It is likely that the association of red-meat consumption with colon cancer is explained either by an inability of epidemiology to detect such a small risk or by combinations of other factors such as greater overweight, less exercise, lower vegetable or dietary fiber intake, and perhaps other habits that differentiate those who eat the most meat from those who eat the least.
Red meat is a nutrient dense food that is an important source of complete protein with all essential amino acids, highly bioavailable iron, zinc, selenium, and B vitamins, especially vitamin B 12 in the diet.
Several of these nutrients are the most common shortfall nutrients in the world that could be alleviated by the consumption of only a few ounces of beef per week Figure 1 ; Klurfeld, Meat has been consumed by humans, sometimes in prodigious amounts, throughout history and is considered by anthropologists as one of the factors that led to evolution of larger brains. In recent decades, many observational studies of people have associated consumption of red or processed meats with a variety of chronic diseases such as multiple types of cancer, various forms of cardiovascular disease, kidney disease, type 2 diabetes, obesity, and total mortality Boada et al.
Consider if a scientist were claiming that a new drug treated all these illnesses. The overwhelming response would be swift and certain that this was not possible. Yet, critics of meat consumption are firmly convinced that it causes multiple harms despite the softness of data supporting such claims, almost all of which are based on epidemiological associations.
These numbers emphasize the nutrient density of red meat. Reproduced from Klurfeld, Epidemiological, or observational, studies provide valuable clues to potential associations between exposure to an agent and development of a disease.
Historically, that is how the sources of infectious disease were traced, such as during a cholera epidemic in London in that John Snow attributed to a contaminated well, or modern outbreaks of food poisoning like E. These relatively clear-cut sources of disease can be identified by epidemiological studies because the risk of infection in an exposed individual is several hundred times that of someone not exposed to the same contamination.
But, correlation does not equal causation. Many strongly correlated factors may have no relation, such as per capita consumption of margarine in the United States and the divorce rate in the state of Maine, which correlated at a level of 0. The 22 members of the working group were all self-nominated; many had spent most of their careers studying the relationship of meat or other dietary factors and cancer. Data used for this exercise were observational studies, animal experiments, and mechanistic studies that might establish a biological link between some component in red or processed meats and development of cancer.
This group concluded that animal experiments were not useful in assessing the evidence because these results had no clear effect in either direction of feeding red or processed meat on tumor development. Therefore, the committee relied upon only observational studies, with supporting information from mechanistic studies.
However, mechanistic studies are not strong evidence of causality; they simply show that some component in meat could affect noncancer endpoints in studies with animals or cell cultures, and plausibly increase the risk of cancer. In addition, the importance of such mechanistic studies in animals should not outweigh the outcomes from animal studies of cancer development. This means that in experiments in which feeding large amounts of bacon or beef does not increase the risk of cancer in animals that are genetically prone to cancer or given a chemical to induce colon cancer, studies of noncancer, potential biological indicators of cancer risk should count less when the totality of the evidence is assessed.
So when evidence of gene damage or oxidative stress in animals is claimed as the supporting mechanisms, but those animals do not get more cancer when fed three times the normal amount of protein combined with a calcium-deficient diet to see an effect, it is illogical to accept the mechanistic studies as confirmation of the epidemiology.
In addition, the IARC subgroup who evaluated mechanisms ignored two studies by one of its members in which bacon fed to rats actually significantly suppressed the precancerous indicators Parnaud et al.
Although the IARC working group on meat and cancer met in October and a two-page summary was published immediately after Bouvard et al. The working group evaluated over epidemiological studies, but only 7 of 14 studies of red meat and 12 of 18 on processed meat found increased risk of colorectal cancer in people eating the most meat. There was insufficient data on meat intake and cancers at other sites in the body for the group to reach a conclusion.
IARC stated that the working group was identifying hazard only—not evaluating the risk of getting colon cancer.
But, this is circular reasoning because the risk among those eating the most meat determined whether meat consumption was deemed a hazard. Another weakness in the conclusion from IARC is that chance, bias, and confounding could not be ruled out with the same degree of confidence for the relation of red-meat consumption and colon cancer, but these three issues were considered unlikely in the linkage of processed-meat intake and colon cancer.
The main reason these differences are not supported is that the same cohort studies provided data on both red and processed meat. Therefore, if chance, bias, and confounding cannot be ruled out for red meat, then those same issues apply to any potential association of processed meat and cancer because the same research data and methods were used from the same subjects.
