Why Is Eating Meat So Damaging to Human Health? Part Two

Acquired Hazards of Meat

This article continues on from Part One. Part Two looks at problems with meat that are not inherent in the meat itself but get attached to it during the life of the animal or in the processing of the meat. By their very natures, some of these problems can be minimized by judicious scrutinization of where a meat animal has been raised and how it has been treated during its life and afterwards in its transition to the table. For instance, you might buy your meat from a farm that does not use growth hormones in their animals. Or you can choose to cook your meats using moist low-heat methods instead of dry high-heat techniques. And of course you can choose not to eat processed meat at all.

 

PROCESSING OF MEAT

Processed meat has been confirmed as a carcinogen with the highest level of evidence and was placed in the “Group 1: Carcinogenic to Humans” category by the World Health Organization in 2015 (1,2). This placement was the result of a formal review by 22 experts from ten countries who looked at over 800 studies from around the world investigating the relationship between meat consumption and cancer and was based mainly on colorectal cancer risk. In their report investigators quantify the risk as an 18% increased risk of developing colorectal cancer for every 50 gm of processed meat consumed daily (1). Note that two or three slices of bacon weigh about 50 gm. There was also data showing increased risk of cancer of the stomach with consumption of processed meat although the evidence was not conclusive (3). Additionally they considered a study done in Taiwan that showed that consumption of processed food and smoked meat by children increase risk of leukemia (4) and a study in Australia that found that the risk for ovarian cancer in women increased as a result of eating processed meat (5).

Evidence is still conflicting about the actual mechanism by which processed meat causes cancer. Some of the possibilities are discussed in other sections of this blog such as the heme iron in meat and the formation of NOCs, HCAs and PAHs (2). Another probable offender is the nitrate that is added to meat during processing to preserve the meat, enhance its flavour and retain a pleasing pink colour. Nitrates themselves are healthy nutrients; the harm comes from the transformation from nitrate to nitrite to nitrosamine that occurs when nitrates combine with the amino acids in meat (6,7). Nitrosamine is known to be a carcinogenic molecule. Even the fumes produced by frying bacon contain nitrosamines in high enough amounts to cause DNA mutations at a rate 350 times more than the fumes from tempeh burgers (8). Plants contain natural nitrates, however nitrosamine is not formed from eating plant-based foods because of phytonutrients such as caffeic acid that are a part of all plants and are capable of blocking nitrosamine formation (9).

Studies show that both red and processed meats increase risk for cardiovascular disease. In one study, consuming one serving of red meat per day increased the risk for heart attack by 31% while five servings of processed meats a week increased the risk by 29% compared to people eating the least amount of meat (10). Another study looked at over 37,000 men and found that consumption of processed meat was significantly associated with increased risk of heart failure (11). The European Epic study followed 448,568 men and women and found that those consuming more than 160 gm per day of processed meat had a 30% increased risk of death from cardiovascular disease compared to those consuming 10 to 20 gm per day (12).

 

GROWTH HORMONES

Information from Health Canada and the US Food and Drug Administration states that growth hormones are approved for use in beef cattle in Canada and for both beef cattle and dairy cattle in the United States (13,14). Hormonal growth promoters can be natural or synthetic products and they are used to increase lean tissue growth. The desired result is faster growth of the whole animal and a healthier, lower fat final product produced at less cost. It is possible to raise beef cattle without the use of growth hormones but the cost of production is increased making beef more expensive.

The governments of the US and Canada claim that hormone residues in beef pose no threat to human health (13,14). Unfortunately this assumption relies on old studies looking at the ability of estrogen to mutate genes and has remained untested by long-term epidemiologic studies. In direct disagreement, the American Public Health Association, the largest association of public health professionals in the world, issued a policy statement in 2009 in opposition to the use of hormone growth promoters in both beef and dairy cattle production due to the mounting evidence of adverse effects on human hormonal systems (15).

In contrast to the governments of the US and Canada, the use of growth hormones is banned in the European Union as is any beef from North America in which growth hormones were used in its production. The European Union’s decision to ban the use of growth hormones is based on two principles (16);
1. The accumulating evidence that even exposure to the very low amounts of hormonally active compounds that remain in meat may disrupt the delicate equilibrium of the human hormonal system at any stage of life.
2. The potential for gene disruption by these compounds and their metabolites.
It is widely recognized that hormone growth promoter residues are present in meat (17,18). They also can persist for weeks to months in manure and feedlot runoff, adding extra hormonal load to the environment (19,20).

