Updated Research and Knowledge - Cutting Edge

[lucky1987]

In the pubmed abstracts I looked up on EGCG, it inhibits both PGD2 and PGE2. I'm not sure why people would speculate that that is going to come out as a net-positive. Are there any hair growth studies of topically applied EGCG that I missed? Those kind of results trump speculation. But if I had to just speculate, EGCG doesn't look like it would be helpful.

I believe you mean the ol, if not go ahead and link the study please

[FADI]

Epigallocatechin-3-gallate (EGCG) from Green Tea

EGCG (usually derived from the dried leaves of green tea) has attained a stellar reputation worldwide for its purported health benefits and weight reduction properties. There is not enough proof of many of these benefits, but green tea in general has become synonymous with good health. So it is no surprise that there are several studies that have concluded EGCG to have a favorable impact on mouse hair as well as on human hair.



Oleuropein (Olive Drupe)

We keep reading about the miracle of olive oil and a Greek/ Mediterranean diet’s positive impact on human lifespan. Now there is yet one more reason to buy olives: a study from earlier this year from South Korea found that topical application of oleuropein induces anagen hair growth in mice. The study is quite technical and it seems like oleuropein stimulates the critical Wnt10b/β-catenin signaling pathway (which is also crucial when it comes to human hair). Oleuropein also upregulates IGF-1, KGF, HGF, and VEGF gene expression in mice. Hopefully they will do a human study on this soon.

[FADI]

Epigallocatechin-3-gallate (EGCG) from Green Tea

EGCG (usually derived from the dried leaves of green tea) has attained a stellar reputation worldwide for its purported health benefits and weight reduction properties. There is not enough proof of many of these benefits, but green tea in general has become synonymous with good health. So it is no surprise that there are several studies that have concluded EGCG to have a favorable impact on mouse hair as well as on human hair.



Oleuropein (Olive Drupe)

We keep reading about the miracle of olive oil and a Greek/ Mediterranean diet’s positive impact on human lifespan. Now there is yet one more reason to buy olives: a study from earlier this year from South Korea found that topical application of oleuropein induces anagen hair growth in mice. The study is quite technical and it seems like oleuropein stimulates the critical Wnt10b/β-catenin signaling pathway (which is also crucial when it comes to human hair). Oleuropein also upregulates IGF-1, KGF, HGF, and VEGF gene expression in mice. Hopefully they will do a human study on this soon.

[bej]

Every study using EGCG shows it reducing PGE2

I believe you mean the ol, if not go ahead and link the study please

OK, I just did a pubmed search, and pulled up every paper that mentions both EGCG and PGE2. In just about every instance, EGCG causes a reduction in PGE2.

This first paper below is the most important one, it's topically applied EGCG to human skin. The second paper below shows that EGCG reduced beta-catenin activity, which is very bad if you want to grow hair. The remaining abstracts just reiterate the point that every time EGCG is put on something, PGE2 goes down, across a wide variety of animals and cell types. I highlighted the relevant parts in bold for easy skimming. In the second to last abstract listed, EGCG even downregulated the PGE2 receptors.

Photochem Photobiol. 1999 Feb;69(2):148-53.

Polyphenolic antioxidant (-)-epigallocatechin-3-gallate from green tea reduces UVB-induced inflammatory responses and infiltration of leukocytes in human skin.

Katiyar SK1, Matsui MS, Elmets CA, Mukhtar H.

