Meat intake and cooking techniques: Associations with pancreatic cancer

University of Minnesota, Minneapolis, MN 55454, USA.
Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis (Impact Factor: 3.68). 10/2002; 506-507:225-31. DOI: 10.1016/S0027-5107(02)00169-0
Source: PubMed


Heterocyclic amines (HCAs), and polycyclic aromatic hydrocarbons (PAHs), formed in temperature and time-dependent manners during cooking of meat, may increase the risk of certain cancers. As these compounds could be carcinogenic for the pancreas, we assessed meat intake, preparation methods, and doneness preferences as risk factors for exocrine pancreatic cancer. In a case-control study (cases=193, controls=674), subjects provided information on their usual meat intake and how it was cooked, e.g. fried, grilled or barbecued (BBQ), etc. Meat doneness preferences were measured using photographs that showed internal doneness and external brownness with a numerical scale. Data were analyzed with unconditional logistic regression. Odds ratios (ORs) increased with increased intake of grilled/BBQ red meat in an analysis adjusted for age, sex, smoking, education, race, and diabetes. Based on amount of BBQ meat consumed, the OR and 95% confidence interval (CI) for the fifth quintile relative to the reference group (quintiles 1 and 2) was 2.19 (1.4, 3.4). Findings were not substantively changed by further adjustment for calories, total fat, fruit and vegetables, or alcohol consumption (from a food frequency questionnaire (FFQ)). Other meat variables did not show statistically significant associations with risk nor did they substantively alter the findings for BBQ. These included total meat, processed meat, total red meat, total white meat, total broiled meat, total fried meat, or total meat cooked by means other than grilling. We conclude that grilled red meat intake is a risk factor for pancreatic cancer and that method of meat preparation in addition to total intake is important in assessing the effects of meat consumption in epidemiologic studies.

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    • "Oreglia, De Stefani, Boffetta, Brennan, and Deneo Pellegrini (2001) linked laryngeal cancer with consumption of red meat due to the production of HAAs. Anderson et al. (2002) revealed that risk of pancreatic cancer is higher in those people who use highly cooked red meat in their routine diet as compared to others who use fruits and vegetables in their regular diet patterns. HAAs also have the potency of causing some other types of cancers like liver and gastrointestinal tract and their production is highly coupled with the well-done cooked meat (Sugimura, 1986). "
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    ABSTRACT: Heterocyclic aromatic amines are compounds produced in meat subjected to high temperature cooking. Formation of these substances is highly influenced by cooking method, cooking time, cooking temperature, and type of meat. Heterocyclic amines contain heterocyclic rings and nitrogen containing groups within their structure. Risks of colon, pancreas, gastrointestinal tract, lung, liver, prostate, skin and breast cancers are decidedly associated with the consumption of heterocyclic amines. These mutagenic compounds can be attenuated by addition of different fruits and vegetable extracts. Several spices and antioxidants can also be used for the reduction of these heterocyclic amines. The level of heterocyclic amines can be reduced by cooking at low temperature and by decreasing the cooking time. Formation of heterocyclic amines can also be prevented by marinating the meat before frying or grilling and by microwave pre-treatments. Objectives of this review are to create awareness about health risks, and to stimulate further research on other suitable ways to reduce the cancer risks associated with the consumption of cooked meat products.
    Lebensmittel-Wissenschaft und-Technologie 11/2014; 59(1):229–233. DOI:10.1016/j.lwt.2014.06.005 · 2.42 Impact Factor
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    • "In addition to total intake, the method of meat preparation is also important. Grilled red meat is a risk factor [90]. Effects of mutagenic heterocyclic amines (HCA) formed during cooking of meat on pancreatic carcinogenesis were studied in the BOP-treated hamster model. "
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    ABSTRACT: Pancreatic cancer is difficult to cure, so its prevention is very important. For this purpose, animal model studies are necessary to develop effective methods. Injection of N-nitrosobis(2-oxopropyl)amine (BOP) into Syrian golden hamsters is known to induce pancreatic ductal adenocarcinomas, the histology of which is similar to human tumors. Moreover, K-ras activation by point mutations and p16 inactivation by aberrant methylation of 5' CpG islands or by homozygous deletions have been frequently observed in common in both the hamster and humans. Thus, this chemical carcinogenesis model has an advantage of histopathological and genetic similarity to human pancreatic cancer, and it is useful to study promotive and suppressive factors. Syrian golden hamsters are in a hyperlipidemic state even under normal dietary conditions, and a ligand of peroxizome proliferator-activated receptor gamma was found to improve the hyperlipidemia and suppress pancreatic carcinogenesis. Chronic inflammation is a known important risk factor, and selective inhibitors of inducible nitric oxide synthase and cyclooxygenase-2 also have protective effects against pancreatic cancer development. Anti-inflammatory and anti-hyperlipidemic agents can thus be considered candidate chemopreventive agents deserving more attention.
    Cancers 12/2011; 3(1):582-602. DOI:10.3390/cancers3010582
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    • "The case-control study of pancreatic cancer conducted from April 1994 to September 1998 in Minnesota has been described in detail elsewhere [16] [17]. Briefly, cases were patients diagnosed with pathologically-confirmed cancer of the exocrine pancreas (International Classification of Disease for Oncology, third edition, code C25). "
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    ABSTRACT: To investigate whether polymorphisms in genes related to oxidative stress act alone or in combination with antioxidants to modulate pancreatic cancer risk. Cases (n=189), ages ≥ 20 years, were ascertained in 1994-1998 from all hospitals in the Twin Cities and the Mayo Clinic. Controls (n=486) were randomly selected from the general population and frequency matched to cases by age and sex. After adjustment for confounders, individuals who were homozygous or heterozygous for the variant allele of SOD2 polymorphism (Ala16Val, rs4880) experienced a 43% lower risk than those who were homozygous for the wild-type allele [OR (95% CI): 0.57 (0.37, 0.89)]. Conversely, an increased risk was observed for the variant allele of hOGG1 polymorphism (Ser326Cys, rs1052133) compared with the wild-type allele [OR (95% CI) for Ser/Cys or Cys/Cys vs. Ser/Ser: 1.57 (1.04, 2.39)]. The protective effect of the variant allele of SOD2 was more pronounced among subjects with a low dietary intake (<median) of lutein/ zeaxanthin, lycopene, α-carotene, and α-tocopherol [OR (95% CI): 0.46 (0.27, 0.81), 0.42 (0.23, 0.75), 0.47 (0.26, 0.85), and 0.48 (0.27, 0.87), respectively]. Individual variations in the capacity to defend against oxidative stress and to repair oxidative DNA damage influence pancreatic cancer risk, and some of these genetic effects are modified by dietary antioxidants.
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