Red Meat and Cancer Risk: A Closer Look at the Evidence

August 10th, 2017|Nutrition|
Red Meat and Cancer - Myolean Fitness

Guest author: Vincent Sparagna (For questions, email at Vincentsparagna@gmail.com)

Reviewed by: Antonis Damianou (myoleanfitness.com), Alex Leaf (leaf-nutrition.com/examine.com), and Sérgio Fontinhas (Big Fitness Project)

The start of the controversy about red meat and cancer

In October 2015, the World Health Organization (WHO) released a report stating that eating processed red meat causes cancer and eating unprocessed red meat probably causes cancer (3,179,193).

Is there, however, an actual cause and effect relationship between the consumption of red meat and cancer?

What are the mechanisms through which red meat may causes cancer?

Is there anything we can do to reduce the potential cancer risk from red meat consumption without completely giving up red meat?

These are some of the questions answered in this article.

But first, here are some of the key takeaways.

Key takeaways

  • Given an otherwise healthy overall lifestyle, moderate red meat consumption is likely fine.
  • Red meat’s dose makes the poison, so it’s wise to moderate red meat intake (particularly, processed red meat).
  • Red meat consumption correlates positively with cancer (mainly colorectal cancer). While consuming red meat may cause cancer, research cannot establish causation, given numerous confounders and lack of intervention studies.
  • Processed red meat and cancer correlate better than unprocessed red meat and cancer.
  • Some authorities recommend consuming “no more than one to two servings per month of processed meats, and no more than one to two servings per week of unprocessed meat” (1); others suggest <300 grams (~10.58 ounces) of red and processed meat per week (187). The World Cancer Research Fund recommends consuming <500 grams (~17.64 ounces) of red meat per week, with very little to no processed red meat (197). There is not sufficient evidence to conclude a definitively safe intake level.
  • Red meat consumption may be carcinogenic through various mechanisms, but your actions can mitigate these risks.
  • Red meat’s link to cancer is pragmatically relevant because you control how much red meat you consume. However, red meat consumption is certainly not the primary factor influencing cancer risk (2).
  • Red meat consumption yields some health benefits, so despite its link to cancer, occasional red meat consumption may improve health.

What type of cancer?

Cancer encompasses a broad number of diseases rather than one uniform condition.

Colorectal cancer (cancer of the colon or rectum) is the third leading cause of cancer-related death in both the United States and world (41,192). Red meat consumption correlates most meaningfully with colorectal cancer.

Less convincing evidence positively correlates red meat consumption with breast, pancreatic, lung, esophageal, gastric, liver, stomach, bladder, head-and-neck, and prostate cancer, as well as non-Hodgkin lymphoma and multiple myeloma (3-40, 45,176,177,187-190,193,197-204,207).

Differentiating between red meats

According to the WHO, “Red meat refers to all mammalian muscle meat, including, beef, veal, pork, lamb, mutton, horse, and goat.” (43).

“Processed meat refers to meat that has been transformed through salting, curing, fermentation, smoking, or other processes to enhance flavour or improve preservation.” (43).

The primary difference is that processed red meat undergoes further processing than red meat.

Red meat and cancer risk classifications

The WHO classifies processed red meat as a group 1 carcinogen and classifies red meat as a group 2A carcinogen (43,179,181,191).

A group 1 carcinogen is defined as “carcinogenic to humans” while a group 2A carcinogen “probably” causes cancer (43,179,181,191).

Cancer Risk Classifications - IARC - Myolean Fitness

Adapted from: IARC (179)

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It is important to note that, for group 1 classifications, the International Agency for Research on Cancer (IARC) states that,

“an agent may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent acts through a relevant mechanism of carcinogenicity.” (215).

Moreover, for group 2A classifications, the IARC states that,

“an agent may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.” (215).

How carcinogenic is red meat?

In a 2017 narrative review, Wolk concluded that consuming 100 grams (~3.53 ounces) of unprocessed red meat per day correlates with increased risk for breast cancer (11%), colorectal cancer (17%), and advanced prostate cancer (19%) (194). Wolk also reported that consuming 50 grams (~1.76 ounces) of processed red meat per day correlates with increased risk of advanced prostate cancer (4%), cancer mortality (8%), breast cancer (9%), colorectal cancer (18%), and pancreatic cancer (19%) (194).

Another meta-analysis from December 2017 reports similar findings to Wolk concerning colorectal cancer (228). This analysis (of 25 studies) discovered a linear dose-response relationship between both processed and unprocessed meat and colorectal cancer risk. Consuming 100 grams of unprocessed red meat per day correlated with a 1.12 relative risk, while consumption of 50 grams of processed meat per day correlated with a 1.17 relative risk (228). Consuming 2 servings of red meat per day or 4 servings of processed meat per day correlated with 1.8-fold colorectal cancer risk. This review also reported that low red meat consumption, paired with a high whole grain, vegetable, fruit, and dairy product consumption, correlated with decreased colorectal cancer risk (228).

Further, Grundy et al (2012) reported that red and processed red meat consumption caused roughly 12% of colorectal cancers in Alberta, Canada (1.5% of all cancers) (195). Of note, roughly 1 in 2 men and 1 in 4 of the study’s women exceeded the World Cancer Research Fund’s 500 gram (~17.64 ounces) red and processed meat per week recommendation (195,190).

