Position statement - Meat and cancer prevention
The term ‘meat’ encompasses a variety of foods, including unprocessed red meat, processed meat, poultry and fish. Unprocessed red meat generally includes beef, veal, pork, mutton and lamb, and processed meat refers to sausages, smoked, cured and salted meats (such as frankfurts, salami, bacon and ham), and canned meats. Processed meat is sometimes referred to as preserved meat.
Australian food regulations define processed meat as a meat product containing not less than 30% meat, where meat either on its own or in combination with other ingredients or additives, has undergone a method of processing other than boning, slicing, dicing, mincing, or freezing. This includes manufactured meat and cured and/or dried meat.
Processed meat differs from unprocessed red meat, in that it may be cured with the addition of preservatives (salt, nitrite or smoke) and/or other additives (phosphate, glutamate or ascorbic acid). Therefore it is possible that the role of unprocessed and processed red meat in carcinogenesis may differ.
The National Health and Medical Research Council dietary guidelines provide recommendations for meat and poultry, grouped along with fish, eggs, tofu, nuts, seeds and legumes. While the guidelines outline the recommended daily intake of food from this grouping, they do not provide advice on the recommended amount of red meat or poultry specifically. The recommended minimum daily intake for food in this group is 2–2½ servings for women and 2½–3 servings for men. One serve is equivalent to
65 g cooked lean red meat, 80 g cooked poultry, 100 g cooked fish, or various amounts of the alternatives within this group.
The guidelines also recommend limiting consumption of foods high in saturated fat, including pies, processed meats and commercial burgers, among other foods.
Lean red meat is an important source of dietary iron, zinc, vitamin B12 and protein in the Australian diet. However, epidemiological evidence suggests that there is a relationship between red and processed meats, and cancer risk. The World Cancer Research Fund (WCRF) estimate that in the UK, 5% of bowel cancer is attributable to high red meat intake, and 10% of bowel cancer is attributable to high intake of processed meat. A recent Australian study estimated that 2,614 cases (18%) of bowel cancers diagnosed in 2010 were attributable to the consumption of red and processed meat.
Major cancer prevention reports have stated that there is convincing evidence that red and processed meat increase the risk of bowel cancer. This position statement summarises the evidence for a relationship between meat consumption and cancer risk.
Views on meat in cancer prevention reports
In 2007, an extensive review on diet and cancer conducted by WCRF found that red meat and processed meat convincingly increased the risk of bowel cancer. Red meat had limited suggestive evidence of an increased risk of oesophageal, lung, pancreatic and endometrial cancer, and likewise, processed meat had limited suggestive evidence of an increased risk of oesophageal, lung, stomach and prostate cancer.
WCRF also found that consumption of grilled or barbecued animal foods was associated with a limited suggestive increased risk of stomach cancer, and that foods containing iron had a limited suggestive increased association with colorectal cancer risk.
WCRF found that the evidence for an association between poultry consumption and cancer risk was too limited in amount, consistency or quality to draw any conclusions.
See Table 1 for a summary of findings from major cancer prevention reports.
Table 1. Conclusions from the major reviews of the epidemiological literature regarding red and processed meat intake and increased cancer risk
|Organisation Review||Meat||Highest Evidence Convincing||Moderate Evidence Probable||Lower Evidence Possible / Limited|
A 2003 expert report by the World Health Organization (WHO) and Food and Agriculture Organisation advised those who are not vegetarian to consume moderate amounts of preserved meat (e.g. sausages, salami, bacon and ham).
A number of meta-analyses have investigated the link between total meat consumption and bowel cancer risk. A summary of the findings of studies investigating the impact of total meat intake is available in Table 2.
Table 2. Relative risk of bowel cancer with high intake of red and processed meat
|Study||n||RR (95% CI)|
|Magalhães et al. 2012||16||1.29 (1.13-1.48) colon|
|1.13 (0.92-1.39) rectal|
|Chan et al. 2011||13||1.22 (1.11-1.34)|
|Norat et al. 2002||24||1.14 (0.99–1.31)|
n = number of studies, RR = relative risk, CI = confidence interval
A 2012 meta-analysis of dietary patterns and cancer risk found that a ‘western’ diet, characterised by high red/processed meat consumption was associated with colon cancer (relative risk (RR)= 1.29, 95% confidence interval (CI)= 1.13-1.48), but not rectal cancer (RR= 1.13, 95% CI= 0.92-1.39).
