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American Journal of Epidemiology Advance Access originally published online on August 9, 2007
American Journal of Epidemiology 2007 166(8):902-911; doi:10.1093/aje/kwm156
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American Journal of Epidemiology © The Author 2007. Published by the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

ORIGINAL CONTRIBUTIONS

A Prospective Study of Fruits, Vegetables, and Risk of Endometrial Cancer

Marjorie L. McCullough1, Elisa V. Bandera2,3, Roshni Patel1, Alpa V. Patel1, Ted Gansler1, Lawrence H. Kushi4, Michael J. Thun1 and Eugenia E. Calle1

1 Epidemiology and Surveillance Research Department, American Cancer Society, Atlanta, GA
2 Cancer Institute of New Jersey, Robert Wood Johnson Medical School, New Brunswick, NJ
3 School of Public Health, University of Medicine and Dentistry of New Jersey, Piscataway, NJ
4 Division of Research, Kaiser Permanente, Oakland, CA

Correspondence to Dr. Marjorie McCullough, Epidemiology and Surveillance Research Department, American Cancer Society, 250 Williams Street, Atlanta, GA 30303-1002 (e-mail: marji-mccullough{at}cancer.org).

Received for publication December 15, 2006. Accepted for publication April 23, 2007.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Case-control studies support a lower risk of endometrial cancer associated with greater vegetable consumption but not fruit consumption. One prospective study suggested an inverse association with fruits and vegetables combined. The authors examined associations for vegetables and fruits separately among women in the American Cancer Society's Cancer Prevention Study II Nutrition Cohort. After exclusions, 41,400 postmenopausal women completed a questionnaire on diet, lifestyle, and medical history at baseline in 1992–1993. Information on diet was updated in 1999; historical dietary information from 1982 was also available. The authors identified 435 eligible cases of endometrial cancer through 2003. In multivariate models, neither fruit consumption (top quintile vs. bottom: rate ratio (RR) = 1.24, 95% confidence interval (CI): 0.90, 1.70; p-trend = 0.30) nor vegetable consumption (RR = 1.21, 95% CI: 0.89, 1.65; p-trend = 0.24) at baseline was associated with risk. Results were similar when diet was cumulatively updated. Only among women who had never used hormone replacement therapy was the risk of endometrial cancer lower in the highest (vs. lowest) tertile of fruit (RR = 0.75, 95% CI: 0.52, 1.07; p-interaction = 0.03, p-trend = 0.11) or vegetable (RR = 0.80, 95% CI: 0.57, 1.13; p-interaction = 0.01, p-trend = 0.29) consumption. This prospective study does not support an association between vegetable or fruit consumption and endometrial cancer.

cohort studies; endometrial neoplasms; fruit; vegetables

Abbreviations: CI, confidence interval; CPS-II, Cancer Prevention Study II; ERT, estrogen replacement therapy; FFQ, food frequency questionnaire; HRT, hormone replacement therapy; RR, rate ratio


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Endometrial cancer is the most common gynecologic cancer in the United States, ranking fourth among all cancers in women in age-adjusted incidence (1). The large international variation in incidence rates indicates that much of the risk is modifiable (2). Most of the major known risk factors for endometrial cancer contribute to prolonged and excessive exposure of the endometrium to estrogens unopposed by progesterone, as occurs with estrogen replacement therapy (ERT) (estrogen without progestin) and obesity.

