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According to the World Health Organisation (WHO), dietary factors are thought to account for as much as 35% of all cancers. The most noticeable correlation between diet and cancer is the fact that people who do not eat meat are much less likely to develop the disease. As shown by large studies, vegetarians are approximately 40% less likely to develop cancer than subjects who eat meat. Another study investigated the link between meat consumption and cancer by observing cancer incidence in Seventh–Day Adventists, a religious group whose members avoid alcohol and tobacco. Approximately half of the population are vegetarian and half still eat meat, allowing for observations regarding the effects of meat-eating, separate from other lifestyle factors. Results indeed demonstrated that there was a significantly lower colorectal cancer risk in the vegetarian subpopulation than in the meat-eaters. A number of hypotheses have been suggested to explain the connection between meat consumption and cancer risk. Meat is devoid of fibre, and other nutrients, that have a protective effect against cancer. It is also high in animal protein and saturated fat, which form carcinogenic compounds such as heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) during processing and/or cooking.,  The major classes of HCAs include amino-imidazo-quinolines and amino-imidazo-quinoxalines (collectively called IQ-type compounds) and amino-imidazo-pyridines such as 2-amino-1-methyl-6- phenylimidazo(4, 5-b)pyridine (PhIP). IQ-type compounds and PhIP are formed from creatine or creatinine (found in all meats), specific amino acids and sugars. These HCAs are formed as meat (including chicken and fish) is cooked, even under normal grilling, frying or roasting conditions, and their formation increases with higher temperatures, and longer cooking times., , ,  One study that included 952 subjects with rectal cancer and 1,205 control subjects found that men and women with the highest consumption of processed or well-cooked meat had an increased risk of rectal cancer. Other research has shown that the high fat content of meat (and other animal products) can increase hormone production within the body, thus increasing the risk of hormone-related cancers, such as breast and prostate cancer. One study found that consumption of a Western diet (especially large amounts of chicken, eggs and meat) increased the serum concentrations of estradiol, a hormone implicated in breast cancer. The American Institute for Cancer Research (AICR) published a review in 2007 of the major studies on food, nutrition and cancer prevention. For cancers of the oesophagus, lung, pancreas, stomach, endometrium, and prostate, it was determined that red meat (beef, pork, or lamb) and processed meat consumption possibly increased cancer risk. For colorectal cancer, a review of the literature determined that there is convincing scientific evidence that red meat, processed meat, saturated/animal fat, and heavily cooked meat all increase cancer risk. The evidence is therefore clear that eating meat, particularly if processed or well cooked, increases the risk of developing cancer. The best option for cancer prevention through diet, therefore, is perhaps to become vegetarian, but this is not acceptable to many people. In which case a decrease in meat consumption (especially processed meats), and a reduction in meat cooking times are more viable options for reducing the risk of cancer development.  Anand, P. et al. (2008) Cancer is a Preventable Disease that requires major lifestyle changes. Pharm Res. 25(9). 2097-116.  Lanou, AJ. & Svenson, B. (2010) Reduced cancer risk in vegetarians: an analysis of recent reports. Cancer Manag Res. 3. 1-8.  Sinha, R. et al. (2009) Meat intake and mortality: a prospective study of over half a million people. Arch Intern Med. 169(6). 562-71.  Orlich, MJ. et al. (2015) Vegetarian dietary patterns and the risk of colorectal cancers. JAMA Intern Med. 175(5). 767-76.  European Commission. (2011) Polycyclic aromatic hydrocarbons - Factsheet. Retrieved November 2016 from, https://ec.europa.eu/jrc/sites/jrcsh/files/Factsheet%20PAH_0.pdf  Knize, MG. et al. (2002) Factors affecting human heterocyclic amine intake and the metabolism of PhIP. Mutat Res. 506-607. 153-62.  Schuirmann, E. & Eichner, K. (1991) [Formation of IQ-compounds in meat and meat products]. Z Ernahrungswiss. 30(1). 56-64.  Skog, KI. et al. (1998) Carcinogenic heterocyclic amines in model systems and cooked foods: a review on formation, occurrence and intake.Food Chem Toxicol. 36(9-10). 879-96.  Thiebaud, HP. et al. (1995) Airborne mutagens produced by frying beef, pork and soy-based food. Food Chem Toxicol. 33(10). 821-8.  Sinha, R. et al. (1995) 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. Cancer Res. 55(20). 4516-9.  Murkovic, M. (2004) Formation of heterocyclic aromatic amines in model systems.J Chromatogr B Analyt Technol Biomed Life Sci. 802(1). 3-10.  Murtaugh, MA. et al. (2004) Meat consumption patterns and preparation, genetic variants of metabolic enzymes, and their association with rectal cancer in men and Women. J Nutr. 134(4). 776-784.  Henderson, BE. & Feigelson, HS. (2000) Hormonal carcinogenesis. Carcinogenesis. 21(3). 427-433.  Sanchez-Zamorano, LM. et al. (2016) The Western dietary pattern is associated with increased serum concentrations of free estradiol in postmenopausal women: implications for breast cancer prevention. Nutr Res. 36(8). 845-54.  AICR.(2007) Food, nutrition, physical activity and the prevention of cancer: a global perspective. Retrieved April 2016 from, http://www.aicr.org/assets/docs/pdf/reports/Second_Expert_Report.pdf