Topical Application Of Oleuropein Induces Anagen Hair Growth In Telogen Mouse Skin.

ChoiGodTsuji

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https://www.ncbi.nlm.nih.gov/pubmed/26060936


METHODOLOGY AND PRINCIPAL FINDINGS:
Oleuropein promoted cultured human follicle dermal papilla cell proliferation and induced LEF1 and Cyc-D1 mRNA expression and β-catenin protein expression in dermal papilla cells. Nuclear accumulation of β-catenin in dermal papilla cells was observed after oleuropein treatment. Topical application of oleuropein (0.4 mg/mouse/day) to C57BL/6N mice accelerated the hair-growth induction and increased the size of hair follicles in telogenic mouse skin. The oleuropein-treated mouse skin showed substantial upregulation of Wnt10b, FZDR1, LRP5, LEF1, Cyc-D1, IGF-1, KGF, HGF, and VEGF mRNA expression and β-catenin protein expression.

CONCLUSIONS AND SIGNIFICANCE:
These results demonstrate that topical oleuroepin administration induced anagenic hair growth in telogenic C57BL/6N mouse skin. The hair-growth promoting effect of oleuropein in mice appeared to be associated with the stimulation of the Wnt10b/β-catenin signaling pathway and the upregulation of IGF-1, KGF, HGF, and VEGF gene expression in mouse skin tissue.


http://www.rdpeptide.net/news/newsview.aspx?id=3869
 

Lucky1987

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Found this post on another forum, guy goes in dept about this stuff, for the people interested:

