Cooking and Health
COOKING VEGETABLES RESULTS IN A SIGNIFICANT LOSS of their nutrient content, a loss that reduces their benefits to human health. The flip-side effect of cooking practices is equally pronounced. An actual threat to human health emerges when meat, dairy, potatoes, and other foods are subjected to high-temperature cooking because heat produces numerous carcinogens.
Let’s take a look at the acrylamides, for starters. They are a class of carcinogens that emerge from the cooking of starchy foods. This chemical was accidentally discovered by Swedish scientists only recently, in 2002, when they closely examined the chemical contents of French fries, potato chips, and other starchy foods after exposure to high heat during frying or baking. This chemical wasn’t detected in uncooked foods or foods that had been boiled. The European Chemical Agency placed acrylamide on its list of potentially hazardous substances in 2010, based on an accumulation of studies showing that it could cause a variety of cancers in laboratory animals, including cancer of the thyroid, oral cavity, mammary glands, uterus, and nervous system. It has also been linked to promoting an elevated risk for atherosclerosis and reproductive disorders.
Other harmful chemical compounds formed during cooking include:
• Phlp, derived from cooked meat, induces cancer of the colon, prostate and mammary gland in animal studies. It is one of the more common of the HCAs.
• HCAs, heterocyclic amines, formed by high temperatures in protein-rich foods that are fried, grilled, or barbecued, and considered a high-risk factor for human cancer, especially colon and breast cancers.
• PAH, polycylic aromatic hydrocarbons, several dozen types of them altogether, found in grilled meat and meat products, and linked to breast cancer in animal experiments.
• AGEs, advanced glycation end products, created when sugars accompanied by proteins or fats are heated, and linked to premature aging, cardiovascular disease, diabetes, kidney and liver disease, and the onset of Alzheimer’s.
• Trans fatty acids formed during the cooking of partially hydrogenated vegetable oils, which is a direct cause of coronary heart disease.
There are also human health risks involved in microwave cooking, particularly when microwaves release the chemical DEHA from plastic containers so it can migrate into food, and when the toxic chemical PFOA, present as a nonstick coating in microwave popcorn bags, migrates during heat exposure.
Effect of charcoal types and grilling conditions on formation of heterocyclic aromatic amines (HAs) and polycyclic aromatic hydrocarbons (PAHs) in grilled muscle foods. Viegas O, et al. Food Chem Toxicol. 2012 Jun;50(6):2128-34. Key Finding: PAH absorption has been linked to both colon cancer and type 2 diabetes, while HA levels have been associated with colon and other cancers. “Grilling muscle foods involves high temperatures that lead to production of cooking toxicants such as Has and PAHs. We quantified HA and PAH levels in well-done meat and fish samples grilled with wood and coconut shell charcoal at 200 degrees C. Higher levels of HAs and PAHs were found in salmon samples. No significant differences were observed for HAs and PAHs in beef samples grilled with both charcoal types. Continuous barbecuing with the same charcoal showed that combustion of fat that dripped along the grilling period contributed to higher formation of HAs and PAHs.”
Heavy metals in raw, fried and grilled Mediterranean finfish and shellfish. Kalogeropoulos N, et al. Food Chem Toxicol. 2012 Oct;50(10):3702-8. Key Finding: “The effect of pan-frying and grilling on the heavy metals Cd, Cr, Cu, Fe, Hg, Ni, Pb and Zn content of popular small Mediterranean finfish and shellfish was studied. The species selected were anchovy, bogue, hake, pciarel, sardine, sand smelt, stripped mullet, mussel, shrimp and squid. Both culinary practices examined resulted in increased metals concentrations compared to those of raw samples. Significant amounts of Fe and Zn were found in the cooked seafood.”
Meat mutagens and breast cancer in postmenopausal women – a cohort analysis. Wu K, et al. Cancer Epidemiol Biomarkers Prev. 2010 May;19(5):1301-10. Key Finding: “Mutagenic compounds produced when meats are cooked at high temperatures have been hypothesized to increase risk of breast cancer. Overall prospective data including results from our study do not provide support for a substantial increase in risk of breast cancer with higher intake of HCAs.”
Meat and meat-related compounds and risk of prostate cancer in a large prospective cohort study in the United States. Sinha R, et al. Am J Epidemiol. 2009 Nov 1;170(9):1165-77. Key Finding: “During 9 years of follow-up (1995-2003), the authors ascertained 10,313 prostate cancer cases in a cohort of 175,343 U.S. men aged 50-71 years. Hazard ratios comparing the fifth intake quintile with the first revealed elevated risks for prostate cancer associated with red and processed meat. Grilling/barbecuing may be one mechanism aong with heme iron, nitrite/nitrate, and benzo{a}pyrene.”
A prospective study of meat, cooking methods, meat mutagens, heme iron, and lung cancer risks. Tasevska N, et al. Am J Clin Nutr. 2009 Jun;89(6):1884-94. Key Finding: “Men and women from the National Institutes of Health-AARP Diet and Health Study with no history of cancer at baseline were monitored for 8 years. Diet was assessed with a 124-item food-frequency questionnaire. We observed a moderate association between meat consumption and lung carcinoma, which might be explained by heme iron intake, high-temperature cooking, and associated mutagens.”
Cured meat, vegetables, and bean-curd foods in relation to childhood acute leukemia risk: a population based case-control study. Liu CY, et al. BMC Cancer. 2009 Jan 13;9:15. Key Finding: “Consumption of cured/smoked meat and fish leads to the formation of carcinogenic N-nitroso compounds in the acidic stomach. A population-based case-control study was conducted of persons between 2 and 20 years old consisting of 145 acute leukemia cases and 370 age- and sex-matched controls. Consumption of cured/smoked meat and fish more than once a week was associated with an increased risk of acute leukemia, perhaps through their contents of nitrites and nitrosamines, while intake of vegetables and soy-bean curd may be protective.”
Meat, eggs, dairy products, and risk of breast cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Pala V, et al. Am J Clin Nutr. 2009 Sep;90(3):602-12. Key Finding: “We investigated the relation of meat, egg and dairy product consumption with breast cancer risk by using data from the European Prospective Investigation into Cancer and Nutrition. Information on diet was collected from 319,826 women. We have not consistently identified intakes of meat, eggs, or dairy products as risk factors for breast cancer. Future studies should investigate the possible role of high-temperature cooking in the relation of red meat intake with breast cancer risk.”
Dietary meat intake in relation to colorectal adenoma in asymptomatic women. Ferrucci LM, et al. Am J Gastroenterol. 2009 May;104(5):1231-40. Key Finding: “Of the 807 eligible women in a cross-sectional multicenter colonscopy screening study, 158 prevalent colorectal adenoma cases and 649 controls satisfactorily completed the validated food frequency and meat questionnaire. There were positive associations between iron and heme iron from meat and colorectal adenoma. Risk was associated with high intake of red meat, pan-fried meat, and heterocyclic amines.”
Xenobiotic metabolizing gene variants, dietary heterocyclic amine intake, and risk of prostate cancer. Koutros S, et al. Cancer Res. 2009 Mar 1;69(5):1877-84. Key Finding: “Among men carrying the A variant gene, the risk of prostate cancer associated with high DiMelQx from cooked meat was 2-fold greater than that with low intake. The observed effect provides evidence to support the hypothesis that heterocyclic amines from meat may act as promoters of malignant transformation.”
Diet and breast cancer in Latin-America. Torres-Sanchez L, et al. Salud Publica Mex. (Spanish). 2009;51 Suppl 2:s181-90. Key Finding: “A systematic search in Mexico identified 27 epidemiological studies that evaluated associations between diet and breast cancer. The research suggests a potential risk associated with elevated caloric consumption, consumption of red meat and processed meats, certain meat cooking techniques, milk and some other dairy products. The impact of specific foods and nutrients on breast cancer incidence is inconclusive. Further research is needed on this topic.”
Cooking temperature, heat-generated carcinogens, and the risk of stomach and colorectal cancers. Ngoan le T, et al. Asian Pac J Cancer Prev. 2009 Jan-Mar;10(1):83-6. Key Finding: “Food change due to cooking temperature and unrecognized heat-formed chemical carcinogens may impact on the risk of stomach and colorectal cancers. A total of 670 cases of stomach and colorectal cancers matched with 672 hospital controls were the subjects of this study. A high intake of roasted meats, bread and bisquit significantly increased the risk of cancer.”
Consumption and health effects of trans fatty acids: a review. Teegala SM, et al. J AOAC Int. 2009 Sep-Oct;92(5):1250-7. Key Finding: “Consumption of industrially produced trans fatty acids remains high in many populations, particularly in developing nations where partially hydrogenated vegetable oils are frequently used for home cooking and among individuals in developed countries having high intakes of bakery or processed foods. Well-controlled observational studies and randomized trials indicate that trans fatty acids consumption adversely affects multiple risk factor for chronic diseases, including numerous blood lipids and lipoproteins, systemic inflammation, endothelial dysfunction, and possibly insulin resistance, diabetes, and adiposity. Consistent evidence from prospective observational studies of habitual trans fatty acid consumption and retrospective observational studies using trans fatty acid biomarkers indicates that trans fatty acid consumption increases risk of clinical coronary heart disease.”