Six hormonal growth promoters are approved in Canada for use in beef cattle. These are the natural hormones progesterone, testosterone and estradiol-17B and the synthetic hormones trenbolone acetate (TBA), zeranol and melengestrol acetate (MGA) (13). Concurrent use of more than one of these steroids is also allowed (21).

Somatotropin is another growth hormone that is naturally occurring in humans and animals and helps in the growth of cells, organs and bones. The synthetic version, known as recombinant bovine somatotropin (rBST), is approved for use in the US for increasing milk production in dairy cattle. It is not approved for sale in Canada due to risk to the animal’s health. However Health Canada states that it does not pose a health risk to humans who drink the milk from a medicated cow (14).

Conflicting with statements from our government, ongoing research has found that hormonally active chemicals such as growth hormones may indeed have adverse effects on human health. One mechanism of this may be through epigenetic changes (22,23). (Epigenetic changes are alterations in the way genes are expressed, possibly due to environmental factors but without any change in DNA). Other study data has shown that muscle extracts from heifers one month after zeranol implantation stimulate human breast cancer cell proliferation in a test tube (24). Furthermore, blood from zeranol-implanted cattle can transform normal human breast cells in a test tube into breast cancer cells within three weeks (25) A 2018 review of this topic concluded that, though there is a lack of systemic study of the effect of growth hormone residues in beef, there is enough evidence regarding their possible effects on cancer growth and alterations of both male and female reproductive functions that use of these hormones should be banned from cattle until their true effects in humans eating the meat are established (26).

 

INFECTIOUS AGENTS IN MEATS

Here is a surprising statistics about cancer. About 20% of human cancers can be linked to infectious agents such as viruses and bacteria (27,28). For instance you are probably aware that HPV (Human Papillomavirus) is a factor in the development of cervical cancer but it is not so well-known that the same virus is implicated in the development of other cancers such as cancer of the mouth, penis and vagina (27). Another culprit is H. Pylori, a bacteria that is an important cause of stomach irritation and ulcers and ultimately gastric cancer (27). Other cancer-linked infectious agents continue to come to light (29).

Viruses infect all animals. Some of these viruses can travel up the food chain and have repercussions on the animal eating the virus-infected meat. In this case, it is ourselves that may be the ones at risk. It has been known for decades that there are cancer-causing viruses in the meat and milk of cattle and in poultry. This is concerning because these viruses are known carcinogens that can survive even high-temperature cooking and pasteurization (30). Both the animal-derived viruses themselves and antibodies to these viruses can be found circulating in the bloodstreams of human beings (31). The fact that they are present within us does not prove that they are causing malignancies but research is continuing to find strong connections. For instance, people who deal with cattle, pigs, sheep and poultry in the meat slaughtering and processing business are at increased risk for the development of and death from a variety of cancers compared with the general US population (32,33). Butchers and meat cutters have a higher incidence of tumours of the brain (34,35). Higher rates of colon and breast cancer are also associated with infectious agents (31,36,37,38). Supporting this concept is the observation that people who avoid dairy products due to lactose intolerance have lower rates of breast and other cancers, although it remains to be proven that other components of milk are not the ones behind this reduction in cancer risk (39).

 

ENDOTOXINS IN MEAT

Inflammation arising from meat, eggs and dairy products has been observed for decades but its specific cause or causes have been difficult to elucidate. A 2011 study shone some light on one potential cause of this inflammation. The study examined common foods looking for evidence of bacterial endotoxins in the food. Endotoxins are lipid substances that were once part of a bacterial cell wall but are released upon death of the cell. The body reacts to these toxins with an immune response which inevitably leads to inflammatory reactions (40). The study found large amounts of endotoxins in pork, poultry and dairy products. This should not be surprising. It is known that animal products often contain bacteria, some benign but others capable of causing disease, most of which are killed by heating or cooking the product (41). Endotoxins however are not destroyed by heat, stomach acid or digestive enzymes. Even boiling meat for two hours straight has no effect on endotoxins (42). So thoroughly cooking meat before eating to kill its bacteria will not get rid of endotoxins. Additionally the presence of saturated fat in the gut appears to give endotoxins a helpful boost in absorption into the body because they can borrow the saturated fat transport system in the gut wall. This double whammy of endotoxins and saturated fat both originate in animal foods that humans eat. It follows that reducing consumption of these foods would be a good solution (43).

