Certain dietary antioxidants such as vitamin E and vitamin C are important for maintaining optimum health. There is now much interest in polyphenolic products of the plant phenylpropanoid pathway as they have considerable antioxidant activity in vitro and are ubiquitous in our diet. Rich sources include tea, wine, fruits and vegetables although levels are affected by species, light, degree of ripeness, processing and storage. This confounds the formulation of databases for the estimation of dietary intakes. Most attention to date has focused on the¯avonoids, a generic term which includes chalcones,¯avones,¯avanones,¯avanols and anthocyanins. There is little convincing epidemiological evidence that intakes of polyphenols are inversely related to the incidence of cancer whereas a number of studies suggest that high intakes of¯avonoids may be protective against CHD. In contrast, numerous cell culture and animal models indicate potent anticarcinogenic activity by certain polyphenols mediated through a range of mechanisms including antioxidant activity,

A sustainable diet that meets dietary requirements for health with lower GHGEs can be achieved without eliminating meat or dairy products or increasing the cost to the consumer.

The data indicate that these subjects had a functional selenium deficit with suboptimal immune status and a deficit in viral handling. They also suggest that the additional 100 microg Se/d may be insufficient to support optimal function.

Cranberry juice consumption did not alter blood or cellular antioxidant status or several biomarkers of lipid status pertinent to heart disease. Similarly, cranberry juice had no effect on basal or induced oxidative DNA damage. These results show the importance of distinguishing between the in vitro and in vivo antioxidant activities of dietary anthocyanins in relation to human health.

In vitro and in vivo laboratory data point to chemoprotective effects of flavonoids on colorectal cancer. However, there has been limited epidemiologic research on the dietary intake of flavonoids and risk of colorectal cancer. Recent expansions of dietary databases to include flavonoid data now make such studies feasible. Association between the six main classes of flavonoids and the risk of colorectal cancer was examined using data from a national prospective case-control study in Scotland, including 1,456 incident cases and 1,456 population-based controls matched on age, sex, and residence area. Dietary, including flavonoid data, were obtained from a validated, self-administered food frequency questionnaire. Risk of colorectal cancer was estimated using conditional logistic regression models in the whole sample and stratified by sex, smoking status, and cancer site and adjusted for established and putative risk factors. After energy adjustment, reductions in colorectal cancer risk associated with the highest quartiles of intake (versus the lowest quartile) were 27% for flavonols [odds ratio (OR), 0.73; P trend = 0.012], 32% for quercetin (OR, 0.68; P trend = 0.001), 32% for catechin (OR, 0.68; P trend < 0.0005); 26% for epicatechin (OR, 0.74; P trend = 0.019), and 22% for procyanidins (OR, 0.78; P trend = 0.031). The significant dose-dependent reductions in colorectal cancer risk that were associated with increased consumption of flavonols, quercetin, catechin, and epicatechin remained robust after controlling for overall fruit and vegetable consumption or for other flavonoid intake. The risk reductions were greater among nonsmokers, but no interaction beyond a multiplicative effect was present. Sex-specific or cancer-type differences were not observed. No risk reductions were associated with intake of flavones (P trend = 0.64), flavonones (P trend = 0.22), and phytoestrogens (P trend = 0.26). This was the first of several a priori hypotheses to be tested in this large study and showed strong and linear inverse associations of flavonoids with colorectal cancer risk. (Cancer Epidemiol Biomarkers Prev 2007;16(4):684 -93)

Epidemiological evidence suggests that diets rich in fruit and vegetables decrease the risk of premature mortality from major clinical conditions, including cancer and heart disease. However, it is not yet clear which components or combination of components in fruit and vegetables are protective and what is their mechanism of action. Such scientific uncertainty does not seem to inhibit the marketing of a huge range of plant-based concoctions, promoted as ‘magic bullets’ for optimum health. For example, the purported health-giving properties of plant polyphenols represent a case in which enthusiastic marketing claims may far exceed the current scientific evidence. Even when good experimental evidence exists, results need to be interpreted with caution in relation to human health benefits, as polyphenols may have limited bioavailability and may also be extensively metabolised. In addition, some polyphenols can be toxic and mutagenic in some cell culture systems. Until more is known about the activity and metabolic fate of polyphenols in the body, it would be better for the consumer to increase fruit and vegetable intake, and also to be wary of claims that these compounds are a panacea for good health.