Wang et al’s (2016) meta-analysis (of 17 prospective cohorts) found that more red and processed meat consumption correlated with increased total, cardiovascular, and cancer mortality risk (202).

The WHO’s report concluded that by not consuming red meat, one’s colorectal cancer risk may decrease by ~18% (3,179). However, it’s very difficult to quantify the correlated risk increase, as meat is one variable in our multifactorial diet. Further, it’s impossible to quantify the exact percentage risk increase, given confounders (e.g. sleep and stress).

Lifestyle factors confounding red meat-consumption-induced colorectal cancer risk include regular smoking, high BMI, and alcohol consumption (6,5,7,9,17,23,25,26,28,35,44-50,190,198,199,212).

Additionally, greater fruit and vegetable consumption correlates with generally reduced cancer risk, confounds red meat’s effects considerably (7,10,11,21,33,36,42,44,51-58,178,198,212). We cannot quantify the degree to which fruit/vegetable consumption (or lack thereof) influences cancer risk in red meat-related trials.

We cannot determine red meat’s carcinogenicity, as observational research lacks the control needed to establish this link (50,59-61). Since many factors alter cancer risk, and cancer takes years to develop, cancer-related randomized trials are difficult to conduct.

Red Meat and Cancer Risk - Graph - Myolean Fitness

Note: All baseline values are derived from the Cancer Statistics Center website.

Baseline cancer risk and absolute risk with red meat consumption

The above graph represents the percentage cancer risk change correlated with consuming ~50 grams (~1.76 ounces) of processed red meat or ~100 grams (~3.53 ounces) of unprocessed red meat per day (except for ovarian, which is ~50-100 grams/week).

For example, the relative risk (risk compared to baseline; expressed as a decimal) for both unprocessed and processed red meat is 1.08 for bladder cancer. As such, compared to baseline (1.0), bladder cancer risk increases by 8% upon consuming ~100 grams of red meat or ~50 grams of processed red meat per day. This doesn’t mean that one’s absolute cancer risk increases by 8%; this means cancer risk increases by 8% of the 2.4% baseline bladder cancer risk. The initial 2.4% absolute risk thus increases by .192% (from 2.4% to 2.592%).

Despite an evident relative risk increase, absolute cancer risk doesn’t increase substantially after consuming 100 grams (~3.53 ounces) of red meat or 50 grams (~1.76 ounces) of processed red meat.

Mechanisms through which red meat may increase cancer risk

In a 2017 paper, Johnson reported several identified mechanisms for meat consumption’s mutagenic effects. Unfortunately, it’s not clear which mechanisms cause cancer in humans. Additionally, the extent to which avoiding red meat decreases cancer risk is unknown (204).

Mechanism 1: NOCs

Processed red meat contains N-nitroso compounds (NOCs). NOCs form endogenously from nitrite and nitrate intake (223).

Upon red meat consumption, heme iron catalyzes N-nitroso compound formation, in a dose-dependent manner (46,63-65,67,74,76,77,131,192). These N-nitroso compounds can potentially damage the gut lining, initiating cell regeneration, which may eventually damage DNA (14,63,78-82,205).

Unprocessed red meat effects gut damage less directly than processed red meat (after curing and smoking). This occurs because processed red meat’s chemicals potentiate faster NOC formation (69,181,192).

What you can do about it: The gut damage caused by NOCs can be reduced or eliminated if the meat is consumed with green vegetables (64). This is because green vegetables contain chlorophyll and/or vitamin C, which may prevent NOC formation (83,54-56). Other high-vitamin C foods should decrease damage as well, though limiting or abstaining from red or processed red meat consumption may help more.

Mechanism 2: High-Heat Chemicals

Heterocyclic amines (HCAs) and Polyaromatic Hydrocarbons (PAHs) form when meat is cooked at high heat or smoked (less so with white meat) (75,93,100-111,181). These heat compounds can damage the gut, and the International Agency for Research on Cancer considers them potentially carcinogenic (98,113,114). Re-heating meat does not seem to contribute to heat compound content (112).

Several genetic mutations (e.g. those involving enzymes NAT1 and NAT2), given their role in HCA metabolism, correlate with increased cancer risk (118-122).

Some researchers suggest that high-heat compounds cannot completely explain the link between colorectal cancer and red/processed meat intake (192). For example, Van Hecke suggests that NOCs and oxidation products better explain red/processed meat’s correlation with colorectal cancer risk (210).

Few studies find significant associations between white meat (e.g. poultry or fish) consumption and cancer (181,189,187,213). Since cooking white meat also creates high-heat chemicals, high-heat chemical concentrations alone, cannot explain (processed) red meat’s carcinogenicity.

Additionally, PAH’s bioaccessibility in meat is under-studied (210), thus its carcinogenic potential is unknown.

However, one may still want to cook red meat at a lower heat. Cooking meat at low heat, reduces advanced glycation end product formation, thereby potentially improving insulin resistance in the obese (224).

What you can do about it: Eating meat with cruciferous vegetables (such as broccoli or Brussels sprouts) or marinating the meat in spices (especially Caribbean spices, such as allspice berries) for 20+ minutes before cooking can reduce HCA and PAH formation; preventing much of the heat-chemical induced damage (115,11,51-53,179).

