brasileirao said:
Are you saying the more you sweat the more hair you will lose. What about oily scalp, I know a few people who do not have oily scalp or skin and still have male pattern baldness.
I am not saying that the increased sweating `causes' hair loss.
I think the sweating efficiency changes in male pattern baldness, reflect the same DHT induced changes in the tissue that cause hair loss. I argue that DHT induced changes in the local tissue fluid pressure effects the size of growing anagen follicles, as i describe in my letter to experts on my theory below.
These same changes in fluid pressure would also alter local sweat secretion, and i think the posted sweating study demonstrates this.
______________________________________________
Dear ---------
I would welcome your opinion on a factor that must, given accepted physiology, have the `final say' in the size of the in vivo anagen follicle. This factor is the basic mechanism in multi-cellular biology of contact inhibition.
My opinion on the role of contact inhibition in anagen follicle size, and the advantages of this in the evolution and function of hair, can be seen here
http://www.hairsite2.com/library/abst-167.htm A slightly modified version of this paper was published in Medical Hypotheses (2002) 59 (5), 522-526. doi:10.1016/S0306-9877(02)00259-1, available on line at
http://www.idealibrary.com
The basic reasoning goes like this.
The amount of hair produced is directly related to the period of anagen, and the size achived by the anagen follicle. In male pattern baldness, the anagen period is shortened, resulting in miniaturised follicles.
In multi-cellular biology, any organ `building' is subject to the ultimate control of normal contact inhibition. Contact inhibition ensures that organs can only be as large as the available space allows. This prevents biological structures from interfering with each other.
As the anagen follicle starts to enlarge, it has to push the surrounding dermal tissue aside. The greater the resistence to movement of the dermal tissue, the earlier normal contact inhibition will `kick in'. If the resistence is high, the anagen enlargement period will be turned off early by contact inhibition, resulting in miniaturised follicles. If the resistence is low, anagen enlargement can continue for longer, resulting in larger follicles and increased hair growth.
The only factor that could `modify' the resistence to movement of the dermal tissue, is the fluid pressure within it. If the fluid pressure is high, the tissue rigidity is increased, and therefore its resistence to movement. Likewise, if the fluid pressure is low, so is the resistence to movement.
This mechanism makes a link with high fluid pressure and reduced hair growth, and low fluid pressure and increased hair growth. In my opinion, hair follicles evolved to `read' the fluid pressure in surrounding tissue to adjust hair production in line with other temperature controls in evolving mammals. Please see "The hydraulic dermal model" section of my paper.
A role of contact inhibition mediated through hydraulic changes in male pattern baldness, does not conflict with in-vitro observations, or the donor dominance observed in transplanted grafts. Sample follicle cells `switched off' by contact inhibition, have been fundamentally altered compared to cells that continue to multiply. EG: samples from terminal hair producing follicles. Any different in-vitro response of such samples to androgens, or other substances is to be expected! The observed Hypoxia in follicle grafts demonstrates no `active' circulation within these grafts. No active circulation means no hydraulic changes! The grafts will remain in the `as transplanted state', demonstrating donor dominance.
In male pattern baldness we have hair loss, immune infiltrate and immune sensitivity, ultimate fibrosis, and tissue thickening. These are all recognised factors in edemous tissue.
http://www.lymphoedema.org.au/lymphoed.htm
One way to increase hair growth according to this mechanism, is to increase the resistence of follicle cells to contact inhibition? The danger here is that these cells would then be far more likely to become tumorous. In my opinion, the results of Fuchs in manipulating the Wnt pathway, confirms a central role of contact inhibition in follicle developement.
http://www.hhmi.org/fuchs/index.html
If you look at other cases of hair loss, the common factor in these conditions is an increase in tissue fluid pressure for one reason or another!
As far as HM like procedures are concerned, i think the implantation itself could create `one off' conditions? There is bound to be some kind of healing process here, and this could very likely allow increased cell multiplication initially, and the developement of a large anagen follicle. We know that an `over production' of cells can occour during the healing process, scar tissue for example?
This predicts a potential problem with follicles generated by HM? If these follicles cycle normally, come the next anagen phase, these would then also come under the influence of normal contact inhibition. If the scalp conditions have not changed, large HM generated follicles could only last for one cycle?
I would welcome your comments on this proposal.
Best Regards,
Stephen Foote.
