I found this, similiar, can get the extract on amazon:
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I have also added 50 mcg of KGF (from Skinactives.com) to 74ml of solution. Don't want to add anything else, as my scalp seems to be ok with the ingredients and percentages currently.Leave a comment:
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Chemical - I am using higher EGCG because I have used at least that strength before, and had no problems. Yes, it dissolves completely in distilled water. It will be a brown color, and stains anything it touches. As for the OL .5%, that's the percentage recommended by SkinActives.com for oleuropein in topical formulations. We'll see how it goes.Leave a comment:
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You really have to forget about emu oil ! There is really no REAL SCIENTIST STUDY about emu oil. Emu oil is just a scam for hairloss, it don't decrease 5AR or DHT
What about Zinc/Zinc Sulphate, Vitamin B6, BetaSitosterol ? It can be a good addition.
In addition, you're attacki AR/5AR/DHT/DKK1 but you should find a way to increase grow factor...because if you want regrowth, you need grow factor (VEGF-> Increased with stemoxydine, but there is FGF ; KGF ; Follistatin).
Look at thistogen : They just play on grow factors...not on DHT and look at the regrowth ! Awesome !
Conclusion : Your idea is good, but now, you should find treatements to add which can increase grow factors ( FGF, KGF, VEGF, FOLLISTATIN, PGE2)Leave a comment:
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If you can use minox then I'd recommend you get your hands on some minox from here: http://www.kirklandminoxidiluk.co.uk/
Then you can just use this oleuropein from amazon uk and this EGCG from amazon uk too. The OL you linked doesnt have a high enough ethanol concentration and likely wont work as effectively as a minox vehicle or a custom Ethanol/PG solution. If you cant use minox then you can use this post from josh as a starting point. Alternatively you can wait for Keeper to organise a OL/EGCG trial with his contact.
Thank you for your kind words, it really makes me happy to know people value the research we are doing here. The biggest motivation is that I think with the combined knowledge and effort of people in this forum we can actually find something that genuinely woks to regrow hair - and keep it. I will indeed be posting more pictures as I see progress. I hope this really works for you and everyone else who's decided go ahead and try this experiment, especially given that its still just experimental research with little real world evidence.
Thats an awfully high amount of OL you're using and EGCG too. I would definitely lower the OL if you can but i not, then I'm interested to see how the higher dose works. I have a few questions. Does the EGCG dissolve well in just water and do you notice any crystal-like residue left after it dries up? I think I will get in contact wit hthe Oleuropein study researchers to find out what happened when they used 3mg OL.
That is an amazing find SriHanuman. According to the study, PGE2 was increased but I couldnt see where they mentioned how it that. They also mentioned minox increasing COX-1 as a mechanism for increasing PGE2, so if G. elliptica increases cox-1 then it wont be anymore useful than using other ways of increasing COX-1/2 production. However it does have strong 5ar inihibitory properties that are dose dependent. The only problem is its quite to find (I didnt look hard enough?).
Rosmarinus officinalis . Its available from amazon uk too. As Brian has shown, rosemary has AR and 5ar suppressive properties making it a potential treatment to stack with EGCG.