One could also simply cook the meat at a lower heat and/or not cook over an open flame (38,43,93,96,101,109,113,114,116,117,209).

Mechanism 3: Iron

Red meat contains abundant iron, which intestinal tract cells oxidize easily, as other compounds don’t bind tightly to iron (64,125,126). Iron oxidation can cause cell damage, and this might explain the link to increased risk of colorectal cancer (127-130).

Heme iron seems to catalyze NOC formation, thus may thereby contribute to cancer risk further (46,63-65,67,74,76,77,131,192,205).

Allison-Sliva highlights that this mechanism isn’t universally relevant to cancer. This is because cooking denatures heme, which creates high plasma hemopexin levels that block its tissue delivery. As such, red meat-derived heme can only contribute to colorectal carcinoma risk, via local effects (208).

What you can do about it: There is no way to mitigate the effect of excess iron from red meat without simply consuming less red meat.

Mechanism 4: TMAO

Trimethylamine N-oxide (TMAO) is a controversial compound that research has linked to colon and colorectal cancer (132,219).

Red meat is high in choline and L-carnitine (amino acid), which gut bacteria may metabolize into TMAO (133,134,194,216,217,218). High TMAO levels correlate with high TMA and DMA levels (216). TMA and DMA risk undergoing nitrosation, which potentially causes cancer (via nitrosated amine formation) (218).

However, TMAO may be a lurking variable, rather than a mechanism causing red meat’s carcinogenicity (218). Evidence of TMAO’s protective effect in carcinogenesis (by correcting mutant protein folding (218,220,221)) supports this assertion.

What you can do about it: The effects that TMAO has on gut health are still largely unknown, though maintaining a healthy gut (by eating a diet rich in fruits and vegetables) can prevent some potential damage from red meat (44,135,7,10,11,21,33,36,42,44,51-58,178,191).

Mechanism 5: Neu5Gc

Human blood contains N-Acetylneuraminic acid (Neu5Ac), but nearly every other mammal’s blood has N-glycolylneuraminic acid (Neu5Gc) type sugars.

Because Neu5Gc and Neu5Ac differ, red-meat derived Neu5Gc ingestion may trigger an immune response, potentiating inflammation and carcinogenesis (137,208).

Human tumors contain high Neu5Gc levels, and Neu5Gc seems carcinogenic to mice. However, we don’t know the dose at which Neu5Gc proves toxic (136,137,222).

What you can do about it: The only way to mitigate the effects of Neu5Gc is to eat less red meat.

Mechanism 6: Environmental Pollutants

Potentially carcinogenic environmental pollutants include: heavy metals, polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs), dioxin-like polychlorinated biphenyls (PCBs), and other persistent organic contaminants (181).

The content of these pollutants differs depending on the processing or cooking method of the meat (181).

Non-red meats typically contain fewer organic compounds, so red meat’s baseline carcinogenic potential is higher (181).

In a 2017 review, Domingo and Nadal outline that certain cooking processes modify red meat’s environmental pollutant content (181-186).

What you can do about it:

Environmental pollutants concentrations depend (mostly) on the food’s baseline pollutant contents, rather than the food’s preparation method. Since environmental pollutants are typically organic, fat-releasing cooking procedures should also reduce red meat’s pollutant concentrations (181,185,186).

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A few important notes on the above mechanisms

Allison-Silva (2016) notes that TMAO, heat compounds, and environmental pollutants are not specific to red meat (208).

Additionally, n-nitroso compounds, heme iron, and heme’s potential to catalyze endogenous nitrosation are specific to red meat. Though, not even these mechanisms explain red meat’s (unique) carcinogenicity to humans, as other carnivores maintain lower risk (208).

Environmental pollutants and infectious agents from dairy cattle may partially explain this discrepancy in risk (208).

Neu5Gc’s metabolic incorporation into red meat consumers’ bodily tissues, followed by inflammation-provoking antibody interactions, potentially explains red-meat induced cancer risk increase (208).

Multiple studies have discovered carcinogenic compounds (e.g. PCDD/Fs, dioxin-like PCBs or PAHs) in raw red meats, which sometimes contain notable carcinogen concentrations (varying with the meat’s type and origin).  Therefore, consuming these meats, processed or not, certainly seems risky. Cooking or processing can only add new carcinogens, or increase concentrations of (e.g. PAHs/HCAs) raw/uncooked meat’s pre-existing carcinogens (181).

