A Story Of Meat & Cancer

Science

Meat & Colorectal Cancer: A Proven Risk?

Posted on February 08, 2019  - By Jacki

Data statistics predict cancer rates are expected to rise
Every year, there are approximately 14 million new cases of cancer. There are 8.2 million cancer-related deaths each year. These statistics, make cancer one of the leading causes of death, globally. To augment the severity of cancer and cancer-related morbidity, is the fact that cancer cases are expected to rise nearly 70% over the next 20 years—meaning there is an expected 22 million new cases a year. In sum, cancer very well could be the leading cause of mortality [1].

Meat consumption is shown to increase cancer risk
Recently, meat consumption has been shown to increase cancer risk, for certain types of cancer. In October of 2015, the International Agency for Research on Cancer (IARC), issued the results on their evaluation of red and processed meat consumption—detailing these meats at some extent, carcinogenic. Beef, veal, lamb, pork and goat, among others are considered red meat. Processed meat, is a product of red meat processing, such as curing, adding preservatives, salting or smoking [2]. Common processed meats include: pastrami, salami, smoked chicken, bacon and ham. The IARC concluded their research by classifying red meat as “probably carcinogenic to humans” (Group 2A). In greater severity, processed meats were and are now classified as “carcinogenic to humans” (Group 1) [3,4].

Studies detail that an increase in meat consumption significantly increases colorectal cancer risk.
Amongst the most prominent studies linking meat consumption to cancers, are those which associate consumption and Colorectal Cancer (CRC). For instance, the European Prospective Investigation into Cancer and Nutrition (EPIC) via a prospective 5 year cohort study, portrayed an increase in CRC risk positively associated with the intake of red and processed meats. This study was carried out and followed 478,040 men and women, across 10 European countries [9]. The study found processed meats to be a bigger culprit in potentiating CRC. In a report which combined three meta-analyses, it was concluded that with consumption at(and with an increase of) 100 grams per day, there is a 12-17% associated increased risk for developing CRC. This study defined the increase in ‘meat’ to include all meats or red meats.
Astoundingly, there was a 49% increased risk between processed meat consumption of just 25 g per day and CRC [11-13]. This studies results are supported by various supplemental studies. Across studies, percentage risk differs, but it remains clear that risk is heightened via dietary intake of meats. For instance, another study, showed that 50 grams of processed meats per day would increase CRC risk by nearly 18% [14]. When combined, these studies and statistics support the reports that both red and processed meats are indeed cancer-causing.

Research has previously detailed three main mechanisms for the carcinogenicity of meat.
The mechanisms behind the interaction between meat and the aggravation of cancer have been investigated. Mechanistically, a study done in 2015 detailed that meat is carcinogenic due to 1) N-nitroso-compounds (NOCs), 2) Polycyclic aromatic hydrocarbons (PAHs), 3) Heterocyclic aromatic amines (HAAs).
How and when are these compounds created?
These processes are posed as threats, as they are included in meat processing methods, including heating meat at high temperatures (HAAs), and smoking or curing (PAH, NOC)[18, 71]. Inflammation, food metabolites and damage of DNA are potential aggravators of meat carcinogenicity [47-50]. Additionally, research scientifically links fat content and iron content in meats to cancer development [2, 43, 51-53]. Beyond these, scientists believe the gut bacteria are involved in the relationship of meat and cancer development[54-60]. Finally, a variety of other mechanisms at play have been suggested, including: heavy metals and others (including but not limited to arsenic, cadmium, mercury, lead, PCB’s) have also been implicated mechanistically[9, 61].

Our Conclusion?
Meat poses a threat to human health. There is need for further studies and investigation, although the topic remains controversial. Despite the weaknesses of the available material and our understanding of this issue, there are many steps the individual can take to derail the toxic effects of meat. These include: perhaps most safely— eliminating red & processed meat from the diet altogether, or, altering cooking processes, limiting meat intake, choosing low-fat meats, eliminating consumptions of processed meats, and consuming vitamins(C & E) and anti-mutagenic additives or food agents with meat intake.