Identification of natural products capable of affording protection against UVB radiation-induced inflammatory responses and generation of oxidative stress may have important human health implications. The UVB exposure-induced skin injury and oxidative stress has been associated with a variety of skin disease conditions including photoaging, inflammation and cancer. Tea is a popular beverage consumed worldwide. In several mouse skin models, topical application as well as oral consumption of green tea has been shown to afford protection against chemical and UVB-induced carcinogenesis and inflammatory responses. In the present study, we investigated in human skin, whether topical application of (-)-epigallocatechin-3-gallate (EGCG), the major polyphenolic constituent in green tea, inhibits UVB-induced infiltration of leukocytes (macrophage/neutrophils), a potential source of generation of reactive oxygen species (ROS), and generation of prostaglandin (PG) metabolites. Human subjects were UVB irradiated on sun-protected skin to four times their minimal erythema dosage (MED) and skin biopsies or keratomes were obtained either 24 h or 48 h later. We found that topical application of EGCG (3 mg/2.5 cm2) before UVB (4 MED) exposure to human skin significantly blocked UVB-induced infiltration of leukocytes and reduced myeloperoxidase activity. These infiltrating leukocytes are considered to be the major source of generation of ROS. In the same set of experiments we found that topical application of EGCG before UVB exposure decreased UVB-induced erythema. In additional experiments, we found that microsomes from EGCG pretreated human skin and exposed to UVB, compared to UVB exposure alone, produced significantly reduced PG metabolites, particularly PGE2. The PG metabolites play a critical role in free radical generation and skin tumor promotion in multistage skin carcinogenesis. Careful microscopic examination of skin sections, stained with hematoxylin and eosin, under higher magnification (x400) also revealed that EGCG pretreated and UVB-exposed human skin contained fewer dead cells in the epidermis with comparison to nonpretreated UVB-exposed skin. Taken together, our data demonstrate that EGCG has the potential to block the UVB-induced infiltration of leukocytes and the subsequent generation of ROS in human skin. This may explain the possible mechanism involved in anti-inflammatory effects of green tea. We suggest that EGCG may be useful as a topical agent for protection against UVB-induced ROS-associated inflammatory dermatoses, photoaging and photocarcinogenesis. Further studies are warranted in this direction.

PMID: 10048310

Toxicol Appl Pharmacol. 2013 Dec 1;273(2):418-24.

Green tea polyphenol, (-)-epigallocatechin-3-gallate, induces toxicity in human skin cancer cells by targeting β-catenin signaling.

Singh T1, Katiyar SK.

The green tea polyphenol, (-)-epigallocatechin-3-gallate (EGCG), has been shown to have anti-carcinogenic effects in several skin tumor models, and efforts are continued to investigate the molecular targets responsible for its cytotoxic effects to cancer cells. Our recent observation that β-catenin is upregulated in skin tumors suggested the possibility that the anti-skin carcinogenic effects of EGCG are mediated, at least in part, through its effects on β-catenin signaling. We have found that treatment of the A431 and SCC13 human skin cancer cell lines with EGCG resulted in reduced cell viability and increased cell death and that these cytotoxic effects were associated with inactivation of β-catenin signaling. Evidence of EGCG-induced inactivation of β-catenin included: (i) reduced accumulation of nuclear β-catenin; (ii) enhanced levels of casein kinase1α, reduced phosphorylation of glycogen synthase kinase-3β, and increased phosphorylation of β-catenin on critical serine(45,33/37) residues; and (iii) reduced levels of matrix metalloproteinase (MMP)-2 and MMP-9, which are down-stream targets of β-catenin. Treatment of cells with prostaglandin E2 (PGE2) enhanced the accumulation of β-catenin and enhanced β-catenin signaling. Treatment with either EGCG or an EP2 antagonist (AH6809) reduced the PGE2-enhanced levels of cAMP, an upstream regulator of β-catenin. Inactivation of β-catenin by EGCG resulted in suppression of cell survival signaling proteins. siRNA knockdown of β-catenin in A431 and SCC13 cells reduced cell viability. Collectively, these data suggest that induction of cytotoxicity in skin cancer cells by EGCG is mediated by targeting of β-catenin signaling and that the β-catenin signaling is upregulated by inflammatory mediators.

PMID: 24096034

Int J Oncol. 2002 Dec;21(6):1275-83.

Inhibitory effects of epigallocatechin-3-gallate on N-nitrosomethylbenzylamine-induced esophageal tumorigenesis in F344 rats.

Li ZG1, Shimada Y, Sato F, Maeda M, Itami A, Kaganoi J, Komoto I, Kawabe A, Imamura M.