Herse the complete list of treatments we have available so far:
Oleuropein: ¬DKK1, ->WNT10b, ->IGF-1, ->BetaCatenin
Emu oil: ¬5ar, ¬DKK1 (via antioxidant activity)
EGCG: ¬Axin, ¬AR, ->BetaCatenin
Rosmarinus Officinalis: ¬AR, ¬5ar (Only rosemary extract not oil or rosmarinic acid)
Gamma Linoleic: ¬5ar (Evening primrose extract)
Procyanidins: ¬PKC, ->BetaCatenin (Apple polyphenols/Grape seed extract)
Forskolin?: ->PKA
Valproic Acid: ¬GSK3b, ->BetaCatenin
Miconazole/Ketoconazole: ¬17bHSD ¬3bHSD
@Kuba197
I would encourage you to ask any questions you may have on the forums so that it may help anyone else who might have the same question. If you truly must contact me in private then: chemxrs at gmail dot com (I hope I dont get in trouble for doing this)Leave a comment:
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Chemical,
Can you give me your e-mail or something that I could contact you.Leave a comment:
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Chemical - I am currently using a 4% (2960 mg EGCG / 50% Green Tea blend, so about 1480 EGCG proper) in 74ml .......5% OL (it's a blend w/20% OL - so about 300mg of Oleuropein proper) ..... 1% Rosemary Ext ... 1% Jojoba Oil .... (.2%) Tea Tree Oil. This is in a distilled water solution. I add maybe 4 ml of 70% ethyl alcohol as well. Apply that, then wait for that to absorb and apply Minox foam, then finish with Ketoconazole 2% cream. I do this 3 times a day if possible. Scalp seems ok with this regimen so far (2 weeks). I would like to use even a higher dose of EGCG blend, but, the hair growth stimulation seems to occur just under the threshold of when the folliculitis starts. So, have to be careful. I don't want to be forced to stop treatments. Scalp feels in harmony and in a positive direction again.Leave a comment:
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Chemical,
I often find myself coming on this website hoping for some sort of miracle cure/new breakthrough treatment/some semblance of hope that I can hold on to. Your knowledge, willingness to explain things in detail and sheer pro-activeness with this awful affliction is great to read, and great to be aware of. Really hoping your hard work and dedication pays off and that you've answered some, if not all of the questions that this sort of hairloss poses.
Have ordered my first lot of EGCG and OL because of this thread. Fingers crossed it works!
Thanks again for your efforts; please post your pictures when you have any updates/progress! I'm not in a situation to post pictures for another 2 months but absolutely will when I can mix my new ingredients with minox.
Jackhammer.Leave a comment:
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Hi chemical
1st thank you for your commitment to the thread.
All very technical and my knowledge of this stuff is next to nothing.
http://www.amazon.co.uk/gp/product/B00B2U9MW4?psc=1&redirect=true&ref_=oh_aui_detailp %20age_o00_s00[/url][/B]
Im in Ireland and cannot get the product above shipped from the U.K.
I have been taking the below as a supplement http://www.comvita.com/products/oliv...-natural/H5488
Would this do mixed with Emu oil?
Appreciate some feedback from all on the thread
Thank you and good luck.Leave a comment:
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How long have you been using VPA, and have you seen any change? Also where did you get the acid form?
PGD2 is quite important for REM sleep and I dont like the idea of messing with neurotransmitters. Thats why I dont like fin either (messes with pregnenolone). If seti can be used effectively topically then that might be ideal. You might also want to increase your EGCG dose too seeing as we're both using very low doses. I'm going to add another cap bumping up the total to 500mg/40ml = 1.25% EGCG.
Indeed, AGA is definitely an androgen mediated disease.
Sorry you're right. I'm using a 0.875% solution. How much EGCG are you using?DOSAGE EQUIVALENCE PERCENT
1mg/mL 0.1%
0.1mg/mL 0.01%
0.01mg/mL 0.001%
0.005mg/mL 0.0005%
@InBeforeTheCure
From those excerpts it seems they are saying having a combination of AR related alleles can predispose individuals to AGA, with EDAR/EDA2R being the most significant predictor. I dont particularly like lookng at nf-kb because its functions are so broad and it plays a hand in alot of signalling cascades which makes it difficult to see the bigger picture. But looking this picture from wikipedia I see PKC activating nf-kb.
I read previously that Andrpgens have the ability to upregulate or maintain AR transcriptional activity. There are feedback loops including GSK3b that try to inhibit AR, but we know PKC can phosphorylate GSK3b possibly preventing the feedback loop. AR also inhibits the PI3K/AKT pathway which prevents the additional degradation of GSK3b. However, inhibiting AR causes an increase in Pi3K/AKT signalling which is good. Without PI3K/AKT, PKA will not be as elevated (?) and PKA is known to upregulate AR. These feedback loops are ridiculously complex and we're only scratching the surface. I just wish it was simpler.The transcription factor nuclear factor (NF)-kappaB, which is implicated in tumorigenesis, functions as an important downstream substrate of mitogen-activated protein kinase, phosphatidylinositol 3-kinase, AKT, and protein kinase C and plays a role in other cancer-associated signaling pathways.
