people with MPB. Since DKK-1 cannot become relevant without DHT and DHT receptor sensitivity, DKK-1 cannot be “a bigger culprit”. It may seem like it can, but this would be impossible.
So, the WNT gene is involved in influencing the effects of the DKK-1 gene. So what? Nothing new or surprising here. Almost every chemical reaction or cellular growth mechanism in the body has multiple genes involved, switching each other on and off.
I don’t mean to be facetious, I just want to point something out:
HM MAKES ALL OF THIS MOOT.
HM takes cells which ARE NOT SUSCEPTIBLE TO DHT (and thus, don’t become involved in the whole DKK-1 mess in the first place), and moves them to the balding areas of the scalp.
HM makes all of the above… DHT… receptor sensitivity… DKK-1… WNT… totally irrelevant.
It’s about replacing bad cells with good.
And the beauty of it is, you don’t even have to understand any of the exceedingly complex gene mechanisms to see that it works.
I like my solutions simple.