I have not much idea what the purpose of hair in mammals, but I have the impression that our existence would be seriously compromised if there were no pilosebaceous units.
What I have clear that we have become the naked ape, but not a bald monkey. We miniaturized body hair but we have enlarged hair on the head. All hair is not the same, the eyebrows, eyelashes are special and only partly be compared with body hair or scalp.
My theory, as you know, could explain not only the pattern of hair loss, but the difference in incidence between the sexes. For me, the hair on the scalp is the same in men and women. And I have in mind all the processes involved in alopecia, hormones, fibrosis, immunology, blood flow, etc.. What I want to explain are the first processes that occur.
I will carefully read your ideas. Do you think that the DHT is necessary to grow healthy hair, not just the body, but the head?
I think you need to go into a lot more detail in support of your idea's Armando. I don't think DHT is necessary to grow hair at all, but it obviously has a major effect on changes in hair growth.
I am posting below about the details of my proposal in male pattern baldness, and the treatment strategy this suggests.
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This is an elaboration in simple terms, upon how this proposed hair adjustment mechanism fits in male pattern baldness. In my following post i will offer my thoughts on current treatments, and the possibilities this mechanism offers for better treatments of male pattern baldness. The proposed mechanism is described here.
http://www.open-science-repository.com/an-evolved-hair-growth-mechanism-in-mammals-implications-in-human-physiology.html
The basic principle is that follicle size is dependent upon the resistence of the surrounding tissue to follicle enlargement, this resistence being modified by changes in local tissue fluid pressures. The recognised molecullar changes in follicles being downstream from this causal action, and not directly rellevant.
When this principle is applied to human androgen related hair growth/loss, it answers the questions according to the scientific requirement of parsimony. Quote "entities should not be multiplied unnecessarily". In this case, an initial action of DHT to increase lymphatic pumping, explains all the downstream effects upon hair growth and related factors. The logic of such an action of androgens on the lymphatics, and how this also explains the associated scalp conditions in male pattern baldness is described in my paper.
Lymphatic vessels drain fluid from tissues by regular contractions. Because the vessels have many one way valves, these contractions move fluid from the tissues to eventualy drain back into the blood circulation. Because of this lymph pumping action, if you wanted to introduce a substance that increased the pumping, this would have to be introduced largely at the extremities of the vessels to balance out over the length of the system.
Any inbalance increasing pumping downstream, would increasingly shut the valves against the flow from the extremities, actually reducing flow in that area. Such opposite effects are common in fluid systems, and this fits with the opposite effect of DHT leading to male pattern baldness in some individuals.
DHT is largely produced near the extremities of lymph vessels, in the dermal tissue. We know DHT is produced from testosterone in hair follicles and sebaceous glands, hair follicles being the largest producer. It stands to reason that there are more DHT producing cells in large hair follicles like scalp follicles. This is how i see the events leading to male pattern baldness.
The rising levels of DHT at puberty increases lymphatic drainage, and increased numbers of these vessels close to hair follicles increases growth through this mechanism. A lot of local DHT is produced by the large scalp follicles, and initially scalp hair growth can increase further. But the amount of the lymph vessels increases lower down, the male pattern baldness area itself is at the extremity of the lymphatics. The increasing DHT feeding into the lower vessels increases drainage here leading to beard growth. The larger follicles of beard growth then add more DHT to the increased lymph vessel pumping lower down. The male pattern baldness area starts to suffer from the back pressure effect, and drainage here reduces increasing risk of lymphedema.
This reduced scalp drainage may or may not lead to male pattern baldness by this mechanism, depending on another related factor. I think the clue to this other factor, is in the recent confirmation that male pattern baldness sufferers are more likely to develope coronary heart disease in later life. The common link would be increased blood pressure feed to the scalp, and perhaps other blood circulation issues.
The fluid balance in tissue depends on a feed and return equation. Reduced lymphatic drainage may not be enough to increase local tissue fluid levels, if the fluid feed is not excessive. The higher the feed pressure, the more likely reduced drainage will lead to increased tissue fluid levels and pressures. I think this is why DHT levels themselves do not equate directly to male pattern baldness in the individual, it's the fluid feed pressure that affects risk of male pattern baldness for a given level of DHT.
How this mechanism of male pattern baldness fits with known and potential treatments, will follow in my next post.
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Following on from my post above, i will discuss traditional treatments for male pattern baldness in the light of this mechanism, and how we might improve the situation.