A 2011 meta-analysis of 13 studies found that high intake or red and processed meats was associated with an increased risk of colorectal (RR= 1.22, 95% CI= 1.11−1.34), colon (RR= 1.19, 95% CI = 1.06−1.34), and rectal cancer (RR= 1.51, 95% CI= 1.31−1.75). This effect was seen to be dose-responsive with risk increasing with the amount of meat consumed.
A 2002 meta-analysis of 24 studies found that high intake of total meat was not significantly associated with an increased risk of bowel cancer (RR= 1.14, 95% CI= 0.99–1.31).
Results from 2005 from the European Prospective Investigation into Cancer and Nutrition (EPIC) study found that high combined intake of red and processed meat was associated with an increased risk of bowel cancer in a dose-responsive manner (hazard ratio (HR)= 1.55, 95% CI= 1.19–2.02) per 100 g/day increase.
Studies of the association between red meat and bowel cancer have reported varying levels of risk. A summary of meta-analyses investigating the link between high intake of red meat and bowel cancer can be found in Table 3.
Table 3. Relative risk of bowel cancer with high intake of red meat
|Study||n||RR (95% CI)|
|Smolińska and Paluszkiewicz 2012||22||1.37 (1.09–1.71) colon|
|1.43 (1.24–1.64) rectal|
|Chan et al. 2011||16||1.10 (1.00−1.21|
|Alexander et al. 2011||25||1.12 (1.04-1.21)|
|Larsson and Wolk 2006||15||1.28 (1.15-1.42)|
|Norat et al. 2002||23||1.35 (1.21–1.51)|
n = number of studies, RR = relative risk, CI = confidence interval
A 2012 meta-analysis of 22 studies assessed the effect of high red meat consumption (>50 g/day) on bowel cancer risk. There was an increased risk of colon cancer (RR= 1.21, 95% CI 1.07-1.37) but not rectal cancer (RR= 1.30, 95% CI 0.90-1.89). For very high intake, consumption more than once daily, there was an increased risk of both colon (RR= 1.37 1.09-1.71) and rectal (RR= 1.43 1.24-1.64) cancer.
A 2011 meta-analysis of 16 studies found that high intake of red meat increased the risk of colon cancer (RR= 1.18, 95% CI= 1.04−1.35), but not colorectal (RR= 1.10, 95% CI = 1.00-1.21) or rectal cancer (RR= 1.14, 95% CI= 0.83−1.56). However, in a dose-response analysis an increase of 100 g red meat/day was statistically significantly associated with increased risk of colorectal (RR= 1.17, 95% CI= 1.05−1.31) as well as colon cancer (RR= 1.17, 95% CI= 1.02-1.33).
A 2011 meta-analysis of 25 prospective studies found that high intake of red meat was associated with a small but significant increase in the risk of colorectal cancer (RR= 1.12, 95% CI= 1.04-1.21) and colon cancer (RR= 1.11, 95% CI= 1.03-1.19), but not rectal cancer (RR= 1.19, 95% CI= 0.97-1.46). The association was only seen in males.
A2006 meta-analysis of 15 studies on red meat consumption and bowel cancer found that high intake was associated with increased risk (RR= 1.28, 95% CI= 1.15-1.42). The association was stronger for rectal cancer (RR= 1.56, 95% CI= 1.25-1.95) than for colon cancer (RR= 1.21, 95% CI= 1.05-1.40). The association for both was dose responsive, with risk increasing with amount consumed.
A 2002 meta-analysis of 23 studies found that red meat was associated with an increased risk of bowel cancer (RR= 1.35, 95% CI= 1.21–1.51). This association was dose-responsive. Results were similar for colon (RR= 1.32, 95% CI= 1.18-1.48) and rectal cancer (RR= 1.36, 95% CI= 1.17-1.57).
Results from 2005 from the EPIC study found that high intake of red meat was not significantly associated with increased risk of bowel cancer in a dose-responsive manner (HR= 1.49, 95% CI= 0.91–2.43) per 100 g/day increase.
