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ORIGINAL RESEARCH COMMUNICATION |
1 From the Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston (HDS, JMG, SL, and JEB); the Departments of Epidemiology (HDS and JEB) and Nutrition (SL), Harvard School of Public Health, Boston; the Massachusetts Veterans Epidemiology Research and Information Center, VA Boston Healthcare System, Boston (HDS and JMG); and the Department of Ambulatory Care and Prevention, Harvard Medical School, Boston (JEB).
2 Supported by research grants AG-15933, CA-47988, HL-43851, HL-65727, and NS-34108 from the National Institutes of Health, Bethesda, MD. 3 Address reprint requests to HD Sesso, Brigham and Women’s Hospital, 900 Commonwealth Avenue East, Boston, MA 02215-1204. E-mail: hsesso{at}hsph.harvard.edu.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Objective: We examined whether flavonoids and selected flavonols and flavones or their food sources are associated with CVD risk.
Design: Women (n = 38 445) free of CVD and cancer participated in a prospective study with a mean follow-up of 6.9 y. On the basis of a food-frequency questionnaire, total flavonoids and selected flavonols and flavones were categorized into quintiles, and food sources were categorized into 4 groups. Relative risks were computed for important vascular events (519 events; excluding revascularizations) and CVD (729 events), including myocardial infarction, stroke, revascularization, and CVD death.
Results: The mean flavonoid intake was 24.6 ± 18.5 mg/d, primarily as quercetin (70.2%). For both CVD and important vascular events, no significant linear trend was observed across quintiles of flavonoid intake (P = 0.63 and 0.80, respectively). No individual flavonol or flavone was associated with CVD. Broccoli and apple consumption were associated with nonsignificant reductions in CVD risk: 25–30% and 13–22%, respectively. A small proportion of women (n = 1185) consuming ≥4 cups (946 mL) tea/d had a reduction in the risk of important vascular events but with a nonsignificant linear trend (P = 0.07).
Conclusions: Flavonoid intake was not strongly associated with a reduced risk of CVD. The nonsignificant inverse associations for broccoli, apples, and tea with CVD were not mediated by flavonoids and warrant further study.
Key Words: Flavonoids • cardiovascular disease • diet • nutrition • women • primary prevention
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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We therefore examined whether flavonoids are associated with incident CVD in a large cohort of female health professionals from the United States. We also evaluated the association between individual selected flavonols and flavones—including quercetin, kaempferol, myricetin, apigenin, and luteolin—plus specific food sources of flavonoids and the risk of CVD.
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SUBJECTS AND METHODS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Intake of flavonoids and food sources
The measurement of total dietary flavonoids and selected flavonols and flavones (in mg/d)—including quercetin, kaempferol, myricetin, apigenin, and luteolin—was based on food tables maintained by the Department of Nutrition, Harvard School of Public Health, Boston. Total flavonoids represent the sum of the individual selected flavonols and flavones. The food tables were originally generated in the Netherlands and later supplemented with values for American foods, including apples, apple juice, onions, tea, red wine, avocado, cantaloupe, watermelon, blueberries, green beans, corn, sprouts, yellow squash, green peppers, and tofu (5). All values were energy-adjusted by using the residual method (21). The SFFQ has been shown among male health professionals to have a high correlation with corresponding dietary records for tea (r = 0.77), apples (r = 0.70), and broccoli (r = 0.46) (5).
Five major food sources of flavonoids—tea, broccoli, apples, onions, and tofu—were considered. A common unit or portion size for each food was specified, and the participants selected from 9 responses ranging from "never or less than once per month" to "≥ 6 per day." Onion intake was represented as "onions as a vegetable, ring, or soup."
Other covariates
On the WHS baseline questionnaire, women also provided self-reports of coronary artery disease risk factors, including age (in y), weight and height (converted to body mass index; in kg/m2), smoking status (categorized as never, former, or current), alcohol use (categorized as rarely or never, 1–3 drinks/mo, 1–6 drinks/wk, or ≥ 1 drink/d), frequency of exercise (categorized as rarely or never, < 1 times/wk, 1–3 times/wk, or ≥ 4 times/wk), parental history of MI at age < 60 y (no or yes), history of hypertension (no or yes), history of diabetes (no or yes), history of hypercholesterolemia (no or yes), and postmenopausal hormone use (categorized as never, former, or current). Other dietary nutrients were also considered, including fruit and vegetable intake (servings/d), total fiber intake (g/d), folate intake (g/d), and saturated fat intake (g/d). Each nutrient was energy-adjusted by using the residual method, as done for total flavonoids and selected flavonols and flavones (21).