Meat and meat mutagens and risk of prostate cancer in the Agricultural Health Study. Koutros S, et al. Cancer Epidemiol Biomarkers Prev. 2008 Jan;17(1):80-7. Key Finding: “Meats cooked at high temperatures, such as pan-frying or grilling, are a source of carcinogenic heterocyclic amines and polycyclic aromatic hydrocarbons. We prospectively examined the association between meat types, cooking methods, meat doneness, and meat mutagens and the risk of prostate cancer in the Agricultural Health Study, with 197,017 person-years of follow-up. Intake of well or very well done total meat was associated with a 1.26-fold increased risk of prostate cancer.”
Dietary patterns and 15-y risks of major coronary events, diabetes, and mortality. Brunner EJ, et al. Am J Clin Nutr. 2008 May;87(5):1414-21. Key Finding: “We analyzed the prospective relation of dietary patterns with incident chronic disease and mortality during 15 y of follow-up of 106,633 person-years at risk among men and women with a mean age of 50 y at the time of dietary assessment. The unhealthy dietary pattern of white bread, processed meat, fries and full-cream milk, compared to the healthy pattern of fruit vegetables, whole-meal bread, low-fat dairy and little alcohol, was associated with increased risk for coronary death or nonfatal myocardial infarction and diabetes.”
Nutrition, total fluid and bladder cancer. Brinkman M, Zeegers MP. Scand J Urol Nephtrol Suppl. 2008 Sep;(218):25-36. Key Finding: “A search of computerized databases was conducted to identify all epidemiological studies published between 1966 and October 2007 on the association between nutrition and bladder cancer. Possible risk factors identified are salted and barbecued meat, pork, total fat, pickled vegetables, salt, soy products, spices and artificial sweeteners.”
Meat and meat-mutagen intake and pancreatic cancer risk in the NIH-AARP cohort. Stotzenberg-Solomon RZ, et al. Cancer Epidemiol Biomarkers Prev. 2007 Dec;16(12):2664-75. Key Finding: “This cohort consisted of 537,302 individuals aged 50 to 71 years with complete baseline dietary data ascertained from a food frequency questionnaire. Men showed a significant 50% increased risks for the highest tertile of grilled/barbecued and broiled meat and significant doubling of risk for the highest quintile of overall meat-mutagenic activity. These findings support the hypothesis that meat intake, particularly meat cooked at high temperatures and associated mutagens, may play a role in pancreatic cancer development.”
Meat intake, preparation methods, mutagens and colorectal adenoma recurrence. Martinez ME, et al. Carcinogenesis. 2007 Sep;28(9):2019-27. Key Finding: “We prospectively assessed the relation between type of meat, meat preparation methods, doneness, a metric of HCAs and other mutagens and colorectal adenoma recurrence among 869 participants in a chemoprevention trial. For recurrence of advanced lesions, significant associations were detected among individuals in the highest when compared with the lowest tertile of intake for pan-fried red meat and well/very well done red meat. Significant positive associations were shown for recurrence of multiple adenomas and the following variables: processed meat, pan-fried meat, well/very well done meat.”
Consumption of trans fats and estimated effects on coronary heart disease in Iran. Mozaffarian D, et al. Eur J Clin Nutr. 2007 Aug;61(8):1004-10. Key Finding: “Partially hydrogenated oils were used extensively for cooking in Iranian homes. Trans fatty acids accounted for 33% of fatty acids in these products, or 4.2% of all calories consumed. Intake of trans fatty acids contributes to a sizeable proportion of coronary heart disease events. Replacement of partially hydrogenated oils with unhydrogenated oils in cooking would likely produce substantial reductions in CHD incidence.”
Dietary mutagen exposure and risk of pancreatic cancer. Li D, et al. Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):655-61. Key Finding: “A total of 626 cases and 530 non cancer controls were frequency matched and dietary exposure information was collected via personal interview using a meat preparation questionnaire. A significantly greater portion of the cases than controls showed a preference to well-done pork, bacon, grilled chicken, and pan-fried chicken, but not to hamburger and steak. A possible synergistic effect of dietary mutagen exposure and smoking was observed among individuals with the highest level of exposure.”
Meat mutagens and risk of distal colon adenoma in a cohort of U.S. men. Wu K, et al. Cancer Epidemiol Biomarkers Prev. 2006 Jun;15(6):1120-5. Key Finding: “Cooking meats at high temperatures and for long duration produces heterocyclic amines and other mutagens. These meat-derived mutagenic compounds have been hypothesized to increase risk of colorectal neoplasia. Our results suggest that mutagens other than heterocyclic amines in cooked meats may also play a role in increasing the risk of distal adenoma.”
Foodstuffs and colorectal cancer risk: a review. Marques-Vidal P, et al. Clin Nutr. 2006 Feb;25(1):14-36. Key Finding: “A systematic review of available prospective studies on dietary intake and colorectal cancer was conducted. Excessive consumption of meat or smoked/salted/processed food appears to be deleterious. The consumption of smoked or salted fish also increases risk for colorectal cancer. The consumption of white meat, fish/seafood and dairy products was mostly unrelated to colorectal cancer risk.”
A review of the toxicology of acrylamide. Exon JH. J Toxicol Environ Health B Crit Rev. 2006 Sep-Oct;9(5):397-412. Key Finding: “Acrylamide (ACR) was recently found to form naturally in foods cooked at high temperature. Acrylamide was shown to be a neurotoxicant, reproductive toxicant, and carcinogen in animal species, though only the neurotoxic effects have been observed in humans.”
Diet and gastric cancer: a case-control study in Shanghai urban districts. Fei SJ, Xiao SD. Chin J Dig Dis. 2006;7(2):83-8. Key Finding: “One hundred and eight-nine patients with gastric cancer and 567 age and sex-matched controls were surveyed with a questionnaire. Increased intake of salted, pickled, fried and smoked foods were risk factors for gastric cancer.”
Comparisons of prostate cancer mortality rates with dietary practices in the United States. Colli JL, Colli A. Urol Oncol. 2005 Nov-Dec;23(6):390-8. Key Finding: “This study found strong positive correlations between prostate cancer mortality and the consumption of total meat; added fats and oils; ice cream; salad/cooking oils; margarine, and vegetable shortening. The link between salad/cooking oil consumption and prostate cancer risk may be consistent with past studies which suggest that mu-linolenic acid (a component of salad/cooking oils) is a suspected risk factor for prostate cancer.”
Dietary habits of patients with coronary atherosclerosis: case-control study. Loke AY, Chan KN. J Adv Nurs. 2005 Oct;52(2):159-69. Key Finding: “A total of 145 consecutive patients scheduled to have coronary angiogram in a regional hospital in Hong Kong completed a self-reported questionnaire on their dietary intake. Patients confirmed as having coronary atherosclerosis were more likely than those with normal coronary vessels to rank deep fry, stir fry, and pan fry as their preferred cooking methods over steaming or boiling.”
Dietary factors and risk of non-hodgkin lymphoma in men and women. Chang ET, et al. Cancer Epidemiol Biomarkers Prev. 2005 Feb;14(2):512-20. Key Finding: “Diet could influence non-hodgkin lymphoma risk by modulating the immune system. We did a population-based case control study. A total of 597 NHL cases and 467 population controls in Sweden completed a food frequency questionnaire. High consumption of dairy products and fried red meat was associated with increased risk of NHL.”
Meat and fat intake as risk factors for pancreatic cancer: the multiethnic cohort study. Nothlings U, et al. J Natl Cancer Inst. 2005 Oct 5;97(19):1458-65. Key Finding: “During 7 years of follow-up, 482 incident pancreatic cancers occurred in 190,545 cohort members. The strongest association was with processed meat. Intakes of pork and of total red meat were both associated with 50% increases in risk. There were no associations of pancreatic cancer risk with intake of poultry, fish, dairy products, eggs, total fat, saturated fat, or cholesterol. Carcinogenic substances related to meat preparation methods might be responsible for the positive association.”
A prospective study of meat and meat mutagens and prostate cancer risk. Cross AJ. Peters U. Kirsh VA. Andriole GL, et al. Cancer Res. 2005 Dec 15;65(24):11779-84. Key Finding: “Using a 137-item food frequency questionnaire, we investigation the association between meat and meat mutagens and prostate cancer risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening. Very well done meat was positively associated with prostate cancer risk. In addition, this study lends epidemiologic support to the animal studies, which have implicated PhlP (produced by high temperature cooking) as a prostate carcinogen.”
Epidemiology of pancreatic cancer: an overview. Ghadirian P, et al. Cancer Detect Prev. 2003;27(2):87-93. Key Finding: “A positive association has been reported between pancreatic cancer risk and dietary intake such as fat and oil, meat, dairy products, and fried foods.”
Intake of conjugated linoleic acid, fat, and other fatty acids in relation to postmenopausal breast cancer: the Netherlands Cohort Study on Diet and Cancer. Voorrips LE, et al. Am J Clin Nutr. 2002 Oct;76(4):873-82. Key Finding: “Statistically significant positive associations were found with total trans fatty acids and risk of breast cancer.”
Dietary patterns and risk for type 2 diabetes mellitus in U.S. men. Van Dam RM, et al. Ann Intern Med. 2002 Feb 5;136(3):201-9. Key Finding: “Participants were 42,504 male health professionals, 40 to 75 years of age, without diagnosed diabetes at baseline. Using a food frequency questionnaire analysis, a ‘western’ diet characterized by higher consumption of red meat, processed meat, French fries, high-fat dairy products, refined grains, and sweets and desserts is associated with a substantially increased risk for type 2 diabetes in men.”
