@marlin
Questo è il post che ha fatto avviare un gb per UK5099. L'utente si definisce un ricercatore con background in Cellular Control Theory e afferma sostanzialmente di essere passato da nw3 a nw1.5 con capelli sparsi nella zona nw0, grazie a UK. E' molto riservato, a detta sua per preservare la privacy e per eventuali problemi legali.
Al di là della questione MPC inhibition, trovo interessante la sua spiegazione della proximity theory, che darebbe un senso un al evoluzione progressiva dell'AGA.
Che ne pensi?
Questo è il post che ha fatto avviare un gb per UK5099. L'utente si definisce un ricercatore con background in Cellular Control Theory e afferma sostanzialmente di essere passato da nw3 a nw1.5 con capelli sparsi nella zona nw0, grazie a UK. E' molto riservato, a detta sua per preservare la privacy e per eventuali problemi legali.
I will post some of my research but not all of it in the interest of time. I have almost cured my Androgenetic Alopecia to baseline, I will not recommend the materials to do so because of legal precariousness, but they've each been discussed throughout the forums at least in a speculative capacity. It is this ensemble of these materials which cures Androgenetic Alopecia. Anything you do is at your own risk and this is in no way a recommendation. The explanation anticipates all and every symptomatic facet of Androgenetic Alopecia hairloss. There are two major causes of the symptoms of Androgenetic Alopecia, the first is namely 5AR sensitivity about the follicles, and the hormones which are aromatized into DHT. DHT kills follicles by triggering Mitochondrial Pyruvate conversion (MPC) [6]. Lack of lactate production has recently been shown to determine the quiescence of the stem cells (note: the mere addition of lactate will not help Androgenetic Alopecia). This quiescence of the stem cells leads to the eventual demise of the follicle by preventing replenishment of the follicle by a mechanism discussed below. The second is evinced by the question which remains, why does a 5AR-inhibitor or otherwise DHT removal not trigger complete rejuvenation of the follicle given that the stem cell exists quiescently? The answer is that a single stem cell follicle itself is unable to signal strongly enough to receive the prolactin/17b-estradiol and other chemicals to participate in the hair cycle, which on trigger switches on MPC inhibition. What is needed is a collection (read density) of follicles (even if fully miniaturized!) to be fully synchronized, this can only happen if each stem cell remains in cycle with each other, where they solicit participation of the next hair cycle [1,2,3,4].
This is why single hair follicle transplants fail and why a minimum density of follicles is required. Additionally, this is why grafts only succeed in adjacency to healthy hair, while regrowth will always occur starting from the adjacent hairs. Finally, this is why hairloss often begins at the temple which has half the density of follicles than everywhere else on the head [7]. As stem cells become dysfunctional, it becomes more difficult for adjacent cells to participate in the next hair cycle. That is, hairloss is an exponential process, accelerating on each new cycle. The goal of Androgenetic Alopecia prevention and rejuvenation of quiescent cells is to then allow hairs to synchronously begin and maintain a hair cycle. This is where the efficacy of lactate hydrogenase medicine (e.g. minoxidil, but it should be clear though that this is not enough if the follicle is DHT treated or otherwise not in cycle) and 5AR inhibition occurs.
1. https://www.sciencedirect.com/scien...8a11500&pid=1-s2.0-S0022519301924749-main.pdf 2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2705329/#R17 (Regeneration only occurs during coordination!) 3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2705329/ 4.https://journals.physiology.org/doi/full/10.1152/physrev.2001.81.1.449 5. https://www.hindawi.com/journals/bmri/2013/957432/ 6. https://www.meta.org/papers/influence-of-5-dihydrotestosterone-and-17-estradio/21812787 7. https://core.ac.uk/download/pdf/82482832.pdf
Men have higher follicular density on the center forehead than the lateral. Please read the original post. Hair should recede in the temples first and then around those areas as follicular density diminishes. Hair loss should also be an accelerating process. Follicular density is less on the crown than it is on the center forehead.
Al di là della questione MPC inhibition, trovo interessante la sua spiegazione della proximity theory, che darebbe un senso un al evoluzione progressiva dell'AGA.
Che ne pensi?