Antioxidant flavonols and ischemic heart disease in a Welsh population of men: the Caerphilly Study.

Antioxidant flavonols and their major food source, black tea, have been associated with a lower risk of ischemic heart disease (IHD) and stroke in Dutch men. We investigated whether flavonol intake predicted a lower rate of IHD in 1900 Welsh men aged 45-59 y, who were followed up for 14 y. Flavonol intake, mainly from tea to which milk is customarily added, was not related to IHD incidence [relative risk (RR), highest compared with lowest quartile: 1.0; 95% CI: 0.6, 1.6; P for trend = 0.996; n = 186] but was weakly positively related to IHD mortality (RR: 1.6; 95% CI: 0.9, 2.9; P = 0.119; n = 131) and cancer mortality (RR: 1.3; 95% CI: 0.7, 2.3; P = 0.150; n = 104) and strongly related to total mortality (RR: 1.4; 95% CI: 1.0, 2.0; P = 0.014; n = 334). Men with the highest consumption of tea (> 1.2 L, or > 8 cups/d) had an RR of 2.4 (95% CI: 1.5, 3.9) of dying in the follow-up period compared with men consuming < 300 mL/d (< 2 cups/d). We conclude that intake of antioxidant flavonols is not inversely associated with IHD risk in the United Kingdom. Possibly, flavonols from tea to which milk is added are not absorbed; experimental evidence suggests that adding milk to tea abolishes the plasma antioxidant-raising capacity of tea. The apparent association between tea consumption and increased mortality in this population merits further investigation.

Dietary magnesium does not predict ischaemic heart disease in the Caerphilly cohort.

OBJECTIVES: To examine the association between dietary magnesium intake and the risk of an ischaemic heart disease (IHD) event. DESIGN: Estimates were made of dietary magnesium intake from food frequency records, supplemented by seven-day weighted intake records. The subsequent incidence of ischaemic heart disease events was recorded. The relative odds of an IHD event was related to base-line magnesium intake. SETTING: Data on dietary magnesium intakes are available for 2172 men aged 45-59 y in the Caerphilly cohort. These have now been followed for ten years since base-line dietary data were collected, and during this time a total of 269 IHD events occurred. Of these, 96 were acute deaths (ICD 410) and 136 were non-fatal myocardial infarctions. RESULTS: The overall mean dietary intake of magnesium was estimated to be 279 (s.d. 83) mg/day. The daily intake of those men who later experienced any IHD event was 266 (s.d. 84) mg/day and this differs from that in men who experienced no IHD event during this time (281 mg, P < 0.05). Men who suffered an acute IHD death had even lower intakes (mean 253 (s.d. 79); P < 0.005). Age, smoking habit, energy intake and alcohol consumption are all significantly associated with both Mg intake and IHD risk and are therefore possible confounding factors. Standardisation for these factors reduces the difference for all IHD events to 2.9 (s.e.m. 3.6) mg Mg/day, P > 0.05, and to 0.9 (s.e.m. 5.8) mg for acute IHD death. Similarly, when the men are ranked into fifths by their daily Mg intake, 70 of the 434 men with the lowest intakes went on to experience an IHD event, compared with only 41 of the 434 men with the highest Mg intakes. The relative odds (RO) for the fifth of men with the lowest intakes, compared with the fifth with the highest intakes, is 1.86 (P < 0.005), but standardisation for the confounding factors leads again to a loss of significance (RO 1.52, P > 0.05). CONCLUSION: Although trends in the data are suggestive, data from the Caerphilly cohort give no certain evidence that dietary magnesium intake is independently predictive of ischaemic heart disease in the population studied.

Factors affecting bone density in young adults.

A 14-y follow-up of 581 children who took part in a randomized controlled trial of the effect of a milk supplement on growth of children was conducted to investigate the supplement's effect on adult bone mineral content (BMC) and density (BMD). BMC and BMD of the nondominant forearm were measured by single-photon absorptiometry in 371 subjects (64%) aged 20-23 y, at a proximal site (shaft of radius and ulna) and at a distal site near the wrist. BMCs and BMDs tended to be higher in the intervention group (NS). Cross-sectionally, BMD was positively associated with body weight (P less than 0.01) in both sexes; inversely associated with alcohol consumption (P less than 0.05), and positively with manual occupation (NS) in men; positively associated with current intakes of calcium (P less than 0.05), vitamin D (P less than 0.01), and sports activity during adolescence (P less than 0.01), and inversely with parity (NS) in women. In multiple linear-regression analysis body weight and sports activity during adolescence were stronger determinants of female BMD than was diet.

Alcohol and platelet aggregation: the Caerphilly Prospective Heart Disease Study.

Intakes of alcohol and saturated fatty acids were determined through a dietary questionnaire from 1600 men (aged 49-66 y) in the Caerphilly Prospective Heart Disease Study. Platelet aggregation induced by thrombin adenosine disphosphate (ADP), and collagen was studied in subjects who had fasted and had not recently taken drugs affecting platelets. In subjects who drank alcohol, the odds ratio of a high response to aggregation was significantly reduced (primary ADP, P less than 0.05; secondary ADP, P less than 0.001; collagen, P less than 0.02). The significance was enhanced by adjusting for smoking and by including only the subjects with a high intake of saturated fatty acids or a low intake of polyunsaturated fatty acids. By contrast, the responsiveness to thrombin was slightly increased at all levels of alcohol consumption. We therefore suggest that part of the effects of alcohol on coronary heart disease may be mediated by a dose-dependent effect on certain platelet functions, modulated by the intake of dietary fat.

Long-term diet modification and platelet activity.

Platelet activity was assessed in a sub-sample of 56 participants in the MRC Diet and Reinfarction Trial (DART). Men whose diets contained a high ratio of polyunsaturated to saturated fatty acids (a P:S ratio of greater than 0.5) showed reduced secondary platelet aggregation to adenosine diphosphate (ADP) in platelet-rich plasma (PRP), and diminished platelet aggregation to ADP in whole blood. A trend of reduced secondary platelet aggregation to ADP with increasing dietary eicosapentaenoic acid was noted, but this was not statistically significant. The results of this study and the MRC Diet and Reinfarction Trial suggest a mediatory role for platelet activity in the relationship between diet and ischaemic heart disease.