Outcome ascertainment
Follow-up in the WHS was accomplished by using annual follow-up questionnaires that were used to update information on compliance, adverse effects to the study agents, health outcomes, and risk factors. Midway through each year-long follow-up period, the participants were also sent a return postcard on which to report any significant problems affecting compliance or recently developed illnesses. Total CVD included MI, coronary artery bypass graft surgery, percutaneous transluminal coronary angioplasty, stroke, and cardiovascular death. The outcome defined as important vascular events was limited to MI, stroke, and cardiovascular disease death. The diagnosis of MI was confirmed by using World Health Organization criteria (22). Revascularization procedures were confirmed by hospital records. A stroke was defined as a typical neurologic deficit, sudden or rapid in onset, lasting > 24 h. CVD death was documented by convincing evidence of a cardiovascular mechanism from death certificates and medical records. All analyses are based on the first confirmed CVD event, and analyses of MI and stroke included death. After a mean follow-up of 6.9 y (range of follow-up: 0.1–7.8 y), morbidity and mortality follow-up rates were 98.9% and 99.9% complete, respectively. A total of 729 CVD cases occurred during this period, including 519 important vascular events.
Data analyses
Measurements of total flavonoid intake, as well as individual flavonols and flavones, were categorized into quintiles on the basis of the overall distribution of intake in women. Participants were first compared according to quintiles of flavonoid intake by using mean values or proportions of baseline coronary artery disease risk factors. Cox proportional hazards were used to model the relative risk (RR) and 95% CI of CVD and important vascular events examining the effect of increasing quintiles of flavonoid intake, with the lowest quintile as the referent. The ≥ 95th percentile compared with the lowest quintile was also compared. Models were first adjusted for age, total energy intake, and randomized treatment assignment. The next model added body mass index, smoking status, frequency of exercise, alcohol use, parental history of MI at age < 60 y, and postmenopausal hormone use. The final multivariate model added dietary factors, including servings of fruit and vegetables and fiber, folate, and saturated fat intakes. Linear trend tests across quintiles of flavonoid intake were tested by using the median for each quintile as an ordinal variable. Analyses of selected flavonols and flavones—including quercetin, kaempferol, luteolin, myricetin, and apigenin—used the same analytic approach as above.
Next, major food sources of flavonoids were a priori categorized: tea intake (none, < 1 cup/d, 1–3 cups/d, and ≥ 4 cups/d); apple intake (none, ≤ 1 apple/wk, 2–6 apples/wk, and ≥ 1 apple/d), broccoli intake [none, ≤ 1 serving/wk, 2–4 servings/wk, and ≥ 5 servings/wk; 1 serving = 1/2 cup (113 g)], onion intake (none, ≤ 1 serving/wk, 2–4 servings/wk, and ≥ 5 servings/wk; 1 serving = 1 onion), and tofu intake [none, 1–3 servings/mo, and ≥ 1 serving/wk; 1 serving = 3–4 oz (85–113 g)]. These analyses included a fourth multivariate model that included total flavonoid intake. Any attenuation in the RRs suggests that flavonoids in the food source are responsible for any benefit, paralleling the analytic approach used for alcohol, HDL cholesterol, and MI (23). In secondary analyses, we examined whether additional variables collected in the WHS that may be potential confounders—including systolic blood pressure, diastolic blood pressure, multivitamin use, and other dietary factors—altered the RRs of CVD. In addition, we considered separate results for the risk of MI and stroke. All analyses were conducted with the use of SAS (version 8; SAS Institute Inc, Cary, NC).
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RESULTS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The baseline characteristics of women were first compared according to quintiles of total flavonoid intake (Table 1
). Women who consumed greater amounts of flavonoids per day tended to be somewhat older, and a greater proportion reported a history of hypertension and diabetes mellitus. Despite the slightly worse CVD risk factors among women consuming greater amounts of flavonoids, a greater proportion of women with higher flavonoid intake exercised more, smoked less, and were current users of postmenopausal hormones. Of the dietary variables, a greater consumption of flavonoids was positively associated with fruit and vegetable intake, fiber intake, and folate intake and negatively associated with saturated fat intake. Other nutrients tended to follow this pattern of a healthier diet in women consuming greater amounts of flavonoids.
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. Women in the second through fifth quintiles of flavonoid intake had no significant linear trend (P = 0.16) after adjustment for age and treatment, although the pattern of the RRs suggested a possible L-shaped inverse association. Further adjustment for lifestyle and medical risk factors weakened the nonsignificant inverse association. Adjustment for dietary factors had little effect on the RRs. When we considered other potentially important CVD risk factors (eg, self-reported blood pressure, self-reported total cholesterol, and age at menopause) or nutrients (eg, multivitamin use and vitamin E intake), they each had a nominal effect on the risk estimates. When hypertension, diabetes, and hypercholesterolemia were considered as intermediate variables, the RRs of CVD for flavonoid intake remained virtually identical when models included these covariates.
