I was wondering the same thing.
Heath et al. estimate that M.P.B. is 77-85% heritable*, so there's room for environmental factors to play a role. Maybe CRH levels could account for some of the 15-23% non-heritable part of M.P.B.?
* Variance in
when you start to lose hair and
how fast you lose it could account for much of the non-heritable part of M.P.B, rather than whether you
ever lose it.
BTW,
CRH is also produced in the skin. Notice that something like UVB can also stimulate its production. Could reducing it be beneficial? Possibly in some cases. Maybe better would be to target the downstream pathway most relevant to M.P.B which, based on other associated genes**, would probably be the intracellular calcium pathway ending in activation of AP-1 -- this is involved in keratinocyte differentiation and proliferation.
**Besides CRHR1, some other M.P.B.-associate genes are: FYN, PIK3R1 (the p85 subunit of PI3K), PLCG1 (PLC-gamma1), ITPR2 (one of the IP3 receptors), PRKCA (PKC-alpha), and FOSL2. These are all known components of the calcium-induced keratinocyte differentiation pathway, some of which are shown in the CRH diagram.
Also, estrogen reduces expression of FOS, GJA1, IL6, and KRT1 while increasing expression of KRT14 -- all consistent with reduced activity of the CRH pathway, especially the parts that act through c-Fos/AP-1.
All those things I mentioned are probably beneficial, except maybe the intracellular calcium...?