michael barry
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Patent..........Curcumin androgen receptor agonist?
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michael barry
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3. Curcumin and Related Compounds
Curcumin was a very effective inhibitor of either the type 1 or type 2 isoenzyme (Table 3, FIG. 3).
TABLE 3 HRED1 HRED1 % HRED2 HRED2 Cell Free Assay Isoenzyme IC50 Inhibition IC50 % Inhibition Compound (uM) @100 uM (uM) @100 uM 1. Curcumin 3 95 5 87 2. Tetrahydrocurcumin 80 56 29 73 3. Demethoxy- >100 23 >100 42 tetrahydrocurcumin 4. 4-hydroxy-3- >100 10 >100 (+60) methoxy- cinnamaldehyde 5. Coniferol >100 10 100 49 6. 4-(4-hydroxy-3- >100 3 >100 4 methoxyphenol)-3- buten-2-one 7. Ferulic Acid >100 0 >100 18 8. Capsaicin >100 0 >100 8 9. Eugenol >100 0 100 50
Commercially available curcumin was chemically reduced with Pt/H2 and the products, tetrahydrocurcumin and demethoxytetrahydrocurcumin, had much less activity than curcumin. However, tetrahydrocurcumin (HZIV 81-2), which is colorless compared to the bright yellow curcumin, had significant activity in the whole cell assay. The structurally related compounds 4-(4-hydroxy-3-methoxyphenol)-3-buten-2-one, ferulic acid, capsaicin, eugenol and coniferyl alcohol had little inhibitor activity (IC50>100 .mu.M) against either isoenzyme highlighting the importance of the diferulolyl structure for activity against 5.alpha.-reductase. Nordihydroguaiaretic acid (NDGA) was also an effective inhibitor of the type 1 (IC50=19 .mu.M) and type 2 (IC50=50 .mu.M) isozymes in cell-free and whole cell assays, but less so than curcumin.
4. Quinones
That appears to claim curcumin acts against alpha five type one and two. I'll try and nail this down.
Curcumin was a very effective inhibitor of either the type 1 or type 2 isoenzyme (Table 3, FIG. 3).
TABLE 3 HRED1 HRED1 % HRED2 HRED2 Cell Free Assay Isoenzyme IC50 Inhibition IC50 % Inhibition Compound (uM) @100 uM (uM) @100 uM 1. Curcumin 3 95 5 87 2. Tetrahydrocurcumin 80 56 29 73 3. Demethoxy- >100 23 >100 42 tetrahydrocurcumin 4. 4-hydroxy-3- >100 10 >100 (+60) methoxy- cinnamaldehyde 5. Coniferol >100 10 100 49 6. 4-(4-hydroxy-3- >100 3 >100 4 methoxyphenol)-3- buten-2-one 7. Ferulic Acid >100 0 >100 18 8. Capsaicin >100 0 >100 8 9. Eugenol >100 0 100 50
Commercially available curcumin was chemically reduced with Pt/H2 and the products, tetrahydrocurcumin and demethoxytetrahydrocurcumin, had much less activity than curcumin. However, tetrahydrocurcumin (HZIV 81-2), which is colorless compared to the bright yellow curcumin, had significant activity in the whole cell assay. The structurally related compounds 4-(4-hydroxy-3-methoxyphenol)-3-buten-2-one, ferulic acid, capsaicin, eugenol and coniferyl alcohol had little inhibitor activity (IC50>100 .mu.M) against either isoenzyme highlighting the importance of the diferulolyl structure for activity against 5.alpha.-reductase. Nordihydroguaiaretic acid (NDGA) was also an effective inhibitor of the type 1 (IC50=19 .mu.M) and type 2 (IC50=50 .mu.M) isozymes in cell-free and whole cell assays, but less so than curcumin.
4. Quinones
That appears to claim curcumin acts against alpha five type one and two. I'll try and nail this down.
michael barry
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A little pubmed on ECGC and Curcumin and androgen receptors and alpha five reductase and DHT
http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
Tres' interessant
http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
Tres' interessant
michael barry
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I found a topical curcumin cream here http://www.springboard4health.com/store ... cumin.html
so where do we buy the non-yellow, stronger curcumin? I could also use that as a topical, since it would not make my hair yellow. Mostly just interested in eating it, for general health. That EGCG could be a good androgen recepter blocker according to another study bryan once posted.
docj077
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I would have to see an in vivo study in humans demonstrating androgen inhibitory activity with curcumin before I'd jump all over it.
If it does work as an internal androgen inhibitor, I certainly haven't noticed anything. My sweet "almost" beard is still as prevalent as ever and I have noticed no other signs of decreased androgen activity. As a topical, maybe it's different.
I use it for it's supposed TGF-beta antagonist abilities.
All that I know is that it doesn't cause brain fog, seems to help my hair as I'm currently only using curcumin, Johnsons Baby shampoo with Vitamin E and honey, and I've starting to use bromelain, but I haven't decided on dosing, yet. I haven't been on propecia now for a few months and that was a very good decision as that stuff really messed with my thyroid hormones.
At least it'll keep me healthy.