How does this compare with known carcinogens? Another indicator of risk is the absolute risk, as opposed to the previously mentioned relative risk. The relative risk is a ratio of the disease rate in the group exposed to the highest amount divided by the rate in the group exposed to the lowest amount but this risk ratio does not reflect the absolute risk of a disease.
The lifetime absolute risk of colon cancer in vegetarians is 4. These numbers are not statistically distinguishable in epidemiological studies. Neither of these was performed by IARC. This finding means that it did not matter how much meat was eaten by the group with the highest intake across different studies; the highest consumers always had a higher cancer risk, suggesting that other factors not measured affected the risk of colon cancer.
In fact, two recent large observational studies comparing vegetarians with meat eaters found no increase of colon cancer risk when adjusting for vegetable intake in one study, or a variety of factors that included socioeconomic status, physical activity, smoking, and alcohol intake Appleby et al.
In other words, people who ate a lot of vegetables and fruit had no increased risk, no matter how much red meat they ate. These results again suggest that there are multiple other lifestyle factors that associate with dietary differences that account for the claimed differences in risk of cancer. A separate recent analysis evaluated health factors associated with meat eating and found that those who ate the most meat weighed more, were less physically active, and had a history of more smoking as well as lower intake of fruits and vegetables Grosso et al.
Those authors concluded that the differences in health behaviors modify the claimed relationship between diet and chronic disease risk. A take-home message might be that there are healthy and unhealthy lifestyles that contribute to colon cancer and other chronic diseases. Those eating the most red or processed meat may be more likely to ignore other health recommendations and have multiple habits that contribute to the risk of disease. One of the weaknesses of most long-term observational studies is the use of a computer-scored food frequency questionnaire to estimate dietary intake.
Many food frequency questionnaires ask only about the frequency of consumption, not serving size. Most people who are asked about their habitual diet for the last year are influenced by what they have eaten over the past few weeks. And, there are very few truly objective tests that can be used to validate whether the questionnaire has accurately captured usual dietary intake. Almost all study questionnaires ask about diet at baseline and assume that it has not changed for the duration of follow-up that can last more than 20 years; such an assumption is demonstrably false.
Another key issue is whether the food frequency questionnaire is adequate for estimating total calories or protein—both critical for studying the effects of meat consumption on health—and both have tests available that can accurately determine how much has been eaten.
The definitive study was done by scientists from the U. National Cancer Institute who concluded that the food frequency questionnaire is not able to evaluate the absolute intake of either energy or protein Schatzkin et al.
A separate issue that potentially weakens the ability of observational studies to provide solid evidence of a causal relationship between a food and a disease outcome is the large number of comparisons in a study. Outcomes prespecified in an analysis are considered more certain whereas those not specified in advance are considered exploratory and require a higher statistical bar to be considered meaningful. However, the large numbers of factors in nutrition studies—for example, food items in a typical food frequency questionnaire, 40 nutrients, and 50 disease endpoints or risk factors—yield a total of , possible outcomes.
Five percent of that number means 20, could be false positives. If we used a higher barrier to declare significance among endpoints not prespecified, such as 0.
In fact, there are existing statistical procedures, widely accepted in genetics and other fields that rely on many simultaneous comparisons that control the false discovery rate but this has never been adopted in the nutrition area.
High numbers of subjects in a study increase the statistical power but may provide a false sense that an association is meaningful. One example from the epidemiology literature clearly designed to show the limitations of standard statistical approaches in large studies used Two of these associations remained statistically significant in the second cohort with relative risks of 1. Observational studies of nutrition and health can contribute to the overall assessment of a causal relationship but because an association is weak evidence, they cannot be used by themselves, or as the primary driver, of any conclusions.
This was made clear more than 50 years ago by Sir A. Hill, who listed nine considerations for conclusions about causality from the scientific literature Hill, The factors were strength, consistency, specificity, temporality, biological gradient, plausibility, coherence, experiment, and analogy; the relationship of meat and cancer only fulfils four of these nine, making it relatively weak and uncertain.
The observational study on meat intake and mortality that critically demonstrated to this author that the association of meat intake with causes of death is not causal was the NIH-AARP Study that followed , older people and recorded 71, deaths Sinha et al.
If one assumes that the food frequency questionnaire was accurate and that diet did not change during 10 years of follow-up both of which are generous assumptions , all causes of death were increased in those eating the most red meat and decreased in people eating the most white meat poultry and fish , except for cardiovascular disease in those eating the most white meat Figure 2 ; Klurfeld, The causes of death were separated into cancer, cardiovascular diseases, accidental, all others, along with total mortality.