Meta-analysis has determined that high red meat consumption is also associated with increased risk of bowel adenoma (RR= 1.24, 95% CI= 1.12-1.36).
A number of meta analyses have been conducted to investigate the link between high intake of processed meats and bowel cancer risk. A summary of findings can be found in Table 4. Over all, high intake of processed meats is associated with an increased risk of bowel cancer.
Table 4. Relative risk of bowel cancer with high intake of red meat
|Study||n||RR (95% CI)|
|Chan et al. 2011||18||1.17 (1.09−1.25)|
|Alexander et al 2010||20||1.16 (1.10-1.23)|
|Larsson and Wolk 2006||14||1.20 ( 1.11-1.31)|
|Norat et al. 2002||23||1.31 (1.13–1.51)|
n = number of studies, RR = relative risk, CI = confidence interval
A 2011 meta-analysis of 18 studies found that high intake of processed meats increased the risk of colorectal (RR= 1.17, 95% CI= 1.09−1.25), colon (RR= 1.19, 95% CI= 1.11−1.29), and rectal cancer (RR= 1.19, 95% C = 1.02−1.39) in a dose responsive manner. The association was dose-responsive for colorectal and colon cancer, but not for rectal cancer.
A 2010 meta-analysis of 20 studies found that high intake of processed meat is associated with increased risk of bowel cancer (RR= 1.16, 95% CI= 1.10-1.23). The association was only significant in males.
A 2006 meta-analysis of 14 studies on red processed consumption and bowel cancer found that high intake was associated with increased risk (RR= 1.20, 95% CI= 1.11-1.31). The association was seen for colon and rectal cancer and was dose responsive, with risk increasing with amount consumed.
A 2002 meta-analysis of the association between processed meat and bowel cancer found evidence of an increased risk with high intake of processed meats (RR= 1.31, 95% CI= 1.13–1.51). The association was significant for colon cancer (RR= 1.22, 95% CI= 1.06-1.39) but not for rectal cancer (RR= 1.21, 95% CI= 0.98-1.50). The risk of bowel cancer was higher for males (RR= 1.57, 95% CI= 1.27-1.93) and was not significant in females (RR= 1.17, 95% CI= 0.95-1.44).
Results from 2005 from the EPIC study found that high intake of processed meat was associated with increased risk of bowel cancer. This association was found to be dose responsive (HR= 1.70, 95% CI= 1.05–2.76) per 100 g/day increase.
Meta-analysis has determined that high processed meat consumption is also associated with increased risk of bowel adenoma (RR= 1.17, 95% CI= 1.08-1.26).
In 2005, the EPIC study showed that poultry consumption was associated with a non-statistically significant reduced risk of bowel cancer (HR= 0.92, 95% CI= 0.76-1.12), colon cancer (HR= 0.89, 95% CI= 0.70-1.13) and rectal cancer (HR= 0.99, 95% CI= 0.71-1.37).
In the EPIC study, fish consumption was associated with a statistically significant reduced risk of bowel cancer (HR= 0.69, 95% CI= 0.54-0.88) and rectal cancer (HR= 0.49, 95% CI= 0.32-0.76), and a non-significant reduced risk of colon cancer (HR= 0.82, 95% CI= 0.60-1.11). The results for fish intake were surprising considering the exposure included both salted and smoked fish, which have been shown to independently increase the risk of some cancers.
A systematic literature review in 2006 found that fish intake was associated with a decreased risk of rectal cancer in case-control studies (pooled odds ratio (OR)= 0.68, 95% CI= 0.48-0.96). A non-significant negative association was found between fish intake and colon cancer in cohort (OR= 0.95, 95% CI= 0.66-1.39) and case-control studies (OR= 0.86, 95% CI= 0.63-1.17), while a small negative association was seen between fish intake and bowel cancer in cohort (OR= 0.95, 95% CI= 0.71-1.28) and case-control studies (OR= 0.99, 95% CI= 0.49-2.03).
A 2006 systematic review found that one out of two cohort studies showed a positive relationship between red meat intake and oesophageal cancer risk. Eighteen case-control studies have investigated meat intake and oesophageal cancer risk, with 11 studies finding a positive association. For processed meat, no cohort studies have reported results for oesophageal cancer. Eight out of nine case-control studies found a positive association between processed meat intake and oesophageal cancer risk.
