Red and processed meat

What it is

Red meat is unprocessed mammalian muscle, such as beef, pork or lamb; processed meat has been salted, cured, fermented or smoked ¹.

Potassium or sodium nitrite (E 249, E 250) is added in curing to fix colour and inhibit microbial growth ².

In the body

Substances in meat, or formed when it is cured or cooked hot, can damage DNA ¹.

Haem catalyses nitrosation and lipid peroxidation in the gut ¹. In 21 volunteers given 420 g of red meat daily for 15 to 21 days, against a vegetarian diet, faecal N-nitroso compounds rose from 193 to 667 μg/day and O6-carboxymethylguanine-positive colonocytes from 22.7% to 55.7% ³.

Meat and meat products are the main dietary source of carcinogenic N-nitrosamines; EFSA judges 95th-percentile intake a health concern ⁴.

Heterocyclic aromatic amines such as PhIP form in meat cooked at high temperature ⁵. Hepatic CYP1A2 N-hydroxylates PhIP; NAT2 or SULT1A1 esterifies the product, which forms the DNA adduct dG-C8-PhIP ⁵⁶.

Bioactivation of PhIPHepatocyte endoplasmic reticulum, then cytosol

PhIP
Cytochrome P450 1A2 (CYP1A2)O2, NADPH via cytochrome P450 reductaseCYP1A2 accounts for an estimated 70% of PhIP metabolism in humans
N-Hydroxy-PhIP
N-acetyltransferase 2 (NAT2)Acetyl-CoAThe ester binds DNA; SULT1A1 and SULT1A2 also activate N-hydroxy-PhIP
N-Acetoxy-PhIP

Gut bacteria cleave carnitine, abundant in red meat, to trimethylamine, which hepatic FMO3 oxidises to trimethylamine N-oxide (TMAO) ⁷⁸⁶. In 113 adults, plasma TMAO rose about threefold after 4 weeks of a red-meat diet against white-meat or meat-free diets ⁸.

Carnitine to trimethylamine N-oxideGut lumen (bacteria), then hepatocyte endoplasmic reticulum

L-Carnitine
Carnitine oxygenase CntA with reductase CntB (gut bacteria)NADHCleaves the C–N bond; another microbial route passes through γ-butyrobetaine
Trimethylamine
Flavin-containing monooxygenase 3 (FMO3)FAD, NADPH, O2FMO3 deficiency causes trimethylaminuria
Trimethylamine N-oxide

What studies show

People who eat more red and processed meat have slightly higher rates of heart disease, bowel cancer and death ⁹¹⁰.

In six US cohorts (29,682 adults, median 19 years), each 2 extra weekly servings (2 against 0 for processed meat and cardiovascular disease) were associated with 30-year absolute risk increases in cardiovascular disease and death of 0.62 and 0.76 percentage points for unprocessed red meat (hazard ratios 1.03 each) and 1.74 and 0.90 for processed meat (1.07 and 1.03) ⁹.

In UK Biobank (mean 5.7 years), colorectal cancer occurred in 274 of 68,359 people (0.40%) eating red and processed meat less than twice a week and 1209 of 192,600 (0.63%) eating it four or more times (adjusted hazard ratio 1.20, 95% CI 1.04 to 1.37), an association confined to men ¹⁰.

