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idontwanttobebalding said:S Foote. said:Has this theoretical treatment grown any hair on the human male pattern baldness scalp yet?
Please understand....I lean more to the "non-direct effect" side....
but, questions must be answered....
there is no light without darkness....
and since no one else is asking you questions.... :whistle:
then I will!
In regards to your question...please check current clinical stage of Follica's approach. It is my understanding that the "wounding" aspect of their treatment is of central importance...however, a topical treatment is an option that, perhaps, may help results. (wounding by a "medical device" speeds FDA approval from my understanding...please correct me if I am wrong!)
I also ran into this study:
http://www.ncbi.nlm.nih.gov/pmc/article ... =pmcentrez
This study speaks to some of the issues we are exploring.....
In this report, we address these key questions in the unperturbed in vivo confines of the normal hair cycle, as well as in response to injury. In so doing, we unearth surprising and dynamic features of the HF-SC niche and its progeny. First, we show that during anagen, the upper ORS remains slow-cycling, like their SC predecessors, while lower ORS cells cycle more rapidly. Moreover, slow-cycling ORS cells survive catagen and contribute mightily to both HG and a new bulge: in fact, they become the main source of SCs used during the next hair cycle. Lacking a DP, the initial bulge ceases to play a major role in homeostasis but can respond to injury. Finally and perhaps most surprisingly, some actively cycling lower ORS cells not only survive catagen, but also home back to the bulge. Like their upper ORS predecessors, these cells retain many HF-SC markers. However, they irreversibly lose their ability to proliferate in normal homeostasis or upon wounding. Instead, they function decisively in hair anchorage during the resting phase and in providing the quiescent signaling cues that control the hair cycle. Our findings define a point along the ORS where cells lose stemness and become irreversibly fated to differentiate or die, and illuminate how downstream SC progeny can provide negative feedback to the niche and restrict SC self-renewal and tissue formation.
Could this help explain where the "negative" growth factors, influenced by androgens "in" the follicle occur, and, how their damaging effects can influence not only the current follicle.......but the "next one" as well?
what are your thoughts on the above study?
And how does your theory work with it?
Thanks for your interest and the links.
What i suggest is that there are two things going on when it comes to hair growth. There is the normal hair cycle, and the mechanism of contact inhibition. I dont think that the hair cycle in itself is the problem in male pattern baldness, i think the anagen phase is switched off early by external pressure, then this modifies the other phases of the cycle. I think if you change the external pressure, the hair cycle can sort itself out.
My concern with the hair multiplication and cell/genetic manipulation experiments, is that these are not going to get around normal contact inhibition, if this is the problem in male pattern baldness.
No one knows much about the pathways involved in contact inhibition, only that this is a basic reaction to cell division and tissue growth in-vivo. This prevents tissue growth from invading the space of other tissues, and all normal cells react to contact inhibition of growth. The central characteristics of cancer cells is they lose this reaction, and this is how they cause damage to healthy tissues.
We do know that the Wnt's pathway, b-catenin, and TGF beta-1 are linked to the contact inhibition process, and these factors have been suggested as relevant in male pattern baldness. Fuchs did a mouse study where she manipulated Wnt's and b-catenin, and grew significant amounts of hair. The problem was the tumor developement that went with it.
In my opinion, there could be ways that HM could work, a wounding process should help because it is thought that contact inhibition is "relaxed" because of injury to allow better healing. Some proposed procedures claim a matrix of some kind to help in tissue growth, basicaly a "mould" that allows tissue growth.
I think there could be easier ways forward with research shifted to the surrounding tissue, and maybe this currect HM research will reach that conclusion?