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We also assessed whether flavonoids were associated with the risk of MI, stroke, and CVD death. There were no significant multivariate linear trends for increasing quintiles of flavonoid intake for the risk of MI, stroke, or CVD death (P for linear trend = 0.89, 0.43, and 0.12, respectively). Compared with women in the lowest quintile of intake, the multivariate RRs (and 95% CIs) for those in the second through fifth quintiles of intake, respectively, were 0.78 (0.49, 1.24), 0.74 (0.46, 1.20), 1.21 (0.78, 1.89), and 0.82 (0.51, 1.33) for MI and 0.62 (0.41, 0.94), 0.74 (0.49, 1.10), 0.76 (0.51, 1.15), and 0.70 (0.46, 1.07) for stroke. In contrast with some previous studies, we found no inverse association between flavonoids and CVD death, with RRs of 0.46 (0.25,0.86), 0.60 (0.33, 1.09), 1.04 (0.62, 1.76), and 1.05 (0.62, 1.78) for the second through fifth quintiles, respectively. To minimize residual confounding, we examined flavonoids and CVD among women with and without a history of hypertension, diabetes, or hypercholesterolemia. No major differences in the pattern of RRs emerged compared with the overall RRs. Finally, coffee intake, which was inversely associated with flavonoid (Spearman’s r2 = -0.15) and tea (Spearman’s r2 = -0.13) intakes, did not confound flavonoid or tea intake in models for CVD.
Each selected flavonol and flavone tended to have only a few major food contributors: for quercetin, onions (27.6%), tea (23.0%), and apples (10.9%); for kaempferol, tea (57.6%) and broccoli (25.8%); for myricetin, tea (51.2%) and beans (36.1%); for apigenin, celery (73.0%); and for luteolin, peppers (83.2%). However, quercetin and kaempferol intakes represented 92.3% of total flavonoid intake in this population of women. No individual flavonol or flavone showed a clear association with total CVD (Table 3), important vascular events, MI, or stroke (data not shown). Adjustment for dietary factors nominally affected the RRs. Only kaempferol intake had a possible U-shaped association with CVD on the basis of the pattern of RRs, which was slightly more pronounced in relation to important vascular events. A reduction in the risk of important vascular events for women above the 95th percentile for myricetin intake was not supported by evidence of similar or intermediate benefits between the 25th and 94th percentiles of myricetin intake (P for linear trend = 0.97).
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). The addition of total flavonoids to models for each flavonoid food source had little effect on the RRs. Increasing tea intake was not associated with the risk of CVD, with a nonsignificant linear trend (P = 0.36). Compared with women consuming no tea, those consuming ≤ 1, 1–3, or ≥ 4 cups/d (946 mL/d) had multivariate RRs of CVD of 1.14 (0.95, 1.36), 1.15 (0.93, 1.42), and 0.74 (0.44, 1.25), respectively. The RRs from age- and treatment-adjusted RRs to multivariate-adjusted RRs were virtually identical, suggesting minimal net confounding by CVD risk factors for tea intake. Only 3.1% of women (6 cases) reported tea consumption of ≥ 4 cups/d, which limited the power and interpretation of a 67% reduction in the risk of important vascular events with a nonsignificant linear trend (P = 0.07). Onion intake was not associated with the risk of CVD or important vascular events.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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On the basis of several in vitro and in vivo studies, flavonoids have shown considerable promise in reducing the risk of CHD by inhibiting LDL cholesterol oxidation (3, 24) and in reducing platelet aggregation (25), ischemic damage (26), or estrogen-like activity (27). The antioxidant potential of all food sources of flavonoids is well established (28). However, data from large clinical trials completed thus far suggest little or no effect of antioxidants on the risk of CHD (29). Data on flavonoids and lipids are often extrapolated from studies examining food-specific effects. Studies of tea have shown little improvement in lipid profiles (30–34) or in platelet aggregation among subjects with CHD (35).
Published studies from Europe—predominantly in men from the Netherlands and Finland—have contributed mixed results on the association between flavonoids and CVD (15). Those studies reporting significant effects tend to show significant linear trends, in contrast with the suggested L-shaped association noted in our data. Hertog et al (13) noted a 68% reduction in CHD mortality for 805 older Dutch men in the highest tertile of flavonoid intake, for which black tea (61%) was the major food source. This association extended to men free of MI at baseline, and updated results noted slightly attenuated but still significant RRs (14). The same cohort also reported reductions in fatal and nonfatal stroke in 552 men initially free of stroke (11). Knekt et al (12) reported an approximate 22% reduction in CHD mortality in Finnish subjects for flavonoids, mainly comprised of quercetin (95%), with onions and apples as the primary food sources. Analyses of another population-based cohort from Finland showed no association between quercetin and stroke in women (10). Another study of 10 054 Finnish subjects indicated an association between higher flavonoid intake and a lower risk of cerebrovascular mortality but not for ischemic heart disease mortality (16). In Finnish male smokers, flavonols and flavones were inversely associated with nonfatal MI but not with stroke or CVD death (8, 9). Finally, a study of Welsh men found no association between flavonoids—predominantly from tea (82%)—and CHD risk (7).
