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  • 1
    Abstract: Chronic inflammation is an important factor in colorectal carcinogenesis. However, evidence on the effect of pro-inflammatory and anti-inflammatory foods and nutrients is scarce. Moreover, there are few studies focusing on diet-gene interactions on inflammation and colorectal cancer (CRC). This study was designed to investigate the association between the novel dietary inflammatory index (DII) and CRC and its potential interaction with polymorphisms in inflammatory genes. Data from the Bellvitge Colorectal Cancer Study, a case-control study (424 cases with incident colorectal cancer and 401 hospital-based controls), were used. The DII score for each participant was obtained by multiplying intakes of dietary components from a validated dietary history questionnaire by literature-based dietary inflammatory weights that reflected the inflammatory potential of components. Data from four important single nucleotide polymorphisms located in genes thought to be important in inflammation-associated CRC: i.e., interleukin (IL)-4, IL-6, IL-8, and peroxisome proliferator-activated receptor-gamma (PPARG) were analyzed. A direct association was observed between DII score and CRC risk (ORQ4 vs. Q1 1.65, 95 % CI 1.05-2.60, and P trend 0.011). A stronger association was found with colon cancer risk (ORQ4 vs. Q1 2.24, 95 % CI 1.33-3.77, and P trend 0.002) than rectal cancer risk (ORQ4 vs. Q1 1.12, 95 % CI 0.61-2.06, and P trend 0.37). DII score was inversely correlated with SNP rs2243250 in IL-4 among controls, and an interaction was observed with CRC risk. Neither correlation nor interaction was detected for other inflammatory genes. Overall, high-DII diets are associated with increased risk of CRC, particularly for colon cancer, suggesting that dietary-mediated inflammation plays an important role in colorectal carcinogenesis.
    Type of Publication: Journal article published
    PubMed ID: 25488145
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  • 2
    Abstract: Unhealthy dietary habits can increase the risk for serious medical conditions, such as cancer, yet the association between diet and breast cancer remains unclear. We investigated whether individual diets based on their inflammatory potential are associated with postmenopausal breast cancer risk by employing an energy-adjusted dietary inflammation index. In a German population-based case-control study, 2887 postmenopausal breast cancer patients (aged 50-74 years, first diagnosed between 2002 and 2005) and 5512 healthy age-matched controls provided information on dietary habits for the year prior to diagnosis (cases) or recruitment (controls) using a 176-items food frequency questionnaire. Associations between the energy-adjusted dietary inflammation index (E-DII) score (both as continuous variable and in quintiles) and risk for breast cancer were assessed using conditional logistic regression adjusted for potential confounders. No significant associations between the E-DII score and postmenopausal breast cancer risk were observed (adjusted OR Q5 vs Q1: 1.01, 95% CI: 0.86-1.17). Associations did not differ by estrogen receptor/progesterone receptor status (ER + PR+: adjusted OR Q5 vs Q1: 1.06, 95% CI: 0.88-1.27; ER + or PR+: OR Q5 vs Q1: 1,07, 95% CI: 0.79-1.45; ER-PR-: OR Q5 vs Q1: 0.87 95% CI: 0.63-1.20). Our results regarding E-DII are consistent with previous studies reporting a lack of association between C-reactive protein, a marker of systemic inflammation, and postmenopausal breast cancer risk. The findings may reflect a real absence of association between dietary inflammatory potential and postmenopausal cancer risk or an underestimation of association due to recall bias. Further investigation is warranted in cohort studies.
    Type of Publication: Journal article published
    PubMed ID: 25987487
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