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Originally Posted by ThisSucksDude
That "DT" massage therapy is pure bullshit.
Didn't the original article say there was full regrowth in 10 MONTHS?
People were doing it for longer than that and couldn't provide photos.
It was just a horseshit article from japan or korea.
I was doing it for a month or two and since no one was giving clear instructions and I was desperate as ****, all I did was end up denting a part of my soft tissue scalp from pressing so hard.
I don't see any downsides to it though (not pressing as hard as you were I guess lol!). I'm not doing the 2x20 mins massage they are talking about, I'm doing a way less time consuming method I made up myself + scalp exercises (I know I know ). And I have halted my hairloss since I started, but as I said earlier it wasn't very aggressive to begin with and yes, I know hairloss isn't always consistent.
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Googled perifollicular fibrosis.. Even more convinced to keep the blood flowing to my scalp now >_>
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It has more to do with the layer of fat under the skin than the skin itself
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Originally Posted by FeelsBad
It has more to do with the layer of fat under the skin than the skin itself
Yeah, I've been reading more into that in the last week. I'm pretty convinced all the big companies battling this are taking the wrong approach.
Seems pretty obvious to me that the hair needs good growing grounds.
EDIT: I don't think more bloodflow to the scalp hurts though, that's where you get the nutrients from after all. (Isn't that what minoxdil does anyway?)
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In a healthy hair follicle cycle the micro environment of the hair follicle communicates with the macro-environment (surrounding tissue). This leads to a tremendous increase of vascularization and adipogenesis in anagen. In telogen there is barely any vascularization at all (almost non-existent) and there is a lack of adipose tissue. These changes lead to a thicker dermis in anagen as you can see on the picture.
Now in AGA you see that the morphology of the hair follicles changes dramatically too. Similar to telogen, but more extreme. Often it is accompanied by inflammation and in late AGA even fibrosis can set in (scar tissue, that can lead to destruction of the hair follicle similar to cicatrial alopecia).
Thus to me it sounds logically that in a bald area the skin is thinner and feels more firm. Although I don't think a study exists that measures the differences in skin thickness.
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Originally Posted by Swooping
In a healthy hair follicle cycle the micro environment of the hair follicle communicates with the macro-environment (surrounding tissue). This leads to a tremendous increase of vascularization and adipogenesis in anagen. In telogen there is barely any vascularization at all (almost non-existent) and there is a lack of adipose tissue. These changes lead to a thicker dermis in anagen as you can see on the picture.
Now in AGA you see that the morphology of the hair follicles changes dramatically too. Similar to telogen, but more extreme. Often it is accompanied by inflammation and in late AGA even fibrosis can set in (scar tissue, that can lead to destruction of the hair follicle similar to cicatrial alopecia).
Thus to me it sounds logically that in a bald area the skin is thinner and feels more firm. Although I don't think a study exists that measures the differences in skin thickness.
Thanks for posting that.. Yeah it's almost infuriating that no one is looking in to it
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This is interesting. Feeling all these scalp sensations, especially over the past few years, has left me wondering about hair loss and vascularization. A follicle that is not producing a fiber doesn't need an ample blood supply, so those vessels are closed off to redirect blood elsewhere, correct. SO, in the event that one starts to regrow hair, through minox or finasteride, there has to be some kind of capillary remodeling, or opening of existing vessels to supply the blood? If this occurs, would you have scalp sensations?
It also reminds me of inflammation. When I had knee surgery I had IDENTICAL feelings as I have had recently in my scalp, just at a larger magnitude. The best way to describe it is, "a slow ant crawling from one point to another directly under your skin".. I would massage my knee and the feeling would go away OR simply move to another location. Is this just stagnant blood working to push through restricted vessels and stimulating neural sensations? It ALWAYS, EVERY DAY, starts at only my left hair line and proceeds towards the middle back. If I scratch it, or massage it, it immediately stops and then proceeds in a different location, as if I just manually moved the blood through a restricted artery. It might sound crazy, but this is the only thing that seems logical to me.
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Send to:
Exp Dermatol. 2016 Jan 19. doi: 10.1111/exd.12941. [Epub ahead of print]
Dermal adipocytes and hair cycling: Is spatial heterogeneity a characteristic feature of the dermal adipose tissue depot?
Kruglikov IL1, Scherer PE2.
Author information
Abstract
Adipocytes are widely distributed in the dermis, in a unique fat depot referred to as dermal white adipose tissue (dWAT). In rodents, dWAT is present as widespread thin layers, whereas in pigs and humans it is present in clusters referred to as "dermal cones" around the pilosebaceous units. This distinct layer of fat cells located above the subcutaneous white adipose tissue is important for proper hair follicle (HF) cycling in rodents. Murine HFs produce spatially restricted synchronous patches after their second postnatal cycle which correlates with a spatial heterogeneity of murine dWAT. Similarly, the cycling of HFs in humans may also be related to the spatial distribution of dWAT, making the difference between murine and human HF cycling of more quantitative than of qualitative nature. This should allow the production of small spatially correlated HF patches in human skin and we propose that this process can be regulated by paracrine signaling and involving a number of signaling modules, including the hedgehog pathway. This pathway is an established player in HF cycling, but is also involved in the regulation of adipogenesis and may therefore be a key regulator of the process across species. We also suggest that the spatial heterogeneity of dWAT is connected not only to HF cycling, but may also be related to other physiological and pathological processes in the skin. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
KEYWORDS:
cycling; dermal adipocytes; hair follicle; human; mosaic; murine; synchronous
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