S Foote. said:
How to put my theory across in simple terms? Well i'll try.
First some personal background.
I am now 54, and i started loosing my hair in my late 20's. Transplants were the only option then (early 80's), and i decided to go down that path (wish i hadn't).
I had four scalp reductions followed by grafts to the frontal area and the central scar left by the reductions. The grafts used were four mm "plugs" (common at the time), and the procedures were carried out at a highly reputable clinic here in England, and the initial results were good.
However my long term experience with these transplants caused me to question the reasons for male pattern baldness, given by the current theory.
The current theory is on the surface supported by the very limited data we have concerning hair transplantation, in particular long term studies don't exist, and the results of some in-vitro studies. The conclusion reached is that hair follicles have some kind of built in "difference" that causes a different "direct" growth response to androgens. However there are a number of serious holes in this conclusion as i have argued before.
Now to my theory.
My background is in engineering systems, and i look at things from the view point of the "whole" system. I think this way of looking at androgen related hair loss/growth, answers the questions the current "molecular" theory cannot.
I have argued the details many times before on these forums, but this is it in a "nutshell" as requested.
The amount of hair growth is dependent upon the size of the follicle reached during the anagen enlargement period of the hair cycle. This expansion of a "pocket" (hair follicle) within the dermal tissue has to move the dermal tissue aside. My original thinking was "what if the dermal tissue doesn't want to move"?
All normal cells respond to a growth control called contact inhibition. Cell multiplication can only happen if there is "space" for this. Not much is known about the molecullar pathway of this process, but we know it effects "ALL" normal cells. Cancer cells lose the contact inhibition response, and this is why they can invade the "space" of other tissues.
The point at which contact inhibition is swiched on must involve a particular degree of resistence or pressure. When this degree of resistence is meet by growing cells, the growth is switched off most likely by changes in the expression of the usual growth factors we know effect cell multiplication.
In the case of hair follicle enlargement, there is another factor as well as the natural resistence of the dermal tissue itself. Because the follicle is an expanding "hollow" pocket in the dermal tissue, there can be a pressure difference.
This is the simple analogy of a ordinary party baloon.
If you push your finger into a party balloon to form a pocket, the amount of resistence depends upon the air pressure within the baloon. If your finger action was "switched off" at a given resistence, this point would be reached sooner the higher the pressure in the baloon. The pocket formed would be smaller.
So according to my theory any changes in the tissue fluid "pressure" around follicles, can effect their anagen size through the normal contact inhibition threshold, and even quite small pressure changes can make a difference.
So where do androgens come into this?
The most consistant action of androgens upon hair in people, is they increase hair growth over the larger part of the body, particularly in certain areas. The beard, groin, and armpit areas also are areas with high levels of lymphatic drainage vessels near the surface. Lymphatic vessels play a central role in the control of the local tissue fluid pressures.
So according to my theory androgens, and DHT in particular must be increasing lymphatic drainage of tissue fluid. This reduces the pressure around the local follicles allowing larger anagen follicles and increased hair growth in these areas.
The lymphatic vessels move tissue fluid by regular contractions, the one way valves in the vessels combined with these contractions "pump" tissue fluid away from the area.
The contractions are due to muscle fibers in the vessel walls. Muscle cells have androgen receptors, so it is perfectly possible for androgens to effect these muscle fibers to increase the rate of "pumping".
Such an action of androgens on lymphatic pumping also makes sense in terms of the "performance" effects of male hormones. Increased lymphatic drainage means increased turnover of fluid around cells, increasing nutrient supply and waste removal in tissues, so enhancing the muscle building action of other androgens.
Once you consider what we know about male pattern baldness in terms of DHT related effects on tissue fluid levels, this makes a lot more sense.
Not everyone developes male pattern baldness, and the time period for male pattern baldness can span many years. According to my theory the development of male pattern baldness in an individual depends upon other characteristics related to the blood feed side of a tissue fluid equasion.
Most of the lymphatic vessels of the head are concentrated lower down, including the beard area. The male pattern baldness pattern area at the top of the head is at the end of the system, and fluid draining from here has to pass through the lower vessels. If DHT increases lymphatic drainage the male pattern baldness area is vunerable because of the increase in pumping and the valves closing against flow from the end of the system (male pattern baldness area).
So increasing levels of DHT can cause an opposite effect of reducing tissue fluid drainage from the male pattern baldness area through fluid dynamic effects. This may or may not cause an increase in the local scalp fluid pressure, depending upon an individuals blood feed characteristics. Too much blood feed and the reduced drainage will increase tissue fluid pressures in the male pattern baldness area, smaller follicles through early contact inhibition and male pattern baldness.
This fluid balance shift can happen quickly or slowly of not at all, depending upon the individuals fluid dynamics. When it does cause hair loss, this only happens as follicles go into the anagen phase. Scalp follicles already in full anagen can not cycle again for years, "then" they become effected by the pressure.
This explains why male pattern baldness cannot be directly related to levels of androgens, and the long time periods involved. The current theory has to have every individual follicle expressing different genes to explain male pattern baldness.
Likewise the in-vitro test results support the involvement of a prior in-vivo change in growth gene related activity in male pattern baldness samples. Contact inhibition causing male pattern baldness is going to change the known growth response gene expressions. So of course then TGF beta-1 etc could be differently expressed from these samples in-vitro.
There are other holes in the in-vitro tests that i have argued before.
The only transplanted follicles that survive in the male pattern baldness area, are those that have had a healing process happen very close to them. The modern very small grafts achieve this. The old large grafts lost most of the hair over time until hair only remained around the edges (where the healing happened). This is known as graft "doughnutting", and is well recognised in the transplantation industry.
The well respected researcher Dr Uno reported that the fibrotic formation around long term male pattern baldness follicles, acted as a barrier to follicle enlargement. This is an example of contact inhibition in follicle growth.
In small graft transplantation, large anagen follicles are selected. When these are transplanted the healing produces a fibrotic shell around the graft. So we have a situation as reported by Uno. Only now this is a large fibrotic shell, that acts as a "mold" to preserve this space for future large anagen follicles.
This prevents the pressure in the dermal tissue from pushing dermal cells into the follicle space causing miniaturisation. In the current HM research, there is talk of an extracellular matrix being necessary to ensure proper follicle growth.
I suggest this happens naturaly in transplantation because of the healing, and is why these large follicles can re-cycle properly in the male pattern baldness area.
Also this "fluid pressure action on follicle size simply explains other known factors in male pattern baldness, the current theory cannot without resorting to added unnecessary complication.
The immunology and fibrosis that developes longer term in male pattern baldness, is a recognised effect of higher tissue fluid levels, as in lymphedema.
The proven sweating differences in tissues where DHT grows hair and male pattern baldness tissue, are also easily explained by this mechanism. Sweating reduces significantly in the beard area where DHT grows hair, but significantly increases in the male pattern baldness area.
Sweat is tissue fluid, so reduced fluid in the beard area will reduce sweating capacity, and increased pressure in the male pattern baldness area will increase sweating capacity, simple.
This fluid pressure/contact inhibition mechanism, simply explains all the factors in DHT related hair growth/loss. The current theory requires unknown and complex mechanisms that go against basic scientific principles.
I hope you now understand my theory. I have not used any references here to try to not distract too much, but i have posted the relevant ones before on these forums, and will again if required.
Regards.
S Foote.