The role of specific dietary factors, including fruit and vegetable consumption, in endometrial carcinogenesis is not well understood (3). Fruits and vegetables contain numerous bioactive compounds, including fiber, folate, vitamins, carotenoids, and phytoestrogens, and have been hypothesized to influence cancer risk through antioxidant activity, modulation of detoxification enzymes, stimulation of the immune system, and modulation of steroid hormone metabolism (4, 5). Seven (6–12) of 10 (6–15) case-control studies reported lower endometrial cancer risk with higher vegetable consumption; five estimates were statistically significant (6, 8–10, 12). Results on the association with fruit have been mixed: Five of 15 case-control studies showed inverse associations (6, 8, 11, 13, 16), three had odds ratios of 1.3 or greater (9, 17, 18), and results from the remaining seven studies were null (7, 10, 12, 14, 15, 19, 20). A recent meta-analysis from a systematic literature review on fruits, vegetables, and endometrial cancer risk suggested an inverse association for vegetable intake (highest category vs. lowest: pooled summary odds ratio = 0.71, 95 percent confidence interval (CI): 0.55, 0.91) and no association for fruit intake (odds ratio = 0.90, 95 percent CI: 0.72, 1.12) (21). Only one prospective cohort study has evaluated this association. Terry et al. (22) examined the combined role of fruit and vegetable consumption in a cohort study of Swedish twins, in which 133 cases of endometrial cancer were identified. Persons reporting a fruit and vegetable consumption of "little or none" as compared with a "large part of the diet" had a rate ratio of 3.1 (95 percent CI: 0.8, 12.7) after adjustment for age, physical activity, weight at enrollment, and parity. Given the small sample and qualitative assessment of diet in that study, it is important to evaluate these associations in other cohort studies.

We examined the association between endometrial cancer and intakes of vegetables and fruits separately in a large US prospective cohort study. Study participants completed three dietary assessments over time, enabling us to update exposures and examine long-term consumption patterns. Because an association between dietary risk factors and endometrial cancer may be overshadowed by hormonal influences, we also examined associations stratified by hormone replacement therapy (HRT), body mass index (weight (kg)/height (m)2), and smoking status. In addition, we examined associations stratified by multivitamin use, because fruits and vegetables may influence risk differently according to background micronutrient exposure.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 References
 
Study population
Women in this study were members of the Cancer Prevention Study II (CPS-II) Nutrition Cohort, established by the American Cancer Society in 1992–1993 for a prospective study of cancer incidence and mortality among 86,404 men and 97,786 women (23). The CPS-II Nutrition Cohort is a subgroup of the approximately 1.2 million participants in CPS-II, a prospective study of cancer mortality established in 1982. In brief, Nutrition Cohort members were CPS-II participants who resided in 21 states with population-based cancer registries (23). Participants were 50–74 years of age at enrollment in 1992 or 1993, when they completed a 10-page confidential, self-administered mailed questionnaire that included questions on demographic, medical, lifestyle, anthropometric, and dietary factors. Follow-up questionnaires were sent to cohort members in 1997, 1999, 2001, and 2003 to update exposure information and to ascertain newly diagnosed cancers. Previous pilot work in this cohort found that sensitivity for a self-report of any cancer was 0.93 (24). The response rate among living cohort members was 89 percent through 2003. The Emory University School of Medicine Institutional Review Board has approved all aspects of the CPS-II Nutrition Cohort study.

Dietary assessment
Baseline FFQ.
In 1992–1993, diet was assessed using a semiquantitative 68-item modified Block food frequency questionnaire (FFQ) (23, 25). The FFQ inquired about portion size (small, medium, or large). Questions on frequency of consumption ranged from "never or less than one serving per month" to "two or more servings per day" for foods and to "six or more servings per day" for beverages. Nutrient intakes were estimated using the Diet Analysis System, version 3.8a (26). The FFQ included summary questions for fruit intake ("Not counting juices, how many servings of fruit did you eat?") and vegetable intake ("Not counting salad or potatoes, how many servings of vegetables did you eat?"); this information is used in the Diet Analysis System to adjust the overall fruit and vegetable consumption estimates upward or downward.

The FFQ was validated using four 24-hour recalls completed at random over a 1-year period among 441 Nutrition Cohort participants (27). Median energy-adjusted, attenuation-corrected Pearson validity correlations ranged from 0.52 to 0.62 for fruits, vegetables, and their subgroups.

