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Has anyone tried this method (below), or does anyone think that these supplements would help?
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Supplemental hair growth?
Has anyone tried this method (below), or does anyone think that these supplements would help?
Comment
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rice bran second study
I read the second study, which confirms RB-SCE as inhibiting the 5-AR enzyme in androgen-responsive organs (the skin organ in this case). the results were "similar to slightly lower than those reported for 2% minoxidil after 48 weeks or 1% pro
-cyanidin B-2 after 16 weeks."
I was also interested in this study in that they published their stack:1
INCI % (as w/w)
----------------------------
Water (aqua), demineralized as 100%
Glycerin 1.0
Hydroxyethyl cellulose 0.5
Tetrasodium EDTA 0.03
C12–14 Pareth-12 2.0
Hyaluronic acid 0.5
Alcohol 15.0
RB-SCE 0.5
PEG-40 castor oil 2.0
Triethanolamine 0.3
INCI = International Nomenclature of Cosmetic Ingredients;
RB-SCE = rice bran supercritical CO2 extract.Comment
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rice bran second study
I read the second study, which confirms RB-SCE as inhibiting the 5-AR enzyme in androgen-responsive organs (the skin organ in this case). the results were "similar to slightly lower than those reported for 2% minoxidil after 48 weeks or 1% pro-cyanidin B-2 after 16 weeks."
I was also interested in this study in that they published their stack:
INCI................................... % (as w/w)
----------------------------- -----------
Water (aqua), demineralized . as 100%
Glycerin................................ 1.0
Hydroxyethyl cellulose............ 0.5
Tetrasodium EDTA................. 0.03
C12–14 Pareth-12................. 2.0
Hyaluronic acid...................... 0.5
Alcohol................................ 15.0
RB-SCE................................ 0.5
PEG-40 castor oil................... 2.0
Triethanolamine..................... 0.3
INCI = International Nomenclature of Cosmetic Ingredients;
RB-SCE = rice bran supercritical CO2 extract.
I did not look at all of these, but i did look at Hyaluronic Acid.
It appears (total guess on my part) that HA may be added due to it's value in cell proliferation and migration, and possible reduction of normally occuring local HA synthesis due to the lowering of TGF-Beta1 by RB-SCE (as noted in the first rice bran study in SriHanuman's post).
This study does mention high molecular weight HA (might be the type used in the RB-SCE study (?)).
"The turnover of HA in most tissues is extraordinarily rapid; the half-life of HA in the skin, which contains about half of all HA in the body, is 1–1.5 days. Thus, the tight control of HA synthesis and degradation is necessary for this turnover and seems to finely balance the amounts of high molecular mass HA (1,000–10,000 kDa) within tissues. On the other hand, an imbalance of synthesis and degradation causes the accumulation of HA with different molecular weights, which is commonly observed in diseases such as arthritis and cancers."
"TGF-β1 conferred the most potent effect on production of high molecular weight HA by up-regulation of HAS expression and down-regulation of HYBID (HYaluronan-Binding protein Involvedin hyaluronan Depolymerization), aka KIAA1199, expression via distinct signaling pathways."Comment
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chemical do you think adding OL to lipogaine would work, only reason im asking is becasue its a diffrent type of vehicleComment
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joshuk, you can whitout problems ;
@Chemical : These studies about rice bran supercritical CO2 extract are very awesome !
It could be a great and cheap addition to our regimen !
Here is a link..if we used at 1%...it could last very long time
Need investigations !Comment
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Here is the full resolution BEFORE/AFTER pic.
When you zoom in you can see some progress, but it's too early to say for sure, in my opinion.
Lemme know what do you think.Comment
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Can really be improve with an AA ( Duta, Fin, RU, CB)Comment
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other dkk1 inhibitors
Review of dkk1:
Dihydrotestosterone-Inducible Dickkopf 1 from Balding Dermal Papilla Cells Causes Apoptosis in Follicular Keratinocytes
"Dickkopf-1 (Dkk-1) is a member of the dickkopf family of proteins that have been shown to be negative regulators of the canonical Wnt-signaling pathway, which has a central role in bone development and formation (see, for example, Glinka et al., Nature 391:357-62 (1998); Fedi et al., J Biol Chem 274(27):19465-72 (1999); Zorn, Curr Biol 11:R592-95 (2001); and Krupnik et al., Gene 238: 301-13 (1999)). Dkk-1 inhibits Wnt signaling through its interaction with the Wnt co-receptors LRP5 or LRP6 and the kremen proteins (see, for example, Bafico et al., Nature Cell Biol 3:683 (2001); Mao et al., Nature 411(17):321 (2001); Mao et al., Nature 417:664 (2002); and Semënov et al., Curr Biol 11:951-61 (2001). By binding LRP5 (LRP6) and kremen proteins, Dkk-1 prevents LRP5 or LRP6 from associating with members of the Wnt pathway and thus prevents Wnt-mediated signal transduction, which in turn results in the inhibition of bone formation.
LRP5 is a key protein in regulating bone mass (see, for example, Gong et al., Cell 107:513-23 (2001); Patel, N Eng J Med 346(20):1572 (2002)). An autosomal recessive disorder characterized by low bone mass (osteoporosis-pseudoglioma syndrome, or “OPPG”) has been identified as being caused by loss-of-function mutations in LRP5 (Gong et al., 2001). In addition, gain-of-function mutations in LRP5 have been shown to result in autosomal dominant high bone mass in humans (Little et al., Am J Human Genetics. 70(1):11-19, 2002). The same mutations in LRP5 that result in high bone mass can interfere with the ability of Dkk-1 to inhibit LRP5 signaling (see, for example, Boyden et al., N Eng J Med. 346(20):1513-1521, 2002). Thus, Dkk-1 is appropriately characterized as being a negative regulator of bone deposition.
In view of the involvement of Dkk-1 in the regulation of bone formation and its role in various other diseases that are associated with bone loss (e.g., cancer and diabetes), there is a need for improved anti-Dkk-1 antibodies for therapeutic use and for other purposes."
other dkk1 blockers:
Horny Goat Weed: "Flavonoids of Herba Epimedii regulate osteogenesis of human mesenchymal stem cells through BMP and Wnt/beta-catenin signaling pathway." http://www.ncbi.nlm.nih.gov/pubmed/19703516
L-ascorbic acid 2-phosphate represses the dihydrotestosterone-induced dickkopf-1 expression in human balding dermal papilla cells. http://www.ncbi.nlm.nih.gov/pubmed/20701628
Preventable effect of L-threonate, an ascorbate metabolite, on androgen-driven balding via repression of dihydrotestosterone-induced dickkopf-1 expression in human hair dermal papilla cells. http://www.ncbi.nlm.nih.gov/pubmed/21034532Comment
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L-ascorbic acid 2-phosphate is possible too buy around 40 dollarsComment
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I have 100g of MAP ( magnesium ascorbyl phosphate), i can inhib DKK-1 too but a member here in a few weeks spoke that Vitamine C was no good hair hairs...Comment
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ALL this info is good ,but makes us a bit confuse.Can someone make a summary of what to use ,how to use ect.Comment
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Would be interesting to have different protocols listed for others to try. That's a lot of work. This stuff is over my head.Comment
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