Nutrition and cancer among American Indians and Alaska natives

Byers, Tim

doi:10.1002/(sici)1097-0142(19961001)78:7<1612::aid-cncr43>3.0.co;2-#

Cited by 13 publications

(3 citation statements)

References 24 publications

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“…Increased risk for colorectal cancer has been associated with inflammatory bowel disease, family history of colorectal cancer, obesity, alcohol consumption, diets high in fats and low in dietary fiber (16), and diabetes (17) and more recently associated with smoking (18,19). Studies of Alaska Native diets over the past 30 years reveal a profile not different from the current average American diet, one of high animal meat and fat consumption (20). A nationwide 2002 Behavioral Risk Factor Surveillance System survey showed that 78% of all Alaska Natives and 75% of both New Mexico Indians and U.S.…”

Section: Discussionmentioning

confidence: 99%

Differences in Cancer Incidence among Indians in Alaska and New Mexico and U.S. Whites, 1993-2002

Kelly

Lanier

Alberts

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Cancer incidence for American Indians and Alaska Natives is typically reported as a single rate for all U.S. indigenous populations combined. Previously reported combined rates suggest that American Indians and Alaska Natives have lower cancer incidence rates compared with the U.S. population. Alaska Native people comprise three major ethnic groups: Eskimo, Indian, and Aleut people. We examined cancer incidence from only Alaska Indians and compared incidence rates with an American Indian population living in New Mexico. These data indicate striking differences in cancer patterns between two American Indian populations. Cancer data for the years 1993 to 2002 for American Indians of New Mexico and U.S. Whites are from the National Cancer Institute Surveillance, Epidemiology, and End Results Program Public-use data set. Data for Alaska Indians are from the Alaska Native Tumor Registry, which is also a Surveillance Epidemiology and End Results Program participant. Overall, cancer incidence rates for all sites combined in New Mexico Indian men and women were lower than U.S. White rates, whereas Alaska Indian men and women exceeded U.S. rates. In comparing Alaska and New Mexico Indians, we observed a 2.5-fold higher incidence of cancer among Alaska Indians. The largest differences between the two Indian populations were noted primarily in cancers associated with tobacco use, including cancers of the oral cavity/pharynx, esophagus (only in men), colon and rectum, pancreas, larynx (men), lung, prostate, and urinary bladder (men). Lung cancer rates in Alaska Indian men and women were 7 and 10 times those of New Mexico Indian men and women. (Cancer Epidemiol Biomarkers Prev

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Section: Discussionmentioning

confidence: 99%

Differences in Cancer Incidence among Indians in Alaska and New Mexico and U.S. Whites, 1993-2002

Kelly

Lanier

Alberts

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Experimental studies have shown that a high-fat diet rich in n-6 polyunsaturated fatty acid (PUFA) and saturated fatty acids (SFA) promoted colon carcinogenesis, particularly in postinitiation or promotional phases and/or both (10,26,28,39). On the other hand, diets rich in n-3 PUFA and n-9 monounsaturated fatty acid (MUFA) have been reported to reduce colon tumorigenesis in both the initiation and postinitiation phases (2,26,29), supporting epidemiological reports showing that an n-3 PUFA-rich diet suppressed the risk of colon cancer in humans (3,7,8). These experimental and epidemiological studies suggested that not only the amount of fat intake but also the composition of ingested dietary fatty acids are crucial factors for colon carcinogenesis.…”

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confidence: 99%

Long-term feeding of various fat diets modulates azoxymethane-induced colon carcinogenesis through Wnt/β-catenin signaling in rats

Fujise¹,

Iwakiri²,

Kakimoto³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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The Wnt signaling pathway plays an essential role in carcinogenesis, and the amount of fat intake and composition of dietary fatty acids are crucial factors for colon carcinogenesis. We investigated whether various dietary fats affected the Wnt signaling pathway of colon tumorigenesis in azoxymethane (AOM)-treated rats. Male Sprague-Dawley rats were given intraperitoneal injections of AOM and supplemented with 10% corn, olive, beef, and fish oil for 44 wk. Aberrant crypt foci (ACF) and tumors were examined at 12 and 44 wk. Normal appearing colon mucosal proliferation and apoptosis were evaluated by 5-bromo-2Ј-deoxyuridine (BrdU) incorporation and percentages of fragmented DNA, respectively. Expressions of ␤-catenin, cyclin D 1, Wnt2, Wnt3, and Wnt5a of normal appearing colon mucosa were analyzed by Western blot analysis. Long-term dietary corn oil and beef tallow increased ACF, tumor incidence, and tumor numbers in AOM-treated rats. In contrast, both olive and fish oil inhibited them. Dietary corn oil and beef tallow increased BrdU incorporation and the expression of cytosolic ␤-catenin and cyclin D 1 and decreased apoptosis in the colon mucosa. Expressions of Wnt2 and Wnt3 in rats fed with beef tallow and Wnt5a in rats fed with corn oil increased with or without AOM-treatment. BrdU-incorporated cells were often observed at the tops of crypts in rats fed with beef tallow, whereas this was not observed in rats fed with the other diet. Long-term high intake of corn oil and beef tallow enhanced cell proliferation through Wnt signaling and modulated the distribution of proliferating cells, which might contribute to promoting effects in colon tumorigenesis. fatty acid