Why you may want to consume red meat

Despite processed or unprocessed red meat’s link to cancer, one might still benefit from red meat consumption:

  • Red meat contains essential nutrients iron, zinc, and vitamin B12 (138-140,190,194,196), thus its consumption helps prevent certain nutrient deficiencies. However, people can obtain these nutrients from other, less potentially carcinogenic sources.
  • Protein plays a vital role in muscle growth (especially when paired with resistance training) (141-145,159,163). Red meat is a great source of protein. Additionally, red meat has a high thermic effect (146), is highly satiating (difficult to overeat; blunts hunger) (139,147,148), and thus may improve weight loss or maintenance (139,146-148). However, other protein sources (such as white meat) may yield similar benefit with less potential risk.
  • Red meat is high in (rare) vitamin K2 (150-155), which potentially kills cancer cells through “oncosis” (killing through oxidation) (156), and may prevent cancer cell formation via autophagy (dead cell matter recycling) (157,158). Unfortunately, I doubt vitamin K2’s benefits outweigh the increased cancer risk correlated with red meat consumption. Additionally, few other vitamin K2 sources exist (only other meats, egg yolks, cheeses, or natto (225,226)).
  • Red meat contains creatine, which might reduce depression (164), enhance brain energetics (165-169), increase muscle growth (161-163, 170,171,180), and improve athletic performance (162, 168,170-175). Vegetarians have lower baseline creatine levels than omnivores (161-163), thus meat consumption likely boosts creatine levels. However, one must consume more red meat than recommended to reap creatine’s benefits, thus I recommend creatine monohydrate supplementation instead.
  • Certain populations can benefit from red meat consumption:
    •  Red meat consumption may tremendously benefit the elderly. Since red meat consumption increases muscle growth when paired with resistance training (159), it helps mitigate sarcopenia (age-related muscle loss). It is prudent to prevent sarcopenia because it contributes to weakness, poor health, and physical ineptitude (160,180).
    • Red meat consumption may enhance growth (mid-arm muscle area), cognitive function (arithmetic performance), and behavior (initiative leadership) in Kenyan children (81). As such, red meat consumption may benefit developing children.
    • Iron deficiency is common (214), and red meat is rich in iron (227), thus red meat consumption may benefit anemics. However, many other dietary iron sources exist.

Conclusion

Most scientific literature indicates a link between red meat and cancer, although we cannot conclude causality without intervention studies. Moreover, there are numerous confounders in this research, making red meat’s carcinogenicity difficult to quantify.

We need more research to establish red meat’s most relevant cancer-inducing mechanisms (specifically for colorectal cancer risk).

Red meat consumption is only one determinant of cancer risk. Reduce general cancer risk by avoiding excessive alcohol consumption, stress, smoking, high BMI, and sleep deprivation. Similarly, it’s prudent to consume fruits and vegetables, while exercising often.

Available evidence indicates that red meat consumption likely increases cancer risk, while processed red meat almost certainly does. However, I doubt red meat increases cancer risk meaningfully if you moderate consumption and maintain healthy lifestyle habits.

