Updated Research and Knowledge - Cutting Edge

[Phoenix7]

This is making my scalp, and area below the hairline shinier... That can't be a good sign, no?

[FADI]

This is making my scalp, and area below the hairline shinier... That can't be a good sign, no?

What do you mean by this ? what is making this shedding?

[Phoenix7]

What do you mean by this ? what is making this shedding?

I'm undecided. The reflectiveness could have just been the solution. I think I'm getting hairs on hairline that weren't there before, definitely am on the sides of the head. However, the front midsection has gone very thin. Hopefully its a big shed before regrowth.

Anyone shed quite badly on the minox/oleuropein?

[Phoenix7]

Oleuropein is a cox-2 inhibitor and inhibits PGE2....

Sketchy as **** that this has been left out of chemical's analysis.

[Sogeking]

Cox-2 inhibition promotes hair growth. Oleuropein is cox-2 inhibitor. In turn by inhibiting cox-2 we are implicitly inhibiting pgd2.
As for shedding. I've been using my mix for a week now. Shedding is the same as pre-use.

Minox is infamous for shedding. Google it. My mix has no minox.

Is it working for me? Not sure yet.

[Phoenix7]

But why obfuscate the fact it inhibits PGE2 in such a detailed analysis? I can't think of a reason. And haven't cox 2 inhibitors been tried and failed already potentially for this very reason?

Been on the minox approaching 2 months so don't think its causing the shed (although can't be sure).

[Sogeking]

But why obfuscate the fact it inhibits PGE2 in such a detailed analysis? I can't think of a reason. And haven't cox 2 inhibitors been tried and failed already potentially for this very reason?

Been on the minox approaching 2 months so don't think its causing the shed (although can't be sure).

WEll so far I found that oleuropein is COX-2 inhibitor. By inhibiting COX-2 you can promote hair growth as noted here:

http://cancerres.aacrjournals.org/content/62/9/2516.full.pdf

Also the study that propmted this thread says that it induces anagen hair growth:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4462586/

The only place I found that mentions pge2 down regulation is this article (well found another study):

http://download.springer.com/static/pdf/79/art%253A10.1186%252Fs12967-014-0219-9.pdf?originUrl=http%3A%2F%2Ftranslational-medicine.biomedcentral.com%2Farticle%2F10.1186%2Fs12967-014-0219-9&token2=exp=1455557573~acl=%2Fstatic%2Fpdf%2F79%2Fart%25253A10.1186%25252Fs12967-014-0219-9.pdf*~hmac=f21e3868ea4491fbcab02bbb095a16c5ed517ea364f1fc707b8e876be2541258

It has a table with PGE2 and an arrow going down. The reference points to an article:

http://www.sciencedirect.com/science/article/pii/S0955286313001782

IT says that hydroxytyrosol reduced PGE2 after:

The increase in prostaglandin E2 and interleukin 1β after reoxygenation were inhibited after incubation of brain slices with HT and after oral administration

So yeah if it were to reduce PGE2 why did oleuropein show induced anagen hair growth? Maybe the incubation of brain slices had some effect on PGE2 down regulation. Or maybe it was administering it orally?
Too many questions. The article is behind paywall. I'm gonna go with the the newest study about anagen hair growth.
As for results. So far there aren't any for me. But I started on 6th Feb.
Of course if you fear this is not helping you then stop using it. Not trying to be glib here. We actually can't say for sure if this will work. Most of the studies were done in mice so basically we are all live guinea pigs for this. Best of luck mate.

Also I am thinking about adding tea tree oil to my concoction (Eth/PG vehicle with OL, ECGC, Rosemary extract, Apple polyphenols) since it helps with seborrheic dermatitis.

[SriHanuman]

Here is what I am using. Vehicle is Eth/Pg/Water and I made 2 concoctions.

First:
- Oleuropein ~0.6mg/ml
- Baicalin ~1mg/ml
- Apple polyphenols ~17mg/ml
- EGCG ~10mg/ml
- Rosemary extract ~1mg/ml
- Rice bran ~0.02mg/ml

I use this in the morning, started a week ago.

Second:
- Oleuropein ~0.6mg/ml
- Baicalin ~1mg/ml
- Fo-Ti ~17mg/ml
- EGCG ~10mg/ml
- Rosemary extract ~1mg/ml

I use this in the evening, started a month ago. There is no minox in any of the concoctions.

Nothing extraordinary to report yet, I maybe seeing more velus hairs and scalp feels great and that's about it for now. I will report back with the experiment if there is any positive results to report about.

[UNBEAT]

anything new??any result using this

[musky]

+1

[Sogeking]

I'm at 2 weeks now. So far nothing to report. I might be having some decrease is shedding but it might be my wishful thinking. I'll be going with this for 3 months then I'll evaluate my results.

[joshuk]

will be starting again next week with an eth/PG mix of OLE/EGCG/APPLE POLY

also recently bought 10g of CB-03-01 which i will be using again as i stopped all hairloss treatments for 2 weeks as i was in hospital. cant really take stuff like that in their haha.

