Dietary modification may affect inflammatory processes and protect against chronic disease. In the present study, we examined the relationship between dietary patterns, circulating carotenoid and tocopherol concentrations, and biomarkers of chronic low-grade systemic inflammation in a 10-year longitudinal study of Scottish postmenopausal women. Diet was assessed by FFQ during 1997–2000 (n 3237, mean age 54·8 (sd 2·2) years). Participants (n 2130, mean age 66·0 (sd 2·2) years) returned during 2007–11 for follow-up. Diet was assessed by FFQ (n 1682) and blood was collected for the analysis of serum high-sensitivity C-reactive protein (hs-CRP), IL-6, serum amyloid A, E-selectin, lipid profile and dietary biomarkers (carotenoids, tocopherols and retinol). Dietary pattern and dietary biomarker (serum carotenoid) components were generated by principal components analysis. A past ‘prudent’ dietary pattern predicted serum concentrations of hs-CRP and IL-6 (which decreased across the quintiles of the dietary pattern; P= 0·002 and P= 0·001, respectively; ANCOVA). Contemporary dietary patterns were also associated with inflammatory biomarkers. The concentrations of hs-CRP and IL-6 decreased across the quintiles of the ‘prudent’ dietary pattern (P= 0·030 and P= 0·006, respectively). hs-CRP concentration increased across the quintiles of a ‘meat-dominated’ dietary pattern (P= 0·001). Inflammatory biomarker concentrations decreased markedly across the quintiles of carotenoid component score (P< 0·001 for hs-CRP and IL-6, and P= 0·016 for E-selectin; ANCOVA). Prudent dietary pattern and carotenoid component scores were negatively associated with serum hs-CRP concentration (unstandardised β for prudent component: − 0·053, 95 % CI − 0·102, − 0·003; carotenoid component: − 0·183, 95 % CI − 0·233, − 0·134) independent of study covariates. A prudent dietary pattern (which reflects a diet high in the intakes of fish, yogurt, pulses, rice, pasta and wine, in addition to fruit and vegetable consumption) and a serum carotenoid profile characteristic of a fruit and vegetable-rich diet are associated with lower concentrations of intermediary markers that are indicative of CVD risk reduction.

There are concerns that weight-loss (WL) diets based on very low carbohydrate (LC) intake have a negative impact on antioxidant status and biomarkers of cardiovascular and metabolic health. Obese men (n 16) participated in a randomised, cross-over design diet trial, with food provided daily, at approximately 8·3 MJ/d (approximately 70 % of energy maintenance requirements). They were provided with two high-protein diets (30 % of energy), each for a 4-week period, involving a LC (4 % carbohydrate) and a moderate carbohydrate (MC, 35 % carbohydrate) content. Body weight was measured daily, and weekly blood samples were collected. On average, subjects lost 6·75 and 4·32 kg of weight on the LC and MC diets, respectively (P < 0·001, sed 0·350). Although the LC and MC diets were associated with a small reduction in plasma concentrations of retinol, vitamin E (α-tocopherol) and β-cryptoxanthin (P < 0·005), these were still above the values indicative of deficiency. Interestingly, plasma vitamin C concentrations increased on consumption of the LC diet (P < 0·05). Plasma markers of insulin resistance (P < 0·001), lipaemia and inflammation (P < 0·05, TNF-α and IL-10) improved similarly on both diets. There was no change in other cardiovascular markers with WL. The present data suggest that a LC WL diet does not impair plasma indices of cardiometabolic health, at least within 4 weeks, in otherwise healthy obese subjects. In general, improvements in metabolic health associated with WL were similar between the LC and MC diets. Antioxidant supplements may be warranted if LC WL diets are consumed for a prolonged period.

Diets rich in flavonoids may reduce the risk of developing colorectal cancer. Flavonoids are widely distributed in foods of plant origin, though in the UK tea is the main dietary source. Our objective was to evaluate any independent associations of total dietary and non-tea intake of four flavonoid subclasses and the risk of developing colorectal cancer in a tea-drinking population with a high colorectal cancer incidence. A population-based case–control study (264 cases with histologically confirmed incident colorectal cancer and 408 controls) was carried out. Dietary data gathered by FFQ were used to calculate flavonoid intake. Adjusted OR and 95 % CI were estimated by logistic regression. No linear association between risk of developing colorectal cancer and total dietary flavonol, procyanidin, flavon-3-ol or flavanone intakes was found, but non-tea flavonol intake was inversely associated with colorectal cancer risk (OR 0·6; 95 % CI 0·4, 1·0). Stratification by site of cancer and assessment of individual flavonols showed a reduced risk of developing colon but not rectal cancer with increasing non-tea quercetin intake (OR 0·5; 95 % CI 0·3, 0·8; Ptrend < 0·01). We concluded that flavonols, specifically quercetin, obtained from non-tea components of the diet may be linked with reduced risk of developing colon cancer.

