Original Article

Prostate Cancer and Prostatic Diseases (2008) 11, 61–66; doi:10.1038/sj.pcan.4500979; published online 22 May 2007

Fruit, vegetable, vitamin A intakes, and prostate cancer risk

G L Ambrosini1, N H de Klerk1, L Fritschi2, D Mackerras3,4 and B Musk1

  1. 1School of Population Health, University of Western Australia, Western Australia, Australia
  2. 2Western Australian Institute for Medical Research, Western Australia, Australia
  3. 3Menzies School of Health Research, Northern Territory, Australia
  4. 4Institute of Advanced Studies, Charles Darwin University, Northern Territory, Australia

Correspondence: GL Ambrosini, School of Population Health (M431), University of Western Australia, 35 Stirling Highway, Crawley 6009, Perth, Western Australia, Australia. E-mail: Gina.Ambrosini@uwa.edu.au

Received 29 January 2007; Revised 16 April 2007; Accepted 17 April 2007; Published online 22 May 2007.



Prostate cancer risk was examined in relation to intakes of fruit, vegetables, β-carotene and retinol. Subjects were a cohort of 1985 men previously to asbestos who participated in a cancer prevention programme of β-carotene and retinol supplements that commenced in July 1990. Diet was assessed at entry to the programme. Ninety-seven cases of prostate cancer were identified during follow-up until the end of 2004. A decreased prostate cancer risk was observed with increasing intakes of vitamin C-rich vegetables, including bell peppers and broccoli. Fruit, other vegetables and vitamin A intakes did not appear to be strong factors in the development of prostate cancer in this study.


nutrition, fruit, vegetables, β-carotene, retinol, vitamin A



Much of the global variation in prostate cancer incidence is thought to be attributable to diet,1 and several observational studies have examined intakes of different fruit and vegetables and prostate cancer risk.2, 3, 4, 5, 6, 7, 8, 9 Although it is widely accepted that a diet rich in fruits and vegetables may protect against some cancers,10, 11 the evidence in relation to prostate cancer is inconclusive.12 However, clinical studies have demonstrated that specific bioactive compounds common to plant foods, including lycopene, β-carotene, vitamin E, vitamin C and various phytoestrogens (for example, soy-derived isoflavonoids), as well as vitamin A and retinoids, may significantly reduce prostate cancer risk or prostate cancer cell growth.12 This study examined the risk of prostate cancer during 12 years of follow-up in relation to intakes of fruit and vegetables, β-carotene and retinol.


Materials and methods


Blue asbestos (crocidolite) was mined and milled in the remote town of Wittenoom Gorge in Western Australia from 1943 until 1966. We have maintained follow-up on cohorts of former workers (n=6908) and residents (n=4890) of Wittenoom Gorge since 1975, to document the epidemiology of asbestos-related diseases including asbestosis, malignant mesothelioma and lung cancer.13 The cohorts and estimation of their cumulative asbestos exposures (residential and occupational) have been described in detail elsewhere.14, 15

In July 1990 all surviving members of the Wittenoom workers cohort who could be traced (n=2373) were invited to take part in a cancer prevention programme to examine the efficacy of β-carotene (synthetic all-trans) and retinol (retinyl palmitate) supplements (hereafter referred to as vitamin A supplements) in reducing the risk of malignant mesothelioma, lung cancer and other cancers.16 The programme was subsequently opened to members of the Wittenoom residents cohort and persons who had experienced an equivalent of at least 3 months of full time occupational exposure to crocidolite elsewhere (that is, not at Wittenoom), for example, carpenters, waterside workers, plumbers. These two groups were not actively recruited.

At entry to the programme, all participants were asked to complete a food frequency questionnaire (FFQ) and to provide smoking, medical and occupational histories. Height and weight was also measured. Former Wittenoom workers were randomly assigned to take either 30mg β-carotene or 7.5mg retinol daily except those with abnormal liver function tests, who were randomized to either 0.75 or 30mg of β-carotene daily. Former Wittenoom residents and all other participants were randomly assigned to receive either 0.75 or 30mg of β-carotene daily. All participants were given 1 year's supply of the randomly allocated vitamin A supplement, and were required to attend a follow-up appointment every 12 months. Preliminary analyses in 1995 established that the 5-year incidence of mesothelioma in former Wittenoom workers was lower in those assigned to retinol compared to those assigned to β-carotene (RR=0.24, 95% CI, 0.07–0.86). This, in combination with overseas trials showing increased rates of lung cancer among smokers taking similar doses of β-carotene,17, 18 led to supplementation with β-carotene being discontinued in 1996. All men were thereafter assigned to 7.5mg of retinol/day only, except those with abnormal liver function, who were supplemented with 0.4mg of retinol/day.