About EBF1, I remember making a post about the relationship between adipocytes and hair. EBF1 is expressed during anagen and also from the study you posted, inhibits ERb. In mice ERb is known to be hair growth suppressive so thats probably a good thing? Or perhaps EBF1 is doing something else behind the scenes.
Theres a disparity between mice ERb receptor distribution and male ERb receptor distribution in the scalp. (females have different ER distribution too) (post).Analysis of Ebf1 mRNA expression using in situ hybridization revealed that Ebf1 is expressed in the DP in mature, growing hair follicles at P4 (Rendl et al., 2005); however, bulge, hair germ, and DP cells lack Ebf1 expression during the initiation of a new anagen during the hair cycle (Figure S3B), when adipogenesis is active. This expression pattern was confirmed by real time PCR on isolated DP cells and epithelial cells (Figure S3C).
I was going over the research on 3b-Diol again and found something I'd missed:
In addition, 3β-adiol is considered a powerful DHT metabolite since its intraprostatic protein level is 100-fold higher than that of estradiol (E2) (29). Notably, 3β-adiol has antiproliferative actions which are not reproduced by 17β-estradiol (30). http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4212017/So Estrogen when applied topically in males doesnt inihibit hair unlike 3B Diol which has antiproliferative actions despite acting via ERb. Regardless of how AR is being increased, preventing the ability of AR to bind to the cell surface and also prevent the intracelluar nuclear trranslocation might be the answer we're looking for. I think given the variation in genetic components, theres a chance these treatments could be hit and miss.We found that 3beta-Adiol not only inhibits PC3-Luc cell migratory properties, but also induces a broader anti-tumor phenotype by decreasing the proliferation rate, increasing cell adhesion, and reducing invasive capabilities in vitro. All these 3beta-Adiol activities are mediated by ERbeta and cannot be reproduced by the physiological estrogen, 17beta-estradiol, suggesting the existence of different pathways activated by the two ERbeta ligands in PC3-Luc cells.
InBeforeTheCure has shown that PGD2 can increase GSK3b, and so it would be incorrect of me to say PGD2 doesnt have a role. I think it has a role but not as significant as the parent mediator of PTGDS, Androgens. I believe we should be focusing more on Androgen as that way we can eliminate multiple bad pathways with one big swoop.
Furthermore, I'd encourage you to read the previous page where I mention cotsarelises findings on actual real world PGD2 expression levels in bald scalp, which shows a modest 2.5-4 fold increase. InBeforeTheCure has also brought to light that 50% if AGA individuals are not sensitive to PGD2 further reinforcing my statement that PGD2 is not the only or most significant factor implicating AGA.
Although the analysis done on mice showed hair phenotype resembling AGA, you can see I've boded the bit that says "15-dPGJ2 was increased 14 fold" in the Ptgs2 overpressed mice. if you look at figure 2F: http://www.ncbi.nlm.nih.gov/pmc/arti...975/figure/F2/
You can see that 15-dPGJ2 is only a small fraction of PGD2, so a 14 fold increase in the metabolite would mean a ridiculously high concentration of PGD2 in the mice. Its not at all surprising that suraphysical levels of PGD2 can retard hair growth. But we have to be realistic here, in AGA humans its not that high anyway. If you inject mice with testosterone or DHT, they also show follicle miniturisation exactly like humans. In fact, anything that reduces BetaCatenin (antibody or what have you) will result in AGA phenotypes. I hope this has clarified my opinion on PGD2's effects on human hair.
