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was observed in rats fed a diet supplemented with geni- stein.286,287 These effects of genistein on the thyroid function are more pronounced when iodine is deficient. Other flavonoids, such as daidzein, quercetin, kaempferol, or naringenin, were also shown to irreversibly inhibit thyroid peroxidase.288 These data are of particular concern for soy-fed babies exposed to particu- larly high doses of isoflavones.289 Vitexin, a C -glycosylflavones abundant in millet, is another inhibitor of thyroid peroxidase. When administered to rats, it increased thyroid weight and de- creased the plasma levels of thyroid hormones.290 It is thought to contribute to the genesis of endemic goiter in West Africa, where millet is a staple food. Most dietary polyphenols have catechol group in their struc- tures and, thus form very stable chelates with ferric ions. This fundamental property explains the inhibition of non-heme iron absorption by polyphenols and polyphenol-containing bever- ages, such as coffee, wine, or tea, as shown in several clinical trials.291−293 As these effects involve direct chelation of iron by polyphenols in the gut, they are only observed when the source of polyphenols is ingested together with the source of iron.294 This is why it is often recommended for people at risk of de- veloping iron deficiencies to drink tea and other polyphenol- rich beverages between the meals rather than during the meals. The effects of polyphenols on iron absorption have been well demonstrated in clinical studies; however, the impact of dietary polyphenols on iron status is not as firmly established in free- living populations.295 In contrast, for other people with a high iron status, the inhibition of iron absorption by polyphenols may be rather beneficial, as high levels of plasma ferritin have been associated to a higher risk of cardiovascular diseases and colon cancer.296 Adverse effects of polyphenol consumption on cardiovas- cular diseases have recently been suggested. High polyphe- nol intake could increase the risk of cardiovascular diseases through an effect on homocysteinemia, an independent risk fac- tor of cardiovascular diseases. The consumption of 2 g chloro- genic acid/d during 1 wk by volunteers significantly increased homocysteinemia.297 Such a dose corresponds to the consump- tion of about 2.5 l coffee/d.1 A similar increase of homocys- teinemia was also observed in L-DOPA-treated Parkinsonian patients.298 Just like chlorogenic acid, L-DOPA contains a cat- echol group and is largely methylated to 3- O -methyldopa with as a consequence, the conversion of the methyl donor S- adenosylmethionine to S-adenosylhomocysteine and homocys- teine. A common L-DOPA dose used in the treatment of Parkin- sonians is 500 mg/d (2.5 mmol/d), a dose close to that used for chlorogenic acid above (5.6 mmol/d). It is not known whether lower polyphenol intakes also affect homocysteinemia. In the future, more attention should be paid to possible ad- verse effects of polyphenol consumption. This is particularly important when considering the growing development of new polyphenol-containing dietary supplements. The consumption of such supplements may lead to particularly high exposure of some specific polyphenols, well above those commonly associ- ated to the diet. The addition of specific polyphenols to different foods should also be strictly controlled to limit their consump- tion to persons for whom an expected health benefit has been well established. More clinical trials and epidemiological stud- ies are needed to better assess the balance between benefits and risks. CONCLUSIONS A protective role of polyphenols against degenerative dis- eases is supported tod by many studies carried out on animals, and different mechanisms of action have been proposed to ex- plain such protective effects. Much progress has also been made on the evaluation of their bioavailability. The significance for human health of all in vitro data obtained on cultured cells or isolated enzymes and receptors will have to be properly re- evaluated in the light of this new knowledge on bioavailability. More human studies are needed to provide definitive proofs of the protective role of polyphenols. Conclusive evidence will largely come from clinical and epidemiological studies. The number of clinical studies so far published is still limited, and the results are often contradictory. If it is clear that the con- sumption of polyphenols improves some oxidative stress related parameters, but the associations between these parameters and disease risk are still not well clarified, we need to identify proper markers of disease risk and demonstrate that they are influenced by the consumption of polyphenols. First, epidemiological data on polyphenols were published approximately 10 yr ago and since then progress has been rela- tively slow because of the lack of food composition tables and lack of validated biomarkers of polyphenol intake. Such tables or biomarkers are needed to evaluate the consumption of polyphe- nols in populations, but their obtention/identification is rendered difficult because of the large number of phenolic compounds present in food. A table for flavonoids based on the surveys of 97 literature sources is now available.299 More research is still needed to cover missing polyphenols and food sources. It is impossible to conclude today that some particular polyphenols offer more health benefits than others and research efforts continue at an increasing pace for all polyphenol classes. All polyphenols share common properties as reducing agents. Most of the dietary polyphenols can chelate iron and other metal ions. As such, they may all trigger common cell responses through mechanisms that have been partly unravelled.21 On the other hand, some polyphenols, like phytoestrogens, show spe- cific properties and may be more indicated for the prevention of specific diseases. More intervention studies are needed to clarify the impact of the most active polyphenols on specific diseases or disease biomarkers. When developping new polyphenol-containing products for specific effects on a given pathology, we will also have to make sure that they do not increase risks for other pathologies. For exemple, resveratrol shows promising anticarcinogenic proper- ties, but it also increases the risk of cardiovascular diseases in mice.300 Quercetin may be effective to prevent different diseases, DIETARY POLYPHENOLS AND DISEASE PREVENTION 297PDF Image | Dietary Polyphenols and the Prevention of Diseases
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