A semi-quantitative FFQ ascertaining usual diet during the previous year was specially designed for the programme to estimate average daily intakes of dietary β-carotene and retinol. The FFQ was posted to study candidates to complete at home and was checked for completeness at their induction interview. This questionnaire was administered to all participants enroling in the programme up until the end of 1996.

The 45 foods (23 fruit and vegetables) included in the FFQ were chosen using a ranking analysis of 7-day diet records from 60 control subjects participating in a local case–control study of renal calculus disease (unpublished data). The ranking criteria were based upon the food's carotene and retinol content, its ability to discriminate these intakes, and other nutritional significance for example, cruciferous vegetables. More detail on the FFQ and agreement between estimates of carotene and retinol intakes and a 28-day diet record have been reported in detail elsewhere.19

The size of a medium serve of each food was specified in the FFQ, and subjects were asked to record their usual serve size as small, medium or large, in relation to this quantity. Serve sizes were derived from those reported in the renal calculus study. There were eight options for the frequency of consumption ranging from ‘never or less than once per month’ up to ‘two or more times per day’. The consumption of fruits and vegetables was collected separately for summer and winter.


All programme participants were followed up for incident prostate cancer diagnosed after enrolment in the programme up until 31 December 2004, or date of death, which ever occurred first. Prostate cancer cases were identified via record linkage with the Western Australian Cancer Registry and the Australian National Cancer Statistics Clearing House. Cancer registration by pathology laboratories is mandatory in Australia and these cancers were histologically confirmed cases classified according to the second edition of the International Classification of Diseases for Oncology.

Statistical analysis

FFQ responses were standardized to a medium serve (for example, small serve=½ medium serve, large serve=1.5 medium serve) before average serves consumed per day or week were calculated for each FFQ item. Total daily fruit and vegetable intake was calculated as the sum of all medium (standardized) fruit and vegetable serves consumed per day. This was truncated to a maximum of 10 serves per day, to reduce the effect of probable incorrect values.20 Less than 1% of respondents reported either total fruit or total vegetable intake greater than 10 serves per day. Weekly intakes of the following groups of fruit and vegetables were calculated: carotene-rich vegetables (carrot, sweet potato, pumpkin, bell peppers), carotene-rich fruits (peaches, apricots, rockmelon), vitamin C-rich fruit (fresh oranges, orange juice, rockmelon) and vitamin C-rich vegetables (peppers, broccoli, spinach). Intake of cooked tomato was estimated by summing weekly serves of tomato sauce (with and without meat), and pizza. Raw tomato intake included fresh tomato and tomato juice. Individual fruit and vegetable intakes were also examined, but only those of interest are reported for brevity. As the FFQ was designed to estimate β-carotene (β-carotene equivalents) and retinol intakes, we also examined prostate cancer risk according to these nutrients. Intakes of β-carotene and retinol were estimated using Australian Food Composition Tables.21

Prostate cancer risk was analysed with Cox proportional hazards models using Stata software version 9.0.22 Dietary intakes were analysed as tertiles created using the ‘xtile’ command in Stata. It was not possible to adjust for energy intakes in our analyses, as the FFQ was not designed to estimate total energy intake. However, the intakes of interest generally have low correlations with energy intake. Each model was adjusted for total fruit and vegetable consumption (serves/day) to determine whether associations between specific fruit or vegetables and prostate cancer risk were independent of overall fruit and vegetable intake. The following potential confounders (measured at baseline) were investigated: age, body mass index (BMI), source of asbestos exposure and smoking status (previous smoker, current smoker or never smoked). To control for randomly assigned vitamin A supplements, an intention-to-treat analysis was conducted, whereby each subject was analysed according to the original supplement assigned to them at entry to the programme. The level for significance was set to 5% for all statistical tests.