Follow-up FFQ.
A 152-item, semiquantitative modified Willett FFQ (28–30) was administered in 1999 to update dietary exposures. For each item, a common food or beverage serving size was specified (e.g., 1/2 cup carrots or one medium apple) and participants were asked how often, on average, they had consumed this amount over the previous year. Nine possible frequency responses ranged from "never or less than once per month" to "four or more times per day" (depending on the item). We computed servings of fruits and vegetables from responses directly marked on the FFQ. The validity and reliability of nutrient and food consumption measured by the FFQ have been documented in similar US populations (28–30).

Historical CPS-II baseline questionnaire.
Dietary questions posed 10 years before baseline (for the parent CPS-II mortality study, in which all CPS-II Nutrition Cohort members were participants) have previously been described (31). Briefly, participants were queried about their consumption of 32 foods using the following format: "On average, how many days per week do you eat the following foods?"

The fruits and vegetables included in the above three surveys are listed in appendix table 1.


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  		TABLE 1. Baseline characteristics of female participants according to fruit and vegetable intake, Cancer Prevention Study II Nutrition Cohort, 1992–2003*

 
Analytic cohort
We excluded from this analysis women who did not return any questionnaires after enrollment in 1992–1993 and were not known to be deceased (n = 3,191) and women who, at baseline, reported a history of uterine cancer (n = 259) or other cancer, except nonmelanoma skin cancer (n = 11,794). Because few participants were premenopausal, we excluded women who were pre- or perimenopausal at baseline (e.g., those who reported that their menstrual periods had not stopped, those who were not sure, or those who left the question blank and were less than age 55 years) (n = 4,291). Women who reported on the baseline questionnaire that their uterus (with or without one or two ovaries) had been removed (n = 29,013) and those with unknown uterine status at baseline (n = 1,710) were excluded. To eliminate the strong impact of estrogen-only HRT (ERT) on endometrial cancer risk and the possibility that reports of ERT use were in error (because ERT use is contraindicated in women with an intact uterus), we excluded women who reported current ERT use in 1992 (n = 1,643) and those with unknown current or past ERT use in 1992 (n = 175). For unverified, self-reported endometrial cancer, we censored follow-up at the last cancer-free survey; when the last cancer-free survey was the baseline survey, these women were excluded from the analysis (n = 27). Cases with missing histologic data, endometrial stromal sarcoma (histology code 8930), adenosarcoma (code 8933), Mullerian mixed tumor (code 8950), endometrial adenofibroma (code 8381), and carcinosarcoma (code 8980) (n = 26) were further excluded because the etiology of these less common tumors is thought to be different from that of endometrial carcinomas. We also excluded women who in 1992 reported extreme values for daily energy intake (<500 kcal/day or >3,500 kcal/day) (n = 823) or had FFQs with 15 percent or more of the 68 questions left blank (n = 3,269). Finally, we excluded women with missing or uninterpretable responses for four or more of the seven fruit items (n = 144) or six or more of the 12 vegetable items (n = 21) in 1992. The final analytic cohort consisted of 41,400 women.

Case ascertainment
We identified and verified 435 incident endometrial cancers (International Classification of Diseases, Ninth or Tenth revision (32, 33), code C54.1) among persons eligible for analysis between the date of enrollment in 1992–1993 and August 31, 2003. Most incident cases of endometrial cancer were initially identified through a self-report of endometrial cancer on any of the questionnaires (n = 406) and were subsequently verified by review of medical records (n = 308) or linkage with state cancer registries (n = 98). An additional 14 cases were ascertained as deaths due to endometrial cancer through linkage with the National Death Index (34). Finally, 15 participants were identified as having endometrial cancer during verification of a different reported cancer, through medical record review (n = 4) or linkage with state cancer registries (n = 11).

We conducted a subanalysis including only type I endometrial cancer (endometrioid carcinoma), since these cases represent cancers in the classic estrogen-driven pathway (35–37). For this analysis, we excluded type II cancers, defined as those with serous papillary or clear-cell histology, and any grade 3 cancers (n = 80), plus those with a missing grade (n = 27) (36), for a total of 328 type I cancers.