Pharyngeal cancer prevention: evidence from a case-control study involving 232 consecutive patients. Escribano Uzcudun A, et al. J Laryngol Otol. 2002 Jul;116(7):523-31. Key Finding: “This was a case-control study conducted in Madrid, Spain, with 232 consecutive patients diagnosed between January 1,1990 and December 31, 1995. A high dietary intake of meat and fried foods were found to be risk factors for pharyngeal cancer.”
Cured and broiled meat consumption in relation to childhood cancer: Denver, Colorado (United States). Sarasua S, Savitz DA. Cancer Causes Control. 1994 Mar;5(2):141-8. Key Finding: “The association between cured and broiled meat consumption by the mother during pregnancy and by the child was examined in relation to childhood cancer. Five meat groups (ham, bacon, or sausage; hot dogs; hamburgers; bologna, pastrami, corned beef, salami, or lunch meat; charcoal broiled foods) were assessed. Exposures among 234 cancer cases and 206 controls were selected in the Denver, Colorado area. Maternal hot-dog consumption of one or more times per week was associated with childhood brain tumor. Among children eating hamburgers one or more times per week was associated with risk of ALL, and eating hot dogs one or more times per week was associated with brain tumors. The results linking hot dogs and brain tumors (replicating an earlier study) and the apparent synergism between no vitamins and meat consumption suggests a possible adverse effect of dietary nitrites and nitrosamines.”
Intake of trans fatty acids and risk of coronary heart disease among women. Willett WC, et al. Lancet 1993 Mar 6;34(8845):581-5. Key Finding: “Trans isomers of fatty acids, formed by the partial hydrogenation of vegetable oils to produce margarine and vegetable shortening, increase the ratio of plasma low-density-lipoprotein to high-density-lipoprotein cholesterol, so it is possible that they adversely influence risk of coronary heart disease (CHD). To investigate this possibility, we studied dietary data from 85,095 participants in the Nurses’ Health Study. During 8 years of follow-up, there were 431 new CHD. Intake of trans isomers was directly related to risk of CHD. Intakes of foods that are major sources of trans isomers (margarine, cookies, biscuits, cake and white bread) were each significantly associated with higher risks of CHD.”
Heavy metals in raw, fried and grilled Mediterranean finfish and shellfish. Kalogeropoulos N, et al. Food Chem Toxicol. 2012 Oct;50(10):3702-8. Key Finding: “The effect of pan-frying and grilling on the heavy metals Cd, Cr, Cu, Fe, Hg, Ni, Pb and Zn content of popular small Mediterranean finfish and shellfish was studied. The species selected were anchovy, bogue, hake, pciarel, sardine, sand smelt, stripped mullet, mussel, shrimp and squid. Both culinary practices examined resulted in increased metals concentrations compared to those of raw samples. Significant amounts of Fe and Zn were found in the cooked seafood.”
Association of Western and traditional diets with depression and anxiety in women. Jacka FN, et al. Am J Psychiatry. 2010 Mar;167(3):305-11. Key Finding: “Key biological factors that influence the development of depression are modified by diet This study examined the extent to which the high-prevalence mental disorders are related to habitual diet in 1,046 women ages 20-93 years randomly selected from the population. A “western” diet of processed or fried foods, refined grains, sugary products, and beer was associated with higher odds for major depression and anxiety disorders. These results demonstrate an association between habitual diet quality and the high-prevalence mental disorders.”
Exposure to polycyclic aromatic hydrocarbons (PAHs), mutagenic aldehydes and particulate matter during pan frying of beefsteak. Sjaastad AK, et al. Occup Environ Med. 2010 Apr;67(4):228-32. Key Finding: “Cooking with gas or electric stoves produces fumes, especially during frying, that contain a range of harmful and potentially mutagenic compounds as well as high levels of fine and ultrafine particles. Naphthalene and mutagenic aldehydes were detected in most of the samples in this study of fumes from the frying of beefsteak. Frying on a gas stove instead of an electric stove causes increased occupational exposure to some of the components in cooking fumes which may cause adverse health effects.” Cooking fumes produced during high temperature frying have been determined to be “probably carcinogenic” by the International Agency for Research on Cancer.
Dietary patterns associated with fat and bone mass in young children. Wosje KS, et al. Am J Clin Nutr. 2010 Aug;92(2):294-303. Key Finding: “Obesity and osteoporosis have origins in childhood and both are affected by dietary intake and physical activity. A total of 325 children contributed data from 13 visits over 4 separate study years. High fried-food intake was related to high fat mass.”
Food intake patterns associated with incident type 2 diabetes: the Insulin Resistance Atherosclerosis Study. Liese AD, etal. Diabetes Care. 2009 Feb;32(2):263-8. Key Finding: “The cohort included 880 middle-aged adults initially free of diabetes. At the 5-year follow-up, 144 individuals had developed diabetes. High intake of the food groups red meat, low-fiber bread and cereal, fried potatoes, eggs, cheese and cottage cheese was positively associated with both biomarkers of type 2 diabetes.”
Chronic intake of potato chips in humans increases the production of reactive oxygen radicals by leukocytes and increases plasma C-reactive protein: a pilot study. Naruszewicz M, et al. Am J Clin Nutr. 2009 Mar;89(3):773-7. Key Finding: “Relatively high concentrations of acrylamide in commonly ingested food products, such as French fries, potato chips, or cereals, may constitute a potential risk of human health. The objective of this pilot study was to investigate the possible connection between chronic ingestion of acrylamide-containing potato chips and oxidative stress or inflammation. Fourteen healthy volunteers were given 160 g of potato chips daily for 4 wk. An increase in acrylamide-hemoglobin adducts in blood was found in all the study subjects. These novel findings seem to indicate that chronic ingestion of acrylamide-containing products induces a proinflammatory state, a risk factor for progression of atherosclerosis.”
Detection of PhlP in grilled chicken entrees at popular chain restaurants throughout California. Sullivan KM, et al. Nutr Cancer. 2008;60(5):592-602. Key Finding: “Heterocyclic amines (HCAs) compounds formed when meat is cooked at high temperatures, particularly through pan frying, grilling or barbequeing, pose a potential carcinogenic risk to the public. It is unclear whether there is any level at which consumption of HCAs can be considered safe. We surveyed at least 9 locations each of 7 popular chain restaurants (McDonald’s, Burger King, Chick-fil-A, Chili’s, TGI Friday’s, Outback Steakhouse, and Applebee’s) in California, collecting one or two entrees from each location. All 100 samples contained PhlP, an HCA. Concentrations were variable within and between entrees and ranged from 0.08 to 43.2 ng/g. When factoring in the weight of the entrees, absolute levels of PhlP reached over 1,000 ng for some entrees.”
Dietary patterns and risk of mortality from cardiovascular disease, cancer, and all causes in a prospective cohort of women. Heidemann C, et al. Circulation. 2008 Jul 15;118(3):230-7. Key Finding: “We prospectively evaluated the relation between dietary patterns and risk among 72,113 women and were followed up from 1984 to 2002. A Western pattern diet reflected high intakes of red meat, processed meat, refined grains, French fries, and sweets/desserts, was associated with a higher risk of mortality from cardiovascular disease (22%), cancer (16%) and all causes (21%) than a prudent diet with high intakes of vegetables and fruit, fish, poultry, and whole grains.”
Major dietary patterns are related to plasma concentrations of markers of inflammation and endothelial dysfunction. Lopez-Garcia E, et al. Am J Clin Nutr. 2004 Oct;80(4):1029-35. Key Finding: “Endothelial dysfunction is one of the mechanisms linking diet and the risk of cardiovascular disease. Markers of inflammation and endothelial dysfunction include C-reactive protein, interleukin 6, E-selectin, sVCAM and SICAM. We conducted a cross-sectional study of 732 women from the Nurses’ Health Study I cohort who were 43-69 y of age and free of cardiovascular disease, cancer, and diabetes mellitus. Dietary intake was documented by using a validated food-frequency questionnaire in 1986 and 1990. A Western pattern diet characterized by higher intakes of red and processed meats, sweets, desserts, French fries, and refined grains showed a positive relation with CRP, interleukin, E-selectin, sICAM and sVCAM. This study suggests a mechanism for the role of dietary patterns in the pathogenesis of cardiovascular disease.”
Dietary corn oil promotes colon cancer by inhibiting mitochrondria-dependent apoptosis in azoxyhmethane-treated rats. Wu B, et al. Exp Biol Med (Maywood). 2004 Nov;229(10):1017-25. Key Finding: “How dietary corn oil is involved in colon carcinogenesis and cancer development is poorly understood. The aim of this study was to investigate whether long-term dietary corn oil promotes colon cancer by inhibiting the tumor suppressor gene p53-mediated mitochondria-dependent apoptosis in male Sprague-Dawley rats. Their diet was supplemented with 10% corn oil for 48 weeks. Long-term dietary corn oil increased aberrant crypt foci at 12 weeks and promoted colon cancer invasion at 48 weeks.”
Prospective study of major dietary patterns and risk of coronary heart disease in men. Hu FB, et al. Am J Clin Nutr. 2000 Oct;72(4):912-21. Key Finding: “This was a prospective cohort of 44,875 men aged 40-75 y without diagnosed cardiovascular disease or cancer at baseline. During 8 y of follow-up, we documented 1,089 cases of CHD. The Western dietary pattern characterized by higher intake of red meat, processed meat, refined grains, sweets and dessert, French fries and high-fat dairy products predict the risk of coronary heart disease independent of other lifestyle variables.”
