It seems i owe you an apology Bryan!
After my reference to eyebrow growth, and your point about terminal growth next to vellous, i wrote a post on notepad to cut&paste later. I don't often do that, but i had been getting cut off line a lot that day. I had thought i had subsequently posted this, but i was distracted and it turns out i overlooked it sorry. :roll:
This is it.
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The central point of my theory is the `in-built' response of the growing anagen follicle to resistence from the surrounding tissue. The growth of any organ is limited by the normal characteristic of contact inhibition. Through contact inhibition, the growing cells meet resistence from the existing cells around this growth. Once a `certain' degree of resistence is meet, the growing cells stop growing.
This characteristic of the contact inhibition of cell growth, is built in to `ALL' normal cells. One of the clinical problems with cancer cells is that they invade other tissues and interfere with other organs, because they have lost `normal' contact inhibition.
I think it is pretty safe to assume that the level of resistence from surrounding tissue, at which growing cells are `switched off' by contact inhibition is a constant. However, other factors can come into play, increasing or reducing the resistence of the surrounding tissue, and so the size of the growing `organ' before contact inhibition kicks in.
Given the `design' of hair follicles and the way the hair cycle works, the `natural' resistence of the tissue around hair follicles, and induced changes in this, `will' create changes in anagen follicle size through contact inhibition, given the basic physics of the system.
It should also be remembered that the hair cycle produces a fresh `batch' of follicle cells each anagen phase, and if these are effected by contact inhibition, this particular batch are likely to retain this induced growth restriction `programing'! Such a characteristic is demonstrated by these cells in-vitro.
However, exposure to androgens of follicle cells in-vitro, does `NOT' directly induce any growth restriction!
The best and most realistic analogy to describe contact inhibition within the follicle `system', is the analogy with a simple party baloon.
If you try to push your finger into a party baloon, a couple of factors are involved in how much `resistence' there is.
Firstly there is the `natural' resistence to movement of the structure of the baloon (the skin). This will offer a `certain' amount of resistence to your finger trying to push into the baloon.
Secondly there is the amount of air pressure in the baloon. This pressure `backs up' the natural resistence of the structure or `skin' of the baloon.
If the structure or skin of the baloon is `weak', the resistence to your finger will be reduced, and you can penetrate the baloon with less resistence. If the pressure in the baloon is also low, the best conditions exist for the maximum penetration of your finger before a `certain' resistence is meet.
Also, if the structure or skin is `weak', any slight changes in internal pressure will make more of a difference to this resistence. If the stucture is `harder' or `tougher' is would take more of a change in pressure to effect the overall resistence.
The other important characteristic of this kind of `system', is that the resistence increases the deeper you push your finger into the baloon! This is a very relevant factor when considering the same principles in the dermis in regard to anagen follicle enlargement.
For the structure or skin of the baloon, consider the dermal tissue. For the pressure behind the skin of the baloon, consider the fluid pressure in the dermal tissue. For your finger, consider the growing anagen follicle trying to push into the dermal tissue!
If the normal contact inhibition of cell growth happens at a constant value of resistence, both the `natural' resistence of the dermal tissue in a particular area, `and' the local tissue fluid pressure, will combine to determine the point at which the resistence to follicle growth reaches the point at which contact inhibition `activates'.
I think hair follicles evolved to take account of contact inhibition of anagen enlargement, to link hair growth with the primary `Hydraulic' temperature control in mammals. This primary temprerature control in the dermis, reduces fluid pressure in cold climates, and increases it in hot climates. This change in resistence `adjusts' hair growth accordingly, and is the reason in evolution for this effect on hair according to my theory.
Why did evolution not just develope a surface structure to produce hair? Why do we have this `pocket' in the dermal tissue system? I think the answer is in this hair growth control system.
I think that apart from rare conditions that can effect the basic hair cycle itself, all hair growth in all species is controlled by the local resistence to anagen enlargement through contact inhibition.
In humans i suggest the factor of the local tissue `toughness' is the major factor in our hair patterns. This can produce the terminal hair growth we see next to vellous growth. Often you can see some intermediate `shorter' growth at this border. Those with Norwood 1 (No loss), can pull back their hair and see shorter hairs in the hairline area.
There is a good example of this mechanism in eyebrow growth.
Eyebrows are seemingly `islands' of hair growth with no apparent association with anything else. But there is a precise association with another factor if you `feel' the tissue this growth comes from!
This hair growth corresponds with an area of `weak' tissue'. You can feel this `softness' compared to the tissue above and below. Boxers can tell us all about how this tissue is easily split!
The tissue resistence factor described above, explains eyebrow hair growth.
I suggest that we have long terminal hair growth on our scalps because of `weak' tissue, and lower fluid pressures in this area, at least pre-puberty. In older bald men, you can often see if you look closely, a change in the surface of the scalp tissue that corresponds to the original hair line.
The down side to this area of weak scalp tissue that produces terminal growth, is that any slight increase in fluid pressure in this area, will more easily increase the resistence of weak tissue as described above. This will more `easily' create smaller follicles through contact inhibition, {male pattern baldness}.
I suggest the primary influence of DHT on changing hair patterns, is through inducing changes in the local tissue pressures.
Again i suggest that the growth of the anagen hair follicle has evolved around the local tissue resistence, and follicles are `very' sensitive to this factor. It doesn't mean that the natural tissue `toughness' differences are going to be obvious, or indeed any changes in the local tissue pressures. But i suggest the evidence is there if we look close enough, as in the eyebrow example.
Going back to the `baloon' analogy. If your finger was able to penetrate to the maximum depth, and then a `tough' structure formed inside the baloon around the `mould' your finger made, any future changes in pressure would not effect `future' finger penetrations. The tough `mould' would preserve the space for your finger!
This is how transplanted anagen follicles survive according to my theory, because of the tough fibrose `shell' formed around it at the time of initial healing.
This post is intended to clear up some points raised about my theory.
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I will try to read any posts as soon as i can, but i am still having some connection and other computer problems. I hope to resolve these over the weekend.
S Foote.