Follow-up ended at the date of diagnosis of endometrial cancer, death, or August 31, 2003, whichever came first. During follow-up, we censored reported but unverified endometrial cancers at the last cancer-free survey. We also censored women at the follow-up survey date of any other verified incident cancer (except nonmelanoma skin cancer), the survey date of newly reported ERT use, and the survey date of self-reported hysterectomy during follow-up.

Statistical analysis
We used Cox proportional hazards models to estimate incidence rate ratios and 95 percent confidence intervals for endometrial cancer in relation to total fruit intake and total vegetable intake (38), as well as botanical and phytochemical subgroups of vegetables and fruits as defined by Smith et al. (39). For age adjustment, we stratified the data on single year of age within each Cox model. Tests for trend for the main exposures were conducted by assigning the median value to each quintile. Covariates included age at menarche, age at menopause, number of livebirths and age at first birth, HRT, smoking, recreational physical activity (metabolic equivalent-hours per week), total energy intake, and body mass index. Body mass index and HRT were modeled as time-varying covariates using information obtained in 1992, 1997, 1999, and 2001. Other variables considered but not included because they did not influence the effect estimates were family history of endometrial cancer (in a mother or sister), history of hypertension, history of diabetes, height, race (97.9 percent of participants were White), education, and consumption of red or processed meat, saturated or total fat, and alcohol.

We used three approaches to examine associations between dietary intake of fruits and vegetables and endometrial cancer. The first used the baseline 1992 FFQ to predict endometrial cancer risk from 1992 to 2003 by quintile of intake. A second, time-dependent analysis used the 1992 FFQ quintiles to predict risk from 1992 to 1999 and then averaged intake from the 1992 FFQ and the 1999 FFQ to create quintiles to predict risk from 1999 to 2003. In the latter analysis, we censored follow-up for women who were missing data from the 1999 FFQ, reported energy intakes of <600 kcal/day or >3,500 kcal/day, or left more than 70 questions blank; this resulted in 10 fewer cases. In our third approach, we used historical information on diet collected in 1982 to examine consistently high intakes (top tertiles in 1982 and 1992) versus consistently low intakes (bottom tertiles in 1982 and 1992) in relation to cancer risk during follow-up from 1992 to 2003.

Potential effect modification of findings by baseline body mass index, HRT, smoking status, and multivitamin use was examined according to fruit and vegetable tertiles from the 1992 survey. To test for any violation of the Cox proportional hazards assumption, we created interaction terms between all main-effects variables and time. Statistical interaction and the Cox proportional hazards assumption were assessed using the likelihood ratio test (40). We also evaluated effect modification by testing the heterogeneity of trends among strata (40). Results from two-sided chi-squared tests were considered statistically significant at p ≤ 0.05.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 References
 
We documented 435 eligible cases of incident endometrial cancer in the cohort during 374,237 person-years of follow-up. The mean age at baseline was 63 years (standard deviation, 6). Median fruit and vegetable intakes in 1992 were 1.6 servings/day (10th–90th percentile distribution, 0.5–3.3) and 1.6 servings/day (10th–90th percentile distribution, 0.7–3.3), respectively. Table 1 provides baseline characteristics according to quintile of fruit and vegetable consumption in 1992. As expected, women with higher fruit and vegetable intakes were more educated, exercised more, took more multivitamin supplements, and smoked less. In addition, use of combined HRT was more common among fruit and vegetable consumers. Women in the highest quintiles of fruit and vegetable intake consumed more energy.