The present study was conducted to assess the inhibitory effects of EGCG (epigallocatechin-3-gallate) on NMBA-induced rat esophageal tumorigenesis and to seek the potential mechanisms. In experiment I, 81 F344 rats were randomly divided into seven experimental groups according to the different regiments of NMBA 1 mg/kg subcutaneously (s.c.) and EGCG 4 mg/kg or 10 mg/kg orally or intraperitoneally (i.p.). The experiment was terminated at 24 weeks. In experiment II, 48 rats were allocated into two groups, each group contained 24 rats, in which the rats were injected with NMBA 1 mg/kg only or a combination of NMBA 1 mg/kg and EGCG 4 mg/kg i.p. Six rats from each group were sacrificed at the 12th, 16th, 20th and 24th week, respectively. The expression of cyclin D1 and cyclooxygenases (COX-2 and COX-1) was detected using semi-quantitative RT-PCR, and the production of prostaglandin E2 (PGE2) was measured by ELISA. In the groups which were treated with EGCG at a dose of 4 mg/kg i.p., or 10 mg/kg both orally and i.p., the mean number of tumors per rat was significantly reduced to 48, 56 and 61%, respectively (p<0.05). The incidence rate of esophageal carcinomas in the rats that were treated with EGCG 4 mg/kg i.p., was significantly lower than that in the rats which only received NMBA 1 mg/kg (p<0.05). The expression of cyclin D1 and COX-2, and the levels of PGE2 were also decreased by EGCG treatment. These results indicated that EGCG significantly inhibits the NMBA-induced rat esophageal carcinogenesis and it inhibitory effects may partly target cyclin D1 and COX-2 expression, and PGE2 production.

PMID: 12429978

Oncol Rep. 2003 Mar-Apr;10(2):421-6.

Promotion effects of hot water on N-nitrosomethylbenzylamine-induced esophageal tumorigenesis in F344 rats.

Li ZG1, Shimada Y, Sato F, Maeda M, Itami A, Kaganoi J, Komoto I, Kawabe A, Imamura M.

This study is to determine the effects of hot water on N-nitrosomethylbenzylamine (NMBA)-induced rat esophageal tumorigenesis model. F344 rats received one treatment of hot water 1 ml/kg and NMBA 1 mg/kg, or a combination treatment of NMBA 1 mg/kg pus hot water 1 ml/kg, or/and EGCG (epigallocatechin-3-gallate) 10 mg/kg. The experiment was concluded at the 20th week. Our results showed that the number of tumors and incidence of carcinomas were significantly increased by hot water (65 degrees C) (p<0.05, p<0.03, respectively), as compared with the group which received NMBA injections only. EGCG treatment did not significantly reduce the number or the size of tumours as the temperature of added hot water increased. In addition, PGE2 production was induced by NMBA, and further significantly increased by added hot water (p<0.05). On the other hand, EGCG slightly decreased the elevated PGE2 production, however, this effect of EGCG was offset by hot water. Our study further confirmed that the drinking of hot beverages increased the risk of esophageal carcinogenesis, and the drinking hot tea will abolish the inhibitory effects of EGCG on this disease.

PMID: 12579283

J Pharmacol Exp Ther. 2005 Dec;315(3):1172-80.

Epigallocatechin-3-gallate impairs chemokine production in human colon epithelial cell lines.

Porath D1, Riegger C, Drewe J, Schwager J.

A major component in green tea, epigallocatechin-3-gallate (EGCG), is reported to interfere with different steps of a number of inflammatory pathways. After oral administration, EGCG is retained in the gastrointestinal tract, where it is thought to exert preventive functions against inflammatory bowel disease and colon cancer. In this study, the human colon adenocarcinoma cell lines HT29 and T84 were used to investigate the effect of EGCG on intestinal inflammation. HT29 and T84 cells were stimulated with tumor necrosis factor (TNF)-alpha to induce the inflammatory condition and to trigger the inflammatory cascade in vitro and treated with EGCG to study its effect on inflammatory processes. The secretion of the chemokines interleukin (IL)-8, macrophage inflammatory protein (MIP)-3alpha, and prostaglandin E2 (PGE2) was determined by enzyme-linked immunosorbent assay. The gene expression level was measured by quantitative real-time polymerase chain reaction. Treatment of TNF-alpha-stimulated HT29 cells with EGCG dose-dependently inhibited the synthesis of IL-8, MIP-3alpha, and PGE2. Treatment with EGCG also inhibited the production of IL-8 and MIP-3alpha in TNF-alpha-stimulated T84 cells. Gene expression analysis in both HT29 and T84 cells revealed that EGCG down-regulates genes involved in inflammatory pathways. This study shows that EGCG acts broadly on the production of chemokines and PGE2 in the chemokine and eicosanoid pathways of colon epithelial cells. Therefore, EGCG might prove useful for the prevention and/or attenuation of colonic disorders.

PMID: 16123309

J Exp Ther Oncol. 2005;5(1):69-78.

EGCG inhibits activation of HER3 and expression of cyclooxygenase-2 in human colon cancer cells.