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“…On the other hand, diets rich in n-3 PUFA and n-9 monounsaturated fatty acid (MUFA) have been reported to reduce colon tumorigenesis in both the initiation and postinitiation phases (Bartoli et al, 2000;Rao et al, 2001, Chapkin et al, 2008, van Beelen et al, 2009and Sarotra et al, 2010, supporting epidemiological reports showing that an n-3 PUFA-rich diet suppressed the risk of colon cancer in humans (Byers, 1996 andCaygill andHill, 1995).…”

Section: Discussionmentioning

confidence: 99%

Dietary fish oil modulates the effect of dimethylhydrazine- induced colon cancer in rats

Rasmy

Khalil²,

Moharib

et al. 2011

Grasas y Aceites

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In order to induce colon cancer, the rats were given a weekly subcutaneous injection of 1,2-Dimethylhydrazine (DMH) at a dose of 20 mg/kg b.w. for five weeks. Afterwards, some of the rats ingested fish oil for either 4 weeks (DMH-FO4 group), or 17 weeks (DMH-FO17 group). The remaining rats continued without any supplementation for the same 4 weeks (DMH4 group), or 17 weeks (DMH17 group). Another two groups of rats did not receive the DMH and were given fish oil (FO17 group) or a normal diet only and considered as the control group (CN group). At the end of the experiment, the rats were sacrificed; and were subsequently subjected to biochemical and molecular biological analyses as well as histopathological examinations. The results showed increased levels of lactate dehydrogenase (LDH), malondialdehyde (MDA) and alkaline phoshatase (ALP) activities in the DMH rats compared to the control. The liver and colonic changes that were induced by DMH were significantly improved through fish oil supplementation in the DMH-FO17 group. The molecular analysis revealed that DMH treatment induced the expression alterations of genes p53, p27 and p21 and increased DNA band patterns related to cancer, while both FO17 and DMH-FO17 groups showed much better results. A histopathological examination of the DMH17 group revealed colon adenocarcinoma and several lesions in rat liver tissues. An improvement in the histopathological picture was seen in the livers and colons of groups DMH-FO17. In conclusion, the present results demonstrated the anti-carciongenic effect of herring fish oil against DMH induced colon carcinogenesis in rats. The inhibitory effect of FO was due to the modulation of elevated biochemical parameters, DNA damage, gene expression and histopathological lesions caused by DMH. KEY-WORDS: Colorectal cancer -DMH -Fish oil -Gene expression -Rats. INTRODUCTIONAmong the factors that contribute to the appearance of cancer, diet plays a fundamental role. Fats are the main component related to the increase in the incidence of cancerous diseases, particularly breast, prostate and colorectal cancer. Colon cancer is one of the leading causes of death in both men and women in Western countries (Parker et al., 1995;and Jemal et al., 2003) and it became the number six leading cause of cancer deaths in Egypt (WHO report, 2006). Several RESUMEN Efecto del aceite de pescado de la dieta en cáncer de colon inducido por dimetilhidrazina en ratas.Este estudio fue realizado para examinar la eficacia de la suplementación de aceite de pescado en la carcinogéne-sis de colon en ratas wistar machos. Para la inducción del cáncer de colon, las ratas fueron tratadas semanalmente con una inyección subcutánea de 1,2-dimethyl hydrazine (DMH) a una dosis de 20 mg/kg de peso durante cinco semana. A continuación, algunas ratas tomaron aceite de pescado durante 4 semanas, o durante 17 semanas (grupo DMH-FO17). Las ratas restantes continuaron sin ningún tipo de suplementación durante las mismas 4 semanas (grupo DMH4), o 17 semanas (grupo DMH17). Otros dos...

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Nutrition and cancer among American Indians and Alaska natives

Cited by 13 publications

References 24 publications

Differences in Cancer Incidence among Indians in Alaska and New Mexico and U.S. Whites, 1993-2002

Differences in Cancer Incidence among Indians in Alaska and New Mexico and U.S. Whites, 1993-2002

Long-term feeding of various fat diets modulates azoxymethane-induced colon carcinogenesis through Wnt/β-catenin signaling in rats

Dietary fish oil modulates the effect of dimethylhydrazine- induced colon cancer in rats

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