As shown in table 2, both fruit and vegetable intake at baseline in 1992–1993 were unrelated to risk of endometrial cancer. This was true in both age-adjusted models and multivariate models, when results were analyzed by number of servings per 1,000 kcal per day, and when examined by decile (data not shown). These findings did not change with cumulatively updated servings, which incorporated information from the 1999 FFQ (data not shown). The association between fruit or vegetable intake and endometrial cancer was not materially different when we limited cases to type I endometrial carcinoma (quintile 5 vs. quintile 1: for fruit, rate ratio (RR) = 0.98, 95 percent CI: 0.63, 1.51 (p-trend = 0.92); for vegetables, RR = 0.97, 95 percent CI: 0.63, 1.50 (p-trend = 0.60)).


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  		TABLE 2. Rate ratio for endometrial cancer according to quintile of fruit or vegetable intake, Cancer Prevention Study II Nutrition Cohort, 1992–2003

 
When we examined long-term consumption patterns from our 1982 and 1992 surveys, there was no statistically significant association between these dietary factors and endometrial cancer risk. The rate ratio associated with being in the top tertile of vegetable intake in both 1982 and 1992 was 0.81 (95 percent CI: 0.57, 1.16), as compared with being in the bottom tertile at both time points. The rate ratio for being in the top tertile of citrus fruit consumption (the only question on fruit asked in 1982) at both time points versus the bottom tertile at both points was 1.21 (95 percent CI: 0.89, 1.64).

Results from the analyses based on quintile of botanical or phytochemical plant food subgroups consumed in 1992 and endometrial cancer risk are provided in table 3. We found increased risk associated with consumption of fruits and vegetables high in lutein and vitamin C (p-trend = 0.04 and p-trend = 0.03, respectively). These results were not appreciably different when we examined cumulatively updated intakes. The largest contributor to lutein-containing vegetables was salad (59 percent), followed by broccoli (32 percent) and spinach (6 percent). When we examined individual foods, consuming salad three times per week as compared with less than once per week was associated with higher risk (RR = 1.46, 95 percent CI: 1.12, 1.91; p-trend < 0.05). For citrus fruits, the largest contributor was orange juice (49 percent); orange juice was nonsignificantly positively related to risk (data not shown). No other individual foods were related to risk (data not shown).


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  		TABLE 3. Multivariate rate ratio for endometrial cancer according to quintile of consumption of plant food subgroups, Cancer Prevention Study II Nutrition Cohort, 1992–2003

 
Relations between fruit and vegetable intakes and endometrial cancer risk were not modified by smoking status, body mass index, or multivitamin use (data not shown). Among women who reported never using HRT, the highest tertiles of fruit and vegetable consumption, as compared with the lowest tertiles, were associated with a slightly lower risk, but the p values for trend were greater than 0.05 (table 4). Among women with a history of ever using HRT, fruit consumption and vegetable consumption were related to a higher risk (p-interaction = 0.03 and p-interaction = 0.01, respectively). Results were similar when we examined a history of ERT or combined HRT use separately. When we excluded the first 2 years of follow-up, the slightly elevated multivariate rate ratios were attenuated for fruits (RR = 1.12) and vegetables (RR = 1.08), and results for lutein- and vitamin C-containing foods were no longer significant (RR = 1.24, 95 percent CI: 0.89, 1.73 (p-trend = 0.13) and RR = 1.16, 95 percent CI: 0.84, 1.60 (p-trend = 0.17), respectively).


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  		TABLE 4. Multivariate rate ratio for endometrial cancer according to fruit or vegetable intake and use of hormone replacement therapy, Cancer Prevention Study II Nutrition Cohort, 1992–2003

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
References
 
In this large prospective cohort study, we did not observe an inverse association between vegetable or fruit intake and endometrial cancer, regardless of timing or method of assessing intake. Persons with the highest intakes of lutein- and vitamin C-containing vegetables were at unexpectedly higher risk of endometrial cancer. In a secondary analysis, women who had never used HRT had an approximately 20–25 percent lower risk of endometrial cancer with fruit or vegetable intake in the highest category versus the lowest, while a somewhat increased risk was observed among ever users of postmenopausal hormones. However, although the interaction was statistically significant, the estimates and trend tests were not.

