Does red meat cause cancer?

Peter Baghurst, Sally Record and Julie Syrette

Abstract

Research reports suggesting high meat consumption is linked with increased incidence of cancers have been the subject of considerable discussion and media attention in recent years. A systematic examination of the epidemiologic literature, however, reveals that the associations between meat consumption and cancer risk are not consistent. Pertinent results from a large number of epidemiologic studies which have examined the relationship between meat consumption and cancers of the stomach, colorectum, breast, prostate gland, kidney and lymphoid organs are presented in extensive tables. Wide variation in the definitions used for the terms ‘meat’ and ‘red meat’ and in the categorisation of consumption level make direct comparison of individual studies difficult. However, it is concluded that any true effect of meat is likely to be small, or even an artefact of a decreased consumption of fruit, vegetables and cereals among high meat consumers.

Mechanisms proposed to explain these associations with cancer risk have been focused in two broad areas. The first of these areas has been concerned with potential adverse effects of dietary fats on cancer risk. Bile acid secretion and conversion of these acids to mutagenic secondary bile acids is increased with high fat intakes; oxidation of fats (especially unsaturated fats) increases generation of damaging free radicals; and specific fats may have unwanted effects on patterns of prostaglandin secretion, on cell-cell communication, and on steroid hormone synthesis. While the relevance of these effects in humans remains unclear, it would seem prudent to choose lean cuts of meat trimmed of selvedge fat which increasingly are becoming available from producers and retailers. However, since fat from all meat products and dishes probably contributes to the average Australian diet around only 20% of total dietary fat, and red meats alone contribute only six to seven per cent, this strategy is unlikely to impact significantly on total fat intakes without simultaneous reductions in fat consumed in the form of dairy products, spreads and sauces.

A second area of potential concern is the production of mutagens in meat by specific cooking methods. Polycyclic aromatic hydrocarbons (PAHs) are generated by incomplete combustion of organic material, and barbecued meat is especially vulnerable to contamination with PAHs generated either from some wood fuels, or from fat dripping from hot meat onto the heat source. It must be noted, however, that PAHs are ubiquitous in the food supply, and cereals, fruits and vegetables, which are typically associated with lower risks of cancer, may be the major dietary contributors of PAHs for many individuals. Heterocyclic amines (HCAs) formed from amino acids, creatinine and the naturally occurring sugars in meats cooked at very high temperatures (as in frying, grilling, or broiling) are also mutagenic, but estimations of the human cancer risk based on animal experiments and typical exposure levels in meat eaters suggest their attributable risk is very low. The finding that HCAs are also formed in white meats such as chicken and fish, whose consumption is often associated with reduced risks of cancer, would suggest that HCAs in the food supply do not contribute materially to the overall human cancer burden. Use of lower temperature cooking methods (stewing, roasting and microwaving) prevents formation of both heterocyclic amines and polycyclic aromatic hydrocarbons.

Micronutrients in meat which are potentially anticarcinogenic include anti-oxidants such as zinc, and the dipeptides carnosine and anserine (not discussed in detail here); while isomers of linoleic acid found in fats from ruminants, and referred to as conjugated linoleic acids have been demonstrated to inhibit cancers in a variety of animal models. Methionine from meat may also be important in maintaining an appropriate level of methylation required for regulation of genes involved in cell proliferation. The relevance of these mechanisms to human health still needs to be quantified.

[Aust J Nutr Diet 1997;54(4Suppl):S1–S44].