Shimizu M1, Deguchi A, Joe AK, Mckoy JF, Moriwaki H, Weinstein IB.

Increased expression of COX-2 appears to play an important role in the development of colorectal cancer. The level of COX-2 expression is regulated by various factors including activation of members of the EGFR family of RTKs. We previously reported that in HT29 human colon cancer cells EGCG, the major biologically active component of green tea, inhibits activation of two members of this family, EGFR and HER2, and multiple downstream signaling pathways. In this study we examined the effects of EGCG on the HER3 RTK and on COX-2 expression in the SW837 human colon cancer cell line that expresses a high level and constitutive activation of HER3 and also expresses a high level of COX-2. Treatment of these cells with 20 microg/ml of EGCG (the IC50 concentration for growth inhibition) caused, within 6 hours, a decrease in the phosphorylated (i.e. activated) forms of not only EGFR and HER2, but also HER3. At 6 to 12 hours there was a decrease in the phosphorylated forms of the downstream signaling proteins ERK and Akt. Within 6 to 12 hours there was a decrease in cellular levels of both COX-2 protein and mRNA, and within 48 hours the cells displayed apoptosis. Reporter assays indicated that EGCG inhibited the transcriptional activities of the COX-2, AP-1, and NF-kappaB promoters. EGCG also caused a decrease in production of PGE2, a major product of COX-2. With a longer incubation time, 96 hours, a very low dose (1.0 microg/ml) of EGCG also caused inhibition of cell growth, inhibition of activation of EGFR, HER2, and HER3, a decrease in the levels of COX-2 and Bcl-xL proteins, and apoptosis. These results provide the first evidence that a low concentration of EGCG can inhibit activation of, at least, three members of the EGFR family of RTKs, and also inhibit COX-2 expression in colon cancer cells. These findings extend our previous evidence that EGCG may be useful in the chemoprevention and/or treatment of colorectal cancer.

PMID: 16416603

Exp Biol Med (Maywood). 2006 Jun;231(6):1123-7.

Antitumor effect of green tea polyphenol epigallocatechin-3-gallate in ovarian carcinoma cells: evidence for the endothelin-1 as a potential target.

Spinella F1, Rosanò L, Decandia S, Di Castro V, Albini A, Elia G, Natali PG, Bagnato A.

The green tea polyphenol, epigallocatechin-3-gallate (EGCG), has been shown to prevent cancer; however, a precise mechanism responsible for tumor growth inhibition has not yet been clearly described. The endothelin (ET) A receptor (ET(A)R)/ET-1 autocrine pathway is overexpressed in ovarian carcinoma and triggers tumor growth, neoangiogenesis, and invasion. These latter tumor-promoting effects are mediated through the activation of cyclooxygenase (COX)-1- and COX-2-dependent pathways by ET-1. In the present study, pretreatment of HEY and OVCA 433 ovarian carcinoma cell lines with green tea and EGCG inhibited ET-1/ET(A)R expression, ET(A)R-mediated COX-1/2 mRNA expression, and COX-2 promoter activity. These effects were associated with a significant reduction in the COX-1/2-derived prostaglandin E2 (PGE2) production. These results provide a novel insight into the mechanism by which EGCG, by affecting ET(A)R-dependent COX-1/2 pathways may inhibit ovarian tumors suggesting that EGCG may be useful in preventing and treating ovarian carcinoma in which activation of ET(A)R by ET-1 plays a critical role in tumor growth and progression.

PMID: 16741061

Biol Pharm Bull. 2008 Mar;31(3):527-30.

Identification of hop polyphenolic components which inhibit prostaglandin E2 production by gingival epithelial cells stimulated with periodontal pathogen.

Inaba H1, Tagashira M, Honma D, Kanda T, Kou Y, Ohtake Y, Amano A.