Our overall null results for the relation between vegetable consumption and endometrial cancer risk are in contrast to the findings of a recent meta-analysis (21) based on 10 case-control studies (6–15). In a meta-analysis of the literature on fruits, vegetables, and endometrial cancer conducted for the upcoming Second World Cancer Research Fund/American Institute for Cancer Research Report on Food, Nutrition, Physical Activity and the Prevention of Cancer, Bandera et al. (21) found a pooled summary odds ratio of 0.71 (95 percent CI: 0.55, 0.91) for the highest levels of vegetable consumption versus the lowest. This estimate is similar to that reported in the 2003 International Agency for Research on Cancer summary on fruits and vegetables (41, 42), which was based on half the number of case-control studies included in the more recent analysis and is congruent with the suggestion that intake of fruits and vegetables "possibly" decreased the risk of endometrial cancer in the earlier 1997 World Cancer Research Fund/American Institute for Cancer Research narrative review (3). Results from a previously published prospective cohort study with 133 cases showed a nonsignificantly increased risk of endometrial cancer among women with a low intake of fruits and vegetables combined; risk estimates for fruits and vegetables were not reported separately (22).

Several potential factors may explain the discrepancy between our findings and those in the case-control literature. Case-control studies are susceptible to recall bias if cases report their diets differently than controls. Another potential difference among studies could be the ranges of fruit and vegetable consumption in the study populations. However, the range of vegetable consumption examined in our study (>2.6 servings/day in the highest quintile vs. <1.0 servings/day in the lowest) was similar to that in a large population-based case-control study (11) in which significant inverse relations were observed (e.g., >3.1 servings of vegetables per day vs. <1.5 servings/day). Other studies examined wider distributions (>404 g/day vs. ≤179 g/day for vegetables; approximately 5 servings/day vs. <2 servings/day) (12). However, our results remained null when we examined intakes in deciles of consumption. Misclassification of exposure from our dietary assessment method cannot totally explain our findings, since the earlier case-control study that found inverse associations (11) used a similar FFQ.

In the United States, phytochemically dense fruits and vegetables comprise a relatively small proportion of overall fruit and vegetable intakes (43). This raises the question of whether examination of "fruits" and "vegetables" combined is specific enough. Nevertheless, certain botanical or phytochemical plant types, such as foods high in lutein and vitamin C, were unexpectedly associated with increased risk of endometrial cancer. This may reflect dietary patterns or other behaviors correlated with contributors to these food subgroups (e.g., salad). When we excluded the first 2 years of follow-up, the rate ratios for these two botanical subgroups were attenuated and no longer statistically significant. This suggests that women may have changed their eating behavior close to diagnosis, perhaps because of symptoms. Chance could also account for the subgroup findings because of the number of exposures examined.

We observed inverse relations between both fruit (RR = 0.75) and vegetable (RR = 0.80) intake and postmenopausal endometrial cancer risk among women who had never used postmenopausal hormone therapy, comparing the highest tertile of intake with the lowest, whereas ever users of HRT were at slightly increased risk. To our knowledge, no previous study has evaluated consumption of fruits and vegetables stratified by hormone use, and this was not a prior hypothesis in our analysis. Because exposure of the endothelium to unopposed estrogen is a major risk factor for endometrial cancer, it is conceivable that any protective effect of plant food constituents (e.g., fiber, phytoestrogens, antioxidants) would be most evident in a low-estrogen environment (postmenopausal women with no HRT use) (44, 45), whereas the potential beneficial effects would be overwhelmed in the presence of high levels of exogenous hormones. Because both fruit consumption and vegetable consumption are correlated with other healthy lifestyle behaviors, it is possible that this interaction reflects uncontrolled confounding. This interaction may also be due to chance.

