What Does Eating Plants Do For Cancer? Part Three

More Possible Dietary Causes of Cancer

Now, in continuation of the last blog, “What Does Eating Plants Do For Cancer? Part Two”, we’ll look at more links of diet with cancer.

HCAs (Heterocyclic amines)
Heterocyclic amines occur when muscle meat (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 (1). The longer the meat is cooked, the more HCAs form (2). Highest production of HCAs occurs when meat is pan-fried and well-done (3). In fact well-done meat is associated with increased risk of many cancers including those of the breast, colon, rectum, esophagus, lung, pancreas, prostate and stomach (3,4,5,6).

HCAs can promote cancer growth from its earliest stages all the way to full malignancy 76). 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 (8). PhIP is also associated with increased risk of colon, esophageal, lung, pancreatic, prostate and stomach cancers (9,10,11,12). 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 (13). 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 (14). Another study showed grilled, barbecued and smoked meat to be associated with increased risk of breast cancer (7). A 2009 study found that consumption of fried meat, beef and processed meat is associated with precancerous damage to breast tissue (15).

The five worst meats to grill are (ordered from worst to better) 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 (2). 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.

PAHs (Polycyclic aromatic hydrocarbons)
These noxious carcinogens are created when meat fat drips onto an open flame causing fire and sizzle that produce the chemical and sears it onto the meat surface. 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 (16,17,18). 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 (19,20).

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 (21,22,23).

Processed meat has been confirmed with the highest level of evidence as a carcinogen and was placed in the “Group 1: Carcinogenic to Humans” category by the World Health Organization in 2015 (24,25). This placement was the result of a formal review by 22 experts from ten countries who looked at over 800 studies investigating meat consumption and cancer from around the world and was based mainly on colorectal cancer risk. In their report they quantify the risk as an 18% increased risk of developing colorectal cancer for every 50 gm of processed meat consumed daily (24). Note that two or three slices of bacon can 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 (26). Additionally a study done in Taiwan has shown that consumption of processed food and smoked meat by children increases risk of leukemia (27) and a study in Australia found that the risk for ovarian cancer in women increased as a result of eating processed meat (28).

Evidence is still conflicting about the actual mechanism by which processed meat causes cancer. Some of the possibilities have already been discussed here such as the heme iron in meat and the formation of NOCs, HCAs and PAHs (24). Another possible 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 (29,30). 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 (31). 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 (32).

Here are a couple of surprising statistics about cancer. About 20% of human cancers can be linked to infectious agents such as viruses and bacteria (33,34). 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 (33). Another culprit is H. Pylori, a bacteria that is an important cause of stomach irritation and ulcers and ultimately gastric cancer (33). More cancer-linked infectious agents continue to come to light (35).

We have 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 (36). Both the animal-derived viruses themselves and antibodies to these viruses can be found circulating in the bloodstreams of human beings (37). 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 (38,39). Butchers and meat cutters have a higher incidence of tumours of the brain (40,41). Higher rates of colon and breast cancer are also associated with infectious agents (37,42,43,44). 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 there are other components of milk that could account for some of this change in cancer risk (45).

The human body is like a finely tuned machine, functioning best in specific conditions. One of these conditions is acid/base balance and our bodies are constantly compensating for challenges to this equilibrium. pH is the actual measurement of acidity in the body. The pH of blood remains remarkably stable, however the pH inside cells and in the spaces between cells can change. As their environment becomes more acidic, enzyme function is disrupted and cells are forced to adjust to this chronic physiological stress in order to survive. (46,47)

The foods and beverages that we consume are a major cause of acidification of the body. This has little to do with the pH of these food items themselves but has everything to do with the acid/base changes caused by food constituents. The early diets of evolving humans consisted of mostly gathered plant matter from the local environment. Plant-based foods are net base-producing foods that help to prevent excess acid in the body and maintain an ideal slightly alkaline body pH of about 7.4 (47). Conversely, the average modern diet in North America is highly acid-producing. While the kidneys and lungs can get rid of most of this excessive acidity, what is left must be neutralized by calcium obtained from within the body. Much of this needed calcium can come from the food that is being eaten daily (calcium absorption is actually increased when eating a diet high in animal protein (48,49)). However, with long-term high protein diets, some calcium will inevitably be leached from the bones and, in severe situations, can cause bone weakening and even osteoporosis (50).

Primary sources of acidity from the diet are sulfur-containing amino acids, salt and phosphoric acid found in soft drinks. Surprisingly, salt, though neutral in pH, accounts for 50% of the net acidity of the average Western diet. This may be due to the impairment by sodium (salt) of the kidney’s ability to excrete acid compounds (46). Sulfur-containing amino acids include methionine, cysteine, homocysteine, and taurine (though only methionine and cysteine are actually incorporated into proteins) and are found mainly in animal-sourced foods such as eggs, meat, poultry, fish and dairy. Consequently a diet high in animal protein and salt and low in fruits and vegetables leads to a low-grade state of acidosis (47).

Cancer is triggered by many different factors both genetic (influenced by the DNA of our genes) and epigenetic (lifestyle factors that change the expression of our genes). Within these factors are micro-environmental and systemic components that can trigger a cascade of events associated with the initiation or aggravation of cancer cell development (47). There is limited evidence that shows a direct link between diet-induced acidosis and cancer. However acid-base equilibrium changes, augmented by other factors such as obesity, metabolic syndrome and inflammation, are known to modify cell metabolism and functions and enhance tumour production and progression.


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2 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.

3 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.

4 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.

5 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.

6 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.

7 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.

8 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.

9 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.

10 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.

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12 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

13 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.

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19 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.

20 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.

21 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.

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23 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.

24 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.

25 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.

26 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.

27 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.

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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.

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