Sources:
1. Stewart, B., Wild, C.P., 2014. World Cancer Report. IARC Press, Lyon, France2014, ISBN: 9789283204299.
2. Lynnette R. Ferguson, Meat and cancer, Meat Science, Volume 84, Issue 2, 2010,Pages 308-313,ISSN 0309-1740,
3. Bouvard, V., Loomis, D., Guyton, K.Z., Grosse, Y., Ghissassi, F.E., Benbrahim-Tallaa, L., Guha, N., Mattock, H., Straif, K., 2015. International agency for research on cancer monograph working group. Carcinogenicity of consumption of red and processed meat. Lancet Oncol. 16, 1599e1600.
4. IARC, 2015.Monographs Evaluate Consumption of Red Meat and Processed Meat. International Agency for Research on Cancer, Press release No. 240, World Health Organization.
9. Marije Oostindjer, et al. The role of red and processed meat in colorectal cancer development: a perspective, Meat Science, Volume 97, Issue 4, 2014, Pages 583-596, ISSN 0309-1740.
11. Larsson, S. C., & Wolk, A. (2006). Meat consumption and risk of colorectal cancer: A meta-analysis of prospective studies. International Journal of Cancer, 119(11), 2657–2664.
12. Norat, T., Lukanova, A., Ferrari, P., & Riboli, E. (2002). Meat consumption and colorectal cancer risk: Dose-response meta-analysis of epidemiological studies. Int J Cancer, 98(2), 241–256.
13. Sandhu, M. S., White, I. R., & McPherson, K. (2001). Systematic review of the prospective cohort studies on meat consumption and colorectal cancer risk: A meta-analytical approach. Cancer Epidemiology, Biomarkers and Prevention, 10(5), 439–446.
14. Lippi, G., Mattiuzzi, C., Cervellin, G., 2016. Meat consumption and cancer risk: a critical review of published meta-analyses. Crit. Rev. Oncol. Hematol. 97, 1e14.
18. de Batlle, et al., 2016. Meat intake, cooking methods and doneness and risk of colorectal tumours in the Spanish multicase-control study (MCC-Spain). Eur. J. Nutr. 2016.
43. Santarelli, R. L., Pierre, F., & Corpet, D. E. (2008). Processed meat and colorectal cancer: A review of epidemiologic and experimental evidence. Nutrition and Cancer, 60(2), 131–144.
47. Hammerling, U., Bergman Laurila, et al N.G., 2016. Consumption of red/processed meat and colorectal carcinoma:possible mechanisms underlying the significant association. Crit. Rev. Food Sci. Nutr. 56, 614e634.
48. Samraj,A.N.,Pearce,O.M.,Laubli,H.,Crittenden,A.N.,Bergfeld,A.K.,Banda,K., Gregg, C.J., Bingman, A.E., Secrest, P., Diaz, S.L., Varki, N.M., Varki, A., 2015. A red meat-derived glycan promotes inflammation and cancer progression. Proc. Natl. Acad. Sci. U. S. A. 112, 542e547.
49. Inoue-Choi, M., Sinha, R., Gierach, G.L., Ward, M.H., 2016. Red and processed meat, nitrite, and heme iron intakes and postmenopausal breast cancer risk in the NIH-AARP Diet and Health Study. Int. J. Cancer 138, 1609e1618
50. Alisson-Silva, F., Kawanishi, K., Varki, A., 2016. 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. Mol. Asp. Med. 51, 16e30.
51. Lin, J., Zhang, S. M., Cook, N. R., Lee, I. M., & Buring, J. E. (2004). Dietary fat and fatty acids and risk of colorectal cancer in women. American Journal of Epidemiology, 160(10), 1011–1022.
52. Schulz, M., Hoffmann, K., Weikert, C., Nothlings, U., Schulze, M. B., & Boeing, H. (2008). Identification of a dietary pattern characterized by high-fat food choices associated with increased risk of breast cancer: The European prospective investigation into cancer and nutrition (EPIC)-Potsdam study [see comment]. British Journal of Nutrition, 100(5), 942–946.
53. Crowe, F. L., Key, T. J., Appleby, P. N., Travis, R. C., Overvad, K., Jakobsen, M. U., et al. (2008). Dietary fat intake and risk of prostate cancer in the European prospective investigation into cancer and nutrition. American Journal of Clinical Nutrition, 87(5), 1405–1413.
54. Huang, X. (2003). Iron overload and its association with cancer risk in humans: Evidence for iron as a carcinogenic metal. Mutation Research, 533(1–2), 153–171.
55. Sesink, A. L., Termont, D. S., Kleibeuker, J. H., & Van der Meer, R. (1999). Red meat and colon cancer: The cytotoxic and hyperproliferative effects of dietary heme. Cancer Research, 59(22), 5704–5709.
56. Nasser, M. I., Bibi, F., Alqahtani, M. H., Chaudhary, A. G., Azhar, E. I., Kamal, M. A., & Yasir, M. (2013). Role of gut microbiota in obesity, type 2 diabetes and Alzheimer's. CNS & Neurological Disorders - Drug Targets (Epub ahead of print).
57. Azcárate-Peril, M.A., Sikes, M., & Bruno-Bárcena, J. M. (2011). The intestinal microbiota, gastrointestinal environment and colorectal cancer: A putative role for probiotics in prevention of colorectal cancer? American Journal of Physiology - Gastrointestinal and Liver Physiology, 301, G401–G424.
58. Magrone, T., & Jirillo, E. (2013). The interplay between the gut immune system and microbiota in health and disease: Nutraceutical intervention for restoring intestinal homeostasis. Current Pharmaceutical Design, 19, 1329–1342.
59. Vipperla, K., & O'Keefe, S. J. (2012). The microbiota and its metabolites in colonic mucosal health and cancer risk. Nutrition Iin Clinical Practice, 27, 624–635.
60. Hildebrandt, M.A., Hoffman, C., Sherrill-Mix, S. A., Keilbaugh, S. A., Hamady, M., Chen, Y., Knight, R., Ahima, R. S., Bushman, F., & Wu, G. D. (2009). High fat diet determines the composition of the murine gut microbiome independently of obesity. Gastroenterology, 137, 1716–1724.
71. Perello , G., Martí-Cid, R., Castell, V., Llobet, J.M., Domingo, J.L., 2010. Influence of various cooking processes on the concentrations of PCDD/PCDFs, PCBs and PCDEs in foods. Food Control 21, 178e185.