Fried, well-done red meat and risk of lung cancer in women (United States). Sinha R, et al. Cancer Causes Control. 1998 Dec;9(6):621-30. Key Finding: “A population-based case-control study of both non-smoking and smoking women was conducted in Missouri. A 100-item food frequency questionnaire with detailed questions on meat consumption was completed by 593 cases and 623 frequency matched controls. We found that consumption of red meat, especially fried and/or well-done red meat, was associated with increased risk of lung cancer.”
Heterocyclic amine content of pork products cooked by different methods and to varying degrees of doneness. Sinha R, et al. Food Chem Toxicol. 1998 Apr;36(4):289-97. Key Finding: “Heterocyclic amines (HCAs) are known mutagens and animal carcinogens produced in meats cooked at high temperatures. We measures the five predominant HCAs in various pork products cooked by different techniques. Highest levels were found in well done and very well done oven-broiled bacon, pan-fried very well done sausage patties, and well done and very well done pan-fried but not broiled pork chops. Hot dogs or ham slices had low or undetectable levels of HCAs.”
High concentrations of the carcinogen 2-amino-1-methyl-6-phenylimidazo-{4,5-b}pyridine (PhlP) occur in chicken but are dependent on the cooking method. Sinha R, et al. Cancer Res. 1995 Oct 15;55(20):4516-9. Key Finding: “The objective of this study was to measure the five predominant HAAs (heterocyclic aromatic amines) which are mutagenic and carcinogenic compounds in chicken cooked by various methods to different degrees of doneness. High levels of PhlP (ranging from 12 to 480 ng/g cooked meat) were found in chicken breasts when panfried, oven-broiled and grilled/barbequed, but not in white roasted or stewed chicken. PhlP concentration increased in skinless, boneless chicken breast with longer cooking time, higher internal temperature and greater degress of surface browning. Certain cooking methods produce PhlP, a known colon and breast carcinogen in rodents, and possibly a human carcinogen, at substantially higher levels in chicken than has been reported previously in red meat.”
Food habits and pancreatic cancer: a case-control study of the Francophone community in Montreal, Canada. Ghadirian P, et al. Cancer Epidemiol Biomarkers Prev. 1995 Dec;4(8):895-9. Key Finding: “A total of 179 cases and 239 controls matched for age, sex, and language (French) were interviewed. Data on food habits, methods of food preparation and preservation, and related information was obtained through a questionnaire. The study found an increased risk of pancreatic cancer associated with a high consumption of salt, smoked meat, dehydrated food, fried food, and refined sugar. An inverse association was found with the consumption of food with no preservatives or additives, raw food, and food prepared by presto or high-pressure cooking.”
Dietary acrylamide exposure of the French population: results of the second French Total Diet Study. Sirot V, et al. Food Chem Toxicol. 2012 Mar;50(3-4):889-94. Key Finding: “Acrylamide is a heat-induced carcinogene compound that is found in some foods consequently to cooking. Acrylamide was analysed in 192 food samples. Highest mean concentrations were found in potato chips.crips, French fries and other fried potatoes, and salted biscuits. Mean acrylamide exposure was assessed for adults and children. A health concern was found. It is therefore advisable to continue efforts to reduce dietary exposure to acrylamide.”
A statistical regression model for the estimation of acrylamide concentrations in French fries for excess lifetime cancer risk assessment. Chen MJ, et al. Food Chem Toxicol. 2012 Oct;50(10):3867-76. Key Finding: “Human exposure to acrylamide through consumption of French fries and other foods has been recognized as a potential health concern. We used cooking temperature and time to estimate acrylamide concentrations in French fries. Based on French fry intake survey data and eight frying temperature-time schemes, results showed that if acrylamide concentration is higher than 168 ppb (parts per billion), the estimated cancer risk for adolescents aged 13-18 years would be already higher than the target excess lifetime cancer risk.”
Effects of chronic oral acrylamide exposure on incremental repeated acquitision (learning) task performance in Fischer 344 rats. Garey J, Paule MG. Neurotoxicol Teratol. 2010 Mar-Apr;32(2):220-5. Key Finding: “This research evaluated the effects of acrylamide on learning task performance in Fischer 344 rats exposed daily beginning prenatally and continuing throughout the lifespan. Acrylamide-exposed rats exhibited altered performance by 4 months of age. From approximately 1-8 months of age over 52 testing sessions, a significant treatment effect was found. Previous findings in these same animals suggest that this decreased response rate could be due to subtle motoric effects or possibly due to decreases in psychomotor speed, but is mostly likely due to motivational effects.”
A prospective study on dietary acrylamide intake and the risk for breast, endometrial, and ovarian cancers. Wilson KM, et al. Cancer Epidemiol Biomarkers Prev. 2010 Oct;19(10):2503-15. Key Finding: “We assessed acrylamide intake among 88,672 women in the Nurses’ Health study using food frequency questionnaires. We observed no association between acrylamide and breast cancer. Risk for endometrial cancer and possibly ovarian cancer was greater among high acrylamide consumers.”
Dietary acrylamide intake and estrogen and progesterone receptor-defined postmenopausal breast cancer risk. Pedersen GS, et al. Breast Cancer Res Treat. 2010 Jul;122(1):199-210. Key Finding: “Acrylamide, a potential human carcinogen, has been discovered in a variety of heat-treated carbohydrate-rich food products. Previously, dietary acrylamide intake was shown to be associated with endocrine-related cancers in humans. We assessed the association between dietary acrylamide intake and risk of postmenopausal breast cancer stratified by estrogen and progesterone-receptor status. This study showed some indications of a positive association between dietary acrylamide intake and receptor-positive breast cancer risk in postmenopausal never-smoking women.”
In vitro investigations of glycidamide-induced DNA lesions in mouse male germ cells and in mouse and human lymphocytes. Hansen SH, et al. Mutat Res. 2010 Feb 1;696(1):55-61. Key Finding: “The industrial compound and food contaminant acrylamide is a probable human carcinogen, also known to induce male-mediated reproductive effects in animals. Most data suggest that its metabolite glycidamide is involved in the observed toxicity. We conclude that there may be differences between mice and humans in acrylamide/glycidamide-induced genotoxicity, and DNA from mouse male germ cells does not appear to be more sensitive to glycidamide than DNA from periperhal blood lymphocytes in vitro.”
Diet-induced obesity in male mice is associated with reduced fertility and potentiation of acrylamide-induced reproductive toxicity. Ghanayem BI, et al. Biol Reprod. 2010 Jan;82(1):96-104. Key Finding: “Acrylamide-induced reproductive toxicity was assessed in obese or lean male mice. Treatment with acrylamide exacerbated male infertility of obese and lean mice, however, this effect was more pronounced in obese mice. Further, females partnered with acrylamide-treated obese mice exhibited a further decrease in the percentage of live fetuses.”
Enhanced fat consumption potentiates acrylamide-induced oxidative stress in epididymis and epididymal sperm and effect spermatogenesis in mice. Zhang JX, et al. Toxicol Mech Methods. 2010 Feb;20(2):75-81. Key Finding: “Acrylamide and high contents of fat could be found co-existent in many foods processed by high temperature, such as deep frying and roasting. This study investigated the effect of enhanced fat consumption on deficits of spermatogenesis induced by acrylamide. These data suggest that enhanced feedings of corn oil and pork fat on mice potentiates acrylamide-induced oxidative stress in the epididymis and epididymal sperm and a subsequent effect on spermatogenesis.”
The carcinogenicity of dietary acrylamide intake: a comparative discussion of epidemiological and experimental animal research. Hogervorst JG, et al. Crit Rev Toxicol. 2010 Jul;40(6):485-512. Key Finding: “Since 2002, it is known that the probably human carcinogen acrylamide is present in commonly consumed carbohydrate-rich foods, such as French fries and potato chips. In this review, the authors discuss the body of evidence on acrylamide carcinogenicity from both epidemiological and rodent studies. Genotoxicity may not be the only mechanism by which acrylamide causes cancer. The estimated risks based on the epidemiological studies for the sites for which a positive association was observed were considerably higher than those based on extrapolations from the rat studies. The observed pattern of increased risks in the rat and epidemiological studies and the decreased risks in the epidemiological studies suggests that acrylamide might influence hormonal systems, for which rodents may not be good models.”
Estimation of the dietary acrylamide exposure of the Polish population. Mojska H, et al. Food Chem Toxicol. 2010 Aug-Sep;48(8-9):2090-6. Key Finding: “The objective of our study was to determine acrylamide content in the Polish foods and to assess the average dietary acrylamide exposure of the Polish population. The main sources of dietary acrylamide in Polish population were as follow: bread supplied 45% of total dietary intake; French fries and potato crisps, 23%, and roasted coffee, 19% of intake.”
Dietary acrylamide intake and the risk of cancer among Finnish male smokers. Hirvonen T, et al. Cancer Causes Control. 2010 Sep 22 {Epub ahead of print}. Key Finding: “The study consisted of 27,111 male smokers, aged 50-69 years, without history of cancer. The men completed a validated dietary questionnaire. Dietary acrylamide intake was positively associated with the risk of lung cancer.”
