Flavonoids in cereals and herbs are thought to reduce incidence of atherosclerosis, osteoporosis, diabetes and some cancers. If they do, could a possible reason be that they reduce the liver's ability to oxidize circulating compounds from foods like caffeine, theobromine.

^{flavanoidsPubMed}
Biochem Pharmacol. 1998 May 1;55(9):1369-75.
Structure-related inhibition of human hepatic caffeine N3-demethylation by naturally occurring flavonoids, by Lee H1, Yeom H, Kim YG, Yoon CN, Jin C, Choi JS, Kim BR, Kim DH.
The effects of flavonoids on caffeine N3-demethylation, a marker activity of CYP1A2, in human liver microsomes were investigated to elucidate the inhibition mechanism and the structure-activity relationship. Caffeine N3-demethylase activity was inhibited by the presence of various flavonoids, whose structures seem to be closely related to the degree of inhibition. Among twenty-one compounds tested, the most active was chrysin with an IC50 value of 0.2 microM. Others had IC50 values ranging from 1 to more than 500 microM. Kinetic analysis revealed that the mechanism of inhibition varied among the flavonoids. The inhibitory effect was postulated to be governed by factors such as the number of hydroxyl groups and glycosylation of these free hydroxyl groups. An increase in the number of free hydroxyl groups reduced the inhibitory effect on P450 activity. Analysis of the quantitative structure-activity relationship (QSAR) showed that the volume to surface area ratio was the most effective factor on the inhibition of caffeine N3-demethylation, and the electron densities on the C3 and C4' atoms exercised significant influence on the inhibitory effect. The calculated inhibitory effect of flavonoids on CYP1A2 activity was highly correlated with the antimutagenicity of flavonoids in 2-amino-3,4-dimethylimidazo[4,5-flquinoline (MelQ)-induced umu response.

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^{homosysteinePubMed}
AHA Recommendation

The American Heart Association has not yet called hyperhomocysteinemia (high homocysteine level in the blood) a major risk factor for cardiovascular disease. We don't recommend widespread use of folic acid and B vitamin supplements to reduce the risk of heart disease and stroke. We advise a healthy, balanced diet that's rich in fruits and vegetables, whole grains, and fat-free or low-fat dairy products. For folic acid, the recommended daily value is 400 micrograms (mcg). Citrus fruits, tomatoes, vegetables and grain products are good sources. Since January 1998, wheat flour has been fortified with folic acid to add an estimated 100 micrograms per day to the average diet. Supplements should only be used when the diet doesn't provide enough.

What is homocysteine, and how is it related to cardiovascular risk?

Homocysteine is an amino acid in the blood. Too much of it is related to a higher risk of coronary heart disease, stroke and peripheral vascular disease (fatty deposits in peripheral arteries).

Evidence suggests that homocysteine may promote atherosclerosis (fatty deposits in blood vessels) by damaging the inner lining of arteries and promoting blood clots. However, a causal link hasn't been established.

How do folic acid and other B vitamins affect homocysteine levels?

Folic acid and other B vitamins help break down homocysteine in the body. Homocysteine levels in the blood are strongly influenced by diet and genetic factors. Dietary folic acid and vitamins B-6 and B-12 have the greatest effects. Several studies found that higher blood levels of B vitamins are related, at least in part, to lower concentrations of homocysteine. Other evidence shows that low blood levels of folic acid are linked with a higher risk of fatal coronary heart disease and stroke.

So far, no controlled treatment study has shown that folic acid supplements reduce the risk of atherosclerosis or that taking these vitamins affects the development or recurrence of cardiovascular disease. Researchers are trying to find out how much folic acid, B-6 and/or B-12 are needed to lower homocysteine levels. Screening for homocysteine levels in the blood may be useful in patients with a personal or family history of cardiovascular disease but who don't have the well-established risk factors (smoking, high blood cholesterol, high blood pressure, physical inactivity, obesity and diabetes).

Although evidence for the benefit of lowering homocysteine levels is lacking, patients at high risk should be strongly advised to be sure to get enough folic acid and vitamins B-6 and B-12 in their diet. They should eat fruits and green, leafy vegetables daily.

This is just one possible risk factor. A physician taking any type of nutritional approach to reducing risk should consider a person's overall risk factor profile and total diet.