Heterocyclic Amine Content of Cooked Meat and Risk of Prostate Cancer

Norrish, Alan; Ferguson, Lynnette R.; Knize, Mark G.; Felton, James S.; Sharpe, Susan J.; Jackson, Rod

doi:10.1093/jnci/91.23.2038

Cited by 164 publications

(105 citation statements)

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“…Epidemiological studies have revealed a link between prostate cancer incidence and mortality and the consumption of red meat and animal fats [62][63][64] . One mechanism by which meats might stimulate cancer development could be related to the formation of hetero cyclic amines (HCAs) 65 .…”

Section: Dietary Factorsmentioning

confidence: 99%

Inflammation in prostate carcinogenesis

et al. 2007

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About 20% of all human cancers are caused by chronic infection or chronic inflammatory states. Recently, a new hypothesis has been proposed for prostate carcinogenesis. It proposes that exposure to environmental factors such as infectious agents and dietary carcinogens, and hormonal imbalances lead to injury of the prostate and to the development of chronic inflammation and regenerative 'risk factor' lesions, referred to as proliferative inflammatory atrophy (PIA). By developing new experimental animal models coupled with classical epidemiological studies, genetic epidemiological studies and molecular pathological approaches, we should be able to determine whether prostate cancer is driven by inflammation, and if so, to develop new strategies to prevent the disease. NIH Public Access Author ManuscriptNat Rev Cancer. Author manuscript; available in PMC 2013 January 23. $watermark-text $watermark-text $watermark-textProstate cancer is the most common non-cutaneous malignant neoplasm in men in Western countries, responsible for the deaths of approximately 30,000 men per year in the United States 1 . The number of afflicted men is increasing rapidly as the population of males over the age of 50 grows worldwide. Therefore, finding strategies for the prevention of prostate cancer is a crucial medical challenge. As men in South East Asian countries have a low incidence of prostate cancer that increases rapidly after immigration to the West, this disease is not an intrinsic feature of ageing. The pathogenesis of prostate cancer reflects both hereditary and environmental components. What are the environmental factors and genetic variations that have produced such an epidemic of prostate cancer? Approximately 20% of all human cancers in adults result from chronic inflammatory states and/or chronic inflammation 2-4 (BOX 1), which are triggered by infectious agents or exposure to other environmental factors, or by a combination thereof. There is also emerging evidence that inflammation is crucial for the aetiology of prostate cancer. This evidence stems from epidemiological, histopathological and molecular pathological studies. The objective of this Review is to take a multidisciplinary approach to present and analyse such studies. Because several reviews related to these topics have been published [5][6][7] , here we will focus on new findings and ideas with the purpose of sparking innovative areas of investigation that might ultimately lead to the prevention of prostate cancer. Enigmas in the aetiology of prostate cancerAs in other cancers, prostate cancer develops through the accumulation of somatic genetic and epigenetic changes, resulting in the inactivation of tumour-suppressor genes and caretaker genes, and the activation of oncogenes 8,9 (TABLE 1). There is also evidence for an underlying genetic instability that might facilitate tumour progression 10,11 . Although these genetic and epigenetic changes are crucial for our understanding of 'how' prostate cancer arises, another key remaining question is 'why'...

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Section: Dietary Factorsmentioning

confidence: 99%

Inflammation in prostate carcinogenesis

et al. 2007

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“…However, recent epidemiological studies concerning HCA intake gave conflicting results. While casecontrol studies conducted in Uruguay and in the USA showed positive correlations between the intake of HCA and the risk of breast (Sinha et al, 2000a;De Stefani et al, 1997b), colon (Sinha et al, 2001;De Stefani et al, 1997a), lung (Sinha et al, 2000b), and gastric cancer (De Stefani et al, 1998a), other groups were not able to detect any association between the intake of HCA and the cancer risk of different sites (Norrish et al, 1999;Augustsson et al, 1999b;Lyon & Mahoney, 1988).…”

Section: Introductionmentioning

confidence: 98%

“…During recent decades, a possible relationship between the methods of meat and fish preparation and the risk of cancer development of different sites has been observed in epidemiological studies (Sinha et al, ,2000a(Sinha et al, ,b,2001Deitz et al, 2000;Norrish et al, 1999;Zheng et al, 1999;De Stefani et al, 1997a,b,1998aProbst-Hensch et al, 1997;Ward et al, 1997;Schiffman & Felton, 1990;Steineck et al, 1990). It has been suggested that heterocyclic amines (HCA) may explain at least some of the observed effect.…”

