Flavonoid intake and risk of chronic disease - Antioxidants

Nutrition Research Newsletter, Oct, 2002

Free oxygen radicals may be involved in several pathologic conditions. Oxidation of low-density lipoproteins (LDLs) is thought to play an important role in the development of atherosclerosis. Free oxygen radicals are apparently involved in different stages of cancer development. Free radicals may contribute to the. autoimmune destruction of beta cells, leading to diabetes, and may impair insulin action. Reactive oxygen species have also been proposed as mediator of inflammatory damage in asthma and in joints in rheumatoid arthritis. Furthermore, it has been suggested that the oxidation of lens proteins by free radicals plays in important role in the process leading to cataract. Flavonoids are products of plant metabolism and have different phenolic structures. They are effective antioxidants because of 'their free-radical scavenging properties and because they are chelators of metal ions; thus, they may protect tissues against free oxygen radicals and lipid peroxidation. Of the few prospective studies in humans that have predicted the effects of flavonoids on cardiovascular disease risk, some showed an inverse association, whereas others showed no association. Studies of cancer have also given contradictory results. In the present cohort, researchers extended the analysis beyond cardiovascular diseases and cancer to other chronic diseases associated with oxidative stress etiology. Flavonones were included in this analysis in addition to flavonols and flavones.

The Finnish Mobile Clinic Health Examination Survey performed multiphasic screening examinations in different regions of Finland during the period 1966 to 1972. A total of 62 440 persons participated, and as part of the study, information on habitual food consumption was obtained from a random sample of 10 054 participants. A dietary history method was used to collect data on habitual food consumption during the year preceding the interview. Flavonoid intakes were estimated, mainly on the basis of the flavonoid concentrations in Finnish foods.

The mean total intake of flavonoids in the total study population was 24.24-26.7. Persons with a higher total flavonoid intake tended to have a lower total mortality. The relative risk (RR)--adjusted for age, sex, geographic area, occupation, blood pressure, smoking, serum cholesterol, body mass index, and diabetes--between the highest and lowest quartiles of intake was 0.92. This association was mainly due to a flavonoid called quercetine. The association tended to persist for quercetine after simultaneous adjustment for the different flavonoids. Of the dietary sources rich in flavonoids, apple, onion, and orange intakes showed the strongest associations. Persons with higher intakes of quercetin had lower mortality from ischemic heart disease. The incidence of cerebrovascular disease was lower at higher kaempferol, naringenin, and hesperetin intakes. Men with higher quercetin intakes had a lower lung cancer incidence, and men with higher myricetin intakes had a lower prostate cancer risk. Asthma incidence was lower at higher quercetin, naringenin, and hesperetin intakes. A trend toward a reduction in risk of type 2 diabetes was associated with higher quercetin intakes.

The results of this study suggest the presence of an inverse association between flavonoid intake and subsequent occurrence of ischemic heart disease, cerebrovascular disease, lung and prostate cancer, type 2 diabetes, and asthma. The potential benefits were mainly ascribed to quercetin, the most potent antioxidant, but also in some cases to kaempferol, myricetin, naringenin, and hesperetin. Although the findings of this study were independent of the intake of antioxidant vitamins, the potential importance of other biologically active compounds in fruit and vegetables on the relation cannot be excluded.

P Knekt, J Kumpulainen, R Jarvinen, H Rissanen, M Heliovaara, A Reunanen, T Hakulinen, A Aromaa. Flavonoid intake and risk of chronic diseases. Am J Clin Nutr 76:560-568 (September 2002) [Correspondence: P Knekt, National Public Health Institute, Mannerheimintie 166, Helsinki 00300, Finland E-mail: paul.knekt@ktl.fi.]