Relative risk was approximated for both sexes combined from tables for risk in each sex provided in Sinha et al. The relative risk of dying from cancer among the highest meat eaters was about 1. The fact that accidents and all other causes of death were increased by red-meat and decreased by white-meat consumption strongly indicates the nonspecific effect of eating these foods. The risk of accidental death was the same as the risk of cancer and risk of a wide-ranging group of 10 causes of death labeled other was significantly higher than that for cancer.
These relationships should make it clear that some confounding factors that associate with high red-meat intake not measured, or simply chance, were more likely explanations than a cause and effect from eating red meat Klurfeld, Relative risk of total mortality among men and women from various causes of death.
Most importantly for the IARC report, two major dietary intervention studies that should have contributed to the assessment of the claimed relationship of red meat and cancer were not considered.
The first was a study of colon polyps, the precancerous growths that greatly increase the likelihood of developing colon cancer. Almost 1, subjects with a recent history of having a polyp removed were divided into a control group that ate their usual diet and a group following a diet characterized by significant decreases in total fat, red, and processed meat along with increases in fruits, vegetables, whole grains, and legumes Schatzkin et al.
Participants were followed for 3 years and at the end of that time, the recurrence of colon polyps was identical in both diet groups. It is possible that the precancerous stage may not have been the proper time for dietary intervention. After 9 years, the rate of colon cancer was almost identical in the low-fat and control-diet groups.
These studies strongly suggest that the observational studies are not supported by dietary intervention studies at either the precancerous or malignant tumor stages of colon cancer. The field of nutrition has a long history of observational studies pointing to a relationship that is not supported by controlled intervention studies that test specific associations.
Examples include claims about cancer with the nutrients beta-carotene, vitamins C or E, and selenium. In fact, beta-carotene in high amounts was shown to significantly increase the risk of lung cancer in smokers, in sharp contrast to what observational studies originally suggested.
Recently, however, there has been public controversy concerning just how healthy eating meat on a daily basis really is, especially red meat. Meanwhile, fears have grown about the amount of fat in all meats, particularly saturated fat. Meat has a very high mineral content including body essentials like magnesium , zinc and iron. Magnesium is important for bone strength as it improves vitamin D synthesis as well as help decrease net acid production.
Most importantly, iron helps to maintain energy levels as well as maximize oxygen transport throughout the body. Red meat and turkey are particularly iron rich. Meat is an excellent source of protein, which is essential for any healthy diet.
It helps build and repair muscle as well as help maintain healthy hair, bones, skin and blood. Due to its High Biological Value HBV , protein obtained from meat is easily digested and thus absorbed quickly and effectively by the body. Red meat , chicken and turkey are extremely high in protein.
Vitamins are vital in maintaining a healthy body. Vitamin E has very strong antioxidant properties and helps reduce damage caused by oxygen to cells thus allowing faster muscle repair and recovery. B vitamins all work together to help convert food into energy but they also have individual uses. B2 is essential for the manufacture of red blood cells, which then transport the oxygen around the body. In addition to offering significant protein, meat provides a wide variety of minerals to support the optimal functioning of your cells and tissues.
For instance, it is an important source of both iron and zinc. Iron helps carry oxygen to and throughout your tissues, while zinc is required for a strong immune system, wound healing and enzyme activity within your cells.
The phosphorus content of meat helps keep your bones strong, the sulfur it contains can be incorporated into new amino acids and the chromium found in meat assists in metabolizing your dietary sugars.
A number of B vitamins are available from the meat you consume. Thiamine, riboflavin, niacin, pantothenic acid and biotin help your cells extract energy from the foods you eat each day.
Vitamin B-6 keeps your nervous and circulatory systems healthy, and it functions in both protein synthesis and protein metabolism. This vitamin also assists in the absorption of vitamin B, another vitamin essential for circulatory and nerve health, as well as energy production. Meat is an especially important source of vitamin B, because, unlike other B vitamins, B is not found in any plant-based foods.
Although you need a limited supply of fats in your diet for good health, the saturated fats found in meat can be detrimental to your well-being. Consuming high levels of saturated fats can increase your risk of atherosclerosis, a condition in which plaque deposits form on the walls of your arteries, and can lead to heart disease. Taking in too many dietary fats, such as from fatty cuts of meat, can result in accumulation of fat stores in and around your organs, causing eventual organ damage.
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