Section: Introductionmentioning

confidence: 99%

“…High-temperature cooking techniques, such as grilling, frying and barbecuing, are more likely to be associated with carcinogen production (Skog et al, 1998). Several reports, focussing on meat preparation by these high-temperature cooking methods, were able to show an increased risk of lung cancer Doneo-Pellegrini et al, 1996), breast cancer (Sinha et al, 2001;Zheng et al, 1998), prostate cancer (Norrish et al, 1999), colorectal tumors Probst-Hensch et al, 1997;Ward et al, 1997;Gerhardsson de Verdier et al, 1991). Apart from the cooking methods, cancer risk was shown to be influenced by the degree of browning of the cooked meat or fish item Zheng et al, 1999;ProbstHensch et al, 1997;Ward et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Cooking of meat and fish in Europe—results from the European Prospective Investigation into Cancer and Nutrition (EPIC)

et al. 2002

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Objectives: There is epidemiologic evidence that the consumption of fried, grilled or barbecued meat and fish that are welldone or browned may be associated with an increased cancer risk. These high-temperature cooking methods are thought to be surrogates for mutagens and carcinogens produced in meat and fish, eg heterocyclic amines or polycyclic hydrocarbons. Since data on food cooking methods are scarce, the aim of this study was to describe the variation in meat and fish cooking methods in different parts of Europe. Design: Using a standardized 24 h recall from a sub-sample of the EPIC cohort (35 644 persons, 35 -75 y old), mean daily intake of meat and fish prepared by different cooking methods and the relative contribution of the cooking methods to the overall cooking of meat and fish was calculated. Results: Whereas frying was more often noted in northern Europe, roasting and stir frying were more often used in the south. Concerning high-temperature cooking methods, their frequency of application varies between 15% in the EPIC cohort of NorthItaly and 49% in the cohort of The Netherlands. Average consumption of fried, grilled and barbecued meat and fish ranges from a low of 12 g=day in the centres in southern Spain to a high of 91 g=day in northern Spain.

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“…Increased risks of colorectal adenoma and adenocarcinoma, and of stomach, breast, lung and PCs have been weakly or clearly associated with potential or estimated HA exposure in most ( Shiffman and Felton, 1990;Gerhardsson de Verdier et al, 1991;Lang et al, 1994;Probst -Hensch et al, 1997;Ward et al, 1997;Kampman et al, 1999;Norrish et al, 1999;Sinha et al, 1998aSinha et al, , 1999Zheng et al, 1998Zheng et al, , 1999, but not all (Lyon and Mahoney, 1988;Muscat and Wynder, 1994;Augustsson et al, 1999 ), case ± control studies investigating possible associations between increased human cancer risk and dietary HA -exposure categories based on self -reported meat -cooking methods and meat -doneness preferences. Positive studies have tended to be those in which interactions among meat types, intake frequencies, cooking methods and /or cooking doneness preferences were reflected in the categories used to classify relative HA -exposure levels (Probst -Hensch et al, 1997;Ward et al, 1997;Sinha et al, 1998bSinha et al, , 1999Zheng et al, 1998 ).…”

Section: Introductionmentioning

confidence: 99%

U.S. dietary exposures to heterocyclic amines*

Bogen

Keating

2001

J Expo Sci Environ Epidemiol

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Heterocyclic amines ( HAs ) formed in fried, broiled or grilled meats are potent mutagens that increase rates of colon, mammary, prostate and other cancers in bioassay rodents. Studies of how human dietary HA exposures may affect cancer risks have so far relied on fairly crudely defined HA -exposure categories. Recently, an integrated, quantitative approach to HA -exposure assessment ( HAEA ) was developed to estimate compound -specific intakes for particular individuals based on corresponding HA -concentration estimates that reflect their meat -type, intake -rate, cooking -method and meat -doneness preferences. This method was applied in the present study to U.S. national Continuing Survey of Food Intakes by Individuals ( CSFII ) data on meats consumed and cooking methods used by > 25,000 people, after adjusting for underreported energy intake and conditional on meat -doneness preferences estimated from additional survey data. The U.S. population average lifetime time -weighted average of total HAs consumed was estimated to be $9 ng / kg / day, with 2 -amino -1 -methyl -6 -phenylimidazo [ 4,5 -b ] pyridine ( PhIP ) estimated to comprise about two thirds of this intake. Pan -fried meats were the largest source of HA in the diet and chicken the largest source of HAs among different meat types. Estimated total HA intakes by male vs. female children were generally similar, with those by ( 0 -to 15 -year -old ) children $25% greater than those by ( 16 + -year -old ) adults. Race -, age -and sex -specific mean HA intakes were estimated to be greatest for African American males, who were estimated to consume $2 -and $3 -fold more PhIP than white males at ages < 16 and 30 + years, respectively, after considering a relatively greater preference for more well -done items among African Americans based on national survey data. This difference in PhIP intakes may at least partly explain why prostate cancer ( PC ) kills $2 -fold more African American than white men, in view of experimental data indicating that PhIP mutates prostate DNA and causes prostate tumors in rats. Journal of Exposure Analysis and Environmental Epidemiology ( 2001 ) 11, 155 ± 168.

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Heterocyclic Amine Content of Cooked Meat and Risk of Prostate Cancer

Abstract: Meat doneness and estimated intake of heterocyclic amines from cooked meat were not clearly associated with prostate cancer risk.

Cited by 164 publications

References 18 publications

Inflammation in prostate carcinogenesis

Inflammation in prostate carcinogenesis

Cooking of meat and fish in Europe—results from the European Prospective Investigation into Cancer and Nutrition (EPIC)

U.S. dietary exposures to heterocyclic amines*

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