  1. Processed And Red Meat Could Cause Cancer? Your Questions Answered
  2. Environmental and heritable factors in the causation of cancer–analyses of cohorts of twins from Sweden, Denmark, and Finland.
  3. Carcinogenicity of consumption of red and processed meat
  4. Well-done red meat, metabolic phenotypes and colorectal cancer in Hawaii
  5. Intake of red meat and heterocyclic amines, metabolic pathway genes and bladder cancer risk
  6. Meat intake, meat mutagens and risk of lung cancer in Uruguayan men
  7. Red and processed meat consumption and the risk of esophageal and gastric cancer subtypes in The Netherlands Cohort Study
  8. Red Meat Consumption and Mortality: Results from Two Prospective Cohort Studies
  9. Meat Consumption and Cancer Risk: a Case-control Study in Uruguay
  10. Meat intake and mortality: a prospective study of over half a million people
  11. Inhibitory effect of marinades with hibiscus extract on formation of heterocyclic aromatic amines and sensory quality of fried beef patties
  12. Processed meat consumption and risk of cancer: a multisite case-control study in Uruguay.
  13. A review and meta-analysis of red and processed meat consumption and breast cancer
  14. Red and processed meat consumption and risk of pancreatic cancer: meta-analysis of prospective studies.
  15. A review and meta-analysis of prospective studies of red and processed meat intake and prostate cancer.
  16. Meat, fish, and colorectal cancer risk: the European Prospective Investigation into cancer and nutrition.
  17. A prospective study of red and processed meat intake in relation to cancer risk.
  18. Meat consumption and risk of colorectal cancer: a meta-analysis of prospective studies.
  19. Red and processed meat and colorectal cancer incidence: meta-analysis of prospective studies.
  20. Meat consumption and mortality – results from the European Prospective Investigation into Cancer and Nutrition
  21. Anatomy of health effects of Mediterranean diet: Greek EPIC prospective cohort study
  22. Association between reported diet and all-cause mortality. Twenty-one-year follow-up on 27,530 adult Seventh-Day Adventists.
  23. Epidemiology of pancreatic cancer in Japan.
  24. Diet, alcohol, coffee and pancreatic cancer: final results from an Italian study.
  25. A cohort study of smoking, alcohol consumption, and dietary factors for pancreatic cancer (United States).
  26. Life-style risk factors for pancreatic cancer in Louisiana: a case-control study.
  27. A case-control study of pancreatic cancer and cigarettes, alcohol, coffee and diet.
  28. A review and meta-analysis of red and processed meat consumption and breast cancer.
  29. Red and processed meat consumption and risk of pancreatic cancer: meta-analysis of prospective studies.
  30. Foods, nutrients and prostate cancer: a case–control study in Uruguay
  31. Dietary factors and risks for prostate cancer among blacks and whites in the United States.
  32. Dietary Factors and Prostatic Cancer
  33. Case-control study of prostate cancer in black patients in Soweto, South Africa.
  34. A prospective study of dietary fat and risk of prostate cancer.
  35. Dietary fat intake and risk of prostate cancer: a prospective study of 25,708 Norwegian men.
  36. Nutrition and prostate cancer.
  37. Prospective study of plasma fatty acids and risk of prostate cancer.
  38. Well-done meat intake and the risk of breast cancer.
  39. Consumption of meat, animal products, protein, and fat and risk of breast cancer: a prospective cohort study in New York.
  40. Frequency of meat and fish intake and risk of breast cancer in a prospective study of 14,500 norwegian women
  41. Meat consumption
  42. Meat consumption and mortality – results from the European Prospective Investigation into Cancer and Nutrition
  43. Q&A on the carcinogenicity of the consumption of red meat and processed meat
  44. Fruits, Vegetables and the Risk of Cancer: a Multisite Case- Control Study in Uruguay
  45. Meat-related mutagens/carcinogens in the etiology of colorectal cancer.
  46. Dietary Red and Processed Meat Intake and Markers of Adiposity and Inflammation: The Multiethnic Cohort Study
  47. Diet and pancreatic cancer: a case-control study.
  48. Red and processed meat consumption and the risk of esophageal and gastric cancer subtypes in The Netherlands Cohort Study.
  49. Metabolic activation and covalent binding to nucleic acids of carcinogenic heterocyclic amines from cooked foods and amino acid pyrolysates.
  50. A review and meta-analysis of prospective studies of red and processed meat intake and prostate cancer
  51. Effect of marinades on the formation of heterocyclic amines in grilled beef steaks.
  52. Effect of beer/red wine marinades on the formation of heterocyclic aromatic amines in pan-fried beef.
  53. Effect of oil marinades with garlic, onion, and lemon juice on the formation of heterocyclic aromatic amines in fried beef patties.
  54. Food sources of nitrates and nitrites: the physiologic context for potential health benefits.
  55. Preventive action of vitamin C on nitrosamine formation.
  56. Potential protective effect of vitamin C on carcinogenesis caused by nitrosamine in drinking water: an experimental study on Wistar rats.
  57. Dietary questions as determinants of mortality: the OXCHECK experience.
  58. Cohort study of diet, lifestyle, and prostate cancer in Adventist men.
  59. Dietary intake of heterocyclic amines and benzo(a)pyrene: associations with pancreatic cancer.
  60. NTP 11th Report on Carcinogens.
  61. Nutritional Epidemiology
  62. Mutational specificities of N-nitrosamines in a host-mediated assay: comparison with direct-acting N-nitroso compounds in vitro and an approach to deducing the nature of ultimate mutagens in vivo.
  63. Diet-induced endogenous formation of nitroso compounds in the GI tract.
  64. Haem, not protein or inorganic iron, is responsible for endogenous intestinal N-nitrosation arising from red meat.
  65. Dietary meat, endogenous nitrosation and colorectal cancer.
  66. Red meat enhances the colonic formation of the DNA adduct O6-carboxymethyl guanine: implications for colorectal cancer risk.
  67. Developing a heme iron database for meats according to meat type, cooking method and doneness level.
  68.  Dose-dependent effect of dietary meat on endogenous colonic N-nitrosation
  69. Total N-nitroso compounds and their precursors in hot dogs and in the gastrointestinal tract and feces of rats and mice: possible etiologic agents for colon cancer.
  70. Risk of colorectal and other gastro-intestinal cancers after exposure to nitrate, nitrite and N-nitroso compounds: a follow-up study.
  71. Dietary exposure and urinary excretion of total N-nitroso compounds, nitrosamino acids and volatile nitrosamine in inhabitants of high- and low-risk areas for esophageal cancer in southern China.
  72. Dietary nitrates, nitrites, and N-nitroso compounds and cancer risk: a review of the epidemiologic evidence.
  73. Nutrition and dietary carcinogens.
  74. Meat and meat-related compounds and risk of prostate cancer in a large prospective cohort study in the United States.
  75. Heterocyclic amines: occurrence and prevention in cooked food.
  76. Effect of white versus red meat on endogenous N-nitrosation in the human colon and further evidence of a dose response.
  77. Reactions of nitrous acid and nitric oxide with porphyrins and haems. Nitrosylhaems as nitrosating agents
  78. DNA damage induced by seven N-nitroso compounds in primary cultures of human and rat kidney cells.
  79. Formation of DNA-damaging N-nitroso compounds from the interaction of calcium-channel blockers with nitrite.
  80. Red meat enhances the colonic formation of the DNA adduct O6-carboxymethyl guanine: implications for colorectal cancer risk.
  81. Meat supplementation improves growth, cognitive, and behavioral outcomes in Kenyan children.
  82. Effect of processed and red meat on endogenous nitrosation and DNA damage.
  83. Green vegetables, red meat and colon cancer: chlorophyll prevents the cytotoxic and hyperproliferative effects of haem in rat colon.
  84. Macromolecular adduct formation and metabolism of heterocyclic amines in humans and rodents at low doses.
  85. Carcinogenicity of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in rats: dose-response studies.
  86. A comparison of the tumors induced by coal tar and benzo[a]pyrene in a 2-year bioassay.
  87. Dietary intake of heterocyclic amines, meat-derived mutagenic activity, and risk of colorectal adenomas.
  88. Analysis of total meat intake and exposure to individual heterocyclic amines in a case-control study of colorectal cancer: contribution of metabolic variation to risk.
  89. Heterocyclic amines, meat intake, and association with colon cancer in a population-based study.
  90. Carcinogenic heterocyclic amines in model systems and cooked foods: a review on formation, occurrence and intake.
  91. Meat intake, heterocyclic amine exposure, and metabolizing enzyme polymorphisms in relation to colorectal polyp risk.
  92. Well-done Meat Intake, Heterocyclic Amine Exposure, and Cancer Risk
  93. Meat, meat cooking methods and preservation, and risk for colorectal adenoma.
  94. Food heating and the formation of heterocyclic aromatic amine and polycyclic aromatic hydrocarbon mutagens/carcinogens.
  95. Cancer risk of heterocyclic amines in cooked foods: an analysis and implications for research.
  96. Role of well-done, grilled red meat, heterocyclic amines (HCAs) in the etiology of human cancer.
  97. Heterocyclic amine content in fast-food meat products.
  98. Some perspectives on the nutritional aspects of breast cancer research. Food-derived heterocyclic amines as etiologic agents in human mammary cancer.
  99. Overview of carcinogenic heterocyclic amines
  100. Food heating and the formation of heterocyclic aromatic amine and polycyclic aromatic hydrocarbon mutagens/carcinogens.
  101. Polycyclic aromatic hydrocarbons in the diet.
  102. The formation and occurrence of polynuclear aromatic hydrocarbons associated with food.
  103. Heterocyclic amine content in beef cooked by different methods to varying degrees of doneness and gravy made from meat drippings.
