michael barry
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http://www.wipo.int/pctdb/en/wo.jsp?ELE ... SPLAY=DESC
"(WO/2007/149312) METHODS AND COMPOSITIONS FOR INHIBITING OR REDUCING HAIR LOSS, ACNE, ROSACEA, PROSTATE CANCER, AND BPH"
That is the title of the patent.
The patent focuses on inhibiting the action of prostaglandin D2 by inhibiting its production or reception via its receptor site. PGD2 is 4.4 times more prevalent in balding scalp than hairy scalp. Shaved mice can have their next growth phase inhibited perpetually with topical application of this substance. The patent makes for interesting reading
....................apparently alot of inflammatory substances are upreged around this particular prostaglandin in androgen-related disorders and Costarialis and his co-counder (long name on that dude) feel its some sort of "lynchpin" in androgen related disorders.
As CollegeChemistryStudent pointed out, DHT is only about twice as prevalent in balding scalp than hirsute scalp, so 4.4 times more Prostaglandin D2 presence in balding scalp and bald scalp over hirsute scalp is even more of a correlation in mathematical terms than DHT, so there really may be a link in the process even if its not total in causality.
Consequently, green tea inhibits some prostaglandin D2 expression:
From PubMed:"
1: Prostaglandins Leukot Essent Fatty Acids. 2004 Jul;71(1):25-31. Links
Antiplatelet effect of green tea catechins: a possible mechanism through arachidonic acid pathway.
Son DJ, Cho MR, Jin YR, Kim SY, Park YH, Lee SH, Akiba S, Sato T, Yun YP.
College of Natural Sciences, Soonchunhyang University, Asan 336-745, South Korea.
We have previously reported that green tea catechins (GTC) showed an antithrombotic activity, which might be due to antiplatelet effect rather than anticoagulation. The present study was performed to investigate the effect of GTC on the arachidonic acid (AA) metabolism in order to elucidate a possible antiplatelet mechanism. GTC inhibited the collagen-, AA- and U46619-induced rabbit platelet aggregation in vitro in a concentration-dependent manner, with IC50 values of 61.0+/-2.5, 105.0+/-4.9 and 67.0+/-3.2 microg/ml, respectively. Moreover, GTC administered orally into rats inhibited the AA-induced platelet aggregation ex vivo by 46.9+/-6.1% and 95.4+/-2.2% at the doses of 25 and 50 mg/kg, respectively. [3H]AA liberation induced by collagen in [3H]AA incorporated rabbit platelets was significantly suppressed by GTC compared to the control. GTC also significantly inhibited the thromboxane A2 (TXA2) and prostaglandin D2 (PGD2) generations induced by addition of AA in intact rabbit platelets. GTC significantly inhibited TXA2 synthase activity in a concentration-dependent manner. Moreover, adenosine triphosphate (ATP) release from dense granule was inhibited by GTC in washed platelets. These results suggest that the antiplatelet activity of GTC may be due to the inhibition of TXA2 formation through the inhibition of AA liberation and TXA2 synthase. Copyright 2004 Elsevier Ltd.
PMID: 15172681 [PubMed - indexed for MEDLINE]"
"(WO/2007/149312) METHODS AND COMPOSITIONS FOR INHIBITING OR REDUCING HAIR LOSS, ACNE, ROSACEA, PROSTATE CANCER, AND BPH"
That is the title of the patent.
The patent focuses on inhibiting the action of prostaglandin D2 by inhibiting its production or reception via its receptor site. PGD2 is 4.4 times more prevalent in balding scalp than hairy scalp. Shaved mice can have their next growth phase inhibited perpetually with topical application of this substance. The patent makes for interesting reading
....................apparently alot of inflammatory substances are upreged around this particular prostaglandin in androgen-related disorders and Costarialis and his co-counder (long name on that dude) feel its some sort of "lynchpin" in androgen related disorders.
As CollegeChemistryStudent pointed out, DHT is only about twice as prevalent in balding scalp than hirsute scalp, so 4.4 times more Prostaglandin D2 presence in balding scalp and bald scalp over hirsute scalp is even more of a correlation in mathematical terms than DHT, so there really may be a link in the process even if its not total in causality.
Consequently, green tea inhibits some prostaglandin D2 expression:
From PubMed:"
1: Prostaglandins Leukot Essent Fatty Acids. 2004 Jul;71(1):25-31. Links
Antiplatelet effect of green tea catechins: a possible mechanism through arachidonic acid pathway.
Son DJ, Cho MR, Jin YR, Kim SY, Park YH, Lee SH, Akiba S, Sato T, Yun YP.
College of Natural Sciences, Soonchunhyang University, Asan 336-745, South Korea.
We have previously reported that green tea catechins (GTC) showed an antithrombotic activity, which might be due to antiplatelet effect rather than anticoagulation. The present study was performed to investigate the effect of GTC on the arachidonic acid (AA) metabolism in order to elucidate a possible antiplatelet mechanism. GTC inhibited the collagen-, AA- and U46619-induced rabbit platelet aggregation in vitro in a concentration-dependent manner, with IC50 values of 61.0+/-2.5, 105.0+/-4.9 and 67.0+/-3.2 microg/ml, respectively. Moreover, GTC administered orally into rats inhibited the AA-induced platelet aggregation ex vivo by 46.9+/-6.1% and 95.4+/-2.2% at the doses of 25 and 50 mg/kg, respectively. [3H]AA liberation induced by collagen in [3H]AA incorporated rabbit platelets was significantly suppressed by GTC compared to the control. GTC also significantly inhibited the thromboxane A2 (TXA2) and prostaglandin D2 (PGD2) generations induced by addition of AA in intact rabbit platelets. GTC significantly inhibited TXA2 synthase activity in a concentration-dependent manner. Moreover, adenosine triphosphate (ATP) release from dense granule was inhibited by GTC in washed platelets. These results suggest that the antiplatelet activity of GTC may be due to the inhibition of TXA2 formation through the inhibition of AA liberation and TXA2 synthase. Copyright 2004 Elsevier Ltd.
PMID: 15172681 [PubMed - indexed for MEDLINE]"