A 2006 meta-analysis found that high intake of processed meat found increased the risk of stomach cancer. This effect was stronger in case-control studies (RR= 1.63, 95% CI= 1.31-2.01) and was not significant in cohort studies (RR= 1.24, 95% CI= 0.98-1.56). For individual processed meats (bacon, sausage and ham) the results were consistent, with studies showing a positive association between high versus low intake of all individual processed meats and the risk of stomach cancer. A dose-response analysis found that the risk of stomach cancer increased when processed meat consumption increased by 30 g per day for both cohort (RR= 1.15, 95% CI= 1.04-1.27) and case-control (RR= 1.38, 95% CI= 1.19-1.60) studies.
A 2006 systematic review found that two out of three cohort studies showed a positive relationship between red meat intake and stomach cancer risk. In addition, 11 out of 16 case-control studies found a positive association between meat intake and stomach cancer risk. For processed meat, four out of six cohort studies have found no association with stomach cancer risk. Ten out of 14 case-control studies found a positive association between processed meat intake and stomach cancer risk.
A 2011 meta-analysis of 15 case-control and two cohort studies found that the association between high fish consumption and reduced gastric cancer risk was not statistically significant (RR= 0.87, 95% CI= 0.71-1.07).
A 2010 meta-analysis of 15 studies for red meat and 11 studies for processed meat assessed the risk of prostate cancer associated with high meat consumption. The study found no link between high intake of red meat and prostate cancer (RR= 1.00, 95% CI= 0.95-1.05). A small increased risk of prostate cancer was associated with processed meat (RR= 1.05, 95% CI= 0.99-1.12), but this funding was potentially confounded by several factors.
A 2004 review of prospective studies found that meat consumption was not consistently associated with prostate cancer risk. Three studies showed an increased risk, one a decreased risk and three a small decreased risk with meat consumption and prostate cancer. Results for fish and poultry were also mixed, however most reported associations for processed meat were positive.
A 2010 meta-analysis of 12 case-control and 12 cohort studies found no association between high fish intake and prostate cancer. However, there was an association between high fish consumption and reduced prostate cancer related mortality (RR= 0.37, 95% CI= 0.18-0.74).
In 2006, a systematic literature review found that the evidence was suggestive that fish intake may be associated with a decreased risk of prostate cancer. For fish intake and prostate cancer risk, the pooled OR for cohort studies was 0.95 (95% CI= 0.84-1.09), and for case-control studies the pooled OR was 0.65 (95% CI= 0.47-0.90).
A 2010 meta-analysis of data from eight cohorts from the Pooling Project publication along with ten other studies investigated the link between meat consumption and breast cancer. The study found no significant association between high red meat intake and breast cancer (RR= 1.02, 95 % CI 0.98-1.07). Weak associations were observed across all meta-analysis models, however the majority were not statistically significant.
In 2006, a systematic literature review found that the evidence was suggestive that fish intake may be associated with a decreased risk of breast cancer. For fish intake and breast cancer risk, the pooled OR for cohort studies was 1.01 (95% CI= 0.83-1.24). For case-control studies however, the pooled OR was 0.82 (95% CI= 0.71-0.96). In addition, many of the studies showed a significant trend (p<0.05) of decreasing risk with higher levels of fish intake.
A 2003 meta-analysis (including nine cohort and 22 case-control studies) investigated the relationship between total meat (red meat, poultry and pork) intake and breast cancer risk. The analysis showed that high versus low meat intake was linked to an increased risk of breast cancer in cohort studies (summary RR= 1.32, 95% CI= 1.12-1.56) and case-control studies (summary RR= 1.13, 95% CI= 1.01-1.25).
A pooled analysis of eight prospective studies in 2002 found that high intake of total meat (RR= 1.08, 95% CI= 0.98-1.19) and white meat (RR= 1.02, 95% CI= 0.91-1.13) appeared to have small non-significant associations with breast cancer, where total meat included eggs. However, high intake of red meat appeared to have a small non-significant negative association with breast cancer (RR = 0.94, 95% CI= 0.87-1.02). There was no significant heterogeneity among studies for total (p= 0.29), white (p= 0.11) and red (p= 0.58) meats.