Trials in free-living populations involving increased consumption of fruit and vegetables are difficult to monitor. We evaluated biomarkers for assessing fruit and vegetable intake and compliance in a 2-year trial. Postmenopausal women were randomised to 300 g additional fruit and vegetables per d (n 66), placebo (n 70) or potassium citrate (n 140). They completed dietary checklists (3-monthly) and food diaries or FFQ (yearly). We measured whole-blood folate, plasma vitamin C and homocysteine (yearly), serum vitamin E and carotenoids (at 12 months) and urinary vitamin K metabolites (yearly). Plasma vitamin C was associated with fruit and vegetable intake at baseline (r +0·31; P < 0·01), remaining significant only for the non-fruit and vegetable group at 12 months (r +0·43; P < 0·01). For the fruit and vegetable group, vitamin C increased by 5·9 μmol/l (P = 0·07) but was not significantly associated with fruit and vegetable intake; vitamin E, β-carotene and β-cryptoxanthin were higher compared with the non-fruit and vegetable group (P < 0·05); and whole-blood folate and the urinary 5C-aglycone metabolite of vitamin K were associated with vegetable intake. For all participants plasma vitamin C increased with increasing fruit and vegetable intakes, reaching a plateau of 90–95 μmol/l at intakes>500 g/d, whereas whole-blood folate, β-carotene and β-cryptoxanthin continued to increase. Concentrations of vitamin C, folate and β-cryptoxanthin were lower and the 7C-aglycone metabolite of vitamin K higher, in smokers compared with non-smokers. Suitable markers for monitoring fruit and vegetable compliance include β-carotene and β-cryptoxanthin. Plasma vitamin C and whole-blood folate may be suitable for monitoring intakes in populations but for monitoring compliance the former may be restricted to low intakes of fruit and vegetables and the latter to vegetable intake.

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 flavonoids, a generic term which includes chalcones, flavones, flavanones, flavanols 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 flavonoids 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, enzyme modulation, gene expression, apoptosis, upregulation of gap junction communication and P-glycoprotein activation. Possible protective effects against heart disease may be due to the ability of some polyphenols to prevent the oxidation of LDL to an atherogenic form although anti-platelet aggregation activity and vasodilatory properties are also reported. However, some polyphenols are toxic in mammalian cells. Thus, until more is known about their bioavailability, metabolism and intracellular location, increasing intakes of polyphenols by supplements or food fortification may be unwise.

Evidence from biochemical and animal models suggests that nutritional antioxidants should inhibit the development of diseases such as CHD and certain cancers. This evidence is not clearly corroborated by intervention studies in human subjects, due, in part, to inadequacies in current analytical methodologies. Although in vitro assays can give useful information on the attributes required by a compound to act as an antioxidant, results may have little nutritional relevance due to limited bioavailability. The determination of antioxidants in blood is often used as a measure of antioxidant status in vivo, but may not necessarily reflect concentrations in target tissues where oxidative stress is greatest. In addition, the accumulation of antioxidants in selective tissues may not be apparent from plasma measurements. Participation in quality-control schemes for antioxidant determination by HPLC allows inter-laboratory comparison of results. Moderation of indices of oxidative damage to lipids, proteins and DNA can provide information on the effectiveness of compounds as nutritional antioxidants. However, most current methods of assessing oxidative stress are subject to confounding factors of non-oxidative origin. Assays for total antioxidant capacity in plasma differ in their type of oxidation source, target and measurement used to detect the oxidized product. They give different results, should never be used in isolation, and results should be interpreted with caution. Until more is known about the activity and metabolic fate of antioxidants, caution should be exercised in the consumption of large amounts of commercially-available antioxidant preparations.

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.

The effects of moderate red wine consumption on the antioxidant status and indices of lipid peroxidation and oxidative stress associated with CHD were investigated. A randomised, controlled study was performed with twenty free-living healthy volunteers. Subjects in the red wine group consumed 375 ml red wine daily for 2 weeks. We measured the total concentration of phenolics and analysed the individual phenolics in the wine and plasma by HPLC with tandem MS. The antioxidant capacity of plasma was measured with electron spin resonance spectroscopy while homocysteine and fasting plasma lipids were also determined. The production of conjugated dienes and thiobarbituric acid-reactive substances (TBARS) were measured in Cu-oxidised LDL. Plasma total phenolic concentrations increased significantly after 2 weeks of daily red wine consumption (P≤0·001) and trace levels of metabolites, mainly glucuronides and methyl glucuronides of (+)-catechin and (−)-epicatechin, were detected in the plasma of the red wine group. These flavan-3-ol metabolites were not detected in plasma from the control group. The maximum concentrations of conjugated dienes and TBARS in Cu-oxidised LDL were reduced (P≤0·05) and HDL cholesterol concentrations increased (P≤0·05) following red wine consumption. The findings from the present study provide some evidence for potential protective effects of moderate consumption of red wine in healthy volunteers.