Chemical;224344 said:
In this post I’ll be describing the effects of Oleuropein on hair follicles and just how awesome this herb is.
I’ll start off with the main study which luckily is a free pubmed article:
Topical Application of Oleuropein Induces Anagen Hair Growth in Telogen Mouse Skin
I’m not going to bother with the cliffs, we’re going to look at the findings in depth because that’s where the devil lives.
What does WNT10b do?
We have our first evidence that oleuropein has the potential to significantly stimulate hair growth in the absence of DKK1.
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Strangely the optimal concentration that achieved the highest percentage of cells with increased proliferation was 20um, instead of the 50um, perhaps theres a biphasic effect? Or maybe a statistical/extraneous anomaly because the two concentrations have similar efficacy. I’ll come back to this.
(Cyc d1 is an indicator of cell cycle progression and correlates with proliferation)
Oleuropein increases BetaCatenin which as we know is a very good thing.
The hairs were physically longer than the tried and proven minoxidil! And there were more follicles in anagen (up from telogen). I’m curious as to what concentration of minoxidil they used and if using higher concentration would’ve yielded better results.
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Oleuropein somehow manages to increase IGF1 (by a lot) and VEGF too. This study shows that oleuropein can increase VEGF via WNT10b, however I’m not sure how IGF-1 was elevated. The figure clearly shows just how much these growth factors are elevated, but I’m surprised minoxidil didn’t come anywhere near close enough to oleuropein in increasing VEGF.
The oleuropein study used 3mg of minoxidil – not sure howthat translates to mumol, maybe someone an help?
Anyways, now comes the best part:
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THIS IS THE ****ING HOLY GRAIL. The rare SYNERGY. When you decrease an inhibitory protein and boost an agonist protein you achieve synergy, where 2 + 2 does not equal 4 (additive) but rather 7. You can see that DKK1 was reduced from control levels. They did not elucidate the actual pathway but if oleuropein targets the gene expression or transcription then this could mean DHT can no longer exert its effects on the hair follicle via DKK1. I am still trying to figure out how this inhibition works because I don’t like believing studies that do not have supporting evidence from other sources. If someone can assist with research I’d be very very grateful.
Lets talk about the dosages and how it translates to human doses.
0.4mg as in 10um? Or 20um? probably 20 as the minimum EFFECTIVE dose. 3mg might have resulted in diminishing returns since they didn’t see dose dependant growth. I believe theres a plateau of diminishing returns and oleuropein isn’t biphasic but that’s still open to debate.
Nothing fancy here, just your standard 50% ethanol, water and propylene glycol. Which means anyone can make an oleuropein vehicle very cheaply. Heck, you could even dissolve it in minoxidil (which is what I’ve been doing).
To conclude the study:
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Imagine what would happen if we combined Minoxidil with this.
A decrease in DKK1 -> more LRP6 available to bind -> the body's natural WNTs can finally work.
Oleuropeins WNT10b upregulation -> increased IGF-1, VEGF, KGF -> BetaCatenin
An increase in VEGF both from oleuropein AND Minoxidil -> more blood vessels to hair follicle, which as I’ve discussed in my first post, leads to increased hair follicle size and growth.
A ridiculous amount of beta catenin from oleuropein and minoxidil combined – does anyone see where I’m going with this?
Thats the agonist side covered, and not to forget:
ketoconazole and miconazole nitrate for 3 beta HSD suppression -> less DHT converted to 3 Beta diol – which is a potent ERBeta agonist -> disinhibition of VEGF pathways and stabilization of HIF-1.
Throw in topical saw palmetto just for safe measure and you’ve got yourself a serious stack.
Bringing me to the part that is most important.
My experiments. First a little bit about myself:
My hairline started receding when I was 17 because I stupidly decided to mess with anabolic steroids (which is where I got my biology knowledge). I used emu oil, and nizoral but didn’t touch minoxidil or finasteride, saw a slight improvement but nothing significant. My father started receding at 30, so I’ve definitely got the genes and would’ve receded eventually even if I hadn’t messed around with my androgens.
I became a NW2 at 18, after using letrozole to boost testosterone to suraphysical levels not realizing it would **** up my hairline. I started using seakelp bioferment, microneedling, emu oil, folligen, and some other supplements. Saw slight improvements but nothing too great.
Then I became a NW3 at 19 when I had the worst shed of my life after a car accident. I was in icu for 2 months and the stress really destroyed my hair. I used emu oil, folligen and microneedling but still wasn’t seeing any significant growth.
Fast forward this year april. I was desperate. So I took the plunge. I decided to go on finasteride, minoxidil (everyday), and ketoconazole cream (everyday). I used emu oil religiously to help with absorption. 2 months in and I saw great regrowth, increased density and I became a NW2.2 ish.
I took the finasteride every 3 days because I didn’t want it to affect my pregnenolone levels too much (I’ve got anxiety and finasteride ED made it worse). I stopped after the 2 month mark. I incorporated iodine into Telogen Effluvium minoxidil thinking it would help. didn’t do sh*t. Kept using minoxidil mixed with emu oil with minor improvements in hair density and decreased shedding.
August 2015, I started putting the pieces together and I had a few breakthroughs in terms of research.
Bought myself Oleuropein capsules from amazon (extra strength), and mixed it with minoxidil. I had one bottle left so I dissolved like 5 capsules into the liquid and gave it a good shake. I also added a few saw palmetto capsules which I regret because it did not dissolve at all. I let it sit for 24 hour then shook it again.
I then used the dropper to mix around 10ml into my emu oil dispenser which was half full (25ml). And that was my treatment. I used it most nights but it was a real pain to keep looking at the ceiling to prevent it from pouring down my forehead. In the morning it would all be absorbed thanks to the minoxidil but there’d be a few remnants of the undissolved saw palmetto and the oleuropein.
Every week I kept adding more drops of the minoxidil (with the dissolved oleuropein and saw) because I wanted to see what would happen. I also used ketoconazole cream 2% (Janssen pharma) twice a day non stop because it was easy to apply.
6 weeks in and I could feel stubble, small prickly hairs. I was ****ing ecstatic. My existing hairs became thicker especially the vertex area, and shedding stopped – (almost completely) but I was still skeptical, I thought it must’ve been a delayed reaction to minoxidil and ketoconazole. My frontal hairline grew a few hairs initially because that’s where I was using it the most, but I wanted to see if this solution actually did anything so I started using it only on my left side and tilting my head to the right to make it pour down to the other side and the backwards to reach the rest of my scalp.
I regret not taking enough pictures before starting although I wasn’t really planning to share this until I genuinely saw an improvement. I’ve got a few shitty pictures taken with a potato before the regimen:
View attachment 43348
( 6 weeks into the regimen):
View attachment 43349
View attachment 43350
The left side was the same as the first pic before the regimen:
View attachment 43351
View attachment 43352
The past few weeks I’ve been really busy with work and have only been using the solution heavily on the weekends (3-5 times a day) to make up for not using it on the weekdays. I've been feeling more stubble, mainly on the left side, and thicker vertex hair. I also got carried away with the oleuropein and now the solution leaves a hard residue after drying so I’ve had to buy more minoxidil and emu oil which should be here this week. I ran out of ketoconazole also so I’ll be starting a proper log with decent pictures now that I’ve got a better phone.
I'll be posting more recent pics tomorrow.
I would strongly recommend people get some ketoconazole in cream form and maybe miconazole too to apply everyday, as often as possible. The reason being, testosterone is always present in the blood, which means DHT is being converted all the time by the hair follicles. You need to keep the hair follicles saturated with antagonists and agonists to keep them from being slowly killed by DKK1/DHT. Agonists like minoxidil and your body's own WNT proteins WILL NOT work if DKK1 has internalized the LRP6 receptors.
I'd also suggest people not to take finasteride systematically because the body will naturally increase testosterone to offset the negative feedback loop, and since finasteride only inhibits ~60%, that increase in testosterone will give 5AR additional substrate to convert into DHT, defeating the whole purpose of finasteride. I'd like to see people try this with RU as an augmentation, since theoretically there should be less DKK1 as a result of impaired AR signalling.
Sorry for the long read.
 
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