 

PERSISTANT ORGANIC POLLUTANTS (POPs)

Persistant Organic Pollutants are toxic man-made chemicals that resist degradation. They persist over long periods of time in the environment and accumulate in the food chain through storage in fatty tissues of humans and animals. POPs are associated with many adverse human health effects such as developmental defects, chronic illness and even death. The majority of persistent organic pollutants also possess the ability to disrupt the normal functioning of the endocrine system. Thus they are called Endocrine Disrupting Chemicals (EDCs) and they can affect important body processes such as the nervous system, immune system and reproductive system (44). Their influences extend to accelerating the development of cancer, heart disease, hypertension, obesity and diabetes (45).

A major source of POPs for human beings is the eating of animal products (46). An example is the POP known as PCB which is found in much higher levels in the meats we eat than in vegetables, fruits or grains (46). Also 90% of human exposure to another POP, dioxin, comes from foods, especially meat, fish, shellfish and dairy products (47).

 

CARCINOGENS IN MEAT PRODUCED DURING COOKING

Heterocyclic amines (HCAs)

Heterocyclic amines occur when muscle meat (from chicken, beef, pork and fish) is cooked over high temperatures such as those found when frying or grilling. The major classes of heterocyclic amines are IQ-type compounds and PhIP. Both of these are formed from the reaction of heat with creatine or creatinine, certain amino acids and sugars found in muscle (48). The longer the meat is cooked, the more HCAs form (49). Highest production of HCAs occurs when meat is pan-fried and well-done (50). HCAs are cancer promotors. Well-done meat is associated with increased risk of many cancers including those of the breast, colon, rectum, esophagus, lung, pancreas, prostate and stomach (50,51,52,53).

HCAs can promote cancer growth from its earliest stages all the way to full malignancy (53). PhIP (2-amino-1-methyl-6-phenylimidazo(4,5)- pyridine) is a well-studied HCA which has potent estrogen-like effects that can fuel breast cancer growth (54). PhIP is also associated with increased risk of colon, esophageal, lung, pancreatic, prostate and stomach cancers (55,56,57,58). A 2005 study followed 29,000 men, confirming that eating high amounts of cooked meat leads to increased risk of prostate cancer, with PhIP most likely the damaging influence (59). Adding to this data is a 2012 interventional study illustrating that long-term, cumulative exposure to PhIP can induce transformation of normal human breast cells into premalignant and malignant stages (61). Another study showed grilled, barbecued and smoked meat to be associated with increased risk of breast cancer (60). A 2009 study found that consumption of fried meat, beef and processed meat is associated with precancerous damage to breast tissue (62).

The five worst meats to grill are (starting with the worst) chicken breast, steak, pork, salmon and hamburger. Chicken produces twice the level of HCAs as does steak and more than 100 times that of hamburger (49).

On a positive note, once exposure to HCAs stops, the body can completely rid itself of these harmful molecules in as little as 24 hours.

 

Polycyclic aromatic hydrocarbons (PAHs)

These noxious carcinogens are created when meat fat drips onto an open flame causing fire and sizzle that produce the chemical and sear it onto the surface of the meat. The longer and hotter the meat is cooked, the more PAHs are produced. PAHs are not found in significant amounts when foods other than meat are cooked at high temperatures.

Cooking methods vary greatly in their ability to produce PAHs. Grilling is the worst, roasting and baking are not quite so risky and boiling creates relatively few PAHs. PAHs are linked to higher rates of colorectal, stomach, pancreatic, breast and prostate cancer (63,64,65). Even exposure to fumes from restaurants which contain high levels of PAHs from the frying and grilling of meats is capable of damaging the DNA of human lung cells (66,67).

HCAs and PAHs cause DNA damage only after they are metabolized by enzymes in the body in a process called bioactivation. The activity of these enzymes differs among people which may lead to variable cancer risks associated with exposure to these carcinogens (68,69,70).

