S Foote. said:
The only mechanism that makes sense of this in terms of mammalian evolution, is that androgens are changing the local tissue "Hydraulics" in line with the dermal model in my early paper.
S Foote.
However, in order for your mechanism to work there is the requirement of muscle hypertrophy in the scalp, which is not a proven phenomenon. The effect must lead to lymphatic obstruction, which is not a proven phenomenon either. Looking at histological specimens from men with male pattern baldness reveals neither process. Nor, is there any evidence for edema of any kind. And, the argument that the edema is so little that it can't be seen doesn't work here. In other parts of the body where edema can lead to hair loss, the edema is always very prevalent before any other process begins.
Another problem that I have here is that there is no increase in the incidence of lymphangiosarcoma in the scalp of men with male pattern baldness. That's a big problem, because lymphatic obstruction has a tendency to lead to such processes. Just ask women that have gone through radical mastectomies.
Histologic specimens also fail to show lymphatic dilation or proliferation of any sort.
The last item that must be considered is the very mechanism that minoxidil uses to decrease blood pressure. Minoxidil is a selective arterial dilator. It would increase blood flow to the scalp, and thus, increase edema if there is indeed a failure of lymphatics.
Your theory is interesting Foote, but I have too many problems with it. Both in terms of the histology and pathology and in terms of the use of minoxidil for male pattern baldness.