Effect of cooking method (baking compared with frying) on acrylamide level of potato chips. Palazouglu TK, et al. J Food Sci. 2010 Jan-Feb;75(1):E25-9. Key Finding: “Baking and frying experiments were conducted at 170, 180 and 190 degrees C using potato slices with a thickness of 1.4 mm. The results showed that acrylamide level of potato chips prepared by frying increased with frying temperature (19.6 ng/g at 170 degrees C, 39 ng/g at 180 degrees C, and 95 ng/g at 190 degrees.) In baking, the highest acrylamide level was observed in potato chips prepared at 170 degrees C (47.8 ng/g at 170 degrees, 19.3 ng/g at 180 degrees C, and 29.7 ng/g at 190 degrees C.) The results showed that baking at 170 degrees C more than doubled the acrylamide amount that formed upon frying at the same temperature.”
Acrylamide monitoring in Switzerland, 2007-2009: results and conclusions. Biedermann M, et al. Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2010 Oct;27(10):1352-62. Key Finding: “Switzerland performed its own monitoring, covering the whole range of products that significantly contain acrylamide (almost 300 samples per year) but focusing on those products that may result in high exposure. No significant change, particularly improvement was noticed, especially regarding those products for which substantial potential for improvement is known.”
Food contaminant acrylamide increases expression of Cox-2 and nitric oxide synthase in breast epithelial cells. Lyn-Cook LE, et al. Toxicol Ind Health. 2010 Aug 16 {Epub ahead of print}. Key Finding: “A potentially harmful effect of the dietary compound acrylamide has been suggested by data indicating its association with increased breast cancer. This study investigated the potential effects of acrylamide in nontumorigenic breast cells by assessing expression levels of inducible nitric oxide synthase and Cox-2 and NOS activity, which are known to be early molecular changes in disease formation. Treatment of cells with acrylamide increased levels of iNOS (both expression and activity) and Cox-2.”
Dietary acrylamide intake and risk of esophageal cancer in a population-based case-control study in Sweden. Lin Y, et al. Int J Cancer. 2010 Aug 16 {Epub ahead of print}. Key Finding: “In a Swedish nationwide, population-based case-control study, data were collected on diet through personal interviews. Among participants in the highest quartile of acrylamide exposure compared to the lowest, the adjusted risk of all esophageal tumors combined was increased, particularly among overweight or obese persons. Regarding squamous cell carcinoma only, a dose-response association was identified. Dietary intake of acrylamide might be a risk exposure for esophageal cancer.”
Toxicity of acrylamide and evaluation of its exposure in baby foods. Erkekoglu P, Baydar T. Nutr Res Rev. 2010 Sep 16:1-11. Key Finding: “Acrylamide can be detected as a contaminant in several foodstuffs including baby foods and infant formulas. It is anticipated that children will generally have intakes that are two to three times those of adults when expressed on a body-weight basis. Though exposure to acrylamide is inevitable, it is necessary to protect infant and children from high exposure. The present review focuses on the several adverse health effects of acrylamide including mutagenicity, genotoxicity, carcinogenicity, neurotoxicity and reproductive toxicity.”
Chronic intake of potato chips in humans increases the production of reactive oxygen radicals by leukocytes and increases plasma C-reactive protein: a pilot study. Naruszewicz M., et al. Am J Clin Nutr. 2009 Mar;89(3):773-7. Key Finding: “Relatively high concentrations of acrylamide {a cooking-induced carcinogen} in commonly ingested food products, such as French fries, potato chips, or cereals, may constitute a risk to human health. Fourteen healthy volunteers were given 160 g of potato chips containing 157 microg acrylamide daily for 4 wk. An increase in acrylamide-hemoglobin adducts in blood was found in all the study subjects. These novel findings seem to indicate that chronic ingestion of acrylamide-containing products induces a proinflammatory state, a risk factor for progression of atherosclerosis.”
Dietary acrylamide intake and the risk of head-neck and thyroid cancers: results from the Netherlands Cohort Study. Schouten LJ, et al. Am J Epidemiol. 2009 Oct 1;170(7):873-84. Key Finding: “Dietary acrylamide was statistically significantly associated with increased risk of oral cavity cancer in female nonsmokers. Dietary acrylamide intake was not positively associated with risk of head-neck and thyroid cancer.”
Acrylamide in selected foods and genotoxicity of their extracts. El-Assouli SM. J Egypt Public Health Assoc. 2009;84(3-4):371-92. Key Finding: “Leukocytes from rat fed Pringles crisps showed extensive DNA damage in comet test. This genotoxicity could not be demonstrated by Pringles in vitro. Continuous surveying of food for acrylamide is necessary to minimize human exposure.”
Lung cancer risk in relation to dietary acrylamide intake. Hogervorst JG, et al. J Natl Cancer Inst. 2009 May 6;101(9):651-62, Key Finding: “We conducted a case-control study among 58,279 men and 62,573 women (aged 55-69 years) in the Netherlands Cohort Study on Diet and Cancer. Acrylamide intake was not associated with lung cancer risk in men but was inversely associated in women, most strongly for adenocarcinoma. This finding suggests that acrylamide is involved in human carcinogenesis through pathways other than genotoxicity.”
Acrylamide decreased dopamine levels and increased 3-nitrotyrosine (3-NT) levels in PC 12 cells. Tareke E, et al. Neurosci Lett. 2009 Jul 17;458(2):89-92. Key Finding: “Acrylamide is a chemical known to produce neurotoxicity in animals, as well as in humans. The mechanism of acrylamide-induced neurotoxicity is not fully known. However, recent studies have revealed that acrylamide affects the dopaminergic system. Our study revealed that acrylamide exposure produced a dose- and time dependent decrease in dopamine levels. The decrease was noted at 24h after exposure to acrylamide.”
imultaneous exposure to dietary acrylamide and corn oil developed carcinogenesis through cell proliferation and inhibition of apoptosis by regulating p53-mediated mitochondria-dependent signaling pathway. Zhang X. Toxicol Ind Health. 2009 Mar;25(2):101-9. Key Finding: “To investigate whether simultaneous exposure to acrylamide and long-term dietary corn oil induces colon cancer by inhibiting the tumor suppressor gene p53-mediate mitochondria-dependent apoptosis in rats, male Sprague-Dawley rats were given introperitoneal injections of acrylamide at does of 10mg/kgbw and diets supplemented with 10% corn oil for 8 weeks. Results suggest that simultaneous exposure to acrylamide and long-term dietary corn oil induces development of colon cancer partly by inhibiting the tumor suppressor gene p53-mediated mitochrondria-dependent apoptosis.”
Dietary acrylamide intake and the risk of renal cell, bladder, and prostate cancer. Hogervorst JG, et al. Am J Clin Nutr. 2008 May;87(5):1428-38. Key Finding: “The Netherlands Cohort Study on diet and cancer includes 120,852 men and women aged 55-69 years. A random subcohort of 5,000 participants was selected and acrylamide intake was assessed with a food frequency questionnaire. After 13.3 years of follow-up, 339, 1210, and 2246 cases of renal cell, bladder, and prostate cancer, respectively, were available for analysis. We found some indications for a positive association between dietary acrylamide and renal cell cancer risk. There were no positive associations with bladder and prostate cancer risk.”
AGE (advanced glycation end products)
Oxidative stress and aging: is methylglyoxal the hidden enemy? Desai KM, et al. Can J Physiol Pharmacol. 2010 Mar;88(3):273-84. Key Finding: “A major precursor of advanced glycation end products is methylglyoxal. AGEs are associated with the aging process and age-related diseases such as cardiovascular complications of diabetes, neurodegenerative diseases and connective tissue disorders. AGEs also increase oxidative stress. Besides causing AGEs formation, MG has a potential role in the aging process through oxidative stress.”
Reaction Metabolites and AGE/RAGE-Mediated Cellular Dysfunction Affect the Aging Process – A Mini-Review. Fleming TH. Humpert PM, et al. Gerontology. 2010 Oct 21 {Epub ahead of print}. Key Finding: “Experimental models have recently provided evidence that reduced detoxification of AGE precursors by the glyoxalase system, engagement of the cellular receptor RAGE and RAGE-dependent sustained activation of the pro-inflammatory transcription factor nuclear factor kB might significantly contribute to the rate of aging and the onset of age-related neurodegenerative, musculoskeletal and vascular diseases.”
RAGE and the pathogenesis of chronic kidney disease. D’Agati V, Schmidt AM. Nat Rev Nephrol. 2010 Jun;6(6):352-60. Key Finding: “The receptor for advanced glycation endproducts, RAGE, has roles in the pathogenesis of renal disorders that are not associated with diabetes, such as obesity-related glomerulopathy, lupus nephritis, and ischemic renal injuries. Accumulating evidence links RAGE to the pathogenesis of nephropathies, indicating that antagonism of RAGE might be a strategy for the treatment of chronic kidney disease.”
Immunohistochemical analysis of human brain suggests pathological synergism of Alzheimer’s disease and diabetes mellitus. Valente T, et al. Neurobiol Dis. 2010 Jan;37(1):67-76. Key Finding: “Our results indicate that Alzheimer’s disease patients present a significant increase of cell damage through a rage-dependent mechanism, suggesting that advanced glycation end products may promote the generation of an oxidative stress vicious cycle, which can explain the severe progression of patients with both pathologies.”
Regulation of advanced glycation end product (AGE)-receptor (RAGE) system by PPAR-gamma agonists and its implication in cardiovascular disease. Yamagishi S, et al. Pharmacol Res. 2009 Sep;60(3):174-8. Key Finding: “There is a growing body of evidence that AGEs and their receptor (RAGE) axis is involved in the pathogenesis of cardiovascular disease. The inhibition of AGE formation, down-regulation of RAGE expression or blockade of the RAGE downstream signaling may be a promising therapeutic target for preventing cardiovascular disease.”