 

ADVANCED GLYCATION END-PRODUCTS (AGEs)

AGEs are highly reactive compounds that promote oxidative stress and inflammation and appear to be linked to development of chronic diseases such as type-2 diabetes, insulin resistance, heart disease, cancer, rheumatoid arthritis and cognitive problems (71,72). AGEs are created in the body when sugars combine with certain amino acids present in proteins in a process called glycation. The formation of AGEs is part of normal metabolism, but when their level becomes excessively high health problems can develop. Both high sugar and fats in the blood as well as inflammation in the body increase the formation of AGEs. As humans age, AGEs accumulate in cells and in the bloodstream due to the previous decades of AGE formation and AGE ingestion. Once formed AGEs add to chronic inflammation and are associated with premature aging. AGEs can clog very small blood vessels, especially in the kidneys, eyes, heart and brain and may be a cause of some of the complications of diabetes (72,73).

AGEs not only form within the body, they also exist in foods. They are naturally a part of uncooked protein-rich animal-derived foods and cooking causes the formation of new AGEs within these same foods. Highest AGE levels are found in beef and cheeses, followed by poultry, pork, fish, lamb, tofu and eggs. Higher fat and aged cheeses (Parmesan and cheddars) contain more AGEs than lower-fat cheeses such as reduced-fat mozzarella, skim milk cheddar and cottage cheeses. High fat spreads (butter, cream cheese, margarine, mayonnaise) are also very high in AGEs followed by oils and nuts. Roasting increases the AGE content of nuts. Carbohydrate-rich foods such as vegetables, legumes, fruits, whole grains, and milk contain relatively few AGEs, even after cooking. Cooking methods that are most prone to accelerating the formation of new AGEs include grilling, roasting, searing, broiling and frying. These dry heat cooking methods can increase the formation of new AGEs by 10 to 100 fold over those of the uncooked state (72,73)

Intake of AGEs can be significantly reduced by eating more legumes, vegetables, fruits, whole grains, and low-fat milk products. It is also helpful to know that certain cooking methods can prevent AGE production. Using moist rather than dry heat for cooking such as steaming, stewing, boiling and poaching and adding acidic ingredients such as lemon juice or vinegar will reduce the generation of new AGEs (72).

It is not completely clear how AGEs exert their deleterious effects on human health. Continuing investigation will add to our knowledge about AGEs and their effects on health as well as the steps that can be taken to minimize the damage they might cause (73,74).

LAST THOUGHTS

I’ll leave the last words to two sources that may reassure you that it really is not necessary to eat meat for health.

The first one comes from The American Dietetic Association that states “appropriately planned vegetarian diets, including total vegetarian or vegan diets, are healthful, nutritionally adequate, and may provide health benefits in the prevention and treatment of certain diseases. Well-planned vegetarian diets are appropriate for individuals during all stages of the life cycle, including pregnancy, lactation, infancy, childhood, and adolescence, and for athletes. A vegetarian diet is defined as one that does not include meat (including fowl) or seafood, or products containing those foods.” They also note that the attributes of a vegetarian diet that may reduce risk of chronic disease include lower intakes of saturated fat and cholesterol and higher intakes of fruits, vegetables, whole grains, nuts, soy products, fiber, and phytochemicals (75).

Secondly, an update on plant-based diets written specifically for physicians points out that healthy eating is best achieved through a plant-based diet that encourages whole, plant-based foods and discourages meats, dairy products and eggs as well as all refined and processed foods. The paper states that “plant-based diets are cost-effective, low-risk interventions that may lower body mass index, blood pressure, HbA1C and cholesterol levels. They may also reduce the number of medications needed to treat chronic diseases and lower ischemic heart disease mortality rates. Physicians should consider recommending a plant-based diet to all their patients, especially those with high blood pressure, diabetes, cardiovascular disease, or obesity.” The conclusion of this article chides physicians who “ignore the potential benefits of good nutrition and quickly prescribe medications instead of giving patients a chance to correct their disease through healthy eating and active living.” Their closing thought is this. “The future of health care will involve an evolution toward a paradigm where the prevention and treatment of disease is centered, not on a pill or surgical procedure, but on another serving of fruits and vegetables.” (76)

 

SOURCES:

1 Bouvard, V., Loomis, D., Guyton, K.Z., Grosse, Y. et al. Carcinogenicity of consumption of red and processed meat. The Lancet Oncology December 2015; 16(16): 1599-1600.