References

Independent research
Turesky RJ. Mechanistic Evidence for Red Meat and Processed Meat Intake and Cancer Risk: A Follow-up on the International Agency for Research on Cancer Evaluation of 2015 Chimia, 2018.
doi:10.2533/chimia.2018.718 PubMed 30376922
Funding and finding
Funding
The research conducted in the author's lab on cooked meat mutagens and colorectal cancer has been supported by National Institutes of Health Grants R01CA122320 and R01CA134700.
Finding
Narrative review. Red meat: unprocessed mammalian muscle meats, including beef, veal, pork, lamb, mutton, horse or goat. Processed meat: meat treated through salting, curing, fermentation, smoking or other processes to enhance flavour or improve preservation. Curing with nitrite can produce carcinogenic N-nitroso compounds, at less than 1 to 130 ppb in cured meats, activated by CYP2E1. Ingested haem can catalyse the nitrosation of endogenous secondary amines and exert pro-oxidative effects by catalysis of lipid peroxidation in the gastrointestinal tract. High-temperature cooking produces heterocyclic aromatic amines, which cytochrome P450 enzymes N-hydroxylate and N-acetyltransferases or sulfotransferases convert to DNA-binding intermediates. Many of these chemicals form DNA adducts.
Regulator
EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS), Mortensen A, Aguilar F, Crebelli R, Di Domenico A, Dusemund B, et al. Re-evaluation of potassium nitrite (E 249) and sodium nitrite (E 250) as food additives EFSA Journal, 2017.
doi:10.2903/j.efsa.2017.4786 PubMed 32625504
Funding and finding
Funding
European Food Safety Authority; requestor: European Commission (Question numbers EFSA-Q-2011-00460 and EFSA-Q-2011-00461).
Finding
Sodium and potassium nitrite are used in curing mixtures to develop and fix the colour of meat, to inhibit microbial growth and to develop characteristic flavours. Acceptable daily intake 0.07 mg nitrite ion/kg body weight per day, based on methaemoglobin formation. Use as food additives supplied about 17% (range 1.5 to 36.0%) of overall nitrite exposure. Margin of exposure for endogenous NDMA formed from nitrite at the ADI 4.2 × 10^5; for preformed NDMA plus NDEA in processed food, below 10,000 in all age groups at high exposure. Nitrosamines formed from nitrite added at authorised levels could not be clearly distinguished from those present without added nitrite. There was evidence linking preformed NDMA with colorectal cancer and some evidence linking nitrite plus nitrate from processed meat with colorectal cancer.
Independent research
Lewin MH, Bailey N, Bandaletova T, Bowman R, Cross AJ, Pollock J, et al. Red meat enhances the colonic formation of the DNA adduct O6-carboxymethyl guanine: implications for colorectal cancer risk Cancer Research, 2006.
doi:10.1158/0008-5472.CAN-05-2237 PubMed 16452248
Funding and finding
Participants
21
Follow-up
15 to 21 days on each diet
Funding
Grant support: UK Medical Research Council grant-in-aid and UK Food Standards Agency.
Finding
Faecal apparent total N-nitroso compounds, vegetarian against red meat diet: 699 ± 120 against 4923 ± 1387 μg/kg (P < 0.0001); output 193 ± 43 against 667 ± 141 μg/day (P = 0.0002). Exfoliated colonocytes staining positive for O6-carboxymethylguanine: 22.7 ± 2.6% against 55.7 ± 3.3% (P < 0.001); faecal N-nitroso compounds correlated with the percentage of positive cells (r = 0.56, n = 55). The red meat was prepared to minimise heterocyclic amine content.
Regulator
EFSA Panel on Contaminants in the Food Chain (CONTAM), Schrenk D, Bignami M, Bodin L, Chipman JK, del Mazo J, et al. Risk assessment of N-nitrosamines in food EFSA Journal, 2023.
doi:10.2903/j.efsa.2023.7884 PubMed 36999063
Funding and finding
Funding
European Food Safety Authority; requestor: European Commission (Question number EFSA-Q-2020-00665).
Finding