(Pre)diabetes, brain aging, and cognition. S Roriz-Filho J, et al. Biochem Biophys Acta. 2009 May;1792(5):432-43. Key Finding: “Chronic hyperglycemia and hyperinsulinemia primarily stimulates the formation of Advanced Glucose Endproducts (AGEs), which leads to an overproduction of Reactive Oxygen Species. Protein glycation and increased oxidative stress are the two main mechanisms involved in biological aging, both being also probably related to the etiopathogeny of Alzheimer’s disease.”
The role of RAGE in amyloid-beta peptide-mediated pathology in Alzheimer’s disease. Schmidt AM, et al. Curr Opin Investig Drugs. 2009 Jul;10(7):672-80. Key Finding: “Relevant preclinical models illustrate that the A beta-RAGE interaction amplifies neuronal stress and the accumulation of A beta, impairs memory and learning, and exaggerates neuroinflammation. These findings suggest that RAGE may mediate a common proinflammatory pathway in neurodegenerative disorders.”
AGE and their receptor RAGE in systemic autoimmune diseases: an inflammation propagating factor contributing to accelerated atherosclerosis. Nienhuis HL, et al. Autoimmunity. 2009 May;42(4):302-4. Key Finding: “Interaction of AGE with RAGE leads to intracellular signaling, and subsequent expression of adhesion molecules, chemokines, pro-inflammatory cytokines and up-regulation of RAGE itself. The AGE-RAGE interaction might act as a pro-inflammatory loop contributing to chronic low grade inflammation rendering these individuals susceptible for development of accelerated atherosclerosis.”
Advanced glycation end products (AGEs) and their involvement in liver disease. Hyogo H, Yamagishi S. Curr Pharm Des. 2008;14(10):969-72. Key Finding: “It is now well established that formation and accumulation of AGEs progress during normal aging, and at an extremely accelerated rate under diabetes, thus being implicated in various types of AGEs-related disorders such as diabetic vascular complications, neurodegenerative diseases and cancers. There are several papers to suggest the involvement of AGEs in various types of liver diseases such as non-alcoholic steatophepatitis.”
Food-derived advanced glycation end products (AGEs): a novel therapeutic target for various disorders. Yamagishi S, et al. Curr Pharm Des. 2007;13(27):2832-6. Key Finding: “The restriction of food-derived AGEs or the inhibition of the absorption of dietary AGEs may be a novel target for therapeutic intervention in the AGE-related disorders such as diabetic vascular complications, neurodegenerative diseases and cancers, and aging.”
Diet-derived advanced glycation end products are major contributors to the body’s AGE pool and induce inflammation in healthy subjects. Uribarri J, et al. Ann NY Acad Sci. 2005 Jun;1043:461-6. Key Finding: “The rate of AGE formation is markedly increased in diabetes mellitus, a condition in which AGEs play a major pathological role. AGEs form during the cooking of foods, primarily as the result of the application of heat. Together with previous evidence from diabetics and renal failure patients, these data suggest that dietary AGEs may play an important role in the causation of chronic diseases associated with underlying inflammation.”
Prevention of diabetic nephropathy in mice by a diet low in glycoxidation products. Zheng F, et al. Diabetes Metab Res Rev. 2002 May-Jun;18(3):224-37. Key Finding: “Intake of high-level, food-derived advanced glycation end products is a major contributor to diabetic nephtropathy in mice. Avoidance os dietary AGEs provides sustained protection against diabetic nephtropathy.”
Orally absorbed reactive glycation products (glycotoxins): an environmental risk factor in diabetic nephropathy. Koschinsky T, et al. Proc Natl Acad Sci USA. 1997 Jun 10;94(12):6474-9. Key Finding: “Daily influx of dietary advanced glycation endproducts (AGEs) may constitute an added chronic risk for renal-vascular injury in diabetes mellitus, and dietary restrictions of AGE food intake may greatly reduce the burden of AGEs in diabetic patients and possibly improve progress.”
PAH (polycyclic aromatic hydrocarbons)
Effect of charcoal types and grilling conditions on formation of heterocyclic aromatic amines (HAs) and polycyclic aromatic hydrocarbons (PAHs) in grilled muscle foods. Viegas O, et al. Food Chem Toxicol. 2012 Jun;50(6):2128-34. Key Finding: PAH absorption has been linked to both colon cancer and type 2 diabetes, while HA levels have been associated with colon and other cancers. “Grilling muscle foods involves high temperatures that lead to production of cooking toxicants such as Has and PAHs. We quantified HA and PAH levels in well-done meat and fish samples grilled with wood and coconut shell charcoal at 200 degrees C. Higher levels of HAs and PAHs were found in salmon samples. No significant differences were observed for HAs and PAHs in beef samples grilled with both charcoal types. Continuous barbecuing with the same charcoal showed that combustion of fat that dripped along the grilling period contributed to higher formation of HAs and PAHs.”
Comparison of polycyclic aromatic hydrocarbons (PAHS) contents in bakery products. Ciemniak A, Witczak A. Rocz Panstw Zakl Hig. (Polish) 2010;61(2):135-40. Key Finding: “PAHs have been found as contaminants in different food categories such as dairy products, smoked and barbequed meat. Processing of food at high temperatures increases the amount of PAHs in the food. Diet is the major source of human to exposure to PAHs, which have carcinogenic potential. The aim of this study was to determine the content levels of 23 PAHs in various sorts of bread. The total concentration of PAHs was varied between 2.61 microg/kg to 43.4 microg/kg.”
Meat Consumption and Risk of Esophageal and Gastric Cancer in a Large Prospective Study. Cross AJ, et al. Am J Gastroenterol. 2010 Oct 26 {Epub ahead of print}. Key Finding: “Red and processed meats could increase cancer risk through several potential mechanisms involving iron, heterocyclic amines, polycyclic aromatic hydrocarbons, and N-nitroso compounds. We found positive associations in this study between red meat intake and esophageal squamous cell carcinoma, and between DiMelQx intake and gastric cardia cancer.”
Health risk assessment on dietary exposure to polycyclic aromatic hydrocarbons (PAHs) in Taiyuan, China. Xia Z, et al. 2010 Oct 15;408(22):5331-7. Key Finding: “Twenty-five kinds of seven categories of foods were sampled and the concentrations of 16 polycyclic aromatic hydrocarbons (PAHs) were determined. The highest level of total PAHs was detected in pork (195.30 ng/g) whereas the lowest concentration was found in milk (8.73 ng/g). The median values of daily exposure doses for children, adolescents, adults and senior males were estimated to be 392.42, 511.01, 571.56, and 532.56 ng/g respectively, whereas those for the above population groups of female were found to be 355.16, 440.51, 487.64, and 444.85 ng/d, respectively. The incremental lifetime cancer risk for all groups indicate a high potential carcinogenic cancer risk.”
Polycyclic aromatic hydrocarbons potentiate high-fat diet effects on intestinal inflammation. Khalil A, et al. Toxicol Lett. 2010 Jul 15;196(3):161-7. Key Finding: “We demonstrate that intestinal inflammation caused by high-fat diet is increased by the contaminant benzo{a}pyrene. Our results suggest that intestinal inflammation may be involved in the onset of type 2 diabetes and that chronic exposure to PAH can increase the risk of type 2 diabetes.”
Influence of smoking parameters on the concentration of polycyclic aromatic hydrocarbons (PAHs) in Danish smoked fish. Duedahl-Olesen L, et al. Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2010 Sep;27(9):1294-305. Key Finding: “A new method for the analysis of 25 polycyclic aromatic hydrocarbon (PAH) compounds in fish was developed, validated, and used for the quantification of PAHs in 180 industrially smoked fish products. The sum concentration of 25 PAHs was highest in smoked herring and mackerel fillets with an average concentration of 320 and 235 microg/kg respectively. Increased combustion temperatures increased PAH levels.”
Exposure to polycyclic aromatic hydrocarbons (PAHs), mutagenic aldehydes, and particulate matter in Norwegian a la carte restaurants. Sjaastad AK, Svendsen K. Ann Occup Hyg. 2009 Oct;53(7):723-9. Key Finding: “The aim of the study was to characterize the exposure regarding polycyclic aromatic hydrocarbons in the breathing zone of the cook during work in Norwegian a la carte restaurants. We conclude that working as a cook in a Norwegian a la carte restaurant involves exposure in components in cooking fumes which may cause adverse health effects.”
Determination of polycyclic aromatic hydrocarbons (PAHs) in commonly consumed Nigerian smoked/grilled fish and meat. Akpambang VO, et al. Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2009 Jul;26(7):1096-103. Key Finding: “Smoking and or grilling, when carried out with traditional methods involving direct contact with wood combustion fumes, is responsible for high contamination levels with carcinogenic PAHs. The aim of this work was to investigate the PAH content of different smoked or grilled meat and fish products commonly consumed in Nigeria. Samples that were smoked or grilled using traditional methods were heavily contaminated with benzo{a}pyrene at levels ranging from 2.4 to 31.2 microg kg. This indicates a potential concern for consumer health.”
Serum polycyclic aromatic hydrocarbons among children with and without asthma: correlation to environmental and dietary factors. Al-Daghri NM. Int J Occup Med Environ Health. 2008;21(3):211-7. Key Finding: “Children from low-income families may be subject to high exposures to PAH which can lead to respiratory disorders. In this study of 75 children we found serum naphthalene and pyreme were significantly elevated among asthmatic children. Significant correlations were elicited between daily meat intake and serum levels of three PAHs. Public health awareness should be enhanced by educating parents to take certain precautions at home, such as preventing indoor smoking and reducing the intake of grilled and smoked meat by children so as to decrease their exposure to carcinogenic PAH.”