2 International Agency for Research on Cancer/World Health Organization. IARC Monographs evaluate consumption of red meat and processed meat. Press Release No. 240. October 26, 2015.

3 Zhao, Z., Yin, Z., Zhao, Q. Red and processed meat consumption and gastric cancer risk: a systematic review and meta-analysis. Oncotarget. 2017 May 2; 8(18): 30563–30575.

4 Liu, C-Y., Hsu, Y-H., Wu, M-T., Pan, P-C., Ho, D-K. Cured meat, vegetables, and bean-curd foods in relation to childhood acute leukemia risk: A population based case-control study. BMC Cancer. 2009; 9: 15.

5 Kolahdooz, F., van der Pols, J.C., Bain, C.J., Marks, G.C. et al. Meat, fish, and ovarian cancer risk: results from 2 Australian case-control studies, a systematic review, and meta-analysis. Am J Clin Nutr June 2010; 91(6): 1752-1763.

6 Hord, N.G., Tang, Y., Bryan, N.S. Food sources of nitrates and nitrites: the physiologic context for potential health benefits. Am J Clin Nutr. 2009 Jul; 90(1):1-10.

7 Katan, M.B. Nitrate in foods: harmful or healthy? Am J Clin Nutr. 2009 Jul; 90(1):11-12.

8 Thiébaud, H.P., Knize, M.G., Kuzmicky, P.A. et al. Airborne mutagens produced by frying beef, pork and a soy-based food. Food Chem Toxicol. 1995 Oct; 33(10): 821-8.

9 Kuenzig, W., Chau, J., Norkus, E., Holowaschenko, H. et al. Caffeic and ferulic acid as blockers of nitrosamine formation. Carcinogenesis. 1984 Mar; 5(3):309-13.

10 Wang, D., Campos, H., Baylin, A. Red meat intake is positively associated with non-fatal acute myocardial infarction in the Costa Rica Heart Study. Br J Nutr. 2017; 118: 303-311.
11 Kaluza, J., Akesson, A., Wolk, A. Processed and Unprocessed Red Meat Consumption
and Risk of Heart Failure: Prospective Study of Men. Circ Heart Fail. 2014; 7:552-557.

12 Rohrmann, S., Overvad, K., Bueno-de-Mesquita, H.B., et al. Meat products consumption
and mortality-results from the European Prospective Investigation into Cancer and Nutrition.
BMC Medicine. 2013; 11: 63-75.

13 https://www.canada.ca/en/health-canada/services/drugs-health-products/veterinary-drugs/factsheets-faq/hormonal-growth-promoters.html

14 https://www.fda.gov/animalveterinary/safetyhealth/productsafetyinformation/ucm055436.htm

15 Policy Statement of the American Public Health Association. Opposition to the Use of Hormone Growth Promoters in Beef and Dairy Cattle Production. Nov 10 2009; Policy Number: 20098

16 European Commissions. Scientific Committee on Veterinary Measures Relating to Public Health. Assessment of Potential Risks to Human Health From Hormone Residues in Bovine Meat and Meat Products; 1999. Available at: http://ec.europa.eu/food/fs/sc/scv/out21_en.pdf.

17 Henricks, D.M., Gray, S.L., Owenby, J.J., et al. Residues from anabolic preparations after good veterinary practice. APMIS. 2001; 109:273–283.

18 Stephany, R.W. Hormones in meat: different approaches in the EU and in the USA. APMIS. 2001; 109:S357–S363.

19 Schiffer, B., Daxenberger, A., Meyer, K., Meyer, H.H.D. The fate of trenbolone acetate and melengestrol acetate after application as growth promoters in cattle: environmental studies. Environ Health Perspect. 2001; 109:1145–1151.

20 Soto, A.M., Calabro, J.M., Prechtl, N.V., et al. Androgenic and estrogenic activity in water bodies receiving cattle feedlot effluent in eastern Nebraska, USA. Environ Health Perspect. 2004; 112:346–352.

21 Orr, R. Growth-Promoting Hormones in Cattle. Manhattan, Kan: International Food Safety Network, Kansas State University, 2001. Available at http://foodsafety.k-state.edu/en/article-details.php?a=4&c=19&sc=162&id=308.

