Natural aromatase inhibitors

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I sent out to our list, Pomogranites effect as an aromatase enzyme. I continued

to read about natural aromatase enzymes.

I found the below list, and Biochanin A, which comes from red clover, chinese

peas also has a very high content as well. Biochanin A is often used to treat

breast cancer, medics are not sure why it helps, Biochanin A will stop or slow

prostrate cancer and certainly lower PSA levels.

I was accused by my second wife of being a bit dense, but it seems to me, if an

aromatase enzyme inhibitor will work against breast and prostrate cancer, as

Anastrozole ie arimidex does on breast cancer. Hence it would be that estrogen

is our enemy when it comes to prostrate cancer. As far as I know, an armatase

inhibitor stops the conversion of testosterone to estrogen. Again to use one

would mean more testosterone and less estrogen in the body.

It would also be much wiser to take red clover and chinese peas rather than

arimidex for either types of cancer, albeit, we would no know the dosage.

I would certainly appreciate anyone chiming in with this, as I found it

profound, noone seems to recognize the obvious.

stay well, david a

Table 2. Ki values of aromatase inhibitors

Inhibitor Ki (?M)

Letrozole 0.0004

Anastrozole 0.011

4-Hydroxyandrostenedione 0.015

4-Benzyl-3-(4'-chlorophenyl)-7-methoxycoumarin 0.084

4-Benzyl-3-(4'-chlorophenyl)-7-hydroxycoumarin 0.23

4-Benzyl-7-methoxy-3-phenylcoumarin 1.1

Aminoglutethimide 2.7

Chrysin 2.6

Naringenin 5.1

7,8-Dihydroxyflavone 10

Biochanin A 12

Biochanin A,,,,,, is huge when it comes to being an aromatase inhibitor ie

Chinese Peas has approximately ten times more Biochanin A, than any other

vegetable.

With exception to Red Clover, which Biochanin A is harvested from and sold as a

health food in china.

The effect of the isoflavones, genistein, daidzein, and biochanin A on the

growth of the LNCaP and DU-145 human prostate cancer cell lines has been

examined. Genistein and biochanin A, but not daidzein, inhibit both serum and

EGF-stimulated growth of LNCaP and DU-145 cells (IC50 values from 8.0 to 27

micrograms/ml for serum and 4.3 to 15 micrograms/ml for EGF), but have no

significant effect of the EGF receptor tyrosine autophosphorylation. In

contrast, tyrphostin 25, a specific EGF receptor tyrosine kinase inhibitor,

inhibits EGF-stimulated growth and EGF receptor tyrosine autophosphorylation in

these whole cells, but does not inhibit serum-stimulated growth. These data

suggest that the mechanism of action of genistein and biochanin A does not

depend on inhibition of EGF receptor tyrosine autophosphorylation, but on a more

distal event in the EGF receptor-mediated signal transduction cascade

Our laboratory has characterized androgen metabolism in an androgen-responsive

prostate cancer cell line (LNCaP) and showed that these cells accumulated

intracellular testosterone primarily as glucuronidated metabolites. Using a

cell-free assay with testosterone as substrate, we showed that LNCaP had

UDP-glucuronosyltransferase (UDPGT) activity. Because dietary factors, such as

flavonoids in soy products, may reduce the risk for hormone-dependent cancers,

we studied the effects of flavonoids on testosterone-UDPGT activity. LNCaP cells

were exposed to selected flavonoids for up to 6 days. The increase in

UDPGT-specific activity was linear over this period. Of the compounds tested,

biochanin A was the most potent, with increased activity at concentration range

0.5-50 µM. Activities were linear for time and protein and were unaffected by

flavonoids added directly to the assay. Kinetics studies showed no change in Km

for testosterone in the face of these large increases in specific activity.

Cellular metabolism of testosterone reflected the increase in enzyme activity.

Intact cells treated with biochanin A produced testosterone-glucuronide from

testosterone at twice the rate of controls. The steroid form of the UDPGT

transcript was expressed in LNCaP cells and was enhanced in biochanin A-treated

LNCaP cells. Additionally, biochanin A markedly decreased prostate specific

antigen (PSA) level against the effect of testosterone on PSA production.

Biochanin A significantly decreased the testosterone-stimulated release of PSA,

presumably because biochanin A increased UDPGT and increased the intracellular

glucuronidation of testosterone. These studies suggest that the modulation of

hormone metabolism by dietary factors may be important in the prevention and

treatment of prostate cancer.