All participants gave their informed consent, and this study was approved by the University of Western Australia's Human Research Ethics Committee and the Clinical Drug Trials Committee of the Sir Charles Gairdner Hospital.



A total of 2183 men enroled in the programme before the end of 1996. Of the 1985 (91%) who completed an FFQ, 49% were former Wittenoom workers, 17% were former Wittenoom residents and 34% were exposed to asbestos elsewhere. During a median of 12.7 years of follow-up, 441 men died, 97 incident cases of prostate cancer were identified, and 35 men were lost to follow-up (could not be traced). Prostate cancer cases were older than non-cases at baseline (P<0.0001), were less likely to be former Wittenoom residents (P=0.001), and were more likely to have been exposed to blue asbestos in occupations outside Wittenoom (P=0.005) (Table 1). As dietary intakes were skewed, Mann–Whitney tests were used to compare median dietary intakes for cases and non-cases (Table 1). There were no differences in total fruit and vegetable intake, but cases had significantly lower median intakes of cooked tomato, broccoli and bell peppers. Estimated β-carotene and retinol intakes did not differ between cases and non-cases.

In multivariate analyses, age (RR=1.06, 95% CI, 1.04–1.09 per year) and source of asbestos exposure were significantly associated with prostate cancer risk. Men exposed to asbestos outside of Wittenoom were at greater risk (RR=2.03, 95% CI, 1.22–3.36) than former workers from Wittenoom. BMI, smoking status and randomly assigned vitamin A supplement were not predictors of prostate cancer risk.

After adjusting for age, source of asbestos exposure and randomly assigned vitamin A supplement, total fruit and vegetable intakes were not related to prostate cancer risk (Table 2). With increasing intakes of vitamin C-rich vegetables, that is peppers, broccoli and spinach, the risk of prostate cancer tended to decrease (P for trend=0.056). For men in the highest tertile of vitamin C-rich vegetable intake (>4 serves/week; 1 serve equivalent to ½ cup), the RR was 0.53 (95% CI, 0.29–0.99). No association was observed between prostate cancer risk and intake of vitamin C-rich fruit, or other groups of fruit and vegetables.

We also analysed individual fruit and vegetable intakes that were used in grouped analyses. None of the fruits examined was associated with prostate cancer risk (not shown). Two vegetables from the vitamin C-rich group showed inverse relationships with prostate cancer risk. A trend was observed across tertiles of bell pepper intake (P=0.007), with men in the highest tertile (>1.5 serves per week; 1 serve equal to ½ cup) having an RR of 0.46 (95% CI, 0.25–0.85). A decreased risk was suggested for men in the highest tertile of broccoli intake (>1.5 serves/week; 1 serve equivalent to ½ cup), with an RR of 0.56 (95% CI, 0.31–1.02, P for trend=0.056). Although cases had significantly lower median intakes of cooked tomato (Table 1), multivariate analyses showed a nonsignificantly decreased prostate cancer risk in the highest tertile of cooked tomato intake (RR=0.67, 95% CI, 0.38–1.16; P for trend=0.134). Intake of raw tomato was not associated with prostate cancer risk, nor was dietary β-carotene or retinol intake (Table 2).



This study has found that prostate cancer risk does not appear to be strongly associated with the intake of β-carotene, retinol, fruits or vegetables, except possibly with vitamin C-rich vegetables such as bell peppers and broccoli. Vitamin C is a strong antioxidant that has been shown to inhibit prostate cancer cell growth in vitro;12 however a protective effect from increased vitamin C intakes against prostate cancer has not been consistently demonstrated in epidemiological studies.23, 24, 25, 26 Furthermore, no effect from vitamin C-rich fruit was observed in this study, even though the bioavailability of vitamin C is usually higher in fruit, due to it being eaten most often raw, rather than cooked.

No association was observed between carotene-rich fruit, carotene-rich vegetables or β-carotene intake and prostate cancer in this study. A 2004 review of dietary intake and prostate cancer concluded that there was no evidence that dietary carotenoids, apart from lycopene and others found in tomato, are associated with prostate cancer risk.27 However, the Health Professionals Follow-Up Study has since published significant inverse associations between β-carotene plasma/diet scores and prostate cancer risk in men aged under 65 years,28 and a multi-centred case–control study in Italy reported a significant inverse relationship between dietary β-carotene and prostate cancer risk.29 Like other studies, our findings do not support a protective role for retinol in prostate cancer.27

There is reasonably consistent evidence that broccoli offers anticarcinogenic effects as a Brassica (cruciferous) vegetable. An epidemiological review published in 2002 concluded that there was modest support that high intakes of Brassica vegetables reduce prostate cancer risk.30 More recently, the Health Professionals Follow-Up Study reported significantly decreased risks for prostate cancer with increasing cruciferous vegetable intakes among men who had a prostate-specific antigen test.4 However, the European Prospective Investigation into Cancer and Nutrition (EPIC), which included over 1000 cases in a cohort of over 130000 men sourced from seven European countries, reported no association in 2004.3

This study found no effect on prostate cancer risk with increased total fruit or vegetable intakes, or both combined. Generally, fruit intake has not been associated with prostate cancer risk.3 Small benefits from increased total vegetable consumption have been reported by several studies,2, 5, 7, 24, 31 but not supported by others.8, 9 In particular, no associations were found in the large EPIC cohort.3 Our findings suggest that intakes of particular vegetable types may be more important than total vegetable intake for the prevention of prostate cancer.

Modest epidemiological evidence supports a protective effect from high intake of cooked tomato against prostate cancer,27, 32, 33 although this remains a controversial area.34 A protective effect has generally been attributed to lycopene which is more bioavailable from cooked tomato than from raw tomato.33 One other cohort study has reported an RR of 0.77 (95% CI, 0.66–0.90) for men consuming high intakes (at least 2 serves per week) of cooked tomato,35 and odds ratios for case–control studies are in the range of 0.46–0.94.33 Our RR of 0.67 for high intake of cooked tomato (>1.8 serves/week) is of similar magnitude, although possibly not significant due to having a smaller sample size.

The fruit and vegetables included in the FFQ used in this study were selected because of their contribution to usual vitamin A intakes in the study population. Therefore ‘total fruit and vegetable’ intakes analysed in this paper may not be directly comparable to typical definitions of total fruit and vegetable intakes. These commonly include contributions from a wider range of fruit and vegetables, as well as potato intake, which contributes to at least 40% of vegetable intake in Australia.36 Therefore, total serves of fruit and vegetables and serves of fruit and vegetable groups may have been underestimated or misclassified by our FFQ, possibly explaining the lack of significant associations observed for these. However, there is no reason to believe that estimates of individual vegetable intakes (for example, broccoli) would have been affected by the questionnaire design.

Repeated assessments of dietary intake might have improved this study, especially given that subjects were taking part in a cancer prevention programme. Participation in the programme could have affected subsequent dietary behaviour in this cohort, and led to a reduction in cancer risk during the follow-up period.

We observed that prostate cancer risk was greater for those men in this study who had not worked at Wittenoom but experienced asbestos exposure in jobs elsewhere. We are currently extracting occupational histories for all men in this study so that we may examine prostate cancer risk according to various occupational exposures. In future it will also be possible to study other lifestyle factors such as physical activity, which could explain the increased risk among other asbestos workers.

Although our results are consistent with other studies, careful interpretation is needed, as some of the results may have arisen by chance due to the number of statistical tests carried out. However, this study does benefit from more than 12 years of follow-up after dietary assessment and the matching of subjects with national cancer records. The cohort design of the study was advantageous for reducing recall bias, particularly as the main focus was mesothelioma and lung cancer, not prostate cancer.

Prostate cancer risk in this study does not appear to be strongly associated with the intake of β-carotene, retinol, fruits or vegetables, except possibly with vitamin C-rich vegetables such as peppers and broccoli. Although the association with cooked tomatoes was not significant, it was consistent with earlier reports.



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Funds for this study were provided by the Western Australian (WA) Cancer Council, the WA Department of Health, the WA Workers’ Compensation and Rehabilitation Commission, Iain and Penny MacGregor, and the Australian National Health and Medical Research Council. We are grateful for research assistance provided by Nola Olsen, Lynne Defrenne, Jan Sleith, Naomi Hammond and Barbara Telfer, and data management provided by Philip Etherington.



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