The association between black tea consumption and iron status was investigated in a sample of African adults participating in the cross-sectional THUSA (Transition and Health during Urbanization of South Africans) study in the North West Province, South Africa. Data were analysed from 1605 apparently healthy adults aged 15–65 years by demographic and FFQ, anthropometric measurements and biochemical analyses. The main outcome measures were Hb and serum ferritin concentrations. No associations were seen between black tea consumption and concentrations of serum ferritin (men P = 0·059; women P = 0·49) or Hb (men P = 0·33; women P = 0·49). Logistic regression showed that tea consumption did not significantly increase risk for iron deficiency (men: OR 1·36; 95 % CI 0·99, 1·87; women: OR 0·98; 95 % CI 0·84, 1·13) nor for iron deficiency anaemia (men: OR 1·28; 95 % CI 0·84, 1·96; women: OR 0·93; 95 % CI 0·78, 1·11). Prevalence of iron deficiency and iron deficiency anaemia was especially high in women: 21·6 and 14·6 %, respectively. However, the likelihood of iron deficiency and iron deficiency anaemia was not significantly explained by tea consumption in sub-populations which were assumed to be at risk for iron deficiency. Regression of serum ferritin levels on tea consumption in women ≤ 40 years, adults with a daily iron intake ≤ 5·80 mg and adults with ferritin levels ≤ 26·60 μg/l, respectively, showed P values in the range of 0·28–0·88. Our findings demonstrate that iron deficiency and iron deficiency anaemia is not significantly explained by black tea consumption in a black adult population in South Africa. Tea intake was also not shown to be related to iron status in several sub-populations at risk for iron deficiency.

Results of population studies suggest that black tea can reduce cardiovascular risk. Effects of black-tea polyphenols to reduce platelet aggregability may help to explain any benefits. Given that black tea is often consumed with and after meals, and man spends much of his life in the postprandial state, the objective of the present study was to investigate the acute effects of ingestion of black tea on postprandial platelet aggregation ex vivo. Twenty healthy participants had platelet aggregation and blood lipids assessed before and 4 h after the ingestion of 50 g dairy fat on two occasions in random order, corresponding to black tea or hot water. Black tea or hot water (one cup) was consumed immediately following the dairy fat, then after 1·5 and 3·0 h. Platelet aggregation ex vivo was assessed in platelet-rich plasma in response to three concentrations of collagen (0·2, 0·6, 2·0 μg/ml) and ADP (2, 4, 8 μM). Urinary concentrations of 4-O-methylgallic acid were used as an indicator that tea polyphenols were absorbed. Serum total cholesterol and triacylglycerol concentrations increased significantly 4 h after ingesting the dairy fat, but there was no significant difference between black tea and hot-water treatments on the cholesterol or triacylglycerol responses. Urinary 4-O-methylgallic acid concentrations were significantly increased following ingestion of black tea (P=0·0001) but not water. Black tea in comparison to hot water did not inhibit collagen or ADP-induced postprandial platelet aggregation. The results of this study do not support the suggestion that reduced postprandial platelet aggregability contributes to any benefits of black tea on cardiovascular risk.

The effect of dietary intake of flavonols (predominantly quercetin) on oxidative DNA damage was studied in thirty-six healthy human subjects (sixteen men, twenty women). The study was a randomised crossover study, comprising two 14 d treatments of either a low-flavonol (LF) or high-flavonol (HF) diet with a 14 d wash-out period between treatments. Subjects were asked to avoid foods containing flavonols, flavones and flavanols during the LF dietary treatment period and to consume one 150 g onion (Allium cepa) cake (containing 89·7 mg quercetin) and one 300 ml cup of black tea (containing 1·4 mg quercetin) daily during the HF dietary treatment. A 7 d food diary was kept during each dietary period and blood samples were taken after each dietary treatment. Products of oxidative damage to DNA bases were measured in DNA from leucocytes. The study had more than 95 % power to detect a change of 20 % in DNA damage products Plasma vitamin C and plasma quercetin concentrations were also measured. No significant differences in intake of macronutrients or assessed micronutrients, measured DNA base damage products, or plasma vitamin C were found between the HF and LF dietary treatments. The plasma quercetin concentration was significantly higher after the HF dietary treatment period (228·5 (SEM 34·7) nmol/l) than after the LF dietary treatment period (less than the limit of detection, i.e. <66·2 nmol/l). These findings do not support the hypothesis that dietary quercetin intake substantially affects oxidative DNA damage in leucocytes.