Evolution of the dietary exposure to polycyclic aromatic hydrocarbons in Catalonia, Spain. Mari-Cid R. Llobet JM, et al. Food Chem Toxicol. 2008 Sep;46(9):3163-71. Key Finding: “The concentrations of 16 polycyclic aromatic hydrocarbons were determined in samples of foodstuffs widely consumed by the population of Catalonia, Spain. The current results were compared with those of a previous survey in 2000. The highest levels of total PAHs were detected in meat and meat products (25.56 microg/kg), oils and fats (23.48 microg/kg) and cereals (20.44 microg/kg). For an average male adult the current dietary intake of the sum of PAHs was higher (12.0 microg/day) than that found in our 2000 survey (8.4 microg/day).”
Polycyclic aromatic hydrocarbons (PAHs) in meat products and estimated PAH intake by children and the general population in Estonia. Reinik M, et al. Food Addit Contam. 2007 Apr;24(4):429-37. Key Finding: “The concentrations of benzo{a}pyrene and 11 other polycyclic aromatic hydrocarbons were analyzed from 322 commercial, cured meat products and 14 home-grilled meat samples. The maximum acceptable concentration of 5 micro kg for benzo{a}pyrene was exceeded in 3.4% of samples. The highest PAH concentrations were detected in home-grilled pork samples. The highest total PAH concentrations detected were 16 microg kg in smoked meat and ham, 19 microg kg in smoked sausage and 6.5 microg kg in smoked chicken samples. “
Joint effects between UDP-glucuronosyltransferase 1A7 genotype and dietary carcinogen exposure on risk of colon cancer. Butler LM, et al. Cancer Epidemiol Biomarkers Prev. 2005 Jul;14(7):1626-32. Key Finding: “The UGT1A7 gene is polymorphic and encodes an enzyme involved in the detoxification of heterocyclic amines (HCA) and polycyclic aromatic hydrocarbons (PAH). Consumption of pan-fried and well-done meat are surrogates for HCA and PAH exposure and are possibly associated with colon cancer. These data suggest that the associations among cooked meat-derived compound exposure and colon cancer are modified by the UGT1A7 genotype.”
Meat-related mutagens/carcinogens in the etiology of colorectal cancer. Cross AJ, Sinha R. Environ Mol Mutagen. 2004;44(1):44-55. Key Finding: “Diets containing substantial amounts of red or processed meats may increase the risk of various cancers, including colorectal cancer. This association may be due to a combination of factors such as the content of fat, protein, iron, and/or meat preparation (e.g., cooking or preserving methods). Red meat may be associated with colorectal cancer by contributing to N-nitroso compound (NOC) exposure. Laboratory results have shown that meats cooked at high temperatures contain other potential mutagens in the form of heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs).”
Polycyclic aromatic hydrocarbons in foods: human exposure through the diet in Catalonia, Spain. Falco G, et al. J Food Prot. 2003 Dec;66(12):2325-31. Key Finding: “The dietary intake of 16 polycyclic aromatic hydrocarbons by the general population of Catalonia, Spain was calculated. Concentrations of PAHs in food samples randomly acquired in seven cities were measured. By food group, the highest levels of total PAHs were detected in cereals (14.5 micro/kg) and in meat and meat products (13.4 micro/kg). The calculated daily intake of PAHs would be associated with a 5/105 increase in the risk for the development of cancer in a male adult with a body weight of 70 kg.”
Environmental toxins and breast cancer on Long Island, I. Polycyclic aromatic hydrocarbon DNA adducts. Gammon MD. Santella RM, et al. Cancer Epidemiol Biomarkers Prev. 2002 Aug;11(8):677-85. Key Finding: “PAH are potent mammary carcinogens in rodents. To examine whether currently measurable PAH damage to DNA increases breast cancer risk, a population-based-case-control study was undertaken. Levels of PAH-DNA adducts was slightly higher among breast cancer cases than among controls.”
Polycyclic aromatic hydrocarbons in the diet Phillips DH. Mutat Res. 1999 Jul 15;443(1-2):139-47. Key Finding: “Polycyclic aromatic hydrocarbons (PAHs), of which benzo{a}pyrene is the most commonly studied and measured, are formed by the incomplete combustion of organic matter. A number of them are carcinogenic and mutagenic and they are widely believed to make a substantial contribution to the overall burden of cancer in humans. Cooking processes can generate PAHs in food. PAHs can also be formed during the curing and processing of raw food prior to cooking. Diet is the major source of human exposure to PAHs.”
Well-done, grilled red meat increases the risk of colorectal adenomas. Sinha R, et al. Cancer Res. 1999 Sep 1;59(17):4320-4. Key Finding: “Red meat or meat-cooking methods such as frying and doneness level have been associated with an increased risk of colorectal and other cancers. It is unclear whether it is red meat intake or the way it is cooked that is involved in the etiology of colorectal cancer. To address this issue, we developed an extensive food frequency questionnaire. A case-control study of colorectal adenomas was conducted at the Naval Medican Center in Bethesda, Md. We found an increased risk of colorectal adenomas associated with higher intake of red meat, most of which was due to the subgroup of red meat that was cooked until well done, very well done and/or high temperature cooking techniques, such as grilling. These results are consistent with the hypothesis that carcinogenic compounds formed by high temperature cooking techniques, such as heterocyclic amines and polycyclic aromatic hydrocarbons, may contribute to the risk of developing colorectal tumors.”
Factors affecting the polycyclic aromatic hydrocarbon content of cereals, fats and other food products. Dennis MJ. Massey RC, et al. 1991 Jul-Aug;8(4):517-30. Key Finding: “Factors affecting PAH concentrations in oils and fats, cereals and related foodstuffs have been investigated. Margarine was the major dietary source of PAHs in the oils and fats total diet group accounting for 70% of the benzo{a}pyrene intake from these commodities.”
HCA (heterocyclic amines) includes PhlP (2-amino-1-methyl-6-phenylimidzo{4,5-b} pyridine) and Others
Red meat and poultry, cooking practices, genetic susceptibility and risk of prostate cancer: results from a multiethnic case-control study. Joshi AD, et al. Carcinogenesis. 2012 Nov;33(11):2108-18. Key Finding: “An association between meat intake and prostate cancer may be due to potent chemical carcinogens that are generated when meats are cooked at high temperatures. We analyzed data for 1096 controls, 717 localized and 1140 advanced prostate cancer cases. We examined nutrient density-adjusted intake of red meat and poultry. Our results support a role for carcinogens that accumulate in meats cooked at high temperatures as potential prostate cancer risk factors, and may support a role for heterocyclic amines (HCAs) in prostate cancer etiology.”
Effect of cooking methods on the formation of heterocyclic aromatic amines in chicken and duck breast. Liao GZ, et al. Meat Sci. 2010 May;85(1):149-54. Key Finding: “In the present study, the effects of various cooking methods, pan-frying, deep-frying, charcoal grilling and roasting on the formation of HAAs in chicken breast and duck breast were studied. Results showed that chicken breast cooked by charcoal grilling contained the highest content of total HAAs, as high as 112 ng/g, followed by pan-fried duck breast (53.3 ng/g), charcoal grilled duck breast (32 ng/g), pan-fried chicken breast (27.4 ng/g), deep-fried chicken breast (21.3 ng/g), deep-fried duck breast (14 ng/g), roasted duck breast (7 ng/g) and roasted chicken breast (4 ng/g). The most abundant HAA was Norhaman.”
Meat Consumption and Risk of Esophageal and Gastric Cancer in a Large Prospective Study. Cross AJ, et al. Am J Gastroenterol. 2010 Oct 26 {Epub ahead of print}. Key Finding: “Red and processed meats could increase cancer risk through several potential mechanisms involving iron, heterocyclic amines, polycyclic aromatic hydrocarbons, and N-nitroso compounds. We found positive associations in this study between red meat intake and esophageal squamous cell carcinoma, and between DiMelQx intake and gastric cardia cancer.”
Dietary exposure to heterocyclic amines in high-temperature cooked meat and fish in Malaysia. Jahurui MH, et al. Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2010 aug;27(8):1060-71. Key Finding: “In this study, the dietary intake of heterocyclic amines in Malaysia and their main sources were investigated. The average daily intake level of heterocyclic amine was 553.7 ng per capita day. The intake of PhlP was the highest. The results reveal that fried and grilled chicken were the major dietary source of HAs in Malaysia.”
The cooked meat-derived mammary carcinogen 2-amino-1-methyl-6-phenylimidazo{4,5-b} pyridine promotes invasive behavior of breast cancer cells. Lauber SN, Gooderham NJ. Toxicology. 2010 Oct 15 {Epub ahead of print}. Key Finding: “The cooked meat derived genotoxic carcinogen PhlP induces cancer of the colon, prostate and mammary gland when fed to rats. Epidemiology studies link these tumours to a Western diet and exposure to heterocyclic amines such as PhlP. We have shown that PhlP is also potently estrogenic and have proposed that this hormonal activity contributes to its target site carcinogenicity. We now postulate that the estrogenic properties of PhlP influence metastatic potential. Our findings emphasize the range and potency of the biological activities associated with this cooked meat product and mechanistically support the tissue-specific carcinogenicity of the chemical.”