Our results fall between those of 2 previous US studies. In the Health Professionals Follow-up Study (HPFS), there were similar medians of flavonoid intake in the lowest and highest quintiles of 34 789 American men. However, the HPFS reported a multivariate RR of CHD of 1.08 in a comparison of the highest compared with the lowest quintiles of flavonoid intake (5). This lack of association also extended to individual flavonols and flavones. In contrast, the Iowa Women’s Health Study reported a significant 32% reduction in CHD death in a comparison of the highest compared with the lowest quintile of flavonoid intake in postmenopausal women (6). With RRs in increasing quintiles of 1.00 (reference), 0.67, 0.65, 0.94, and 0.68 in the Iowa Women’s Health Study—which indicate the lack of a significant linear trend (P = 0.25)—these results parallel the L-shaped association noted for flavonoids and important vascular events in our study. Broccoli, even at low intakes (as in our study), was the only flavonoid food source with a similar inverse association with CHD death. Onion intake, a major contributor of flavonoids, was not ascertained in the Iowa Women’s Health Study.
The ubiquitous nature of flavonoids in fruit and vegetables provides an impetus to focus on the major flavonoid food sources. Previous studies on flavonoid food sources and CVD have largely focused on tea, red wine, soy products, and chocolate. However, of these foods, only tea is a major source of flavonoids. Early case-control studies of tea consumption found no association with CHD or MI (36–38), but the lack of an effect may reflect the low prevalence of heavy tea consumption. Some (13, 15, 30, 39), but not all (5, 6, 9), more recent cohort studies report an inverse association between tea and CHD. The US Food and Drug Administration allowed for health claim labels on soy products, stating that "soy protein included in a diet low in saturated fat and cholesterol may reduce the risk of CHD by lowering blood cholesterol levels" (40). However, despite evidence that soy and tofu products may improve lipid profiles (41, 42), few studies have linked soy products with a reduction in CVD risk (43). Too few US women consumed tofu in the early 1990s to enable us to draw meaningful conclusions from our data.
Because thousands of flavonoids occur in fruit and vegetables, with 6 major classes (44), it is difficult to isolate any single flavonoid as being more strongly associated with the risk of CVD than any other. An important caveat to assessing the existing literature on flavonoids and the risk of CVD is that catechins and isoflavones are not included within the food-composition tables generating the flavonoid data for this study and most previous studies. Although tea is the main dietary source of catechins (45, 46), is strongly correlated with catechins (r = 0.98), and was recently shown to be inversely associated with CVD among men (47), whether our findings for tea would also reflect what would have been observed for catechin intake requires additional studies. Furthermore, the present database underestimates the flavonoid contributions from red wine and chocolate. In this regard, total flavonoid intake may have been underestimated. However, the US Department of Agriculture plans to expand this database, eventually allowing for a more comprehensive quantification of dietary flavonoid intake.
Another important consideration is that misclassification in the measurement of dietary factors may bias our results. Any misclassification would not be expected to affect our finding that the effect of flavonoid food sources is not mediated by flavonoids, because the addition of flavonoids into models yielded identical RRs. Most Western studies on tea emphasize black tea; however, the increasing popularity and consumption of green and oolong teas merit investigation. The SFFQ used in our study did not specifically include green or oolong tea to be considered in these analyses, but the intake of these types of tea was very low in the early 1990s in US women. Higher flavonoid intake may only be a surrogate for other uncontrolled dietary factors inversely associated with CVD (34). It may instead be more important to consume a flavonoid-rich diet consisting of many food sources, reflecting the cardiovascular benefits of a diet rich in fruit and vegetables (20, 48). However, additional control for dietary factors nominally affected the RRs. Finally, some of the reported RRs had wide 95% CIs, losing significance because of either insufficient power or comprehensive control for potential confounding variables.
In conclusion, data from the WHS indicate a nonsignificant L-shaped association between higher flavonoid intake and CVD risk after control for known lifestyle and dietary factors, with similar RRs at or above the second quintile of intake. For important vascular events, there was a greater magnitude of risk reduction associated with flavonoid intake and a similar L-shaped pattern of RRs. The nonsignificant inverse associations of broccoli, apples, and tea consumption with CVD and important vascular events do not appear to be mediated by flavonoids but warrant further study.
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ACKNOWLEDGMENTS |
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HDS and SL contributed to the data analysis and the writing of the manuscript and JMG and JEB contributed to the study design, data collection, and writing of the manuscript. None of the authors had any financial or personal conflicts of interest.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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