A 2007 meta-analysis on meat intake and endometrial cancer risk suggested that meat, particularly red, may be associated with an increased risk of endometrial cancer, however the definition of meat varied substantially among both cohort and case-control studies and several case-control studies did not adjust for energy intake.
For highest versus lowest consumption categories, case-control studies showed there was a modest association between meat intake (type unspecified) and endometrial cancer (OR= 1.39, 95% CI= 1.13-1.71). The same finding was noted from a dose-response analysis, in which the OR for an increase in meat intake of 100 g/day was 1.26 (95% CI= 1.03-1.54). For red meat intake, case-control studies showed that a high intake (OR= 1.48, 95% CI= 1.22-1.80) and an increase in intake of 100 g/day (OR= 1.51, 95% CI= 1.19-1.93) was associated with an increased risk of endometrial cancer. Data for processed meat was not pooled, however three case-control studies found inconsistent results.
In addition, the meta-analysis showed that a high versus low intake of poultry (OR= 0.96, 95% CI= 0.72-1.29) and an increase in poultry intake of 100 g/day (OR= 1.03, 95% CI= 0.32-3.28) was not strongly associated with endometrial cancer risk. Likewise an increase in fish intake of 100 g/day was not strongly associated with endometrial cancer risk (OR= 1.04, 95% CI= 0.55-1.98). However individual study results for both poultry and fish intake were heterogeneous (p<0.01).
Potential mechanisms of action
The following hypotheses have been proposed to explain the association between meat consumption and cancer risk, particularly bowel cancer. However, none of these hypotheses have been confirmed in human experiments:
- A high iron intake may cause oxidative damage and hence induce tumours by catalysing the production of hydroxyl radicals.
- Nitrogenous residues from meat are available for N-nitrosation by colonic bacteria, thereby increasing the formation of ammonia and N-nitrosocompounds (NOC). Ammonia is a promoter of carcinogenesis and NOC have been shown to induce the formation of DNA adducts in human colonocytes. Meat or fish processed by the addition of nitrites and by smoking or direct-fire drying may contribute even further to the production of NOC. Endogenous production of NOC is increased with the consumption of red meat, but not white meat or fish. The difference may be related to the higher haem content of red meat which can act as a nitrosating agent under certain conditions.
- Heterocyclic amines (HCAs) formed when meat, fish or poultry are cooked are known to be absorbed from the human gastrointestinal tract and have been shown to be large-bowel carcinogens in animal models and to produce adducts in mammary tissue of rodents. Different amounts of HCAs are produced according to duration and temperature of the cooking method, with higher levels of HCAs found in meat cooked using high-temperature methods such as grilling, pan-frying and barbecuing. Therefore, cooking method rather than the type of meat may be a more important determinant of cancer risk. In addition, differences in genotype may also play a role in the association between HCA exposure and colorectal cancer. For HCAs to bind to DNA and hence initiate carcinogenesis, they must be activated by N-acetyltransferase (NAT) enzymes. Differences in an individual’s capacity to metabolise HCA may explain inconsistency in the relationship between meat consumption and risk of colorectal cancer, where rapid NAT acetylators may have a higher risk of colon cancer than slow NAT acetylators.
- Polycyclic aromatic hydrocarbons (PAHs) formed from the incomplete combustion of organic material, may induce the formation of DNA adducts and interfere with apoptosis. PAHs are in a wide variety of foods, however higher levels are found in foods that have been exposed to combustion products and foods that have been charred or burned when cooked at high-temperatures.
- The total fat content of meat may contribute to an increased production of bile acids in the colonic lumen. Bile acids metabolised into the secondary bile acid, deoxycholic acid, may act as tumour promoters by increasing cell proliferation in the colonic mucosa. However epidemiological studies have not consistently shown an association with dietary fat intake and cancer risk.
- The low ratio of polyunsaturated to saturated fatty acids in meat fat may contribute to hyperinsulinaemia. Exposure to elevated blood-insulin levels may promote the growth of colon tumours which has been demonstrated in a rat model.
- Fish, particularly those high in omega-3 polyunsaturated fatty acids, may be protective against colorectal cancer as these fatty acids have been shown to reduce cell proliferation and aberrant crypt formation, probably by modifying the inflammatory response.