  104. Heterocyclic amine content of pork products cooked by different methods and to varying degrees of doneness.
  105. Cooking procedures and food mutagens: a literature review.
  106. High concentrations of the carcinogen 2-amino-1-methyl-6-phenylimidazo- [4,5-b]pyridine (PhIP) occur in chicken but are dependent on the cooking method.
  107. BENZO(A)PYRENE AND OTHER POLYNUCLEAR HYDROCARBONS IN CHARCOAL-BROILED MEAT.
  108. 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, a Carcinogen in High- Temperature-Cooked Meat, and Breast Cancer Risk
  109. Mutagens from the cooking of food. II. Survey by Ames/Salmonella test of mutagen formation in the major protein-rich foods of the American diet.
  110. Influence of creatine, amino acids and water on the formation of the mutagenic heterocyclic amines found in cooked meat.
  111. Heterocyclic-Amine Mutagens/Carcinogens in Foods
  112. Effect of cooking time on mutagen formation in smoke, crust and pan residue from pan-broiled pork
  113. Analysis of 200 food items for benzo[a]pyrene and estimation of its intake in an epidemiologic study.
  114. Genotoxicity of heat-processed foods.
  115. Effect of cruciferous vegetable consumption on heterocyclic aromatic amine metabolism in man.
  116. Meat intake and cooking techniques: associations with pancreatic cancer.
  117. Heterocyclic Amine Content in Restaurant-Cooked Hamburgers, Steaks, Ribs, and Chicken
  118. Meat, metabolic genotypes and risk for colorectal cancer.
  119. Polymorphisms of cytochrome P450 1A2 and N-acetyltransferase genes, meat consumption, and risk of colorectal cancer.
  120. Metabolic activation of carcinogens and expression of various cytochromes P450 in human prostate tissue
  121. N-Acetyltransferase expression and DNA binding of N-hydroxyheterocyclic amines in human prostate epithelium
  122. Expression in human prostate of drug- and carcinogen-metabolizing enzymes: association with prostate cancer risk.
  123. Role of free radicals and catalytic metal ions in human disease: an overview.
  124. Iron and colorectal cancer risk: human studies.
  125. Iron and colorectal cancer risk in the α-tocopherol, β-carotene cancer prevention study
  126. Iron-overload induces oxidative DNA damage in the human colon carcinoma cell line HT29 clone 19A.
  127. Available Iron in Response to Dietary Iron Supplementation Are Associated with Changes in Crypt Cell Proliferation in Rat Large Intestine
  128. Dietary iron enhances the tumor rate in dimethylhydrazine-induced colon carcinogenesis in mice
  129. Influence of dietary iron overload on cell proliferation and intestinal tumorigenesis in mice.
  130. Beef meat and blood sausage promote the formation of azoxymethane-induced mucin-depleted foci and aberrant crypt foci in rat colons.
  131. Heme iron from meat and risk of colorectal cancer: a meta-analysis and a review of the mechanisms involved.
  132. A genome-wide systems analysis reveals strong link between colorectal cancer and trimethylamine N-oxide (TMAO), a gut microbial metabolite of dietary meat and fat
  133. Trimethylamine and Trimethylamine N-Oxide, a Flavin-Containing Monooxygenase 3 (FMO3)-Mediated Host-Microbiome Metabolic Axis Implicated in Health and Disease
  134. Dietary compound linked to heart disease may be influenced by gut microbiome
  135. Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis
  136. Involvement of a non-human sialic Acid in human cancer.
  137. A red meat-derived glycan promotes inflammation and cancer progression.
  138. Red meat consumption: An overview of the risks and benefits
  139. Red meats: Time for a paradigm shift in dietary advice
  140. https://data.oecd.org/agroutput/meat-consumption.htm
  141. Leucine Regulates Translation Initiation of Protein Synthesis in Skeletal Muscle after Exercise
  142. Nutritional and regulatory roles of leucine in muscle growth and fat reduction.
  143. Amino acids: metabolism, functions, and nutrition
  144. Branched-chain amino acids activate key enzymes in protein synthesis after physical exercise.
  145. Branched chain amino acids activate messenger ribonucleic acid translation regulatory proteins in human skeletal muscle, and glucocorticoids blunt this action.
  146. A high-protein diet for reducing body fat: mechanisms and possible caveats.
  147. The satiating power of protein—a key to obesity prevention?
  148. Protein, weight management, and satiety
  149. Dietary intake of vitamin K and risk of prostate cancer in the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC-Heidelberg)
  150. Vitamin k contents of meat, dairy, and fast food in the u.s. Diet.
  151. Measurement of K vitamins in animal tissues by high-performance liquid chromatography with fluorimetric detection.
  152. Quantitative measurement of tetrahydromenaquinone-9 in cheese fermented by propionibacteria.
  153. Vitamin K content of foods and dietary vitamin K intake in Japanese young women.
  154. Determination of phylloquinone and menaquinones in animal products with fluorescence detection after postcolumn reduction with metallic zinc.
  155. Quantitative measurement of vitamin K2 (menaquinones) in various fermented dairy products using a reliable high-performance liquid chromatography method.
  156. https://en.wikipedia.org/wiki/Ischemic_cell_death
  157. Growth inhibitory effects of vitamin K2 on colon cancer cell lines via different types of cell death including autophagy and apoptosis.
  158. Apoptosis of liver cancer cells by vitamin K2 and enhancement by MEK inhibition.
  159. Protein-enriched diet, with the use of lean red meat, combined with progressive resistance training enhances lean tissue mass and muscle strength and reduces circulating IL-6 concentrations in elderly women: a cluster randomized controlled trial
  160. Sarcopenia: An Undiagnosed Condition in Older Adults. Current Consensus Definition: Prevalence, Etiology, and Consequences
  161. Vegan diets: practical advice for athletes and exercisers
  162. Effect of creatine and weight training on muscle creatine and performance in vegetarians.
  163. Effect of creatine supplementation and a lacto-ovo-vegetarian diet on muscle creatine concentration.
  164. Open-label adjunctive creatine for female adolescents with SSRI-resistant major depressive disorder: a 31-phosphorus magnetic resonance spectroscopy study.
  165. Effect of creatine supplementation and sleep deprivation, with mild exercise, on cognitive and psychomotor performance, mood state, and plasma concentrations of catecholamines and cortisol.
  166. The influence of creatine supplementation on the cognitive functioning of vegetarians and omnivores.
  167. Oral creatine monohydrate supplementation improves brain performance: a double-blind, placebo-controlled, cross-over trial.
  168. Creatine supplementation, sleep deprivation, cortisol, melatonin and behavior.
  169. Prevention of traumatic headache, dizziness and fatigue with creatine administration. A pilot study.
  170. Effects of acute creatine monohydrate supplementation on leucine kinetics and mixed-muscle protein synthesis
  171. Global and targeted gene expression and protein content in skeletal muscle of young men following short-term creatine monohydrate supplementation.
  172. Effect of creatine supplementation on jumping performance in elite volleyball players.
  173. Skill execution and sleep deprivation: effects of acute caffeine or creatine supplementation – a randomized placebo-controlled trial.
  174. Does oral creatine supplementation improve strength? A meta-analysis.
  175. Global and targeted gene expression and protein content in skeletal muscle of young men following short-term creatine monohydrate supplementation.
  176.  Intakes of red meat, processed meat, and meat-mutagens increase lung cancer risk
  177.  A prospective study of red and processed meat intake in relation to cancer risk.
  178. Eat to live, not live to eat.
  179. IARC, 2015. Monographs Evaluate Consumption of Red Meat and Processed Meat. International Agency for Research on Cancer, Press release No. 240, World Health Organization.
  180. Exercise and nutritional interventions for improving aging muscle health.
  181. Carcinogenicity of consumption of red meat and processed meat: A review of scientific news since the IARC decision.
  182. Occurrence of halogenated flame retardants in commercial seafood species available in European markets
  183. Exposure to perfluorinated compounds in Catalonia, Spain, through consumption of various raw and cooked foodstuffs, including packaged food
  184. Effects of various cooking processes on the concentrations of arsenic, cadmium, mercury, and lead in foods.
  185. Concentrations of polybrominated diphenyl ethers, hexachlorobenzene and polycyclic aromatic hydrocarbons in various foodstuffs before and after cooking.
  186. Influence of various cooking processes on the concentrations of PCDD/PCDFs, PCBs and PCDEs in foods
  187. Meat consumption and cancer risk: a critical review of published meta-analyses
  188. The World Cancer Research Fund report 2007: A challenge for the meat processing industry
  189. Meat subtypes and their association with colorectal cancer: Systematic review and meta-analysis
  190. Processed meat: the real villain?
  191. Meat: The balance between nutrition and health. A review
  192. Mechanisms Linking Colorectal Cancer to the Consumption of (Processed) Red Meat: A Review
  193. A critical overview on the biological and molecular features of red and processed meat in colorectal carcinogenesis
  194. Potential health hazards of eating red meat
  195. Cancer incidence attributable to red and processed meat consumption in Alberta in 2012
  196. The impact of red and processed meat consumption on cancer and other health outcomes: Epidemiological evidences
  197. Animal foods
  198. Diet and the risk of head-and-neck cancer among never-smokers and smokers in a Chinese population
  199. A review and meta-analysis of prospective studies of red and processed meat, meat cooking methods, heme iron, heterocyclic amines and prostate cancer
  200. Food of animal origin and risk of non-Hodgkin lymphoma and multiple myeloma: A review of the literature and meta-analysis