IntroductionHyperuricemia is a strong risk factor for gout. The incidence of gout and hyperuricemia has increased recently, which is thought to be, in part, due to changes in diet and lifestyle. Objective of this study was to investigate the association between plasma urate concentration and: a) food items: dairy, sugar-sweetened beverages (SSB) and purine-rich vegetables; b) related nutrients: lactose, calcium and fructose.MethodsA total of 2,076 healthy participants (44% female) from a population-based case-control study in Scotland (1999–2006) were included in this study. Dietary data was collected using a semi-quantitative food frequency questionnaire (FFQ). Nutrient intake was calculated using FFQ and composition of foods information. Urate concentration was measured in plasma.ResultsMean urate concentration was 283.8±72.1 mmol/dL (females: 260.1±68.9 mmol/dL and males: 302.3±69.2 mmol/dL). Using multivariate regression analysis we found that dairy, calcium and lactose intakes were inversely associated with urate (p = 0.008, p = 0.003, p = 0.0007, respectively). Overall SSB consumption was positively associated with urate (p = 0.008), however, energy-adjusted fructose intake was not associated with urate (p = 0.66). The intake of purine-rich vegetables was not associated to plasma urate (p = 0.38).ConclusionsOur results suggest that limiting purine-rich vegetables intake for lowering plasma urate may be ineffectual, despite current recommendations. Although a positive association between plasma urate and SSB consumption was found, there was no association with fructose intake, suggesting that fructose is not the causal agent underlying the SSB-urate association. The abundant evidence supporting the inverse association between plasma urate concentration and dairy consumption should be reflected in dietary guidelines for hyperuricemic individuals and gout patients. Further research is needed to establish which nutrients and food products influence plasma urate concentration, to inform the development of evidence-based dietary guidelines.

Objective: To determine the potential antioxidant effect of rutin (quercetin-3-O-b-rutinoside) supplementation. Design: A 6-week randomized single-blind placebo controlled trial was conducted; 500 mg rutin supplement was compared to an equivalent amount of glucose placebo. In addition, a pharmacokinetic study was carried out. Setting: The Rowett Research Institute, Aberdeen, UK. Subjects: Eighteen healthy non-obese normocholesterolaemic female volunteers in the age range 18 ± 48 y. Main outcome measures: Plasma¯avonoids, ascorbic acid, tocopherols and carotenoids, plasma antioxidant capacity, lymphocyte DNA damage, blood chemistry and haematology, liver function tests, urinary malondialdehyde, 8-hydroxy-2H -deoxyguanosine and 8-iso-prostaglandin F 2a . Results: Eighteen volunteers completed the trial. Rutin supplementation did not induce any adverse changes in blood chemistry or indices of liver function. Plasma¯avonoids were signi®cantly elevated in the rutinsupplemented group. Endogenous oxidation of pyrimidines was signi®cantly decreased in both rutin-and placebo-treated volunteers. There was no signi®cant change in the level of urinary 8-hydroxy-2 H -deoxyguanosine or urinary malondialdehyde in either group. A linear correlation was observed between urinary malondialdehyde and urinary 8-iso-prostaglandin F 2a (R 0.54, P`0.01). Conclusion: Six weeks' rutin supplementation signi®cantly elevated the levels of three plasma¯avonoids (quercetin, kaempferol and isorhamnetin) but there was no signi®cant change in plasma antioxidant status. The decrease in the level of endogenous base oxidation in lymphocyte DNA seen in both the placebo-and rutinsupplemented subjects may re¯ect seasonal changes in other dietary antioxidants.