Factors to consider when evaluating the literature on meat and cancer risk
Cut and quality of meat
Studies do not always collect information on the type of meat cut typically used (or species of fish), and if the meat consumed was lean or fatty.
Studies do not usually take into account the cooking method of meat and the doneness level e.g. raw versus well done. Differences in cooking method possibly may explain inconsistencies in the relationship between meat consumption and colorectal cancer. Given the effect of cooking method on HCAs and PAHs it may be important to include information on cooking method in dietary data.
Differences in meat definition
Different studies may define “total meat”, “red meat”, “white meat” and “processed meat” to include slightly different meat categories, which makes it difficult to compare results across studies.
Other lifestyle and dietary factors
It is difficult to separate the independent role of individual foods when studying cancer incidence and other health outcomes. The relative risk estimates for meat and cancer could also be affected by other eating and lifestyle patterns, such as:
- fruit and vegetable intake;
- dietary fibre intake;
- dietary fat intake (particularly total and saturated fat intake);
- body mass index; and
- physical activity levels.
For example, a higher intake of meat may be linked with an increased cancer risk because the diet of those eating large quantities of meat may contain inadequate fruit, vegetables and fibre. Many epidemiological studies on meat and cancer risk do not comprehensively control for all potential confounding factors.
Current consumption levels in Australian adults
The 2011–2012 National Nutrition and Physical Activity Survey (NNPAS) reported that seven out of ten Australians consumed meat, poultry and game products and dishes the day before the survey. This category includes beef, sheep, pork, poultry, sausages, processed meat (e.g. salami) and mixed dishes where meat or poultry is the major component.
NNPAS reported that chicken was the most commonly consumed meat within this category with 31% of people eating chicken the day before the survey, this was followed by beef (21%), processed meat (22%), sausages (7%), lamb and bacon (5% each). Meat, poultry and game provided 14% of total energy intake. Males were slightly more likely than females to consume meat, poultry and game (72% and 66% respectively).
Compared with data from the 1995 National Nutrition Survey, consumption of meat appears to have decreased. In 1995 most adults (85% of men and 77% of women) ate some meat, poultry or game on the day of the survey. Between 1983 and 1995, mean daily intake of red meat and pork declined for both men and women; whereas mean daily intake of poultry and seafood increased.
Contribution of meat to the Australian diet
Meat is an important source of iron, particularly haem iron in the diets of females. It contributes 16% and 11% of total iron intake in adult males and females respectively. Iron is an essential mineral required for formation of haemoglobin.
Meat is a major source of zinc, contributing a third and a quarter of total zinc intake in adult males and females respectively. Zinc is present in many tissues and plays a role in enzyme reactions and maintaining the immune system.
Meat is an important source of protein, contributing a quarter and a fifth of total protein intake in adult males and females respectively. Protein is involved in the growth and repair of cells.
Meat also contributes to the intake of vitamin B12, thiamin, riboflavin, niacin, phosphorus and magnesium. These nutrients are involved in essential chemical reactions including cell growth and repair, metabolism, and nerve and muscle function.
Meat contributes 14% and 11% of total fat in adult males and females respectively. Meat contributes 15% and 11% of saturated fat in adult males and females respectively. Fat is energy dense and therefore over consumption leads to weight gain and saturated fat raises cholesterol levels.
Cancer Council recognises that red meat is an important contributor to dietary iron, zinc, vitamin B12 and protein in the Australian diet.
Cancer Council recommends people:
More studies are needed on the association between meat and cancer risk. In the future, there is a need for more studies that:
- Investigate the differences found between cohort and case-control studies.
- Use a standard set of definitions for different meat categories.
- Collect and report separate data for unprocessed and processed meat.
- Collect and report data on the cooking method used.
- Adequately control for potential confounding factors such as fruit, vegetable, fibre and fat intake, body weight, and physical activity levels.
- Systematic reviews that assess and report on the quality of individual studies
Position statement details
This position statement was reviewed and approved by the Public Health Committee in October 2007 and updated October 2013.
This position statement was reviewed by:
- Allison Hodge
- Dallas English
- Hayley Griffin
- Jenny Atkins
- Udani Abeypala
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