Assessment of 10 carcinogenic N-nitrosamines occurring in food (NDMA, NMEA, NDEA, NDPA, NDBA, NMA, NSAR, NMOR, NPIP, NPYR), assumed equally potent; BMDL10 10 μg/kg body weight per day from rat liver tumours induced by NDEA. Exposure 0 to 208.9 ng/kg body weight per day across surveys, age groups and scenarios. Meat and meat products were the main contributing food category, 7 to 100% of exposure across surveys excluding cooked unprocessed meat and fish and 20 to 99% including them. Margins of exposure at the 95th percentile 3337 to 48; highly likely (98 to 100% certain) to be below 10,000 for all age groups, which raises a health concern.
Independent research
Bellamri M, Walmsley SJ, Turesky RJ. Metabolism and biomarkers of heterocyclic aromatic amines in humans Genes and Environment, 2021.
doi:10.1186/s41021-021-00200-7 PubMed 34271992
Funding and finding
Funding
R01CA122320 and the National Cancer Institute Cancer Center Support Grant CA077598 supported a portion of the research conducted in the Turesky Laboratory.
Finding
Narrative review. Heterocyclic aromatic amines form during high-temperature cooking of meat, poultry and fish, in amounts that increase with cooking time and temperature; PhIP and AαC can reach 50 ppb or more in well-done meat and poultry. In model systems with amino acids and sugars, creatine or creatinine is the precursor of the imidazo moieties of the aminoimidazoarenes, which are more potent mutagens than the amino acid pyrolysates. Hepatic CYP1A2 accounts for an estimated 70% of PhIP metabolism in humans, mainly by N-oxidation to genotoxic N-hydroxy-PhIP. Most N-hydroxy-heterocyclic amines are bioactivated by human NAT2 to reactive esters; N-acetoxy-PhIP is stable enough to isolate; SULT1A1 and SULT1A2 catalyse binding of N-hydroxy-PhIP to DNA. The proposed reactive intermediate is the heteroaryl nitrenium ion; N-hydroxy-PhIP forms the adduct N-(2′-deoxyguanosin-8-yl)-PhIP (dG-C8-PhIP).
Textbook or database
UniProt Consortium. UniProt: the Universal Protein Knowledgebase in 2025 Nucleic Acids Research, 2025.
doi:10.1093/nar/gkae1010 PubMed 39552041
Funding and finding
Funding
National Human Genome Research Institute (NHGRI) [HG002273]; Office of the Director, NIH OD [U24HG007822]; National Institute of Allergy and Infectious Diseases (NIAID); National Institute on Aging (NIA); National Institute of General Medical Sciences (NIGMS) [R35GM141873]; National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); National Eye Institute (NEI); National Cancer Institute (NCI); National Heart, Lung, and Blood Institute (NHLBI); Biotechnology and Biological Sciences Research Council (BBSRC) [BB/T015608/1]; National Science Foundation's Directorate for Biological Sciences [BB/X002179/1]; Open Targets; Horizon 2020 - Research and Innovation Framework Programme [825575]; State Secretariat for Education, Research and Innovation (SERI); European Molecular Biology Laboratory (EMBL) Australia. Funding for open access charge: National Institutes of Health.
Finding
Reviewed human entries, release 2026_03, read through rest.uniprot.org on 2026-10-21. MB (P02144), myoglobin: monomeric haem protein of the muscle sarcoplasm that stores oxygen and facilitates its diffusion within muscle; reversibly binds oxygen through a pentacoordinated haem iron; has nitrite reductase activity. FMO3 (P31513): hepatic enzyme of the endoplasmic reticulum and microsomal membrane, cofactor FAD; trimethylamine + NADPH + O2 = trimethylamine N-oxide + NADP+ + H2O (EC 1.14.13.148); TMA is generated by gut microbiota from dietary precursors including L-carnitine; deficiency of FMO-mediated N-oxidation causes trimethylaminuria. CYP1A2 (P05177): hepatic cytochrome P450 of the endoplasmic reticulum, haem cofactor, using O2 and electrons from NADPH via cytochrome P450 reductase; catalyses the N-hydroxylation of heterocyclic amines. NAT2 (P11245): cytoplasmic; an N-hydroxyarylamine + acetyl-CoA = an N-acetoxyarylamine + CoA (EC 2.3.1.118); bioactivates several known carcinogens. SULT1A1 (P50225): cytoplasmic sulfotransferase using 3'-phosphoadenylyl sulfate; mediates the metabolic activation of carcinogenic N-hydroxyarylamines to reactive intermediates that form DNA adducts.