Red and processed meat consumption and risk of bladder cancer: a dose–response meta-analysis of epidemiological studies

  1. Red and processed meat consumption and mortality: dose–response meta-analysis of prospective cohort studies
  2. Association Between Consumption of Red and Processed Meat and Pancreatic Cancer Risk: A Systematic Review and Meta-analysis
  3. The cancer risk related to meat and meat products
  4. Consumption of Red/Processed Meat and Colorectal Carcinoma: Possible Mechanisms Underlying the Significant Association
  5. A red meat-derived glycan promotes inflammation and cancer progression
  6. Red and processed meat, nitrite, and heme iron intakes and postmenopausal breast cancer risk in the NIH-AARP Diet and Health Study
  7. Human risk of diseases associated with red meat intake: Analysis of current theories and proposed role for metabolic incorporation of a non-human sialic acid
  8. Meat intake, cooking methods and doneness and risk of colorectal tumours in the Spanish multicase-control study (MCC-Spain)
  9. Increased oxidative and nitrosative reactions during digestion could contribute to the association between well-done red meat consumption and colorectal cancer
  10. Polycyclic Aromatic Hydrocarbons (PAHs) and their Bioaccessibility in Meat: a Tool for Assessing Human Cancer Risk
  11. European Code against Cancer 4th Edition: Diet and cancer
  12. Meat, Fish, Poultry, and Egg Intake at Diagnosis and Risk of Prostate Cancer Progression
  13. Iron deficiency anaemia
  14. Occupational Safety and Health Administration
  15. Effect of egg ingestion on trimethylamine-N-oxide production in humans: a randomized, controlled, dose-response study.
  16. Formation of methylamines from ingested choline and lecithin.
  17. TMAO: A small molecule of great expectations
  18. Plasma choline metabolites and colorectal cancer risk in the Women’s Health Initiative Observational Study.
  19. Rescue of the neuroblastoma mutant of the human nucleoside diphosphate kinase A/nm23-H1 by the natural osmolyte trimethylamine-N-oxide
  20. Substrate rescue of DNA polymerase beta containing a catastrophic L22P mutation.
  21. N-Glycolylneuraminic acid in human tumours
  22. Dietary Components Related to N-Nitroso Compound Formation: A Prospective Study of Adult Glioma
  23. Oral AGE restriction ameliorates insulin resistance in obese individuals with the metabolic syndrome: a randomised controlled trial
  24. Nutritional Intake of Vitamins K1 (Phylloquinone) and K2 (Menaquinone) in The Netherlands
  25. Dietary Intake of Menaquinone Is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study
  26. Iron in red meat-friend or foe.
  27. Food groups and risk of colorectal cancer.

