Old Baldy said:
I'm showing you respect because you geniunely believe in a form of the hydraulic theory. You use the lympathic system to get there. That wasn't the theory in my youth. In my youth they just said sebum was choking or blocking the hair follicle. Your theory is more thought out.
I also mentioned the vacum cleaner device where you put a bag over your head and attached it to your vacum cleaner. It was supposedly going to "clear" out the clogged follicles. A far cry from your theory where you feel the lymphatic system creates internal pressures that choke off the follicles. I assume you feel the lymphatic system creates this "pressure" out of its reaction to DHT?
Medical research doesn't point to that happening but your theory is a far cry from the quackery I heard as a kid. You can't even compare the two.
Your theory is far more technical and thought out than the "hydraulic" or "clogging" theories I heard as a kid.
I disagree with your theory only from reading about DHT and male pattern baldness as it is viewed currently by the medical community. Being a layman that's all I really have to go by. But don't compare your theory to the quackery types of hydraulic theories I heard when I was a child. They are simply not the same thing.
My main concern with your point of view is why you reject the mountainous amount of opinions from the medical community stating DHT has a direct effect on the hair follicles. Not a direct effect on some other system that then affects the hair follicles.
Bryan accepts those findings from the medical community, you don't.
OK Old Baldy, i'am sorry if i read you wrong, and i will answer your main point, which is a fair question.
You say:
"My main concern with your point of view is why you reject the mountainous amount of opinions from the medical community stating DHT has a direct effect on the hair follicles. Not a direct effect on some other system that then affects the hair follicles."
I think the big problem historicaly in hair loss research, is that key experiments have not been considered. in the context of a `complete' scientific theory. The danger of not considering `particular' experimental results in the context of a complete theory, is that assumptions can be made, about the `true' significance of certain experiments.
In this case it has been shown that androgens directly reduce the growth of male pattern baldness follicle cells in-vitro. So because we know male pattern baldness is related to androgens, it is easy to go Ah-Ah androgens are having a direct effect!
The same principle applies in the donor dominance issue. One type of transplantation seemed to show that follicles must be inherently `different' in the way they respond to androgens. So there again the conclusion was that androgens are creating male pattern baldness `directly'.
This `hypotheses' has been around for over 60 years, and is still the currently accepted `mechanism' as you know.
The problem in my opinion is that the direct action idea cannot logicaly explain any of the other observations in DHT related hair growth/ loss. Any sound theory `has' to do this according to the scientific rules! I have argued the points of contention as i see them in this and other threads.
If this was mainstream science, the interpretation of the initial experiments would be re-thought to see if there was another reason for the results, that made sense of the `whole' observations.
My `Hydraulic' theory was developed to try to explain `ALL' the relevant issues in DHT related hair growth/loss, in accordence with the rules of theories. The basic argument is here
http://www.hairsite2.com/library/abst-167.htm
According to this, there are possible alternative explainations for what we see in both transplantation, and the in-vitro experiments.
If the cells in male pattern baldness follicles have been subject to normal `in-vivo' contact inhibition by an in-direct action of DHT, their `WHOLE' programed growth response has been altered! They are therefore likely to continue to demonstrate a growth restricted response in-vitro, to any number of substances. What the in-vitro experiments show `FOR SURE', is that androgens are not directly `CHANGING' the existing growth response of any of the samples. The direct theory, and the current donor dominance interpretation, says that androgens should directly change the growth response!
The point i would make to people is really this.
The direct theory has serious flaws for a number of reasons, and the range of experiments necessary to confirm `ANY' theory have just not been done yet in my opinion. Now that more and more professional hair loss researchers are questioning the assumptions of the existing theory, we might get these experiments done! Meanwhile, just don't take what `ANYONE' says on internet sites as `gospel' without reference to the recognised rules of science!
For reference, below is the letter i sent to experts for comments on my theory, that Dr Sawaya replied to.
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.