If it does work as an internal androgen inhibitor, I certainly haven't noticed anything. My sweet "almost" beard is still as prevalent as ever and I have noticed no other signs of decreased androgen activity. As a topical, maybe it's different.
I use it for it's supposed TGF-beta antagonist abilities.
All that I know is that it doesn't cause brain fog, seems to help my hair as I'm currently only using curcumin, Johnsons Baby shampoo with Vitamin E and honey, and I've starting to use bromelain, but I haven't decided on dosing, yet. I haven't been on propecia now for a few months and that was a very good decision as that stuff really messed with my thyroid hormones.
At least it'll keep me healthy.
docj077, how long were you on propecia? If it was a year, you can learn a lot from this experiment, since people usually fall to baseline fast after getting off. you'll know in 6 months.
BTW, even dutasteride does not reduce my body hair density, so i don't think you can draw that conclusion about curcumin. And I suspect hampster flank is more responsive than human body parts.
BTW, even dutasteride does not reduce my body hair density, so i don't think you can draw that conclusion about curcumin. And I suspect hampster flank is more responsive than human body parts.
docj077
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collegechemistrystudent said:
Six months on propecia. My free T4 levels became elevated and I experienced all the signs and symptoms of hyperthyroidism, so I stopped the drug and my physical manifestations of the disease went away. My thyroid iodine uptake scan was negative, so I know that there is nothing wrong with my thyroid gland.
For me, any drug that inhibits androgens in any way will decrease both the growth rate and the density of all androgen dependent hair on my body when taken internally. On propecia, my arms hair, armpit hair, pubic hair, and eye brow hair all thinned rapidly. Maybe I'm just an odd case, I don't know.
As for my hair returning to baseline, I really don't think my hair has changed for the worse. I don't use anything in it anymore to style it and using my baby shampoo, as well, has really reduced any signs of inflammation including pain or itching. I've also noticed that the oil production on my scalp has dropped way below the level it was at when I was using either tree trea oil shampoo, revivogen, or my other organic shampoo. My hair is soft, and yet, my scalp isn't oily. I haven't had that phenomenon since I was a kid.
Really, I don't think that propecia did anything for me except for maybe a little maintenance. I was pretty unimpressed, but at least I know now that I can't take the stuff. Plus, that experience has helped me refocus my efforts.
michael barry
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Doctor,
If curcumin and green tea can outdo gamma linolenic acid in keeping hamster flank organs small.......................then they can do topical spironolcatone in doing it as well. Bryan has posted about GLA outdoing Sprio and cyterperone acetate on flank organs.
I'll have to look for his post online concerning that, its been a long time since Ive read it. I never noticed any difference physiologically whatsoever on propecia, but DID notice a difference when taking internal green tea extract. Gave me the blahs, a little diarreaha, less libido.
The only way I could think that you could test green tea topically woudl be on some body hair. I know it decreases sebum when used topically. Why Im a little hesitant about green tea is that it inhibits angiogenesis, which we really need with hair (guys with baldness genetics need all the help they can get). I'll post that old post from Bryan if I can find it online somewhere.
If curcumin and green tea can outdo gamma linolenic acid in keeping hamster flank organs small.......................then they can do topical spironolcatone in doing it as well. Bryan has posted about GLA outdoing Sprio and cyterperone acetate on flank organs.
I'll have to look for his post online concerning that, its been a long time since Ive read it. I never noticed any difference physiologically whatsoever on propecia, but DID notice a difference when taking internal green tea extract. Gave me the blahs, a little diarreaha, less libido.
The only way I could think that you could test green tea topically woudl be on some body hair. I know it decreases sebum when used topically. Why Im a little hesitant about green tea is that it inhibits angiogenesis, which we really need with hair (guys with baldness genetics need all the help they can get). I'll post that old post from Bryan if I can find it online somewhere.
docj077
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michael barry said:
I need to see an actual histological section of someone with male pattern baldness before I could jump to any conclusions. I briefly saw one on the internet and I took from it what I could.
Seeing a section would tell me if green teas angiogenesis inhibitory abilities really even matter, because I need to know if blood vessels in the dermis are even effected. If they aren't, it doesn't matter as the epidermis has no real blood flow anyway. The epidermis is like that for a reason...to prevent blood flow to cancers that may potentially metastasize.
Also, I can't remember if you're the one interested in edema in the scalp, but there are two easy ways to see edema in a scalp section. First, look in the dermis at the collagen. If it is widely scattered with large open areas, then there is edema fluid there. Most of the section will demonstrate that phenomenon. Second, look at the dermis. Look for a phenomenon known as spongiosis. This is demonstrated by gaps in the keratinocytes.
From what I've seen, male pattern baldness demonstrates neither process.
michael barry said:
GLA inhibits 5ar, like finasteride does. spironolactone and cyterperone block the androgen receptors. It is wrong to compare the three head to head. And spironolactone is much better than cyterperone. I forgot what is wrong with cyterperone, but it is not an option.
spironolactone competes with testosterone, whereas GLA does not. As for these other things, curcumin also only inhibits 5ar. EGCG, though, inhibits the androgen receptor. Or rather, even when pure DHT was added to hampster flank with EGCG, the grouth was inhibited 97% compared to the grouth with the eGCG. I wish they had compared it head to head with RU.