Further Reading:

  1. https://examine.com/nutrition/is-processed-meat-bad-for-me/
  2. https://examine.com/nutrition/scientists-just-found-that-red-meat-causes-cancer–or-did-they/
  3. https://examine.com/nutrition/does-red-meat-cause-cancer/
  4. https://examine.com/nutrition/how-can-i-make-red-meat-healthier/

More on nitrate:

  1. http://pubs.rsc.org/en/content/articlelanding/1975/c310.1039/c39750000884#!divAbstract
  2. https://examine.com/supplements/nitrate/

More on L-carnitine:

  1. https://examine.com/supplements/l-carnitine/

More on vitamin K2:

  1. https://honey-guide.com/2014/03/10/menaquinones-k2-and-phylloquinone-k1-content-of-animal-products-and-fermented-foods/
  2. http://www.k-vitamins.com/index.php?page=Cancer
  3. The Ultimate Vitamin K2 Resource
  4. https://wholehealthsource.blogspot.com/search?q=vitamin+k2

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4 Comments

  1. Marouane 10/08/2017 at 10:16 pm - Reply

    Great article! Keep it up

    • Myolean Fitness 11/08/2017 at 9:59 am - Reply

      Thanks!

      Vincent did all the work!

  2. Bunny Clapton 24/02/2018 at 12:11 am - Reply

    So very useful, thank you. My husband has colorectal cancer and wanted to understand what may have contributed to its development. He was/is a great meat eater while a not-great vegetable and fruit eater. However, he is also thin, non-smoking, active, occasional wine consumer.

    • Myolean Fitness 24/02/2018 at 12:17 am - Reply

      Hi and thanks for your comment,

      I hope that your husband kicks the cancer’s butt!

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