Strengths of this analysis include the prospective nature of the study, the relatively large size of the cohort, and the repeated measures of dietary intake. By asking about dietary intake years before diagnosis with endometrial cancer, we eliminated the possibility of recall bias influencing the effect estimates. Another advantage of cumulative updating of dietary data during follow-up is reduction of misclassification (46). Finally, we were able to censor women during follow-up at the date of hysterectomy, something that was not done in the only previous cohort study to report on this association (22). Limitations of this analysis include a relatively homogenous cohort and the use of different dietary assessment instruments over time.

In summary, the results of this large prospective study of postmenopausal women do not replicate earlier case-control study findings of an inverse association between vegetable and fruit consumption and endometrial cancer risk. While it is possible that fruits and/or vegetables influence risk in certain subgroups of the population (e.g., never users of HRT), this cohort study does not support a major role for fruits and vegetables in endometrial cancer prevention.


APPENDIX TABLE 1. Fruits and vegetables included in three surveys administered to the Cancer Prevention Study II (CPS-II) Mortality Cohort and the CPS-II Nutrition Cohort, 1982–1999

CPS-II Mortality Cohort—baseline questionnaire (1982) CPS-II Nutrition Cohort
Baseline food frequency questionnaire (1992) Follow-up food frequency questionnaire (1999)
Fruits
Citrus fruits/juices Oranges*,{dagger} Oranges*,{dagger}
Orange or grapefruit juice*,{dagger} Orange juice*,{dagger}
Grapefruit juice*
Grapefruit*,{ddagger} Grapefruit*,{ddagger}
Cantaloupe§ Cantaloupe§
Apples, applesauce, pears Fresh apples or pears
Applesauce
Other fruit juices Other fruit juices
Apple juice or cider
Any other fruit, including bananas or fruit cocktail Bananas
Peaches, apricots, or plums
Strawberries, fresh, frozen, or canned{dagger}
Blueberries, fresh, frozen, or canned
Raisins or grapes
Prunes
Avocados
Vegetables
Baked beans, lima beans, pinto beans, kidney beans, chili Beans or lentils, baked or dried
Peas or lima beans
Tomatoes Tomatoes, tomato juice{ddagger} Tomatoes{ddagger}
Tomato or V8 juice{ddagger}
Spaghetti, lasagna, other pasta with tomato sauce (assuming that 40% of the weight was tomato sauce){ddagger} Tomato sauce (e.g., spaghetti sauce){ddagger}
Salsa, picante or taco sauce{ddagger}
Cabbage, broccoli, Brussels sprouts Broccoli{dagger},#,** Broccoli{dagger},#,**
Brussels sprouts{dagger},#
Cabbage, coleslaw, sauerkraut# Cabbage or coleslaw#
Green leafy vegetables Mustard greens, turnip greens, collards§,#,** Kale, mustard, or chard greens§,#,**
Spinach§,** Spinach, cooked §,**
Spinach, raw as in salad§,**
Green salad** Iceberg or head lettuce
Romaine or leaf lettuce§,**
Carrots Carrots or mixed vegetables containing carrots§ Carrots, raw§
Carrots, cooked, or carrot juice§
Sweet potato/yams§ Yams or sweet potatoes§
Squash, corn Any other vegetables, including green beans, corn, or peas Mixed vegetables, stir-fry, vegetable soup
Corn
Dark orange (winter) squash§
String beans
Cauliflower
Celery
Green or red peppers
Onions as a garnish or in a salad
Onions as a vegetable, rings or soup
Mushrooms
Eggplant, zucchini or other summer squash
Vegetable and tomato soup, including vegetarian, beef, minestrone

* Rutaceae (citrus) botanical family.

{dagger} Foods high in vitamin C (>50 mg/100 g).

{ddagger} Foods high in lycopene (>750 µg/100 g).

§ Foods high in ß-carotene (>1,900 µg 100 g).

Campbell Soup Company, Camden, New Jersey.

# Cruciferae (mustard) botanical family.

** Foods high in lutein/zeaxanthin (>1,000 µg/100 g).


   ACKNOWLEDGMENTS
 
Conflict of interest: none declared.


   References
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

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