In 2015, a Working Group of the International Agency for Research on Cancer [IARC] classified ‘processed meat’ as a Group 1 carcinogen, concluding that a review of epidemiological and supporting population-based case-control studies provided ‘sufficient evidence’ that high consumption of processed meat causes colorectal cancer [1]. The IARC concluded that consumption of ‘red meat’ lacked clear associations with colorectal cancer in high quality studies, and thus limited evidence for carcinogenicity of red meat; factoring in mechanistic studies, however, the Working Group classified red meat consumption as ‘probably carcinogenic to humans’ [1].

It’s important to define what differentiates ‘red meat’ and ‘processed meat’. Red meat includes unprocessed mammalian muscle meats from beef, veal, lamb, mutton, pork, or goat meat, which is typically consumed cooked [1]. Processed meat includes the use of methods like salting, curing, smoking or other industrial processes to enhance flavour and preservation [1]. “High” consumption is defined as >200g/d, while the mean intake for meat eaters is 50-100g/d [1].

To be classified as “carcinogenic to humans”, the IARC prioritizes epidemiological studies, supported by population-based case-control studies, which have to accumulate to a point where there are ‘consistent associations…in different populations, which make chance, bias, and confounding unlikely as explanations…’ for the results other than that the agent – in this case processed meat – causally increases risk for cancer [1].

For the purposes of this article, ‘red meat’ as defined by the IARC will be referred to as unprocessed meat. Processed meat will retain its IARC definition.


But Association Isn’t Causation?

This is true. But the statement should never be used to summarily dismiss an observation. Observational epidemiology has provided the “proof” for causation in relation to cancer before, with regard to cigarette smoking: we didn’t wait for randomised controlled trials to prove smoking causes cancer.

Observational epidemiology is a powerful tool in health sciences, so if we can “convict” smoking using this tool, why can’t we do the same for meat? Because diet is a complex interplay of multiple factors and variables. Cigarettes, on the other hand, are a clearly identifiable agent that increase risk independent of other variables like diet, BMI, age, and lifestyle. In light of sensationalist media headlines following the IARC decision, it’s important to reemphasize the recent publication in the International Journal of Cancer that “meat consumption is not tobacco smoking” [2].

One of the primary issues with the IARC analysis is the lack of clear associations from the studies with diet patterns as a whole. The limitations of looking at single nutrients or standalone foods in relation to multifactorial disease processes, without regard to the overall diet pattern, is now a recognized issue in nutrition science [3]. This is particularly relevant to the role of meat in the diet, as high levels of processed meat are inversely associated with overall diet quality, in particular low intakes of fibre, vegetables and fruit, and greater likelihood of smoking [4][5].

An example of this issue can be seen in meat eaters’ diametrically opposed paradigm: vegetarianism. Several recent epidemiological studies have failed to find that vegetarian diets reduce risk of colorectal cancer, total cancers, or all-cause mortality compared to non-vegetarian diets [6][7]. Have vegetarian diets suddenly become a risk factor? No, these studies are highlighting limitations in how we quantify disease risk relative to dietary exposure. For example, in the Oxford-EPIC study in the U.K., subjects were divided according to 4 strata: those who ate meat, fish but no meat, dairy and/or eggs but no meat or fish, and no animal produce at all [6]. Colorectal cancer rates overall in the cohort were 13% lower than the national average, but interestingly vegetarians in this cohort had rates of colorectal cancer similar to the national average [6]. In contrast, meat eaters had a moderate mean intake – 78g and 69g for men and women, respectively – and had vegetable and fruit intake which, although less than the vegetarian groups, was still higher than average [6]. In this regard, it would appear that the diet as a whole of those who consumed meat was relatively nutritionally balanced.

What the Oxford-EPIC study is really giving us insight into is the false nutritional dichotomy that the healthfulness of a diet is defined by the presence or absence of meat. It should be emphasised that this study is not an outlier, and multiple prospective studies have found no difference in risk for colorectal cancer between vegetarians and non-vegetarians [8]. This should not be interpreted as a reflection of the respective diets, which are difficult to quantify as a whole through the methodology used in prospective studies, but as a reflection of issues with binary constructs based around meat consumption or lack thereof, and a failure to quantify key variables [9]. An example of this issue can be found in a recent large Australian cohort study, where there was no difference in all-cause mortality between vegetarian and non-vegetarian subjects [7]. Attempting to isolate the health effects of diet from other variables which the Oxford-EPIC study did not do, the researchers subcategorized non-meat eaters into vegetarians, semi-vegetarians and pesco-vegetarians; yet meat eaters were divided dichotomously by eating meat or not eating meat [7][9].

Consequently, typifying the limitation of research in this area, there were no means of quantifying meat intake relative to quality (processed vs. unprocessed), dose or frequency of consumption, or relative to vegetable and fruit intake: the subdivisions afforded to vegetarian diets have yet to be applied to meat-inclusive diets [9]. Another important observation is that defining a diet by the absence of meat gives rise to a false rebuttable presumption of healthfulness in a vegetarian diet: the authors in this study, however, were sharp to recognise that “vegetarian” defined by the absence of meat may still encompass conventional unhealthy foods in the typical Western diet [7]. Indeed, it is noted that the mere label of “vegetarian” defined simply by the absence of meat gives no indication of healthfulness of the diet pattern: refined grains, added sugars, trans fats, french fries, sodas, and sodium are all vegetarian [3].

Thus, we can see the issues with the IARC undertaking – although a noble review of over 800 epidemiological studies, together with supporting case-control and mechanistic studies – in determining the carcinogenic potential or unprocessed and processed meats. We should take their conclusions seriously, but consider them directive of a deeper analysis. In particular, the inconsistencies in relation to unprocessed meats are borne out in the population-based studies highlighted above and present a number of issues, namely:

  1. The healthfulness of a diet is not dichotomous, defined by the presence or absence of red meat;
  2. The diet pattern as a whole is more relevant than presence or absence of a standalone food;
  3. We need to look closer at the nuances in the picture of red meat and health.

Let’s look deeper at these nuances.


A Closer Look at Diet Patterns

In 1978 a paper was published in the Journal of the National Cancer Institute entitled, ‘Diet in the epidemiology of cancer of the rectum and colon’ [10] in which no association was found between consumption of beef or other meat in men with colorectal cancer compared to healthy controls, but increases in risk were found with reduced frequency of vegetable consumption. The greatest reduction in risk was associated with frequent consumption of cruciferous vegetables in particular, specifically cabbage, Brussels sprouts and broccoli [10].

This paper is instructive, coming at a time where a pivotal change was occurring in the typical adult diet in Western industrialised countries. Data from the National Health and Nutrition Examination Survey [NHANES] in the United States indicates that from 1977 to 1996, the typical diet increased significantly in overall dietary energy, with the food groups contributing most to increased energy density including salty snacks, soft drinks, pizza, with significant contributions from candy, fruit drinks, french fries, cheeseburgers, and Mexican food [11]. The increase in consumption of these foods reflected an increase in the proportion of calories consumed away from home, with adults consuming up to 30% of daily energy from restaurants and fast-food establishments [11]. Of particular note, the consumption of meat consumed alone, i.e. as a meal, decreased significantly: the data showed that hamburgers and cheeseburgers consumed in 1996 were primarily consumed in a restaurant or fast-food establishment [11]. In conjunction with this shift to convenience energy-dense foods, beneficial components of diet declined significantly. Data indicates that less than 14% of US adults meet vegetable requirements, a paltry 1.5 cup per day serving is not even achieved by over 50% of the population [12].

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