[noisette]

Topical Treatment of Hair Loss with Formononetin by Modulating Apoptosis.

Kim MH1,*Choi YY1,*Lee JE1,*Kim K2,*Yang WM1.

Author information

1College of Korean Medicine and Institute of Korean Medicine, Kyung Hee University, Seoul, Korea.2Department of Ophthalmology, Otorhinolaryngology and Dermatology of Korean Medicine, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.

Abstract

Formononetin is one of the main components of red clover plants and its role on hair regrowth against hair loss has not been established yet. In the present study, we assessed the potential effects of formononetin on alopecia, along with impaired hair cycles by induction of apoptosis-regression.Depilated C57BL/6 mice were used for monitoring the hair cycles. Formononetin (1 and 100 µM) was topically treated to the dorsal skin for 14 days. Topical formononetin treatment induced miniaturized hair follicles to recover to normal sizes. Tapering hair shaft began to grow newly, emerging from the hair follicles by formononetin. In addition, formononetin inhibited the activation of caspase-8 and decreased the procaspase-9 expression. As a result of formononetin treatment, anti-apoptotic Bcl-2 was up-regulated, whereas pro-apoptotic Bax and p53 were down-regulated, resulting in a decrease of caspase-3 activation. Formononetin showed the obvious inhibition of apoptosis under terminal deoxynucleotidyl transferase dUTP nick end labeling staining thereafter.Taken together, our findings demonstrate that formononetin exerted the hair regrowth effect on hair loss, in which the underlying mechanisms were associated with Fas/Fas L-induced caspase activation, thus inhibiting apoptosis.

Georg Thieme Verlag KG Stuttgart · New York

[Seuxin]

Thanks Noisette !

Sadlly, it's only on mices...
Formononetin appear to be expansive...

Maybe have to find a natural component who contain it (red clover plants powder ?)

http://www.starwest-botanicals.com/category/red-clover-blossoms/

[musky]

Yo McChemical dog you have misinterpreted this study

http://www.ncbi.nlm.nih.gov/pubmed/1632630

5 alpha-Dihydrotestosterone, the principal androgen mediating prostate growth and function in the rat, is formed from testosterone by steroid 5 alpha-reductase. The inactivation of 5 alpha-dihydrotestosterone involves reversible reduction to 5 alpha-androstane-3 beta,17 beta-diol by 3 beta-hydroxysteroid oxidoreductase followed by 6 alpha-, 7 alpha-, or 7 beta-hydroxylation. 5 alpha-Androstane-3 beta,17 beta-diol hydroxylation represents the ultimate inactivation step of dihydrotestosterone in rat prostate and is apparently catalyzed by a single, high-affinity (Km approximately 0.5 microM) microsomal cytochrome P450 enzyme. The present studies were designed to determine if 5 alpha-androstane-3 beta,17 beta-diol hydroxylation by rat prostate microsomes is inhibited by agents that are known inhibitors of androgen-metabolizing enzymes. Inhibitors of steroid 5 alpha-reductase (4-azasteroid analogs; 10 microM) or inhibitors of 3 beta-hydroxysteroid oxidoreductase (trilostane, azastene, and cyanoketone; 10 microM) had no appreciable effect on the 6 alpha-, 7 alpha-, or 7 beta-hydroxylation of 5 alpha-androstane-3 beta,17 beta-diol (10 microM) by rat prostate microsomes. Imidazole-type antimycotic drugs (ketoconazole, clotrimazole, and miconazole; 0.1-10 microM) all markedly inhibited 5 alpha-androstane-3 beta,17 beta-diol hydroxylation in a concentration-dependent manner, whereas triazole-type antimycotic drugs (fluconazole and itraconazole; 0.1-10 microM) had no inhibitory effect. The rank order of inhibitory potency of the imidazole-type antimycotic drugs was miconazole greater than clotrimazole greater than ketoconazole. In the case of clotrimazole, the inhibition was shown to be competitive in nature, with a Ki of 0.03 microM. The imidazole-type antimycotic drugs inhibited all three pathways of 5 alpha-androstane-3 beta,17 beta-diol hydroxylation to the same extent, which provides further evidence that, in rat prostate microsomes, a single cytochrome P450 enzyme catalyzes the 6 alpha-, 7 alpha-, and 7 beta-hydroxylation of 5 alpha-androstane-3 beta,17 beta-diol. These studies demonstrate that certain imidazole-type compounds are potent, competitive inhibitors of 5 alpha-androstane-3 beta,17 beta-diol hydroxylation by rat prostate microsomes, which is consistent with the effect of these antimycotic drugs on cytochrome P450 enzymes involved in the metabolism of other androgens and steroids.

Ketocanzole and miconazole inhibited the HYDROXYLATION of beta-diol, this means less beta-diol will be converted into it's hydroxy metabolites, which means if you use Keto there will be MORE beta-diol lying around. Food for thought dog.