Independent research
Zhu Y, Jameson E, Crosatti M, Schäfer H, Rajakumar K, Bugg TD, et al. Carnitine metabolism to trimethylamine by an unusual Rieske-type oxygenase from human microbiota Proceedings of the National Academy of Sciences of the United States of America, 2014.
doi:10.1073/pnas.1316569111 PubMed 24591617
Funding and finding
Funding
This work is supported by the Royal Society (RG2011/R1) and partially by the Natural Environment Research Council (NE/I027061/1).
Finding
A two-component Rieske-type oxygenase/reductase, CntA and CntB, encoded in a carnitine utilisation gene cluster in 39 human microbiota reference genomes, cleaves the C-N bond of carnitine to trimethylamine and a four-carbon compound. Deletion of cntA or cntB abolished trimethylamine formation from carnitine in A. baumannii; purified CntA and CntB with NADH were necessary and sufficient in vitro. CntB is a predicted NAD(P)-dependent reductase with flavin and plant-type [2Fe-2S] ferredoxin domains; CntA carries a Rieske [2Fe-2S] centre and a mononuclear iron centre, and its glutamate 205 is essential for catalysis.
Independent research
Wang Z, Bergeron N, Levison BS, Li XS, Chiu S, Jia X, et al. Impact of chronic dietary red meat, white meat, or non-meat protein on trimethylamine N-oxide metabolism and renal excretion in healthy men and women European Heart Journal, 2019.
doi:10.1093/eurheartj/ehy799 PubMed 30535398
Funding and finding
Registration
NCT01427855
Participants
113
Follow-up
4 weeks on each of three isocaloric diets
Funding
This work was supported by the National Institutes of Health and the Office of Dietary Supplements [R01 HL103866 to S.L.H., R01 HL126827 and R01 DK106000 to W.H.W.T. and S.L.H., RO1 HL106003 to R.M.K. and N.B., R01 HL130819 to Z.W. S.L.H. is also partially supported by an award from the Leducq Foundation.] and The University of California, San Francisco (UCSF) Clinical and Translational Science Unit.
Finding
Carnitine is enriched in red meat; the red meat diet contained 3.8-fold and 7.9-fold more carnitine than the white meat and non-meat diets. After 4 weeks, plasma TMAO rose about threefold on the red meat diet against the white meat or non-meat diets (P < 0.0001), with median absolute increases of 5.9 and 5.7 μM against non-meat and white meat; urine TMAO also rose. Red meat reduced the fractional renal excretion of TMAO (P < 0.05) and increased that of carnitine, γ-butyrobetaine and crotonobetaine. Isotope tracers (n = 13) showed more TMA and TMAO formed from carnitine, not choline, on the red or white meat diet than on the non-meat diet. Saturated fat did not affect TMAO. Plasma TMAO fell within 4 weeks of stopping red meat. The authors state that the direct contribution of TMAO to cardiovascular disease pathogenesis in humans is unclear.
Independent research
Zhong VW, Van Horn L, Greenland P, Carnethon MR, Ning H, Wilkins JT, et al. Associations of Processed Meat, Unprocessed Red Meat, Poultry, or Fish Intake With Incident Cardiovascular Disease and All-Cause Mortality JAMA Internal Medicine, 2020.
doi:10.1001/jamainternmed.2019.6969 PubMed 32011623
Funding and finding
Participants
29,682
Follow-up
median 19.0 years (interquartile range 14.1 to 23.7)
Funding
This study was funded in part by a postdoctoral fellowship to Dr Zhong from the American Heart Association Strategically Focused Research Networks (14SFRN20480260). The Lifetime Risk Pooling Project was funded by grant R21 HL085375 from the NIH/NHLBI and by the Northwestern University Feinberg School of Medicine. The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.
Finding
