Flavonols cardiovascular effects

In the following sections we will review some of the targets of flavonols that, in our opinion, are the most relevant to explain their cardiovascular effects. 

A modest but not significant inverse correlation between the intake of flavonols and flavones and subsequent mortality rates was found in a prospective cohort study of US Health Professionals by Rimm et al [206]. The authors do not exclude that flavonoids have a protective effect in men with established coronary heart disease although strong evidence was missing. Also other studies failed to demonstrate a significant statistical association between the intake of polyphenols and CHD. In Great Britain for instance coronary and total mortality even rose with the intake of the major flavonol source, tea [207], The most likely explanation for the latter observation is that in this study tea consumption merely acted as a marker for a lifestyle that favours the development of cardiovascular disease. Indeed, men with the highest intake of tea and flavonols tended to be manual workers, and they smoked more and ate more fat [208],... 

In summary, the evidence for the preventive effect of flavonols in cardiovascular disease is growing based on mechanistic, animal, epidemiological, and short-term intervention studies. However, we must learn from the lessons with dietary antioxidants, the last word awaits large-scale intervention clinical trials. 

Several cohort studies have been performed in which the relationships between flavonoid intake and the risk of coronary heart disease have been investigated. The studies have shown that the mortality from coronary heart diseases (CHD) is inversely correlated with the intake of flavonoids in the diet. Hollman and Katan (1998) summarize that in three out of five cohort studies, in addition to one cross-cultural study, flavonoids from the flavonol and flavone subgroups demonstrated a protective role toward cardiovascular disease. The protective effect of the flavonoids is partly explained by the inhibition of LDL oxidation and by reduced platelet aggregability. As reviewed by Cook and Samman (1996), there are several possible routes as to how LDL is oxidized by free radicals generated in the cells and how the oxidized LDL initiates and promotes atherosclerosis in the human body. 

Flavonols Quercetin, kaempferol and myricetin and their glycosides (rutin, etc.) Widely distributed. Main sources Onions, apples, tea, red grapes, and broccoli, citrus fruits and maize. Antiproliferative effect [69], Inhibition of angiogenesis [108], Cardiovascular properties [115, 116], protection of DNA damage [60, 137, 138.]. 10-500... 

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