According to the proposed mechanism, male pattern baldness is caused by DHT induced lymphedema. The recognised effects of lympedema on tissue matches the known conditions in male pattern baldness, as refered to in my paper. The normal obvious swelling of edema does not develope in the scalp, because this is a relatively thin curving tissue that naturaly resists tissue expansion. What this means is a high pressure relative to the degree of tissue expansion, and this is reflected in the recognised scalp tightness in male pattern baldness.
I think the higher scalp fluid level in male pattern baldness also explains how we have been mislead in the diagnoses of the pathway involved. We know that there are higher levels of DHT in the bald area compared to the hairy sides. We also know that every now and then, it is discovered there are also higher levels of other substances in the bald scalp. The latest here being PGD2.
Increased fluid levels in a tissue, will also mean increased levels of anything being transported in that fluid. That dosen't mean these substances are causal in male pattern baldness. Logicaly, the miniaturised follicles in male pattern baldness just cannot produce more DHT than large follicles in hairy areas. I think this is why using topical 5ARI's in the male pattern baldness area does very little, they are being used in the wrong place. The systematic 5ARI's like Propecia work better for this reason, but then you have the side effects.
This mechanism also explains why we get contrary advice on when to start treatments for male pattern baldness. They say with most treatments the sooner the better, but in transplantation the advice is often wait as long as you can for the best results. This fits in very well with this mechanism.
If you are trying to re-enlarge the shrinking follicles, you need to act quickly before the surrounding tissue toughens due to developing fibrosis, also known to be caused by edema. This explains why the longer male pattern baldness goes on, the harder it is to reverse. In transplantation you want fibrosis formation in the scalp. Because this will help stabilise the tissue against further expansion, and form a better protective scaffold around the transplanted follicles.
As i refer to in my paper the common factor in treatments shown to have 'some' effect, is a reduction of fluid levels in the male pattern baldness area. I should add low level lasers to this list, as these have also been demonstrated to reduce fluid levels in lymphedema.
In my opinion, this mechanism also explains why the current research into the HM type procedures, is going nowhere. These are not targeting the problem, in that hair follicles have evolved to adjust their size according to the resistence of the surrounding tissue. Trying to go against the normal tissue growth controls creates a paradox, in that the more effective the procedure, the more likely it will not be licensed for safety reasons. There may be a case for a technology that grows whole large follicles outside of the body. These then being used in conventional transplantation. But i think there is potential for better, safer, and cheaper alternative treatments than this in the future.
They say that the myths and 'old wives tales' about something, often have a grain of truth in them? There has always been the 'poor blood supply to the follicles' notion about male pattern baldness. We get idea's to increase follicle blood supply, hanging upside down, scalp exersises, massage, various electrical devices etc. We know it is not an issue of blood supply to the follicles because of transplantation. However, i think what these things can contribute to is better circulation in the scalp tissue, helping to reduce the fluid levels.
In particular i think a good massage method is very worthwhile. This can help to move excess fluid, and break down fibrosis. Avoid any topical that causes irritation and further inflamation. Use cool water when washing the area, and generally treat the scalp as an edemous tissue.
According to this mechanism we need to target two things to treat male pattern baldness effectively. The DHT induced scalp drainage restriction, and the high pressure scalp blood feed.
The real target for topical 5ARI's is not the male pattern baldness area, but the hairy area's of the scalp and face. This is where the excess DHT is produced that triggers the process of male pattern baldness. I think this is why Nizoral shampoo has been supprising in its effect on male pattern baldness. It is used on the whole scalp, and in effect the face/beard area. It should be possible to produce better 5ARI effective products for this purpose. This better targeting of topicals could make it possible to avoid systematic 5ARI's and their side effects altogether. Topicals for the male pattern baldness area, should be aimed at reducing the inflammation/fibrosis element that hinders the reversal of male pattern baldness, and may help to reverse longer term male pattern baldness.
There is already a surgical procedure that dramaticaly reduces excess blood supply to the scalp. This has been used to good effect in seborrheic alopecia. http://www.ncbi.nlm.nih.gov/pubmed/157397 Note the statement that "the condition of the hair follicle is strikingly improved". It may be argued that this is because of other factors, but such a follicle response to reduced blood feed in the scalp, is in line with the mechanism described here.
This would of course need to be further researched and approved for use in male pattern baldness. But this kind of procedure along with the 5ARI method above, would be the future of more effective male pattern baldness treatment according to the evidence for this proposed mechanism.
