It could work but if does increase hair then you'd notice hair everywhere. OL and EGCG work differently when taken orally and I cant vouch for their oral effectiveness on hair growth. Theres not alot of research on oral supplements increasing scalp hair growth in AGA unfortuneately. You're much better off using them topically since they are quite soluble and have low-ish molecular weights.
Good question. Simply dissolving in a solution does not mean it will permeate the skin. The molecular weight in addition to solubility properties are a much predictor of topical absorption. This is a probabilistic model where complete absorption and equal tissue distribution is not guaranteed. Ethanol has the ability to strip the skin of lipids and enhance the absorption of molecules. Heres a post I made on minox/OL molecular weight and absorption.
I apologise, you are correct. It is indeed the DP1, so CRTH2 anatagonists shouldnt be a problem. I think I need you to correct mistakes in my analysis lol.
Two receptors for EDA were found that are specific for the two isoforms EDA-A1 and EDA-A2: EDAR and EDA2R, respectively. EDA-A1 and its receptor EDAR are capable of activating the NF-κB pathway and are implicated in hair growth. EDA2R is capable of activating the NF-κB pathway and also through TRAF3,6, JNK (c-Jun N-terminal kinase), which activates c-Jun. Mutations in EDA and EDAR give rise to ectodermal dysplasia, a clinical syndrome characterized by loss of hair, sweat glands, and teeth, whereas mutations in EDA2R do not. Recently, a preliminary report suggested that EDAR may influence hair thickness in Asians, A scan for genetic determinants of human hair morphology: EDAR is associated with Asian hair thickness.
EDA2R could influence the onset of AGA through the activation of the NF-κB pathway or by c-Jun, which has been shown to be critical for AR transactivation. Moreover, in adult mice, EDA2R is also expressed in the hair bulb and in differentiating hair matrix (Botchkarev and Fessing, 2005).
Our previous studies suggest that the proto-oncoprotein c-Jun is an AR coactivator that stimulates AR transactivation by mediating receptor dimerization and subsequent DNA binding. (study)
So this means in the presence of AR, anything that wants to activate AKT via PI3K will be unsuccessful. This includes IGF-1, shh, EGF (wiki). Beautiful diagram here: https://en.wikipedia.org/wiki/File:M...thway-v1.7.svg
But does this mean beard DPC do not inhibit PI3K via PTEN in response to AR activation? Apparently PTEN deficiency results in accelerated hair follicle morphogenesis and enhanced AKT(PKB) activation (study). Very interesting.
Heres some more research on ERb and hair.
Recent in vitro studies have shown that 17β-estradiol inhibits female scalp hair shaft elongation (Nelson 2006), although stimulation occurs in hair follicles derived from frontotemporal male scalp (Conrad et al 2004). In addition, in female hair follicles the phytoestrogen, genistein inhibits hair shaft elongation to a similar extent as 17β-estradiol. Since genistein preferentially binds to ERβ, this opens the possibility that the inhibition of hair growth in response to 17β-estradiol may be mediated via ERβ rather than ERα (Nelson 2006). Therefore the development of selective estrogen receptor ligands may provide important clinical applications for the prevention and treatment of disorders of hair growth.
ERbeta was the major steroid receptor expressed in human skin. It was highly expressed in epidermis, blood vessels and dermal fibroblasts, in contrast to ERalpha and AR. In the hair follicle, ERbeta expression was localized to nuclei of outer root sheath, epithelial matrix and dermal papilla cells, in contrast to ERalpha, and the AR, which was only expressed in dermal papilla cells.
Anyways, I want to know what role ERa has in male DPC. ERb can increase proliferation of existing hair, but does it secrete growth factors in a paracrine manner? Or does ERa promote WNT activation by itself in DPC to prolong anagen?
It can! This is excellent research SriHanuman. Unfortuneately I cant use this because I'm trying a different stack, so I wont be able to gauge its effectiveness. People who cant use minox might find fo-ti useful.
Thank you! We're uncovering so much research that I think it is already leading to something.
Update
Last week I increased the EGCG concentration totalling 12.5mg/ml. The hairs that I grew using minox + OL are 100% terminal. Really wasnt expecting results this fast. I'm seeing more tiny vellus hairs along nw1 hairline and the skin turning grey/green. My nw1/0 hairs grow sideways, as in they come out of the skin at very low degree angles. My nw0 is hairline is completely bald atm so it might be harder to regrow. I'm not sure if my aggressive micro-needling (3mm derma pen) last year has caused scarring. I hope not because I'd be devastated.
Bear in mind I'm using the MXOLCG once a day at night because of work and laziness, and Ketoconazole in the morning. During the weekends I use MXOLCG 3x day. If only I could use minox 3x a day everyday... I try to use Emu oil every two days, and I'll be adding the Gamma Linoleic Acid to the Emu oil (which has minox in it already). I'll be posting pics soon. I am tempted to use Rosemary but I'll wait.
I'm also going to ask the moderators to let me edit my first post so I can reorganise the research for people to find easily.
Leave a comment: