- 1 Key messages
- 2 Background
- 3 Rationale
- 4 Views on fruit and vegetables in cancer prevention reports
- 5 Epidemiological evidence
- 6 Potential mechanisms of action
- 7 Recommendations
- 8 How much fruit and vegetables should we be eating?
- 9 Current Australian consumption levels
- 10 Cancer survivors
- 11 Organic fruit and vegetables
- 12 Future research
- 13 Position statement details
- 14 References
The protective effects of fruit and vegetables against cancers, as well as other diseases such as heart disease and type 2 diabetes, led to the promotion of fruit and vegetables consumption as a previous national public health priority.
Fruit and vegetables are high in nutrients such as fibre, vitamins and minerals. In addition they contain antioxidants and phytochemicals, which are chemicals found in plants such as flavonoids, carotenoids and lignans. It is probably a combination of these nutrients and phytochemicals found together in whole foods that helps to reduce the risk of chronic diseases rather than one anti-cancer component, although many different mechanisms have been proposed. Single nutrients identified from the analysis of epidemiological studies have usually been unsuccessful when investigated further in trials, making the whole food approach more appropriate to prevention advice.
Fruit and vegetables also play an important role in weight management due to their low energy density, high fibre content and capacity to displace higher energy foods from the diet. Obesity is a known risk factor for cancer of the bowel, kidney, pancreas, oesophagus, endometrium and breast (in post-menopausal women). Evidence suggests that obesity may also be linked to cancer of the gallbladder and liver. Therefore fruit and vegetables may reduce the risk of cancer directly through the provision of specific anti-carcinogenic agents and indirectly through their role in weight management.
The International Agency for Research on Cancer (IARC) concluded that 5–12% of cancers could be attributed to low fruit and vegetable consumption. Australian data suggests that 2% of cancers were attributable to low consumption of fruit and vegetables. In terms of health care costs, it has been estimated that low vegetable intake (less than four serves per day) accounts for 17% of the cost of bowel cancer, 2% of the cost for breast cancer, and 9% of the cost of lung and of prostate cancer. An Australian study found that 21% of the cost of lung cancer and 4% of the cost of breast cancer has been attributed to lower fruit intake (less than three serves per day).
In 2009, WCRF analysed the proportion of cancers attributable to low fruit and vegetable consumption for those cancers for which there was probable evidence of a link, based on the 2007 report. These numbers give some indication of what proportion of cancers can be prevented by increased fruit and vegetable intake on a population level. Data from the US, UK, Brazil and China were analysed (see Table 1 for an overview of UK estimates).
Table 1. UK population attributable fractions (PAF) of cancers associated with low fruit and vegetable intake
|Mouth, larynx and pharynx||Vegetables||34%|
Many cancer organisations worldwide, together with a number of National Dietary Guideline committees have recommended a daily intake of five to seven serves of fruits and vegetables to reduce cancer risk. Therefore it is important for the Cancer Council to evaluate the evidence on fruit, vegetables and cancer prevention in order to develop its messages and recommendations.
This position statement summarises epidemiological evidence from major cancer prevention reports, meta-analyses and systematic reviews that examined the relationship between fruit and vegetable consumption and cancer risk. In addition to the meta-analyses and systematic reviews identified, several cohort studies were also considered, including the published results of the European Prospective Investigation into Cancer and Nutrition (EPIC) study. A major strength of EPIC is the wide range of fruit and vegetable intakes that have been assessed.
Views on fruit and vegetables in cancer prevention reports
Several major reports have investigated the relationship between fruit and vegetable intake and cancer risk, finding that there is moderate probable evidence of an association fruit and vegetable consumption and decreased risk for a number of cancer types (see Table 2). This level of evidence is regarded as sufficient to inform population health recommendations. On the whole, evidence that vegetables are protective is stronger than for fruits, but this may simply reflect the generally greater consumption of vegetables worldwide or the different mix of nutrients obtained from them.
Table 2. Conclusions from major cancer prevention reports regarding the cancer protective effect of fruit and vegetables
|Organisation review||Highest evidence
|Lower evidence |
|WCRF/AICR (2007)||Mouth (f & v)
Pharynx (f & v)
Larynx (f & v)
Oesophagus (f & v)
Stomach (f & v)
|Nasopharynx (f & v) |
Colon & rectum (f & v)
|IARC (2003)||Oesophagus (f & v)
Colon & rectum (v)
|Mouth (f & v) |
Pharynx (f & v)
Larynx (f & v)
Kidney (f & v)
Colon & rectum (f)
|WHO/FAO (2003)||Oral Cavity (f & v)
Oesophagus (f & v)
Stomach (f & v)
Colon & rectum (f & v)
f = fruit; v = vegetables
In 2007, the World Cancer Research Fund and the American Institute of Cancer Research (WCRF/AICR) published an update of their conclusions regarding fruit and vegetables in their Report on Food, Nutrition Physical Activity and the Prevention of Cancer. The report found that there was probable evidence of a protective effect by fruit and vegetables for cancer of the mouth, pharynx, larynx, oesophagus and stomach, and fruit also probably protected against lung cancer (see Table 2). There was limited suggestive evidence that fruit and vegetables reduced the risk of nasopharyngeal and bowel cancer, fruit lowered the risk of pancreatic and liver cancer and vegetables reduced the risk of lung, ovarian and endometrial cancer.
For particular types of fruits and vegetables, WCRF found probable evidence that allium vegetables protect against stomach cancer, garlic probably protected against bowel cancer and foods containing lycopene probably protected against prostate cancer. A more recent review by WCRF in 2014 concluded that links between prostate cancer and foods containing lycopene have been downgraded from strong evidence of a decreased risk to no conclusion possible. There was limited suggestive evidence that carrots lowered the risk of cancer of the cervix.
IARC reviewed the evidence relating to cruciferous vegetables, isothiocyanates and indoles in 2004 and found that for human studies:
- There was limited evidence that cruciferous vegetables reduced the risk of stomach and lung cancer.
- There was inadequate evidence that cruciferous vegetables reduced the risk for cancers at all other sites.
- There was inadequate evidence to assess the independent effects of isothiocyanates and indoles on human cancer risk, as opposed to their combined effects with other compounds in cruciferous vegetables.
In 2003, IARC found probable evidence that a high intake of vegetables reduced the risk of oesophageal and bowel cancer, while a high intake of fruit probably reduced the risk of oesophageal and stomach cancer (see Table 1). However IARC rated the evidence for an association between vegetable intake and cancer of the mouth, pharynx, larynx, kidney, stomach, lung and ovary and the evidence for an association between fruit intake and cancer of the mouth, pharynx, larynx, kidney, bowel and bladder as possible.
Similarly, the World Health Organization (WHO) suggested that a high intake of fruit and vegetables probably reduced the risk of cancers of the oral cavity, oesophagus, stomach and bowel (see Table 2). WHO recommended an intake of at least 400 g of fruit and vegetables daily (in addition to potatoes).
The conclusions from WHO and IARC differed from earlier reviews by WCRF/AICR and the United Kingdom Department of Health Committee of the Medical Aspects of the Food Supply (COMA) because of the inclusion and consideration of more prospective studies published since these original reviews were undertaken. In recent years it has been increasingly apparent that the protective association between fruit and vegetable intake and cancer is much stronger in case-control studies than in cohort studies. Furthermore, randomised controlled trials involving fruit and vegetable intake, notably for bowel cancer, have not demonstrated any benefit. Case-control studies are known to be prone to recall and selection bias, however the length of follow-up in cohort studies can also potentially limit the interpretation of their results.
Results published in 2001 from the EPIC study showed that significant health gains are made from even a small increase in fruit and vegetable intake. Increasing intakes of fruit and vegetables by just 50 g a day (equivalent to 2/3 cup cooked vegetables or 1/3 of a piece of fruit) was associated with a reduction in cancer risk of around 20%.
Recent reviews and meta-analyses suggest that fruit and vegetables may protect against oral, laryngeal, oesophageal, bowel and lung cancer. Fruit consumption may also lower the risk of stomach and bladder cancer. Fruit and vegetables do not appear to be associated with a lower risk of prostate, breast or ovarian cancer.
All cancers combined
The association between fruit and vegetable intake and the risk of major chronic disease was examined in the Nurses Health Study and Health Professionals Study. There was no association between the consumption of fruit and vegetables and cancer incidence. The relative risk (RR) of cancer based on a continuous measure for the increment of five serves per day of total fruit and vegetable intake was 1.00 (95% confidence interval (CI)= 0.95-1.05). Interestingly, five serves of fruit and vegetables were protective against cardiovascular disease (RR= 0.88, 95% CI= 0.81-0.95).
A 2006 meta-analysis of 15 case-control studies and one cohort study found a statistically significant reduction in oral cancer risk for each portion of fruit (combined adjusted odds ratio (OR)= 0.51, 95% CI= 0.40-0.65) and vegetable consumed (combined adjusted OR= 0.50, 95% CI= 0.38-0.65). Similar results were found when results were pooled from 12 studies that adjusted for age, sex, smoking and alcohol intake (OR for fruit= 0.49, 95% CI= 0.39-0.63; OR for vegetables= 0.43; 95% CI= 0.31-0.59). Interestingly citrus fruit appeared to provide greater protection than overall fruit consumption (OR= 0.38, 95% CI= 0.26-0.56).
A meta-analysis completed in 2003 found that in case-control studies (nine studies on fruit and seven studies on vegetable consumption), both fruit (RR= 0.53, 95% CI= 0.37-0.76) and vegetables (RR= 0.84, 95% CI= 0.67-1.07) provided protection against oral cancer, with fruit providing a statistically significant result.
In the only meta-analysis identified for laryngeal cancer, fruit consumption provided a significant protective effect (RR= 0.73, 95% CI= 0.64-0.84), while vegetables appeared to provide a very small non-significant reduction in risk (RR= 0.92, 95% CI= 0.83-1.02) in case-control studies (five studies on fruit and seven studies on vegetable consumption).
A 2013 meta-analysis of 32 studies involving 10,037 cases of oesophageal cancer found that vegetable intake and fruit intake were both associated with a lower risk of oesophageal cancer.The decrease in risk was significant for vegetable intake (RR= 0.56, 95% CI= 0.45-0.69) and for fruit intake (RR= 0.53, 95% CI= 0.44-0.64).
An earlier meta-analysis, completed in 2003, which included one cohort study and 12 case-control studies, similarly indicated a significant protective association for fruit (RR= 0.72, 95% CI= 0.62-0.83) and vegetables (RR= 0.89, 95% CI= 0.82-0.97) with oesophageal cancer.
The effect of fruit and vegetable intake on the risk of adenocarcinoma of the oesophagus was investigated as part of the EPIC study. A non-significant inverse association was found for total vegetable consumption (hazard ratio (HR)= 0.71, 95% CI= 0.34-1.48), total fruit intake (HR= 0.94, 95% CI= 0.49-1.80) and citrus fruit consumption (HR= 0.73, 95% CI= 0.39-1.37).
An increase of 100 g per day of total vegetables (HR= 0.72, 95% CI= 0.32-1.64), total fresh fruit (HR= 0.84, 95% CI= 0.60-1.17) and citrus fruit (HR= 0.77, 95% CI= 0.46-1.28) also showed a non-significant inverse association with oesophageal cancer. A limitation of the EPIC study was that the number of oesophageal cancer cases was small, which limits the statistical power of the study.
A 2013 meta-analysis of sixteen case-control and six prospective studies found that high consumption of cruciferous vegetables is associated with reduced stomach cancer risk (RR= 0.81; 95% CI= 0.75-0.88).
In 2005, a meta-analysis which included 14 cohort studies on the association between stomach cancer and the consumption of fruit (13 studies) and vegetables (eight studies) found a slight non-significant protective effect for fruit (RR= 0.89, 95% CI= 0.78-1.02), while only a very small non-significant inverse relationship was found for vegetable consumption (RR= 0.98, 95% CI= 0.86-1.13). The strongest association was seen in those studies with a follow-up period >10 years for fruit (RR= 0.66, 95% CI= 0.73-0.93) and vegetables (RR= 0.71, 95% CI= 0.53-0.94). Fruit consumption had a non-significant negative effect on mortality (RR= 0.88, 95% CI= 0.70-1.09), while vegetable consumption had a small non-significant positive effect on mortality (RR= 1.02, 95% CI= 0.78-1.33) in those studies with a follow-up period ≥10 years.
A meta-analysis from 2003 included seven cohort studies and 24 case-control studies regarding fruit consumption and stomach cancer, and five cohort studies and 17 case-control studies regarding vegetable consumption and stomach cancer. All but one of these cohort studies was included in the meta-analysis mentioned above.
The combined analysis of case-control and cohort studies found a statistically significant protective result for both fruit (RR= 0.74, 95% CI= 0.69-0.81) and vegetable (RR= 0.81, 95% CI= 0.75-0.87) consumption. Fruit (RR= 0.69, 95% CI= 0.62-0.77) and vegetable (RR= 0.78, 95% CI= 0.71-0.86) intake was significantly protective in case-control studies. However, this result was weaker and non-significant in cohort studies (RR for fruit= 0.89, 95% CI= 0.73-1.09; RR for vegetables= 0.89, 95% CI= 0.75-1.05).
The effect of fruit and vegetable intake on the risk of gastric cancer was investigated as part of the EPIC study. The range of fruit and vegetable intakes varied greatly between the lowest intakes and highest intakes. There was very little evidence for a protective association between fresh fruit (HR= 0.99, 95% CI= 0.68-1.42) and stomach cancer, while there was a non-significant inverse association for citrus fruit (HR= 0.88, 95% CI= 0.63-1.24) and a non-significant positive association for vegetables (HR= 1.15, 95% CI= 0.78-1.70) and stomach cancer.
The relationship between specific fruit and vegetable types and stomach cancer has been investigated in a number of analyses.
Meta-analysis of 19 case-control and two cohort studies has indicated that high levels of allium vegetables (such as onions, garlic and shallots) reduced the risk for stomach cancer (OR= 0.54; 95% CI= 0.43-0.65).
Review of 14 studies (12 case control and two cohort studies) has found that high intake of citrus fruit is associated with a reduction in the risk of stomach cancer (OR= 0.72; 95% CI= 0.64-0.81).
Meta-analysis of 21 studies investigating tomato and lycopene consumption found that there is an associated decrease in stomach cancer risk. High versus low consumption of tomato product was associated with reduced the risk for gastric cancer stomach cancer risk (OR= 0.73; 95% CI= 0.60-0.90). Similar results were found for lycopene consumption (OR=0.88; 95% CI=0.67-1.16) and serum lycopene (OR= 0.79; 95% CI=0.59-1.07).
The Pooling Project of Prospective Studies of Diet and Cancer analysed 14 studies to investigate the link between fruit and vegetable intake and colon cancer risk. No significant association was seen for vegetables (RR= 0.94, 95% CI= 0.86 to 1.02), fruit (RR= 0.93, 95% CI= 0.85 to 1.02), or total fruits and vegetables (RR= 0.91, 95% CI= 0.82 to 1.01).
In contrast, a meta-analysis 19 prospective studies demonstrated a small but significant decreased risk for bowel cancer with high intake of vegetables (RR=0.91, 95% CI= 0.86-0.96), fruit (RR=0.90, 95% CI= 0.83-0.98) and total fruit and vegetables (RR=0.92, 95%, CI= 0.86-0.99). The associations were specific to colon cancer.
A 2003 meta-analysis revealed a small decreased risk of bowel cancer, which was significant for higher intakes of fruit and vegetables when all studies were pooled (see Table 3). This protective effect was significantly stronger in case-control studies than in cohort studies. In the analyses by cancer site (colon versus rectum), cohort studies found a significant protective effect of vegetables on colon but not rectal cancer. There was insufficient data from case-control studies to calculate the RR for rectal cancer and fruit consumption. Fruit consumption showed stronger protection against rectal cancer than colon cancer in cohort studies.
Table 3. Results from meta-analysis on fruit and vegetable and bowel cancer
|n||RR (95% CI)||n||RR (95% CI)|
|Bowel||All studies||31||0.94 (0.90-0.98)||46||0.91 (0.86-0.97)|
|Cohort||16||0.96 (0.90-1.01)||17||0.96 (0.90-1.05)|
|Case-control||15||0.93 (0.87-0.99)||29||0.87 (0.80-0.95)|
|Colon||All studies||19||0.94 (0.89-1.00)||27||0.91 (0.83-1.00)|
|Cohort||9||0.97 (0.91-1.04)||11||0.91 (0.86-0.96)|
|Case-control||10||0.90 (0.82-0.99)||17||0.90 (0.78-1.03)|
|Rectal||All studies||-||-||9||0.95 (0.80-1.11)|
|Cohort||5||0.88 (0.81-0.96)||5||1.06 (0.90-1.25)|
RR= relative risk, CI= confidence interval and n = number of studies
In contrast to these results, a randomised controlled trial found that over four years those following a diet low in fat (20% of total calories) and high in fibre (18 g fibre per 1000 kcal), fruit and vegetables (3.5 servings per 1000 kcal) did not have a different rate of recurrent bowel adenomas when compared to those that were instructed to follow their usual diet and were given a brochure containing general healthy eating advice (unadjusted RR= 1.00, 95% CI= 0.90-1.12). While the dietary assessment data did indicate that the intervention and control groups differed substantially in the consumption of fruit and vegetables, the intervention period was relatively short. It is also possible that dietary intervention might only affect the growth of adenomas once they occur.
Most recently, a large cohort study showed that (over a five year follow-up period) for highest versus lowest intake categories, vegetable intake was significantly associated with a reduced risk of bowel cancer (RR= 0.82, 95% CI= 0.71-0.94), and total fruit and vegetable intake was associated with a non-significant reduced risk of bowel cancer in men (RR= 0.91, 95% CI= 0.78-1.05). In particular, green leafy vegetables were associated with a significantly lower risk of bowel cancer in men (RR= 0.86, 95% CI= 0.74-0.99). However in women, vegetable intake (RR= 1.12, 95% CI= 0.90-1.38) and total fruit and vegetable intake (RR= 1.08, 95% CI= 0.86-1.35) were associated with a non-significant increased risk of bowel cancer. Fruit intake alone was associated with a small non-significant increased risk of bowel cancer in both men (RR= 1.06, 95% CI= 0.91-1.23) and women (RR= 1.09, 95% CI= 0.88-1.36). The difference in results for men and women may be due to reporting errors, as women may be more likely to over report foods perceived as healthy.
Meta-analysis of seven cohort and six population-based case-control studies investigating the link between cruciferous vegetable intake and prostate cancer risk indicated that high consumption is associated with reduced risk of prostate cancer (RR=0.90; 95% CI= 0.85-0.96). However, this effect was not seen in the cohort studies analysed (RR= 0.95; 95% CI= 0.88-1.02).
A meta-analysis which included 10 cohort or nested case-control studies and 11 case-control studies on the association between prostate cancer and tomato, tomato products or lycopene intake showed moderate protection against prostate cancer among those who consumed large amounts of raw tomato (RR= 0.89, 95% CI= 0.80-1.00). Interestingly, cohort studies showed a greater protective effect (RR= 0.71, 95% CI= 0.57-0.87) than case-control studies (RR= 0.98, 95% CI= 0.86-1.00).
A similar trend was also seen for lycopene intake. The RR of prostate cancer among those who consumed large amounts of lycopene was 0.89 (95% CI= 0.81-0.98). Again cohort studies showed a larger protective effect (RR= 0.84, 95% CI= 0.75-0.95) than case-control studies (RR= 0.98, 95% CI= 0.83-1.16). Cooked tomatoes appeared to provide even greater protection, which could be due to increases in concentration or improved availability of lycopene (RR= 0.81, 95% CI= 0.71-0.92). In addition, increasing concentrations of serum lycopene showed greater protection against prostate cancer than that of dietary lycopene intake (RR= 0.74, 95% CI= 0.59-0.92). This effect was even stronger for case-control studies (RR= 0.55, 95% CI= 0.32-0.94). The influence of dietary lycopene intake on serum lycopene concentrations was not explored in this meta-analysis, however other studies have shown that dietary sources of lycopene can increase serum lycopene levels and reduce oxidative stress effectively.
The association between fruit and vegetable consumption and prostate cancer risk was investigated as part of the EPIC cohort study. The consumption of fruit, vegetables, cruciferous vegetables and combined total fruits and vegetables with prostate cancer risk was examined, however no significant associations were found. The RR in the highest quintile of consumption compared with the lowest quintile was 1.06 (95% CI= 0.84-1.34) for fruits, 1.00 (95% CI= 0.81-1.22) for vegetables, 1.00 (95% CI= 0.79-1.26) for fruits and vegetables combined and 1.01 (95% CI= 0.83-1.23) for cruciferous vegetables. A recent review by WCRF in 2014 which included only randomised controlled trials and cohort studies concluded that the evidence for links between foods containing lycopene and prostate cancer was limited-no conclusion possible.
A meta-analysis of 11 case-control and two cohort studies indicated that high intake of cruciferous vegetables was associated with a reduced risk of breast cancer (RR= 0.85, 95% CI= 0.77-0.94). However, it was noted that the number of studies was limited and as such, further investigation was recommended.
A second meta-analysis of 15 prospective studies concluded that high intake of fruits, and fruits and vegetables combined, but not vegetables, is associated with a small reduction in breast cancer risk. The RR for the highest versus the lowest intake was 0.89 (95 % CI= 0.80-0.99) for fruits and vegetables combined, 0.92 (95 % CI= 0.86-0.98) for fruit alone, and 0.99 (95 % CI= 0.92-1.06) for vegetables alone.
There was no significant association found between breast cancer risk and vegetable intake, fruit intake or fruit and vegetable juice consumption in the EPIC cohort study. RR estimates (adjusted for breast cancer risk factors) for comparisons of the highest versus the lowest quintiles were 0.98 (95% CI= 0.84-1.14) for total vegetables, 1.09 (95% CI= 0.94-1.25) for total fruit and 1.05 (95% CI= 0.92-1.20) for fruit and vegetable juice.
When vegetable intake was divided into specific groupings (leafy, fruiting, root, cabbages, mushrooms and garlic and onions) there was also no evidence for a significant inverse association between intake and breast cancer risk. Adjusted RR estimates ranged from 0.98 (95% CI= 0.85-1.14) for mushrooms to 1.18 (95% CI= 1.01-1.38) for cabbage.
A meta-analysis completed in 2003 found that fruit did not provide protection against breast cancer, however this was not the case for vegetables. Increasing fruit consumption by 100 g/day (which is approximately one serve per day) had very little association with breast cancer risk (RR= 0.99, 95% CI= 0.98-1.00), whereas increasing vegetable consumption by 100 g/day did slightly lower the risk of breast cancer (RR= 0.96, 95% CI= 0.94-0.98). Case-control studies showed a protective effect of vegetables (RR= 0.86, 95% CI= 0.78-0.94), but not cohort studies (RR= 1.00, 95% CI= 0.97-1.02). Fruit consumption was not found to be significantly protective in either the pooled estimate from case-control studies (RR= 0.92, 95% CI= 0.84-1.01) or cohort studies (RR= 0.99, 95% CI= 0.98-1.00).
In a meta-analysis, total fruit and vegetable intake was not significantly associated with ovarian cancer risk. Twelve cohort studies were included in this analysis. The pooled multivariate RR comparing the highest versus the lowest quartiles of intake showed little association for total fruit (RR= 1.11, 95% CI= 0.89-1.37) and total vegetable (RR= 0.88, 95% CI= 0.71-1.09) consumption with ovarian cancer cases that occurred within the first five years.
When fruit and vegetable intake were represented as per 100 g/day (which is approximately one serve per day), the RR values for total fruits, total vegetables and total fruits and vegetables had no association with ovarian cancer. When grouped according to classes of fruit and vegetables, no statistically significant association was found. A marginally significant association with the consumption of green leafy vegetables for a 100 g increment was found (pooled multivariate RR= 0.88, 95% CI= 0.76-1.00).
The relationship between lung cancer and dietary carotenoids was investigated by analysing the primary data from seven large cohort studies in North America and Europe as part of the Pooling Project of Prospective Studies of Diet and Cancer. The intakes of five carotenoids (α-carotene β-carotene, β-cryptoxanthin, lutein and lycopene) were inversely associated with lung cancer risk. The associations were similar after adjustment for various variables but were attenuated and no longer significant after additional adjustment for smoking status, duration and quantity. Only the inverse association between β-cryptoxanthin intake and lung cancer risk remained statistically significant (RR= 0.76, 95% CI= 0.67-0.86, p <0.001). This result did not change after adjustment for intakes of vitamin C, folate, other carotenoids or multivitamin use, and was also consistent for smoking status. Therefore foods high in β-cryptoxanthin, such as orange juice, oranges and papaw, may modestly lower the risk of lung cancer.
The effect of fruit and vegetable consumption and lung cancer risk was also investigated as part of the EPIC study. There was a significant inverse association between fruit consumption and lung cancer risk, but no association was found for vegetable consumption after adjustment for age, smoking, height, weight and gender. The HR for lung cancer and fruit consumption was 0.60 (95% CI= 0.46-0.78, p value <0.01). This relationship was strengthened when lung cancers diagnosed in the first two years of follow-up were excluded from the analysis (HR= 0.50, 95% CI= 0.36-0.70). The HR for lung cancer and vegetable consumption was 1.00 (95% CI= 0.76-1.30). There was a non-significant inverse association between leafy vegetables and lung cancer risk (HR= 0.89, 95% CI= 0.66-1.19), and a non-significant positive association between cruciferous vegetables and lung cancer risk (HR= 1.21, 95% CI= 0.92-1.60).
When data was divided into smoking status (current, ex-smokers, life-long non-smokers), fruit consumption provided a significant inverse association with lung cancer for smokers (HR= 0.51, 95% CI= 0.35-0.73) and life-long non-smokers (HR= 0.33, 95% CI= 0.13-0.83). There was a small non-significant positive relationship seen for fruit consumption and lung cancer for ex-smokers (HR= 1.07, 95% CI= 0.65-1.76). Vegetable consumption appeared to have a non-significant inverse association with lung cancer for smokers (HR= 0.80, 95% CI= 0.55-1.17), little association for life-long non-smokers (HR= 0.99, 95% CI= 0.45-2.21) and a non-significant positive association for ex-smokers (HR= 1.29, 95%, CI= 0.78-2.14).
The association between fruit and vegetable intake and the risk of lung cancer was investigated as part of the Pooling Project of Prospective Studies of Diet and Cancer. Fruit consumption was highest among never smokers and lowest among current smokers. For vegetables, intakes among never and past smokers were generally similar and exceeded intakes among current smokers. Significantly reduced risks of lung cancer were observed among those with higher total fruit (RR= 0.44, 95% CI= 0.38-0.50, p trend <0.001), total vegetable (RR= 0.71, 95% CI= 0.63-0.80, p trend <0.001) and total fruit and vegetable intakes (RR= 0.48, 95% CI= 0.43-0.54, p trend <0.001) on age-adjusted analysis. This result was slightly weaker, although still significant when smoking status (never, past, current) was taken into account (RR total fruit= 0.66, 95% CI= 0.58-0.75, p trend <0.001; RR total vegetables= 0.81, 95% CI= 0.72-0.92, p trend 0.004; RR total fruit and vegetables= 0.67, 95% CI= 0.59-0.77, p trend <0.001).
In 2003, a meta-analysis found that vegetable consumption appeared to provide significant protection against lung cancer (RR= 0.89, 95% CI= 0.82-0.93) with case-control studies (RR= 0.85, 95% CI= 0.77-0.92) showing a stronger protection compared to cohort studies (RR= 0.92, 95% CI= 0.84-1.07). Fruit consumption also provided significant protection against lung cancer (RR= 0.85, 95% CI= 0.78-0.92). This was also reflected in case-control studies (RR= 0.83, 95% CI= 0.74-0.94) and cohort studies (RR= 0.86, 95% CI= 0.78-0.94). Interestingly, fruit consumption appeared to have a significant protective effect in men that was not found in women. The results for vegetables did not differ by sex.
Meta-analysis of five cohort and five case-control studies found that overall cruciferous vegetables intake was associated with a decreased risk of bladder cancer (RR= 0.80; 95% CI= 0.69-0.92), but this effect was not seen in the cohort studies analysed (RR= 0.86; 95% CI= 0.61-1.11).
A second meta-analysis indicated that fruit consumption provided significant protection against bladder cancer (RR= 0.81, 95% CI= 0.73-0.91), which was consistent across five case-control (RR= 0.82, 95% CI= 0.70-0.94) and three cohort studies (RR= 0.80, 95% CI= 0.65-0.99). Vegetable consumption showed a non-significant inverse association across all studies (RR= 0.91, 95% CI= 0.82-1.00), case-control (RR= 0.90, 95% CI= 0.78-1.03) and cohort studies (R R= 0.92, 95% CI= 0.75-1.14).
A meta-analysis of 14 studies analysing the effect of fruit and vegetable consumption on pancreatic cancer risk has demonstrated that there is no association between fruit or vegetable consumption, or total fruit and vegetable consumption and pancreatic cancer. It was noted that in most prospective studies, inverse associations were weak and imprecise due to small numbers of cases.
Meta-analysis of one cohort study and 16 case-control studies indicated a decreased risk of endometrial cancer associated with consumption of vegetables (OR=0.90 95%, CI=0.86-0.95) and cruciferous vegetables (OR=0.79 95%, CI=0.0.69-0.90), but not for fruit (OR=0.97, CI=0.92-1.02).
Potential mechanisms of action
Many possible mechanisms have been proposed to account for protection by fruit and vegetables, particularly as the terms “fruit” and “vegetable” include a broad range of foods, and fruit and vegetables contain a large range of biologically active compounds. Protective dietary components include fibre, vitamins, minerals, antioxidants and phytochemicals like carotenoids, flavonoids, isoflavonoids, allium compounds and dithiolthiones.
- helping to reduce the oxidative damage to DNA caused by free radicals;
- interacting with carcinogens e.g. reducing the formation and activation, as well as assisting with the detoxification of carcinogens; and
- altering the activity of various metabolising enzymes and affecting cellular mechanisms important in cancer development.
Table 4 provides a comprehensive list of the possible anti-carcinogenic mechanisms of nutrients found in fruit and vegetables.
|Phytochemical||Proposed mechanism||Food source|
|Vitamins C and E, carotenoids, polyphenols||Antioxidant protection against oxidative damage to DNA, cellular macromolecules and membranes.||Fruit and vegetables generally: especially yellow and orange; citrus fruit; berries.|
|Dithiolthiones, isothiocyanates, allium compounds||Increases Type II detoxifying enzymes (e.g. glutathione S transferase).||Cruciferous vegetables:|
broccoli, cauliflower, cabbage, brussel sprouts, kohlrabi; allium vegetables: onions, leeks, chives.
|Vitamin C, allium compounds||Reduces bacterial formation of nitrosamines from nitrate in stomach. Decreases Type 1 activating enzymes (e.g. aryl hydroxylase).||All fruit and vegetables (Vitamin C) particularly:|
blackcurrants, guava, citrus, kiwi fruit, broccoli, sprouts; allium vegetables: onions, leeks, chives.
|Folic acid||Preserve integrity of DNA and ensure optimum DNA methylation.||Green leafy vegetables; avocado; oranges.|
|Carotenoids, flavonoids||Induction of cell differentiation.||Yellow/orange fruits and vegetables:|
carrots, sweet potato, mango, pumpkin, red capsicum, rockmelon, paw paw, tomato;
Dark green vegetables:
silverbeet, spinach, broccoli, dark green lettuce, Chinese greens (e.g. bok choy), kale, parsley, basil.
|Soluble fibre, resistant starch||Decreases concentrations of secondary bile acids, which modify the enzyme activities of intestinal bacteria.
Fermentation, which produces short-chain fatty acids that may inhibit carcinogenesis via effects on colonic pH and increased availability of butyrate.
|All fruits and vegetables (including legumes) particularly:|
Soluble fibre such as dried apricots, dried figs, prunes, quince, okra, cabbage, carrot, broccoli, leeks, brussel sprouts, beetroot, lychees, peas, mulberries, asparagus, lemons, oranges, swede, parsnip, dates, plums.
Resistant starch such as corn, bananas, peas, potato, sweet potato, broad beans.
|Insoluble fibre||Dilutes carcinogens by increasing faecal bulking.
Reduces interaction of carcinogens with mucosal cells by increasing stool transit time.
|All fruits and vegetables, particularly:|
guava, quince, peas, dried figs, corn, broad beans, berries, dates, pears, prunes, cabbage, spinach , pineapple, broccoli, onion, leek, asparagus, turnip, swede, beetroot, squash, brussel sprouts, okra, carrots, pumpkin, rhubarb, green beans.
|Cancer Council supports the Australian Dietary Guidelines that recommend eating plenty of fruit and vegetables. Because knowledge is still incomplete about the ways in which phytochemicals may reduce cancer risk and their potential relevance to specific tissues and to particular stages of cancer development, Cancer Council also recommends that people eat a variety of different fruit and vegetables to obtain maximum benefits.
In defining the variety of fruits and vegetables to recommend, attention should be paid to their phytochemical content as well as to the epidemiological evidence concerning their protective potential. On this basis fruits should include citrus fruits, coloured fruits (especially red, yellow and orange) and berries, while vegetables should include cruciferous and allium types, dark-green leafy vegetables and red/yellow/orange vegetable types. The value of eating raw and cooked vegetables instead of taking dietary supplements has been repeatedly shown. Therefore both cooked and raw vegetables should be recommended in a cancer protective diet.
The definitions for fruit in many studies include fruit juices. The cancer protective phytochemicals are preserved in fresh fruit and vegetable juices and some phytochemicals may be more bioavailable in juices rather than whole fruits and vegetables. However the fibre is removed in most vegetable and fruit juices and also in dietary supplements, and fibre is thought to be protective against bowel cancer. Therefore fruit and vegetables are best consumed whole, rather than as a juice or individual nutrients in a supplement form. As well, studies suggest that antioxidant supplements are not protective and may in fact increase overall mortality.
How much fruit and vegetables should we be eating?
The population recommendation of at least two serves of fruit and five serves of vegetables daily is appropriate for cancer prevention. For many Australians, this means doubling their current intake. Table 5 shows examples of a serve of fruit and vegetables, as specified in the Australian Dietary Guidelines.
Table 5. Sample fruit and vegetable serving sizes in the Australian Dietary Guidelines
|Fruit||1 serve equals:
|Vegetables||1 serve equals:
As stated in the 2007 WCRF/AICR review, there is no convincing evidence that higher intakes of fruit and vegetables are harmful, and almost all findings are to the contrary. Protection is often, but not always, found in the upper quartile or quintile of consumption, which in many studies equates approximately to the recommended two to three servings of fruit and four to five servings of vegetables.
Because some of the proposed mechanisms for how fruit and vegetables protect against cancer work at the early stages of cancer development and initiation, and most cancers develop over many years, it is important that a protective diet begins in childhood and extends into adulthood.
In addition to their anti-carcinogenic activity, fruit and vegetables play an important role in weight regulation due to their low energy density and fibre content. As obesity emerges as a major risk factor for several cancers, the importance of fruit and vegetables will continue to strengthen.
Current Australian consumption levels
The 2011–2012 National Nutrition and Physical Activity Survey (NNPAS) found that, while 75% of Australians report eating vegetables, only 6.8% consumed the recommended usual intake of vegetables. The group least likely to eat the recommended number of serves of vegetables was men aged 19–30 years (1.6%). Just over half (54%) of Australians consumed the recommended serves of fruit with females (58%) more likely than males (50%) to meet the recommendation.
These statistics mirror results from the 2007–08 National Health Survey which found that 93% of Australian adults did not consume the two serves of fruit and five serves of vegetables per day recommended in the NHMRC Dietary Guidelines for Australian Adults. While 56% of females aged 15 and over, and 46% of males aged 15 and over in Australia met the recommended daily intake of fruit, only 10% of females and 7% of males met the recommended daily intake of vegetables.
In 2011, 52% of adults in NSW consumed two or more serves of fruit each day and 9% of adults reported consuming five or more serves of vegetables each day. Both proportions were lower in males than females.
The 2011–2012 NNPAS found that children aged 2–3 years were the age group most likely to meet requirements, however only half (49%) usually consume the recommended number of servings per day. Children aged 2–8 years had the highest rate of fruit consumption and were most likely to met daily requirements for fruit consumption.
This mirrors earlier data showing that vegetable consumption was highest among children ages 4–8 years, with 22% of children in this age group meeting consumption levels recommended in the NHMRC dietary guidelines. And data showing that fruit and vegetable consumption drops steeply in older children.
The barriers to consuming fruit and vegetables include high prices (especially of fruit), time taken to prepare vegetables, inadequate supply and quality, concerns about pesticides, and social and domestic household changes which result in less time being available to prepare food. Concerns about pesticides are almost certainly unwarranted as Australian produce consistently shows low levels of chemical residues and contaminants, which are well below acceptable safety limits.
There are a small number of studies indicating that diet may play a role in preventing cancer progression and recurrence in people who already have cancer, however intervention studies with cancer end-points are few in number and further research is needed before definitive dietary advice can be given to cancer patients.
For more information, see the Cancer Council Australia position statement: Benefits of healthy diet and physical activity for cancer survivors.
Organic fruit and vegetables
Organic foods are produced without using synthetic chemicals such as pesticides, fertilisers, hormones and antibiotics or genetic modification. There is also an emphasis on appropriate land management and use of renewable resources and conservation practices. Reasons why people choose organic fruits and vegetables include reduced environmental impact, avoidance of genetic modification, better flavour and taste, perceived health benefits or just personal preference. However organic foods are more expensive than conventional foods, and there is also potentially higher wastage due to a shorter shelf life of some products.
It is difficult to measure accurately the nutritional content of organic versus conventionally grown food due to the variables that affect the end product. Such variables include types of fertilisers used, soil types, harvesting methods, transport and storage. However it appears that organic produce may provide higher levels of vitamin C and lower nitrate levels compared with conventionally produced fruits and vegetables.
Presently there is no evidence to suggest that organic fruit and vegetables are more effective in reducing cancer risk than conventionally grown fruit and vegetables. Therefore the consumption of all fruits and vegetables should be encouraged, whether they are organic or not. The consumption of organic fruit and vegetables are an individual’s choice. It is recommended that all fruits and vegetables be washed and peeled where appropriate to remove possible pesticide residue and possible microbial growth.
More studies are needed on the association between fruit, vegetables and cancer risk. In the future, there is a need for more studies that:
- Are prospective and include a very large follow-up period;
- Examine the reasons for differences seen between cohort and case-control study results;
- For certain cancers, investigate further the difference in risk for men and women;
- Explore the risk associated with sub-groups of fruit and vegetables e.g. citrus fruit, green leafy vegetables, cruciferous vegetables;
- Consider broad dietary patterns e.g. those that eat small amounts of fruit and vegetables may also eat small amounts of dietary fibre;
- Investigate ways in which individual phytochemicals may reduce cancer risk;
- Examine whether fruit and vegetables play a role in preventing cancer progression and recurrence in people who already have cancer; and
- Identify intermediate biomarkers that are suitable for inferring cancer outcomes or use the molecular profile of certain cancers (e.g. bowel) as endpoints in order to help clarify inconsistent results in the literature.
Position statement details
This position statement was reviewed and approved by the Public Health Committee August 2007 and updated November 2014.
This position statement was reviewed by:
- Bruce Armstrong
- Finlay Macrae
- Vicki Flood
- Simone Lee
- Freddy Sitas
- Carla Saunders
- National Health and Medical Research Council. Australian dietary guidelines. Canberra: NHMRC; 2013 Available from: http://www.nhmrc.gov.au/_files_nhmrc/publications/attachments/n55_australian_dietary_guidelines_130530.pdf.
- Vainio H, Bianchini F. IARC monographs on the evaluation of carcinogenic risks to humans, volume 6. Weight control and physical activity. Lyon: International Agency for Research on Cancer; 2002 Available from: http://www.iarc.fr/en/publications/pdfs-online/prev/handbook6/Handbook6-0.pdf.
- World Cancer Research Fund, American Institute for Cancer Research. Food, nutrition, physical activity, and the prevention of cancer: a global perspective. Washington DC: AICR; 2007.
- World Health Organization, Food and Agriculture Organization. Diet, nutrition and the prevention of chronic diseases. Geneva, Switzerland: WHO; 2003. Report No.: WHO technical report series 916. Available from: http://apps.who.int/iris/bitstream/10665/42665/1/WHO_TRS_916.pdf.
- International Agency for Research on Cancer. IARC handbooks on cancer prevention, vol. 8: Fruit and vegetables. Lyon: IARC; 2002.
- Begg S, Vos T, Barker B, Stevenson C, Stanley L, Lopez AD. The burden of disease and injury in Australia 2003. Canberra: AIHW; 2007. Report No.: Cat. no. PHE 82. Available from: http://www.aihw.gov.au/publication-detail/?id=6442467990.
- Marks GC, Pang G, Coyne T, Picton P. Cancer costs in Australia - the potential impact of dietary change. Canberra: Australian Food and Nutrition Monitoring Unit, Commonwealth Department of Health and Aged Care; 2001 Available from: http://www.health.gov.au/internet/main/publishing.nsf/Content/F660EB8C551A8578CA256F190004C4EC/$File/cancercosts.pdf.
- World Cancer Research Fund, American Institute for Cancer Research. Policy and action for cancer prevention. Food, nutrition, and physical activity: a global perspective. Washington DC: AICR; 2009 Available from: http://www.dietandcancerreport.org/cancer_resource_center/downloads/chapters/pr/Introductory%20pages.pdf.
- World Cancer Research Fund International. Continuous Update Project Report: Diet, Nutrition, Physical Activity, and Prostate Cancer. World Cancer Research Fund International; 2014 Available from: http://www.wcrf.org/sites/default/files/Prostate-Cancer-2014-Report.pdf.
- International Agency for Research on Cancer. IARC handbook of Cancer Prevention, volume 9: cruciferous vegetables, isothiocyanates and indoles. Lyon: IARC; 2004.
- World Cancer Research Fund, American Institute for Cancer Research. Summary: food nutrition and the prevention of cancer: a global perspective. Washington, DC: AICR; 1997.
- Nutritional aspects of the development of cancer. Report of the Working Group on Diet and Cancer of the Committee on Medical Aspects of Food and Nutrition Policy. Rep Health Soc Subj (Lond) 1998;48:i-xiv, 1-274 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/9599404].
- Khaw KT, Bingham S, Welch A, Luben R, Wareham N, Oakes S, et al. Relation between plasma ascorbic acid and mortality in men and women in EPIC-Norfolk prospective study: a prospective population study. European Prospective Investigation into Cancer and Nutrition. Lancet 2001 Mar 3;357(9257):657-63 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/11247548].
- Hung HC, Joshipura KJ, Jiang R, Hu FB, Hunter D, Smith-Warner SA, et al. Fruit and vegetable intake and risk of major chronic disease. J Natl Cancer Inst 2004 Nov 3;96(21):1577-84 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/15523086].
- Pavia M, Pileggi C, Nobile CG, Angelillo IF. Association between fruit and vegetable consumption and oral cancer: a meta-analysis of observational studies. Am J Clin Nutr 2006 May;83(5):1126-34 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/16685056].
- Riboli E, Norat T. Epidemiologic evidence of the protective effect of fruit and vegetables on cancer risk. Am J Clin Nutr 2003 Sep;78(3 Suppl):559S-569S [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/12936950].
- Liu J, Wang J, Leng Y, Lv C. Intake of fruit and vegetables and risk of esophageal squamous cell carcinoma: a meta-analysis of observational studies. Int J Cancer 2013 Jul 15;133(2):473-85 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/23319052].
- González CA, Pera G, Agudo A, Bueno-de-Mesquita HB, Ceroti M, Boeing H, et al. Fruit and vegetable intake and the risk of stomach and oesophagus adenocarcinoma in the European Prospective Investigation into Cancer and Nutrition (EPIC-EURGAST). Int J Cancer 2006 May 15;118(10):2559-66 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/16380980].
- Wu QJ, Yang Y, Wang J, Han LH, Xiang YB. Cruciferous vegetable consumption and gastric cancer risk: a meta-analysis of epidemiological studies. Cancer Sci 2013 Aug;104(8):1067-73 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/23679348].
- Lunet N, Lacerda-Vieira A, Barros H. Fruit and vegetables consumption and gastric cancer: a systematic review and meta-analysis of cohort studies. Nutr Cancer 2005;53(1):1-10 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/16351501].
- Zhou Y, Zhuang W, Hu W, Liu GJ, Wu TX, Wu XT. Consumption of large amounts of Allium vegetables reduces risk for gastric cancer in a meta-analysis. Gastroenterology 2011 Jul;141(1):80-9 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/21473867].
- Bae JM, Lee EJ, Guyatt G. Citrus fruit intake and stomach cancer risk: a quantitative systematic review. Gastric Cancer 2008;11(1):23-32 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/18373174].
- Yang T, Yang X, Wang X, Wang Y, Song Z. The role of tomato products and lycopene in the prevention of gastric cancer: a meta-analysis of epidemiologic studies. Med Hypotheses 2013 Apr;80(4):383-8 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/23352874].
- Koushik A, Hunter DJ, Spiegelman D, Beeson WL, van den Brandt PA, Buring JE, et al. Fruits, vegetables, and colon cancer risk in a pooled analysis of 14 cohort studies. J Natl Cancer Inst 2007 Oct 3;99(19):1471-83 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/17895473].
- Aune D, Lau R, Chan DS, Vieira R, Greenwood DC, Kampman E, et al. Nonlinear reduction in risk for colorectal cancer by fruit and vegetable intake based on meta-analysis of prospective studies. Gastroenterology 2011 Jul;141(1):106-18 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/21600207].
- Schatzkin A, Lanza E, Corle D, Lance P, Iber F, Caan B, et al. Lack of effect of a low-fat, high-fiber diet on the recurrence of colorectal adenomas. Polyp Prevention Trial Study Group. N Engl J Med 2000 Apr 20;342(16):1149-55 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/10770979].
- Park Y, Subar AF, Kipnis V, Thompson FE, Mouw T, Hollenbeck A, et al. Fruit and vegetable intakes and risk of colorectal cancer in the NIH-AARP diet and health study. Am J Epidemiol 2007 Jul 15;166(2):170-80 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/17485731].
- Liu B, Mao Q, Cao M, Xie L. Cruciferous vegetables intake and risk of prostate cancer: a meta-analysis. Int J Urol 2012 Feb;19(2):134-41 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/22121852].
- Etminan M, Takkouche B, Caamaño-Isorna F. The role of tomato products and lycopene in the prevention of prostate cancer: a meta-analysis of observational studies. Cancer Epidemiol Biomarkers Prev 2004 Mar;13(3):340-5 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/15006906].
- Rao AV. Processed tomato products as a source of dietary lycopene: bioavailability and antioxidant properties. Can J Diet Pract Res 2016 Jul 29;65(4):161-5 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/15596034].
- European Prospective Investigation into Cancer and Nutrition (EPIC), Key TJ, Allen N, Appleby P, Overvad K, Tjønneland A, et al. Fruits and vegetables and prostate cancer: no association among 1104 cases in a prospective study of 130544 men in the European Prospective Investigation into Cancer and Nutrition (EPIC). Int J Cancer 2004 Mar;109(1):119-24 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/14735477].
- Liu X, Lv K. Cruciferous vegetables intake is inversely associated with risk of breast cancer: a meta-analysis. Breast 2013 Jun;22(3):309-13 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/22877795].
- Aune D, Chan DS, Vieira AR, Rosenblatt DA, Vieira R, Greenwood DC, et al. Fruits, vegetables and breast cancer risk: a systematic review and meta-analysis of prospective studies. Breast Cancer Res Treat 2012 Jul;134(2):479-93 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/22706630].
- van Gils CH, Peeters PH, Bueno-de-Mesquita HB, Boshuizen HC, Lahmann PH, Clavel-Chapelon F, et al. Consumption of vegetables and fruits and risk of breast cancer. JAMA 2005 Jan 12;293(2):183-93 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/15644545].
- Koushik A, Hunter DJ, Spiegelman D, Anderson KE, Arslan AA, Beeson WL, et al. Fruits and vegetables and ovarian cancer risk in a pooled analysis of 12 cohort studies. Cancer Epidemiol Biomarkers Prev 2005 Sep;14(9):2160-7 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/16172226].
- Männistö S, Smith-Warner SA, Spiegelman D, Albanes D, Anderson K, van den Brandt PA, et al. Dietary carotenoids and risk of lung cancer in a pooled analysis of seven cohort studies. Cancer Epidemiol Biomarkers Prev 2004 Jan;13(1):40-8 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/14744731].
- Manzi F, Flood V, Webb K, Mitchell P. The intake of carotenoids in an older Australian population: The Blue Mountains Eye Study. Public Health Nutr 2002 Apr;5(2):347-52 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/12020387].
- Miller AB, Altenburg HP, Bueno-de-Mesquita B, Boshuizen HC, Agudo A, Berrino F, et al. Fruits and vegetables and lung cancer: Findings from the European Prospective Investigation into Cancer and Nutrition. Int J Cancer 2004 Jan 10;108(2):269-76 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/14639614].
- Smith-Warner SA, Spiegelman D, Yaun SS, Albanes D, Beeson WL, van den Brandt PA, et al. Fruits, vegetables and lung cancer: a pooled analysis of cohort studies. Int J Cancer 2003 Dec 20;107(6):1001-11 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/14601062].
- Liu B, Mao Q, Lin Y, Zhou F, Xie L. The association of cruciferous vegetables intake and risk of bladder cancer: a meta-analysis. World J Urol 2013 Feb;31(1):127-33 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/22391648].
- Koushik A, Spiegelman D, Albanes D, Anderson KE, Bernstein L, van den Brandt PA, et al. Intake of fruits and vegetables and risk of pancreatic cancer in a pooled analysis of 14 cohort studies. Am J Epidemiol 2012 Sep 1;176(5):373-86 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/22875754].
- Bandera EV, Kushi LH, Moore DF, Gifkins DM, McCullough ML. Fruits and vegetables and endometrial cancer risk: a systematic literature review and meta-analysis. Nutr Cancer 2007;58(1):6-21 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/17571962].
- Greenwald P, Clifford CK, Milner JA. Diet and cancer prevention. Eur J Cancer 2001 May;37(8):948-65 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/11334719].
- Talalay P, Fahey JW. Phytochemicals from cruciferous plants protect against cancer by modulating carcinogen metabolism. J Nutr 2001 Nov;131(11 Suppl):3027S-33S [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/11694642].
- Heber D. Vegetables, fruits and phytoestrogens in the prevention of diseases. J Postgrad Med 2004 Apr;50(2):145-9 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/15235216].
- Johnson IT. Micronutrients and cancer. Proc Nutr Soc 2004 Nov;63(4):587-95 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/15831131].
- Smith TA. Carotenoids and cancer: prevention and potential therapy. Br J Biomed Sci 1998 Dec;55(4):268-75 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/10436544].
- National Health and Medical Research Council. Nutrient reference values for Australia and New Zealand including recommended dietary intakes. Canberra: NHMRC; 2006 Available from: http://www.nhmrc.gov.au/_files_nhmrc/publications/attachments/n35.pdf.
- Englyst HN, Cummings JH. Improved method for measurement of dietary fiber as non-starch polysaccharides in plant foods. J Assoc Off Anal Chem 1988 Jul;71(4):808-14 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/2458334].
- Record S. Personal communication on resistant starch. CSIRO Australia; 2002.
- Link LB, Potter JD. Raw versus cooked vegetables and cancer risk. Cancer Epidemiol Biomarkers Prev 2004 Sep;13(9):1422-35 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/15342442].
- Helser MA, Hotchkiss JH, Roe DA. Influence of fruit and vegetable juices on the endogenous formation of N-nitrosoproline and N-nitrosothiazolidine-4-carboxylic acid in humans on controlled diets. Carcinogenesis 1992 Dec;13(12):2277-80 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/1473234].
- Xu GP, Song PJ, Reed PI. Effects of fruit juices, processed vegetable juice, orange peel and green tea on endogenous formation of N-nitrosoproline in subjects from a high-risk area for gastric cancer in Moping County, China. Eur J Cancer Prev 1993 Jul;2(4):327-35 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/8358285].
- McEligot AJ, Rock CL, Shanks TG, Flatt SW, Newman V, Faerber S, et al. Comparison of serum carotenoid responses between women consuming vegetable juice and women consuming raw or cooked vegetables. Cancer Epidemiol Biomarkers Prev 1999 Mar;8(3):227-31 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/10090300].
- Steinmetz KA, Potter JD. Vegetables, fruit, and cancer prevention: a review. J Am Diet Assoc 1996 Oct;96(10):1027-39 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/8841165].
- European Prospective Investigation into Cancer and Nutrition, Bingham SA, Day NE, Luben R, Ferrari P, Slimani N, et al. Dietary fibre in food and protection against colorectal cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC): an observational study. Lancet 2003 May 3;361(9368):1496-501 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/12737858].
- Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C. Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis. JAMA 2007 Feb 28;297(8):842-57 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/17327526].
- National Health and Medical Research Council. Australian Guide to Healthy Eating. Canberra: NHMRC; 2013 Jan 13 Available from: http://www.nhmrc.gov.au/_files_nhmrc/publications/attachments/n55i_australian_guide_to_healthy_eating.pdf.
- Australian Bureau of Statistics. Australian Health Survey: Nutrition First Results - Foods and Nutrients, 2011-12. Canberra: ABS; 2014 May 9. Report No.: 4364.0.55.007. Available from: http://www.abs.gov.au/ausstats/abs@.nsf/mf/4364.0.55.007?OpenDocument.
- Australian Bureau of Statistics. National Health Survey: summary of results (re-issue), 2007-08. ABS cat. no. 4364.0. Canberra: ABS; 2009.
- Australian Bureau of Statistics. National health survey 2007-2008: summary of results. Canberra: ABS; 2009. Report No.: 4364.0. Available from: http://www.abs.gov.au/AUSSTATS/abs@.nsf/mf/4364.0.
- Centre for Epidemiology and Research. 2010 report on adult health from the New South Wales population health survey. Sydney: NSW Department of Health; 2011 Available from: http://www0.health.nsw.gov.au/resources/publichealth/surveys/pdf/hsa_10pub.pdf.
- Commonwealth Scientific Industrial Research Organisation, Preventative Health National Research Flagship, University of South Australia. 2007 Australian National Children’s Nutrition and Physical Activity Survey - main findings. Canberra: Commonwealth of Australia; 2008 Available from: http://www.health.gov.au/internet/main/publishing.nsf/content/66596E8FC68FD1A3CA2574D50027DB86/$File/childrens-nut-phys-survey.pdf.
- Cox DN, Beaumont-Smith N, Baghurst K. An issues paper on barriers to the consumption of vegetables and fruits. Canberra: Commonwealth Department of Health and Aged Care; 1999.
- Food Standards Australia New Zealand. The 23rd Australian Total Diet Study. Canberra: FSANZ. 2011. Canberra: FSANZ; 2011 Available from: http://www.foodstandards.gov.au/publications/documents/FSANZ%2023rd%20ATDS_v8_.pdf.
- Davies AA, Davey Smith G, Harbord R, Bekkering GE, Sterne JA, Beynon R, et al. Nutritional interventions and outcome in patients with cancer or preinvasive lesions: systematic review. J Natl Cancer Inst 2006 Jul 19;98(14):961-73 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/16849679].
- Williams CM. Nutritional quality of organic food: shades of grey or shades of green? Proc Nutr Soc 2002 Feb;61(1):19-24 [Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/12002790].