6963 incident cardiovascular events and 8875 deaths. Hazard ratios and 30-year absolute risk differences per 2 servings a week (2 against 0 servings a week for the nonmonotonic association of processed meat with cardiovascular disease). Cardiovascular disease: processed meat HR 1.07 (95% CI 1.04 to 1.11), ARD 1.74% (0.85% to 2.63%); unprocessed red meat HR 1.03 (1.01 to 1.06), ARD 0.62% (0.07% to 1.16%); poultry HR 1.04 (1.01 to 1.06), ARD 1.03% (0.36% to 1.70%); fish HR 1.00 (0.98 to 1.02). All-cause mortality: processed meat HR 1.03 (1.02 to 1.05), ARD 0.90% (0.43% to 1.38%); unprocessed red meat HR 1.03 (1.01 to 1.05), ARD 0.76% (0.19% to 1.33%); poultry HR 0.99 (0.97 to 1.02); fish HR 0.99 (0.97 to 1.01). Results read from the abstract in PubMed Central.
Independent research
Bradbury KE, Murphy N, Key TJ. Diet and colorectal cancer in UK Biobank: a prospective study International Journal of Epidemiology, 2020.
doi:10.1093/ije/dyz064 PubMed 30993317
Funding and finding
Participants
475,581
Follow-up
mean 5.7 years (maximum 8.6)
Funding
This work was supported by Girdlers' New Zealand Health Research Council Fellowship (K.E.B.), Cancer Research UK (T.J.K.; C8221/A19170 and 570/A16491), the UK Medical Research Council (T.J.K.; MR/M012190/1) and the Wellcome Trust [T.J.K.; Our Planet Our Health, project: Livestock, Environment and People (LEAP) (205212/Z/16/Z)]. The funders did not influence the design of the study, analysis or interpretation of the data, the writing of this report or the decision to publish.
Finding
2609 incident colorectal cancers. Red and processed meat (Figure 1): less than twice a week, mean 21 g/day, 274 cases among 68,359 participants; 4 or more times a week, mean 76 g/day, 1209 cases among 192,600; adjusted HR 1.20 (95% CI 1.04 to 1.37); per 50 g/day 1.17 (1.04 to 1.32). Red meat per 50 g/day 1.18 (1.00 to 1.39); processed meat per 25 g/day 1.19 (1.03 to 1.38). Heterogeneity by sex (P = 0.008): positive association in men, none in women. Poultry and fish were not associated. Fibre from bread and breakfast cereals, highest against lowest fifth, HR 0.86 (0.76 to 0.98).
Industry-funded
Alexander DD, Weed DL, Miller PE, Mohamed MA. Red Meat and Colorectal Cancer: A Quantitative Update on the State of the Epidemiologic Science Journal of the American College of Nutrition, 2015.
doi:10.1080/07315724.2014.992553 PubMed 25941850
Funding and finding
Funding
This manuscript was partially funded by Meat & Livestock Australia (MLA). MLA did not contribute to the writing, analysis, or interpretation of study findings.
Finding
High against low red meat intake, 27 cohorts: summary relative risk 1.11 (95% CI 1.03 to 1.19), heterogeneity P = 0.014, I2 33.6%. Associations attenuated in models of fresh red meat separated from processed meat, in better adjusted models, in women and outside the United States. Categories of median intake above 100 g/day (6 studies): 1.20 (1.11 to 1.29); categories up to 100 g/day 1.00 to 1.03, not significant; each 70 g increment (13 studies) 1.05 (0.97 to 1.13). The authors conclude that red meat intake does not appear to be an independent predictor of colorectal cancer risk.
Expert consensus
Bouvard V, Loomis D, Guyton KZ, Grosse Y, El Ghissassi F, Benbrahim-Tallaa L, et al. Carcinogenicity of consumption of red and processed meat Lancet Oncology, 2015.
doi:10.1016/S1470-2045(15)00444-1 PubMed 26514947
Funding and finding
Funding
not stated
Finding
Red meat: unprocessed mammalian muscle meat such as beef, veal, pork, lamb, mutton, horse or goat. Processed meat: meat transformed through salting, curing, fermentation, smoking or other processes to enhance flavour or improve preservation. More than 800 epidemiological studies assessed. Colorectal cancer: positive associations with red meat in 7 of 14 cohorts and with processed meat in 12 of 18 cohorts; a meta-analysis of 10 cohorts gave relative risks of 1.17 (95% CI 1.05 to 1.31) per 100 g/day of red meat and 1.18 (1.10 to 1.28) per 50 g/day of processed meat. Processed meat classified as carcinogenic to humans (Group 1) on sufficient evidence for colorectal cancer; chance, bias and confounding judged unlikely explanations. Red meat classified as probably carcinogenic to humans (Group 2A) on limited evidence in humans and strong mechanistic evidence; chance, bias and confounding could not be ruled out with the same confidence. Mechanistic evidence: haem iron mediates formation of N-nitroso compounds and lipid oxidation products in the digestive tract; 300 or 420 g/day of red meat increased putative N-nitroso-derived DNA adducts in two intervention studies; meat heated at high temperature contains heterocyclic aromatic amines, which are genotoxic.