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On the topic of AR, I found a study talking about synergistic effects of 5ar inibitors and AR antagonists:
So if I use a 5ar antagonist alongside EGCG theoretically there should be even greater AR suppression. EGCG can inhibit AR to an extent, but when DHT binds to AR its effects are order of magnitudes greater than T. I'm not taking anything strong enough to inhibit 5ar. I found out that Gamma Linoleic acid can inhibit 5ar quite well (study).Progesterone (P), a 5 alpha RI, and spironolactone (SL), an ARI, produced a dose responsive decrease in SGS at topical concentrations of 0.01% to 5.0%. At concentrations of 1, 3, and 5%, P and SL combinations produced neither an additive nor synergistic inhibition of SGS. At very low concentrations of up to 0.10%, neither P nor SL alone produced any effect on SGS. When combinations of these two steroids were applied at low concentrations, SGS decreased unilaterally to approximately 50%. This synergy occurred best at a P:SL ratio of 1:2. The lower effective concentrations of P may be explained by its greater percutaneous absorption. Synergy was also demonstrated at low concentrations with other antiandrogens: cyproterone acetate, canrenone, hydroxyflutamide, and N-N-diethyl-4-methyl-3-oxo-4-aza-5 alpha-androstane- 17 beta-carboxamide.
I've bought some Evening Primrose Oil gel capsules which I'll be adding to my Emu oil for use at night and in the morning before work after the MXOLCG has dried. Emu oil also has potential to reduce 5ar due its Beta-Sitosterol contents.Leave a comment:
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Chemical, you say PGD2 does not play the major role, but what about the fact that genetically altered mice which overexpress Ptgs2 phenocopy AGA?
Transgenic mice overexpressing Ptgs2 in the epidermis phenocopy AGA
Given the correlation of increased levels of PGD2 with balding scalp in humans and the presumptive inhibitory role of PGD2 on the mouse follicle, we hypothesized that mice with high levels of PGD2 in the skin might develop features of AGA. Because Ptgs2 (cyclooxygenase 2, prostaglandin G/H synthase) is the enzyme upstream to Ptgds, we further hypothesized that mice overexpressing Ptgs2 would have elevated PGD2 levels. Transgenic mice that overexpress Ptgs2 in the epidermis had been developed previously for carcinogenesis studies. The hair follicles in these K14-Ptgs2 transgenic mice were noted to enter catagen prematurely, and these mice reportedly developed alopecia and sebaceous gland enlargement (14, 23).
We further analyzed the skin and hair follicles of the K14-Ptgs2 mouse. These mice developed alopecia, which was evident as a decrease in the normal murine pelage coat compared to control (Fig. 5, A and B). By histology, we also detected sebaceous gland hyperplasia as indicated by enlarged sebocytes clustered around the hair follicle (Fig. 5, C and D). The hair follicles in the K14-Ptgs2 mice were miniaturized compared to controls (Fig. 5, C and D), and these follicles bore a marked resemblance to the miniaturized follicles in human bald scalp.
To determine the prostaglandin content in the alopecic skin of the K14-Ptgs2 mice, we measured prostaglandin levels by HPLC-MS during the anagen phase of the hair follicle cycle. PGE2 was elevated in the K14-Ptgs2 mice compared to age-matched wild-type controls, as was previously shown using immunoassays measuring PGE2 and PGF2α content in biopsied mouse skin (14, 24). PGD2 was also elevated and was more abundant than PGE2 in both wild-type and K14-Ptgs2 mice. 15-dPGJ2 was elevated in K14-Ptgs2 mice compared to controls and demonstrated the largest fold increase (~14-fold), although baseline values were low (5.7 ng/g tissue) (Fig. 5E). We found low levels (18.4 ng/g tissue) of PGF2α, and an absence of prostacyclin (6k-PGF1α) and thromboxane (TxB2) (Fig. 5E), which are not known to be present in normal skin. Together, the balding phenotype in these mice is likely a result of the overwhelming PGD2 and 15-dPGJ2 inhibitory effects on the hair follicle, despite the presence of PGE2, a known promoter of hair growth (20).Leave a comment:
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