Came across this,thought it would be of intrest.

To assess the effects of testosterone on the risk of developing atherosclerosis, male mice lacking the LDLR (LDL receptor) and fed a high-cholesterol diet, a model of human atherosclerosis, were studied.1

The researchers found that fatty-streak-lesion formation (an early stage of atherosclerosis) in the aorta was greater in castrated animals than in animals with intact testes or in castrated animals that were supplemented with testosterone. These results were similar to earlier work by others with castrated, cholesterol-fed rabbits.

The particularly interesting part of the study was the determination of whether it was testosterone itself that produced the antiatherogenic effect or whether it was the conversion of testosterone to estradiol by the aromatase enzyme that was responsible. Aromatase has been shown to be present in endothelial cells and vascular smooth muscle cells, as well as other tissues. Thus, local conversion of testosterone to estradiol can take place in blood vessels. The results showed that in the testis-intact animals given an aromatase inhibitor, there was a greater extent of early lesion formation than in the testis-intact animals receiving only vehicle. They also found that the castrated mice supplemented with testosterone and simultaneously given an aromatase inhibitor had significantly increased lesion formation compared to the castrated mice given testosterone alone. Thus, the conversion of testosterone to estradiol was required for the atheroprotective effect of testosterone.

In a later study of testosterone and diet-induced atherosclerosis in mice2 expressing or not expressing CETP [cholesteryl ester transfer protein (important for the export of cholesterol from cells)], the researchers found that castration resulted in 1.7-fold higher levels of antioxidized LDL antibodies than sham-operated (operated upon but not actually castrated). Diet-induced atherosclerosis studies showed that testosterone deficiency increased by 100%, and CETP expression reduced by 44%, the size of aortic lesion area in castrated mice. The authors stated that [a]romatization of testosterone into 17beta-estradiol seems to be an important determinant of the beneficial effects of androgens observed in men and mice.

It is also relevant to know that many polyphenols inhibit aromatase. One study3 reported that aromatase was inhibited in cultures of choriocarcinoma-derived JAR cells by chrysin (a flavone), naringenin (a flavanone), daidzein and genistein (isoflavones), kaempferol, myricetin, quercetin, and rutin (flavonols), catechin, epicatechin, and epigallocatechin-3-gallate (flavanols), and resveratrol (a stilbene). Chrysin, naringenin, and quercetin were the most potent polyphenols in inhibiting aromatase activity. In addition, red wine (but not white wine), green tea, and black tea also inhibited aromatase. These effects may contribute to the anticarcinogenic effects of these polyphenols and beverages in, for example, breast and prostate cancers. Another paper4 reported inhibition of aromatase activity by flavonoids, with apigenin (found in parsley, celery, and many other plants), chrysin, and hesperidin (found in grapefruit, especially the rind) having the greatest activity.

One advantage of the local conversion of testosterone to estradiol by aromatase in blood vessels is that it avoids the negative effects of systemic estrogen treatment in males. The moral of this story is that, unless required for treatment of a serious condition, such as cancer, men should probably not take powerful systemic aromatase inhibitors. We have seen no indication, however, of an increased cardiovascular risk in heavy tea drinkers or in moderate drinkers of red wine.


Nathan et al. Testosterone inhibits early atherogenesis by conversion to estradiol: critical role of aromatase. Proc Natl Acad Sci USA 98(6):3589-93 (2001).
Casquero et al. Atherosclerosis is enhanced by testosterone deficiency and attenuated by CETP expression in transgenic mice. J Lipid Res 47(7):1526-34 (2006).
Monteiro et al. Modulation of aromatase activity by diet polyphenolic compounds. J Agric Food Chem 54:3535-40 (2006).
Jeong et al. Inhibition of aromatase activity by flavonoids. Arch Pharm Res 22(3):309-12 (1999).

from Life Extension News vol.9,no.3 August 2006