22 vom Saal FS, Belcher SM, Guillette LJ, et al. 2007. Chapel Hill Bisphenol A expert panel consensus statement: integration of mechanisms, effects in animals and potential impact to human health at current exposure levels. Reprod Toxicol. 2007; 24:131–138.

23 Swan SH, Kruse RL, Fan L, et al.; the Study for the Future of Families Research Group. Semen quality in relation to biomarkers of pesticide exposure. Environ Health Perspect. 2003;111:1478–1484.

24 Ye, W., Xu, P., Zhong, S., Threlfall, W.R., Frasure, C., Feng, E., Li, H. et al. Serum harvested from heifers one month post-zeranol implantation stimulates MCF-7 breast cancer cell growth. Exp Ther Med. 2010 Nov; 1(6):963-968.

25 Liu, S., Lin, Y.C. Transformation of MCF-10A human breast epithelial cells by zeranol and estradiol-17beta. Breast J. 2004 Nov-Dec; 10(6):514-521.

26 Senthil Kumar, V., Rajan, C., Divya, P.,Sasikumar, S. Adverse effects on consumer’s health caused by hormones administered in cattle. International Food Research Journal 25(1): 1 – 10 (February 2018)

27 DeFlora, S., Bonanni, P. The Prevention of infection-associated cancers. Carcinogenesis. 2011 Jun; 32(6): 787–795.

28 Zhang, X., Zhang, Z., Zheng, B., He, Z., Winberg, G., Ernberg, I. An update on viral association of human cancers. Arch Virol. 2013 Jul ;158(7): 1433-43.

29 Pagano, J.S., Blaser, M., Buendia, M.A., Damania, B., Khalili, K., Raab-Traub, N.,Roizman,B. Infectious agnets and cancer: criteria for a causal relation. Semin Cancer Biol. 2004 Dec;14(6):453-71.
Infectious agents and cancer: criteria for a causal relation.

30 Peretti, A., Fitzgerald, P.C., Bliskovsky, V., Buck, C.B., Pastrana,D.V. Hamburger polyomaviruses. J Gen Virol. 2015 Apr; 96(Pt 4):833-839.

31 Laurent, S., Esnault, E., Dambrine, G., Goudeau, A., Choudat, D., Rasschaert, D. Detection of avian oncogenic Marek’s disease herpesvirus DNA in human sera. J Gen Virol. 2001 Jan; 82(Pt 1):233-240.

32 Johnson, E.S., Cancer mortality in workers employed in cattle, pigs, and sheep slaughtering and processing plants. Environ Int. 2011 Jul; 37(5):950-959.

33 Johnson, E.S., Ndetan, H.,Lo,K.M. Cancer mortality in poultry slaughtering/processing plant workers belonging to a union pension fund. Environ Res. 2010 Aug; 110(6):588-594.

34 Ruder, A.M., Waters, M.A., Carreon, T., et al. The Upper Midwest Health Study: industry and occupation of glioma cases and controls. Am J Ind Med. 2012; 55(9):747–755.

35 De Roos, A.J., Stewart, P.A., Linet, M.S. et al. Occupation and the risk of adult glioma in the United States. Cancer Causes Control. 2003; 14(2):139–150

36 zur Hausen, H., de Villiers, E.M. Dairy cattle serum and milk factors contributing to the risk of colon and breast cancers. Int J Cancer. 2015 Aug 15; 137(4):959-67.

37 zur Hausen, H. Red meat consumption and cancer: reasons to suspect involvement of bovine infectious factors in colorectal cancer. Int J Cancer. 2012 Jun 1; 130(11):2475-2483.

38 Buehring, G.C., Shen, H.M., Jensen, H.M., Jin, D.L., Hudes, M., Block, G. Exposure to Bovine Leukemia Virus Is Associated with Breast Cancer: A Case-Control Study. PLOS One September 2, 2015

39 Ji, J., Sundquist, J., Sundquist, K. Lactose intolerance and risk of lung, breast and ovarian cancers: aetiological clues from a population-based study in Sweden. Br J Cancer. 2015 Jan 6; 112(1): 149–152.

40 Meseguer, V., Alpizar, Y.A, Luis, E., Tajada, S., Denlinger, B., Fajardo, O. et al. TRPA1 channels mediate acute neurogenic inflammation and pain produced by bacterial endotoxins. Nature Communications 2014; 5(3125).