Well-done meat intake, heterocyclic amine exposure, and cancer risk. Zheng W, Lee SA. Nutr Cancer. 2009;61(4):437-46. Key Finding: “High intake of meat, particularly red and processed meat, has been associated with an increased risk of a number of common cancers such as breast, colorectum, and prostate in many epidemiological studies. Heterocyclic amines (HCAs) are a group of mutagenic compounds found in cooked meats, particularly well-done meats. The majority of studies done over the past 10 years have shown that high intake of well-done meat and high exposure to meat carcinogens, particularly HCAs, may increase the risk of human cancer.”
Quantification of heterocyclic amines from thermally processed meats selected from a small-scale population-based study. Busquets R, et al. Mol Nutr Food Res. 2008 Dec;52(12):1408-20. Key Finding: “Heterocyclic amines (HAs) are potent mutagens that form at high temperatures in cooked, protein-rich food. Due to their frequent intake, these compounds are considered a risk factor for human cancer. Food-frequency questionnaires designed to provide data on parameters that affect HA formation were used to survey a small population (459 persons) from Barcelona, Spain. Subsequently, the most-consumed food items named were cooked according to the preferences of the population surveyed and analyzed for HAs. In the population studied, the estimated intake via consumption of 13 meat dishes was 285.6 ng of mutagenic HAs per capita a day. PhlP was the HA to which the population was most exposed, mainly from fried chicken and griddled beef. When the co-mutagens norharman and harman are included, the mean daily intake of HAs rises to 475.6 ng per capita and day.”
Detection of PhIP in grilled chicken entrees at popular chain restaurants throughout California. Sullivan KM, et al. Nutr Cancer. 2008;60(5):592-602. Key Finding: “Hetercocyclic amines (HCAs) compounds formed when meat is cooked at high temperatures particularly through pan frying, grilling, or barbequeing, pose a potential carcinogenic risk to the public. It is unclear whether there is any level at which consumption of HCAs can be considered safe. We surveyed at least 9 locations each of 7 popular chain restaurants (McDonald’s, Burger King, Chick-fil-A, Chili’s, TGI Friday’s, Outback Steakhouse and Applebee’s) in California, collecting one or two entrees from each location. Entrees were analyzed for PhlP (a HCA compound). All 100 samples contained PhlP. Concentrations were variable within and between entrees and ranged from 0.08 to 43.2 ng/g. When factoring in the weight of the entrees, absolute levels of PhlP reached over 1,000 ng for some entrees.”
The cooked meat derived genotoxic carcinogen 2-amino-3-methylimidazo{4,5-b}pydridine has potent hormone-like activity: mechanistic support for a role in breast cancer. Lauber SN, Gooderham NJ. Cancer Res. 2007 Oct 1;67(19):9597-602. Key Finding: “In view of the strong association between estrogen, progesterone, prolactin, and breast cancer, the PhlP repertoire of hormone-like activities provides further mechanistic support for the tissue-specific carcinogenicity of the chemical. Furthermore, the recent epidemiology studies that report an association between consumption of cooked red meat and premenopausal and postmenopausal human breast cancer are consonant with these observations.”
Joint effects between UDP-glucuronosyltransferase 1A7 genotype and dietary carcinogen exposure on risk of colon cancer. Butler LM, et al. Cancer Epidemiol Biomarkers Prev. 2005 Jul;14(7):1626-32. Key Finding: “The UGT1A7 gene is polymorphic and encodes an enzyme involved in the detoxification of heterocyclic amines (HCA) and polycyclic aromatic hydrocarbons (PAH). Consumption of pan-fried and well-done meat are surrogates for HCA and PAH exposure and are possibly associated with colon cancer. These data suggest that the associations among cooked meat-derived compound exposure and colon cancer are modified by the UGT1A7 genotype.”
Dietary exposure to heterocyclic amines in a Chinese population. Wong K, et al. Nutr Cancer. 2005;52(2):147-55. Key Finding: “HAAs formed in meat during high-temperature cooking have been associated with risk of colorectal and breast cancer. Incidence of these cancers is increasing in Singapore, a country with 77% ethnic Chinese. The purpose of this study was to estimate HAA levels in the Chinese diet and individual levels of exposure. Twenty-five samples of meat and fish cooked as commonly consumed were analyzed. The estimated mean daily exposure to HAA was 49.95 ng/day; this was 50% higher among younger (20-39 yr) compared with older individuals. Seven specific meat-cooking method combinations contributed 90.1% of this intake, namely, pan-fried fish, pork, and chicken, deep-fried chicken as well as fish, roasted/barbequed pork, and grilled minced beef.”
Heterocyclic amines: Mutagens/carcinogens produced during cooking of meat and fish. Sugimura T, et al. Cancer Sci. 2004 Apr;95(4):290-9. Key Finding: “Research leading to the discovery of a series of mutagenic and carcinogenic heterocyclic amines (HCAs) was inspired by the idea that smoke produced during cooking of food, especially meat or fish, might be carcinogenic. More than ten kinds of HCAs actually produced by cooking or heating of meat or fish have now been isolated and their structures determined, most being previously unregistered compounds. They are highly mutagenic and are also mutagenic in vitro and in vivo toward mammalian cells. HCAs have now been chemically synthesized and subjected to long-term animal testing. When HCAs were fed in the diet, rodents developed cancers in many origins, including colon, breast and prostate, and one HCA produced hepatomas in monkeys. Advice to the general public about how to reduce the carcinogenic load imposed by HCAs would be an important contribution to cancer prevention.”
Meat-related mutagens/carcinogens in the etiology of colorectal cancer. Cross AJ, Sinha R. Environ Mol Mutagen. 2004;44(1):44-55. Key Finding: “Diets containing substantial amounts of red or processed meats may increase the risk of various cancers, including colorectal cancer. This association may be due to a combination of factors such as the content of fat, protein, iron, and/or meat preparation (e.g., cooking or preserving methods). Red meat may be associated with colorectal cancer by contributing to N-nitroso compound (NOC) exposure. Laboratory results have shown that meats cooked at high temperatures contain other potential mutagens in the form of heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs).”
Dietary intake of heterocyclic amines, meat-derived mutagenic activity, and risk of colorectal adenomas. Sinha R, et al. Cancer Epidemiol Biomarkers Prev. 2001 May;10(5):559-62. Key Finding: “We found an elevated risk of colorectal adenomas associated with high intake of certain HCAS. Further, mutagenic activity from cooked meat consumption, a measure that integrates all of the classes of mutagens, was strongly associated with risk and explained the excess risk with intake of well-done red meat.”
Well-done, grilled red meat increases the risk of colorectal adenomas. Sinha R, et al. Cancer Res. 1999 Sep 1;59(17):4320-4. Key Finding: “Red meat or meat-cooking methods such as frying and doneness level have been associated with an increased risk of colorectal and other cancers. It is unclear whether it is red meat intake or the way it is cooked that is involved in the etiology of colorectal cancer. To address this issue, we developed an extensive food frequency questionnaire. A case-control study of colorectal adenomas was conducted at the Naval Medican Center in Bethesda, Md. We found an increased risk of colorectal adenomas associated with higher intake of red meat, most of which was due to the subgroup of red meat that was cooked until well done, very well done and/or high temperature cooking techniques, such as grilling. These results are consistent with the hypothesis that carcinogenic compounds formed by high temperature cooking techniques, such as heterocyclic amines and polycyclic aromatic hydrocarbons, may contribute to the risk of developing colorectal tumors.”
Heterocyclic amine content in beef cooked by different methods to varying degrees of doneness and gravy made from meat drippings. Sinha R. Rothman N, et al. Food Chem Toxicol. 1998 Apr;36(4):279-87. Key Finding: “We measured five HCAs (IQ, MelQ, MelQx, DiMelQx, and PhlP) in different types of cooked beef. Steak and hamburger patties were pan-fried, oven-broiled, and grilled/barbequed to four levels of doneness (rare, medium, well done or very well done) while beef roasts were oven cooked to three levels of doneness (rare, medium or well done). MelQx content increased with doneness under each cooking condition for steak and hamburger patties, up to 8.2 ng/g. PhlP was the predominant HCA produced in steak (1.9 to 30 ng/g) but was formed only in very well done fried or grilled hamburger. DiMelQx was found in trace levels in pan-fried steaks only, while IQ and MelQ were not detectable in any of the samples. Roast beef did not contain any of the HCAs, but the gravy made from the drippings from well done roasts had 2 ng/g of PhlP and 7 ng/g of MelQx.”
Cancer risk of heterocyclic amines in cooked foods: an analysis and implications for research. Layton DW, et al. Carcinogenesis. 1995 Jan;16(1):39-52. Key Finding: “Heterocyclic amines are formed as pyrolysis products during the cooking of meats/fish. These substances are potent mutagens and are carcinogens in laboratory animals. We estimated the average intakes of HAs, based on analyses of the concentrations of HAs in cooked foods and data from a dietary survey of the US population and quantified the cancer potencies of the individual compounds using dose-response data from animal bioassays. Dietary intakes of the five principal HAs in descending order were PhlP, A Alpha C, MelQx, DiMelQx, and IQ. The carcinogenic potencies, in contrast, were almost the reverse order: IQ, DiMelQx, MelQx, PhlP, A alpha C. Nearly half (46%) of the incremental risk of cancer was due to ingestion of PhlP. Consumption of meat and fish products contributed the most (approximately 80%) to total cancer risk.”