Chronic marginal periodontitis is a destructive inflammatory disease caused by an imbalance between bacterial virulence and host defense ability, resulting in eventual tooth exfoliation. Porphyromonas gingivalis, a major periodontal pathogen, triggers a series of cellular inflammatory responses including the production of prostaglandin E2 (PGE2), which causes periodontal destruction; thus, anti-inflammatory reagents are considered beneficial for periodontal therapy. In the present study, we examined whether hop- and apple-derived polyphenols (HBP and ACT, respectively) inhibit PGE2 production by human gingival epithelial (HGE) cells stimulated with P. gingivalis components. HGE cells were stimulated with P. gingivalis membrane vesicles, and the effects of HBP, ACT and epigallocatechin gallate (EGCg) on PGE2 production by HGE cells were evaluated using an enzyme-linked immunosorbent assay. HBP and EGCg significantly inhibited PGE2 production, whereas ACT did not. By further fractionation steps of HBP to identify the effective components, 3 components of HBP, 2-[(2-methylpropanoyl)-phloroglucinol]1-O-beta-D-glucopyranoside (MPPG), quercetin 3-O-beta-D-glucopyranoside (isoquercitrin), and kaempferol 3-O-beta-glucopyranoside (astragalin), were found to be elements which significantly inhibited cellular PGE2 production. These results suggest that HBP is a potent inhibitor of cellular PGE2 production induced by P. gingivalis, and HBP may be useful for the prevention and attenuation of periodontitis.

PMID: 18310924

PLoS One. 2011;6(10):e25224.

Green tea catechins reduce invasive potential of human melanoma cells by targeting COX-2, PGE2 receptors and epithelial-to-mesenchymal transition.

Singh T1, Katiyar SK.

Melanoma is the most serious type of skin disease and a leading cause of death from skin disease due to its highly metastatic ability. To develop more effective chemopreventive agents for the prevention of melanoma, we have determined the effect of green tea catechins on the invasive potential of human melanoma cells and the molecular mechanisms underlying these effects using A375 (BRAF-mutated) and Hs294t (Non-BRAF-mutated) melanoma cell lines as an in vitro model. Employing cell invasion assays, we found that the inhibitory effects of green tea catechins on the cell migration were in the order of (-)-epigallocatechin-3-gallate (EGCG)>(-)-epigallocatechin>(-)-epicatechin-3-gallate>(-)-gallocatechin>(-)-epicatechin. Treatment of A375 and Hs294t cells with EGCG resulted in a dose-dependent inhibition of cell migration or invasion of these cells, which was associated with a reduction in the levels of cyclooxygenase (COX)-2, prostaglandin (PG) E(2) and PGE(2) receptors (EP2 and EP4). Treatment of cells with celecoxib, a COX-2 inhibitor, also inhibited melanoma cell migration. EGCG inhibits 12-O-tetradecanoylphorbol-13-acetate-, an inducer of COX-2, and PGE(2)-induced cell migration of cells. EGCG decreased EP2 agonist (butaprost)- and EP4 agonist (Cay10580)-induced cell migration ability. Moreover, EGCG inhibited the activation of NF-κB/p65, an upstream regulator of COX-2, in A375 melanoma cells, and treatment of cells with caffeic acid phenethyl ester, an inhibitor of NF-κB, also inhibited cell migration. Inhibition of melanoma cell migration by EGCG was associated with transition of mesenchymal stage to epithelial stage, which resulted in an increase in the levels of epithelial biomarkers (E-cadherin, cytokeratin and desmoglein 2) and a reduction in the levels of mesenchymal biomarkers (vimentin, fibronectin and N-cadherin) in A375 melanoma cells. Together, these results indicate that EGCG, a major green tea catechin, has the ability to inhibit melanoma cell invasion/migration, an essential step of metastasis, by targeting the endogenous expression of COX-2, PGE(2) receptors and epithelial-to-mesenchymal transition.

PMID: 22022384

J Inflamm (Lond). 2014 Mar 28;11(1):8

Expression of pro-inflammatory mediators is inhibited by an avocado/soybean unsaponifiables and epigallocatechin gallate combination.

Ownby SL1, Fortuno LV, Au AY, Grzanna MW, Rashmir-Raven AM, Frondoza CG.

BACKGROUND:
Osteoarthritis (OA) is characterized by inflammation, joint immobility, and pain. Non-pharmacologic agents modulating pro-inflammatory mediator expression offer considerable promise as safe and effective treatments for OA. We previously determined the anti-inflammatory effect of an avocado/soybean unsaponifiables (ASU) and epigallocatechin gallate (EGCG) combination on prostaglandin E2 (PGE2) production and nuclear factor-kappa B (NF-κB) translocation. The aim of this study was to evaluate the effects of ASU + EGCG on pro-inflammatory gene expression.