Expert consensus
Johnston BC, Zeraatkar D, Han MA, Vernooij RWM, Valli C, El Dib R, et al. Unprocessed Red Meat and Processed Meat Consumption: Dietary Guideline Recommendations From the Nutritional Recommendations (NutriRECS) Consortium Annals of Internal Medicine, 2019.
doi:10.7326/M19-1621 PubMed 31569235
Funding and finding
Registration
PROSPERO CRD42017074074; PROSPERO CRD42018088854
Funding
Primary Funding Source: None. Grant support: Dr. El Dib received a São Paulo Research Foundation (FAPESP) (2018/11205-6) scholarship and funding from the National Council for Scientific and Technological Development (CNPq 310953/2015-4) and the Faculty of Medicine, Dalhousie University.
Finding
The panel suggests that adults continue current unprocessed red meat consumption and continue current processed meat consumption (weak recommendations, low-certainty evidence); 11 of 14 panellists voted for each, 3 for a weak recommendation to reduce. For a decrease of 3 servings a week of unprocessed red meat: 12 randomised trials (54,000 participants) gave low- to very low-certainty evidence of little or no effect on cardiometabolic outcomes and cancer; 23 cohorts (1.4 million participants) gave 1 to 6 fewer major cardiovascular events and cases of type 2 diabetes per 1000 persons over an average 10.8 years; 17 cohorts (2.2 million) gave 7 fewer lifetime cancer deaths per 1000. For processed meat: 1 to 12 fewer cardiometabolic events per 1000 (10 cohorts, 778,000 participants) and 1 to 8 fewer cancer events per 1000 over a lifetime (31 cohorts, 3.5 million). The panel did not rate up for dose-response because of potential residual confounding. Randomised trials were limited by small differences in meat consumption between groups.
Funding unknown
No authors listed. Correction: Nutritional Recommendations (NutriRECS) on Consumption of Red and Processed Meat Annals of Internal Medicine, 2020.
doi:10.7326/L19-0822 PubMed 31887739
Funding and finding
Funding
not stated
Finding
Published online 31 December 2019, in print 4 February 2020. On the disclosure forms of the six NutriRECS articles on red and processed meat, Bradley Johnston did not indicate a grant from Texas A&M AgriLife Research to fund investigator-driven research related to saturated and polyunsaturated fats; the funding period started within the 36-month reporting period of the ICMJE disclosure form. The updated forms include this grant and funding from the International Life Science Institute (North America) that ended before the 36-month reporting period.
Industry-funded
Erickson J, Sadeghirad B, Lytvyn L, Slavin J, Johnston BC. The Scientific Basis of Guideline Recommendations on Sugar Intake: A Systematic Review Annals of Internal Medicine, 2017.
doi:10.7326/M16-2020 PubMed 27992898
Funding and finding
Registration
PROSPERO CRD42015029182
Funding
This project was funded by the Technical Committee on Dietary Carbohydrates of ILSI North America. The authors wrote the protocol, the scope of which was reviewed and approved by ILSI; and conducted the study independently from ILSI. The abstract states that the funding source is primarily supported by the food and agriculture industry.
Finding
9 guidelines with 12 recommendations; each advised less consumption of foods containing nonintrinsic sugars. Guidelines scored poorly on AGREE II for rigour of development, applicability and editorial independence; 5 recommendations set limits from less than 25% to less than 5% of energy; quality of the supporting evidence was low to very low. The authors concluded that the guidelines do not meet criteria for trustworthy recommendations.

Updated 2026-10-21