No abstract

The epidemiologic literature on the relationship between vegetable and fruit consumption and human cancer at a variety of sites is reviewed systematically. A total of 13 ecologic studies, nine cohort studies, and 115 case-control studies are included. Cancer of all sites, cancers of lung, breast, colon, rectum, esophagus, larynx, oral cavity and pharynx, stomach, pancreas, prostate, bladder, ovary, endometrium, cervix, and thyroid, as well as mesothelioma and gestational trophoblastic disease, are considered. Relevant data from clinical trials, animal, and in vitro studies are included. It is concluded that consumption of higher levels of vegetables and fruit is associated consistently, although not universally, with a reduced risk of cancer at most sites. The association is most marked for epithelial cancers--particularly those of the alimentary and respiratory tracts--and, currently, is weak to nonexistent for hormone-related cancers. The association exists for a wide variety of vegetables and fruit with some suggestion that raw forms are associated most consistently with lower risk. Possible mechanisms by which vegetable and fruit intake might alter risk of cancer and possible adverse effects of vegetable and fruit consumption will be considered in Part II of this review.

The epidemiologic literature on the relationship between vegetable and fruit consumption and human cancer at a variety of sites was reviewed systematically in Part I. It was concluded that consumption of higher levels of vegetables and fruit is associated consistently, although not universally, with a reduced risk of cancer at most sites, and particularly with epithelial cancers of the alimentary and respiratory tracts. Possible mechanisms by which vegetable and fruit intake might alter risk of cancer are addressed here. A large number of potentially anticarcinogenic agents are found in these food sources, including carotenoids, vitamins C and E, selenium, dietary fiber, dithiolthiones, glucosinolates and indoles, isothiocyanates, flavonoids, phenols, protease inhibitors, plant sterols, allium compounds, and limonene. These agents have both complementary and overlapping mechanisms of action, including the induction of detoxification enzymes, inhibition of nitrosamine formation, provision of substrate for formation of antineoplastic agents, dilution and binding of carcinogens in the digestive tract, alteration of hormone metabolism, antioxidant effects, and others. It appears extremely unlikely that any one substance is responsible for all the associations seen. Possible adverse effects of vegetable and fruit consumption are also examined. One way to consider the relationships reviewed here is to hypothesize that humans are adapted to a high intake of plant foods that supply substances crucial to the maintenance of the organism, but only some of which are currently called 'essential nutrients.' Cancer may be the result of reducing the level of intake of foods that are metabolically necessary--it may be a disease of maladaptation.

To investigate the relation of dietary intakes of sucrose, meat, and fat, and anthropometric, lifestyle, hormonal, and reproductive factors to colon cancer incidence, data were analyzed from a prospective cohort study of 35,215 Iowa (United States) women, aged 55-69 years and without a history of cancer, who completed mailed dietary and other questionnaires in 1986. Through 1990, 212 incident cases of colon cancer were documented. Proportional hazards regression was used to adjust for age and other risk factors. Risk factors found to be associated significantly with colon cancer included: (i) sucrose-containing foods and beverages other than ice cream/milk; relative risks (RR) across the quintiles = 1.00, 1.73, 1.56, 1.54, and 2.00 (95% confidence intervals [CI] for quintiles two and five exclude 1.0); (ii) sucrose; RR across the quintiles = 1.00, 1.70, 1.81, 1.82, and 1.45 (CI for quintiles two through four exclude 1.0); (iii) height; RR = 1.23 for highest to lowest quintile (P for trend = 0.02); (iv) body mass index; RR = 1.41 for highest to lowest quintile (P for trend = 0.03); and (v) number of livebirths, RR = 1.59 for having had one to two livebirths and 1.80 for having had three or more livebirths compared with having had none (P for trend = 0.04). These data support hypotheses that sucrose intake or being tall or obese increases colon cancer risk; run contrary to the hypothesis that increased parity decreases risk; support previous findings of no association with demographic factors other than age, cigarette smoking, or use of oral contraceptives or estrogen replacement therapy; and raise questions regarding previous associations with meat, fat, protein, and physical activity.

Previous epidemiologic studies have shown an inverse association between vegetable and fruit consumption and colon cancer risk; few of these studies have been prospective or have focused on women. This report describes results from a prospective cohort study of 41,837 women aged 55-69 years who completed a 127-item food frequency questionnaire in 1986 and were monitored for cancer incidence for 5 years via the State Health Registry of Iowa. After specific exclusion criteria were applied, 212 colon cancer cases and 167,447 person-years were available for analysis. Intakes of 15 vegetable and fruit groups and dietary fiber were the major factors of interest. Consumption of garlic was inversely associated with risk, with an age- and energy-adjusted relative risk of 0.68 (95% confidence interval (CI) 0.46-1.02) for the uppermost versus the lowermost consumption levels. Inverse associations were also observed for intakes of all vegetables and dietary fiber; age- and energy-adjusted relative risks for the uppermost versus the lowermost intake quartiles were 0.73 (95% CI 0.47-1.13) and 0.80 (95% CI 0.49-1.31), respectively. Associations for the other vegetable and fruit groups were less remarkable.