41 Waters, A.E., Contente-Cuomo, T., Buchhagen, J., Liu, C.M., Watson, L., Pearce, K., Foster, J.T., Bowers, J., Driebe, E.M., Engelthaler, D.M., Keim, P.S., Price, L.B. Multidrug-Resistant Staphylococcus aureus in US Meat and Poultry. Clin Infect Dis 2011; 52(10): 1227-1230.

42 Erridge, C. The capacity of foodstuffs to induce innate immune activation of human monocytes in vitro is dependent on food content of stimulants of Toll-like receptors 2 and 4. Br J Nutr. 2011 Jan; 105(1):15-23.

43 Harte, A.L., Varma, M.C., Tripathi, G., McGee, K.C., Al-Daghri, N.M., Al-Attas, O.S. et al. High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects. Diabetes Care. 2012 Feb; 35(2):375-382.

44 Damstra, T. Potential effects of certain persistent organic pollutants and endocrine disrupting chemicals on the health of children. J Toxicol Clin Toxicol. 2002; 40(4):457-465.

45 Ljunggren, S.A., Helmfrid, I., Salihovic, S., van Bavel, B., Wingren, G., Lindahl, M., Karlsson, H. Persistent organic pollutants distribution in lipoprotein fractions in relation to cardiovascular disease and cancer. Environ Int. 2014 Apr;65:93-99.

46 Domingo, J.L, Nadal, M. Carcinogenicity of consumption of red and processed meat: What about environmental contaminants? Environ Res. 2016 Feb; 145:109-115.

47 World Health Organization Fact Sheet: http://www.who.int/news-room/fact-sheets/detail/dioxins-and-their-effects-on-human-health

48 Jagerstad, M., Skog, K., Grivas, S., Olsson, K. Formation of heterocyclic amines using model systems. Mutat Res. 1991; 259(3-4):219-233.

49 Sinha, R., Rothman, N., Brown, E.D. et al. High concentrations of the carcinogen 2-amino-1-methyl-6-phenylimidazo-[4,5] pyridine [PhlP] occur in chicken but are dependent on the cooking method. Cancer Res. 1995; 55: 4516-4519.

50 Butler, L.M., Sinha, R., Millikan, R.C., Martin, C.F. et al. Heterocyclic amines, meat intake, and association with colon cancer in a population-based study. Am J Epidemiol 2003;157(5): 434-445.

51 Murtaugh, M.A., Ma, K.N., Sweeney, C., Caan, B.J., Slattery, M.L. Meat Consumption patterns and preparation, genetic variants of metabolic enzymes, and their association with rectal cancer in men and women. J Nutr. 2004; 134(4): 776-784.

52 Gooderham, N.J., Murray, S., Lynch, A.M. et al. Food-derived heterocyclic amine mutagens: variable metabolism and significance to humans. Drug Metab Dispos. 2001; 29: 529-534.

53 Sinha, R., Peters, U., Cross, A.J. et al. Meat, meat cooking methods and preservation, and risk for colorectal adenoma. Cancer Res. 2005; 65: 8034-8042.

54 Rashmi,S.,Gustafson, D.R., Kulldorff, M. et al. 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, a Carcinogen in High- Temperature-Cooked Meat, and Breast Cancer Risk. JNCI: Journal of the National Cancer Institute August 2000; 92(16): 1352–1354.

55 Ward, M.H., Sinha,R., Heineman, E.F., Rothman, N. et al. Risk of adenocarcinoma of the stomach and esophagus with meat cooking method and doneness preference. Int J Cancer. 1997 Mar 28; 71(1):14-9.

56 Cross, A.J., Freedman, N.D., Jiansong, R., Ward, M.H. et al. Meat consumption and risk of esophageal and gastric cancer in a large prospective study. Am J Gastroenterol. 2011 Mar; 106(3): 432–442.

57 Lam, T.K., Cross, A.J., Consonni,D., Randi, G. et al. Intakes of red meat, processed meat, and meat-mutagens increase lung cancer risk. Cancer Res. 2009 Feb 1; 69(3): 932–939.

