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CURCUMIN, A 5 ALPHA REDUCTASE TYPE 2 INHIBITOR
Another mechanism by which curcumin benefits those with hair loss has been elucidated. In addition to its ability to down-regulate the inflammatory cytokine, tgf-b, and its likely effects on Substance P, which was detailed in an Italian patent in our last update, it has been shown to specifically inhibit 5 alpha reductase type 2, the enzyme responsible for the conversion of testosterone into dihydrotestosterone(DHT).
This newly identified mechanism would, by itself, appear to suggest that systemic, oral use of Curcumin would have significant benefits for hair growth. 5 alpha reductase type 2 is predominately responsible for the amount of DHT in circulation, and is the mechanism by which Propecia functions. The beauty of Curcumin is that it addresses multiple other mechanisms for hair growth and instead of side effects has significant health and anti-aging benefits.
Recent advances in Curcumin formulation have resulted in an enhanced bio-availability and a significantly improved sustained retention time in the body confirmed by human clinical trials. A 400 mg capsule of this new Bio-Curcumin, is the functional equivilant of 2772mg of a 95% Curcumin extract.
Curcumin as Type II inhibitor
Establishment of type II 5a-reductase over-expressing cell line as an inhibitor screening model.
Sunhyae Janga, Young Leea, Seong-Lok Hwangb, Min-Ho Leeb, Su Jin Parkb, In Ho Leeb, Sangjin Kangb, Seok-Seon Rohc, Young-Joon Seoa, Jang-Kyu Parka, Jeung-Hoon Leea and Chang Deok Kima, , aDepartment of Dermatology and Research Institute for Medical Sciences, School of Medicine, Chungnam National University, Daejeon, Republic of Korea bLG Household and Health Care Research Park, Daejeon, Republic of Korea cOriental Medical College of Daejeon University, Daejeon, Republic of Korea Received 2 November 2006; accepted 14 March 2007. Available online 22 June 2007.
Abstract Dihydrotestosterone (DHT) is the most potent male hormone that causes androgenetic alopecia. The type II 5a-reductase is an enzyme that catalyzes the conversion of testosterone (T) to DHT, therefore it can be expected that specific inhibitors for type II 5a-reductase may improve the pathophysiologic status of androgenetic alopecia. In this study, we attempted to establish the reliable and convenient screening model for type II 5a-reductase inhibitors. After transfection of human cDNA for type II 5a-reductase into HEK293 cells, the type II 5a-reductase over-expressing stable cells were selected by G418 treatment. RT-PCR and Western blot analyses confirmed that type II 5a-reductase gene was expressed in the stable cells. In in vitro enzymatic assay, 10 µg of stable cell extract completely converted 1 µCi (0.015 nmol) of T into DHT. The type II 5a-reductase activity was inhibited by finasteride in a dose-