>>Are you saying that the inflamation part of male pattern baldness should be addressed first before we go after the DHT. I read up on all that information and what Im confused about is that if balding men had some sort of lymphedema we would be slow healers to bruises and/or swelling. I think you have brought up a good point which opens the doors to the benefits of Cu-peptides in helping ease inflamation. But I dont see how you can discredit DHT all together. <<
Hi Tony.
I don't discredit DHT at all, i propose a basic DHT `trigger' that accounts for `ALL' the related observations. I think this trigger is DHT induced edema in the male pattern baldness area. Remember that the scalp is a reletively thin tissue that curves around the skull, so it is `well supported' and it would take a lot of pressure to create `obvious' clinical edema in the male pattern baldness area. But all the signs of increased fluid pressures and levels are there, as described in the lymphedema link in my post. In my opinion, the inflamation in male pattern baldness is just a consequense of the same increased fluid pressure that causes the follicle miniaturisation, `NOT' the cause of the miniaturisation. But the inflamation then tends to make the edema worse and the fibrosis also inhibits follicle enlargement as stated in the original post in this thread. So the inflamation component is an important contributing factor in my opinion, and has to be addressed.
Perhaps this letter i have been sending to experts for comments will explain my theory better. A link to my paper is in the letter.
Regards.
S Foote.
_________________________________________
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.