58 Stolzenberg-Solomon, R.Z., Cross, A.J., Silverman, D.T., Schairer, C. et al. Meat and Meat-Mutagen Intake and Pancreatic Cancer Risk in the NIH-AARP Cohort . Cancer Epidemiol Biomarkers Prev 2007; 16(12). December 2007

59 Cross, A.J., Peters, U., Kirsh, V.A., Andriole, G.L. et al. A prospective study of meat and meat mutagens and prostate cancer risk. Cancer Res 2005; 65(24): 11779-11784.

60 Steck, S.E., Gaudet, M.M., Eng, S.M., Britton, J.A. et al. Cooked meat and risk of breast cancer – lifetime versus recent dietary intake. Epidemiology 2007; 18(3): 373-382.

61 Choudhary, S., Sood, S., Donnell, R.L., Wang, H.C. Intervention of human breast cell carcinogenesis chronically induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine. Carcinogenesis April 2012; 33(4): 876-885.

62 Rohrmann, S., Lukas Jung, S.U., Linseisen, J., Pfau, W. Dietary intake of meat and meat-derived heterocyclic aromatic amines and their correlation with DNA adducts in female breast tissue. Mutagenesis 2009; 24(2): 127-132.

63 Mastrangelo, G., Fadda, E., Marzia, V. Polycyclic aromatic hydrocarbons and cancer in man. Environ Health Perspect. 1996 Nov; 104(11): 1166–1170.

64 World Cancer Research Fund. Food, nutrition, physical activity, and the prevention of cancer: A global perspective. American Institute of Cancer Research. Washington, DC: 2007

65 Norat, T., Riboli, E. Meat consumption and colorectal cancer: a review of epidemiologic evidence. Nutr Rev. 2001; 59(2):37-47.

66 Chen, J.W., Wang, S.L., Hsieh, D.P., Yang, H.H., Lee, H.L. Carcinogenic potencies of polycyclic aromatic hydrocarbons for back-door neighbours of restaurants with cooking emissions. Sci Total Environ 2012; 417-418:68-75.

67 Yang, S.C., Jenq, S.N., Kang, Z.C., Lee, H. Identification of benzo(a)pyrene7,8-diol9,10-epoxideN2-deoxyguanosine in human lung adenocarcinoma cells exposed to cooking oil fumes from frying fish under domestic conditions. Chem ResToxicol. 2000; 13(10): 1046-1050.

68 Sinha, R., Rothman, N., Mark, S.D. et al. Lower levels of urinary 2-amino-3,8-dimethylimidazo[4,5-f]-quinoxaline (MeIQx) in humans with higher CYP1A2 activity. Carcinogenesis 1995; 16(11):2859–2861.

69 Moonen, H., Engels, L., Kleinjans, J., Kok, T. The CYP1A2-164A–>C polymorphism (CYP1A2*1F) is associated with the risk for colorectal adenomas in humans. Cancer Letters 2005; 229(1):25–31.

70 Butler, L.M., Duguay, Y., Millikan, R.C. et al. Joint effects between UDP-glucuronosyltransferase 1A7 genotype and dietary carcinogen exposure on risk of colon cancer. Cancer Epidemiology, Biomarkers and Prevention 2005; 14(7):1626–1632.

71 Jiao, L., Kramer, J.R., Chen, L., Rugge, M., Parente, P., Verstovsek, G., Alsarraj, A., El-Serag, H.B. Dietary consumption of meat, fat, animal products and advanced glycation end-products and the risk of Barrett’s oesophagus. Aliment Pharmacol Ther. 2013 Oct; 38(7):817824.

72 Uribarri, J., Woodruff, S., Goodman, S., Cai, W., Chen, X., Pyzik, R., Yong, A., Striker, G.E., Vlassara, H. Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet. J Am Diet Assoc. 2010 Jun; 110(6): 911–916.

73 http://www.berkeleywellness.com/healthy-eating/food-safety/article/abcs-ages-advanced-glycation-end-products

74 Luevano-Contreras, C., Chapman-Novakofski, K. Dietary Advance Glycation End Products and Aging. Nutrients. 2010 Dec; 2(12): 1247–1265.

Promoting a healthy adventurous lifestyle powered by plants and the strength of scientific evidence.

My name is Debra Harley (BScPhm) and I welcome you to my retirement project, this website. Over the course of a life many lessons are learned, altering deeply-rooted ideas and creating new passions.

Leave a Comment