FINDINGS:
Articular chondrocytes from carpal joints of mature horses were pre-incubated for 24 hours with control media alone or ASU (8.3 μg/mL) + EGCG (40 ng/mL), followed by one hour activation with interleukin-1 beta (IL-1β, 10 ng/mL) and tumor necrosis factor-alpha (TNF-α, 1 ng/mL). Total cellular RNA was isolated and real-time PCR performed to measure IL-1β, TNF-α, interleukin-6 (IL-6), cyclooxygenase-2 (COX-2), and interleukin-8 (IL-8) gene expression. Intracellular localization of NF-κB was analyzed by immunohistochemistry and Western blot. Pre-treatment with ASU + EGCG significantly (P < 0.001) decreased gene expression of IL-1β, TNF-α, IL-6, COX-2, and IL-8 in cytokine-activated chondrocytes. Western blot and immunostaining confirmed NF-κB translocation inhibition.

CONCLUSIONS:
We demonstrate that ASU + EGCG inhibits cytokine-induced gene expression of IL-1β, TNF-α, IL-6, COX-2, and IL-8 through modulation of NF-κB. Our results indicate that the activity of ASU + EGCG affects a wide array of inflammatory molecules in addition to decreasing PGE2 synthesis in activated chondrocytes. The responsiveness of chondrocytes to this combination supports its potential utility for the inhibition of joint inflammation.

PMID: 24678847

[Seuxin]

Yeah, ECGC is just antioxydants, it's shitty for hair, useless, and bad since it inhibe pge2 ! No news about chemical...maybe he's totally bald...

[ledhead]

Bej what are your thoughts on Oleuropein?

[ledhead]

Nvm saw your post on the other page. I am using about 5-7 drops in a 3ml application of adenogen mixed with RU

[SriHanuman]

In the pubmed abstracts I looked up on EGCG, it inhibits both PGD2 and PGE2. I'm not sure why people would speculate that that is going to come out as a net-positive. Are there any hair growth studies of topically applied EGCG that I missed? Those kind of results trump speculation. But if I had to just speculate, EGCG doesn't look like it would be helpful.

http://www.bettinamoritz.com.br/alunos/artigos/cha_verde_cabelo.pdf

[Sogeking]

if you never had velus hair there, then this is a improvement ?

I mean that is an improvement, however those velus hair aren't doing me much good.
I guess I'll have to wait and see how this turns out.
About two weeks ago I also added some small amount of castor and rice bran oil to the mix.

[bej]

Bej what are your thoughts on Oleuropein?

The data available look good, for mouse studies and human hair cell culture. The alterations in gene expressions look very desirable. It would be nice to see this tested in humans.

I ordered some Olive Leaf Extract with 20% Oleuropein. Unfortunately, it would be very crude for a topical. I put some extract in pure ethanol, and it had almost no solubility. The powder in the capsules appeared to be a fine olive-green. But it doesn't look so fine when you try to dissolve it. The solution turns green, so something dissolves a little bit. But it largely settles out with a fine greenish-brown powder, a heftier white powder, and a whole bunch of gnarly green chunks. If pure Oleuropein was available, I'd revisit this, but until then, I'm not pursuing it.

[bej]

Bej what are your thoughts on Oleuropein?

The data available look good, for mouse studies and human hair cell culture. The alterations in gene expressions look very desirable. It would be nice to see this tested in humans.

I ordered some Olive Leaf Extract with 20% Oleuropein. Unfortunately, it would be very crude for a topical. I put some extract in pure ethanol, and it had almost no solubility. The powder in the capsules appeared to be a fine olive-green. But it doesn't look so fine when you try to dissolve it. The solution turns green, so something dissolves a little bit. But it largely settles out with a fine greenish-brown powder, a heftier white powder, and a whole bunch of gnarly green chunks. If pure Oleuropein was available, I'd revisit this, but until then, I'm not pursuing it.

[Seuxin]

A first solution will be to made a tincture of oleuropein....or to buy directly a high dosed tincture.
Second solution, if you have oleuropein as powder is to try to coumpound a cream, maybe with an HRT Cream. But i think a tincture will be better...

[Diffuse Danny]

I add a heaped teaspoon of Oleuropein powder into an 84ml bottle of Garnier fructis stemox, it dissolves quickly and perfectly

[79BirdofPrey]

Can anyone share where one can purchase some quality Oleuropein here in the states? Thanks.

[ryan82]

The key is the oleuropein for the velus hair and not EEGC ?