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- Tetens, Inge, et al.
(författare)
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Dietary intake and main sources of plant lignans in five European countries
- 2013
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Ingår i: Food & Nutrition Research. - : TAYLOR & FRANCIS LTD. - 1654-6628 .- 1654-661X. ; 57
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Tidskriftsartikel (refereegranskat)abstract
- Background: Dietary intakes of plant lignans have been hypothesized to be inversely associated with the risk of developing cardiovascular disease and cancer. Earlier studies were based on a Finnish lignan database (Fineli (R)) with two lignan precursors, secoisolariciresinol (SECO) and matairesinol (MAT). More recently, a Dutch database, including SECO and MAT and the newly recognized lignan precursors lariciresinol (LARI) and pinoresinol (PINO), was compiled. The objective was to re-estimate and re-evaluate plant lignan intakes and to identify the main sources of plant lignans in five European countries using the Finnish and Dutch lignan databases, respectively. Methods: Forty-two food groups known to contribute to the total lignan intake were selected and attributed a value for SECO and MAT from the Finnish lignan database (Fineli (R)) or for SECO, MAT, LARI, and PINO from the Dutch database. Total intake of lignans was estimated from food consumption data for adult men and women (19-79 years) from Denmark, Finland, Italy, Sweden, United Kingdom, and the contribution of aggregated food groups calculated using the Dutch lignin database. Results: Mean dietary lignan intakes estimated using the Dutch database ranged from 1 to 2 mg/day, which was approximately four-fold higher than the intakes estimated from the Fineli (R) database. When LARI and PINO were included in the estimation of the total lignan intakes, cereals, grain products, vegetables, fruit and berries were the most important dietary sources of lignans. Conclusion: Total lignin intake was approximately four-fold higher in the Dutch lignin database, which includes the lignin precursors LARI and PINO, compared to estimates based on the Finnish database based only on SECO and MAT. The main sources of lignans according to the Dutch database in the five countries studied were cereals and grain products, vegetables, fruit, berries, and beverages.
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| 2. |
- Wang, Xiaoliang, et al.
(författare)
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Mendelian randomization analysis of C-reactive protein on colorectal cancer risk
- 2019
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Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 48:3, s. 767-780
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Tidskriftsartikel (refereegranskat)abstract
- Background: Chronic inflammation is a risk factor for colorectal cancer (CRC). Circulating C-reactive protein (CRP) is also moderately associated with CRC risk. However, observational studies are susceptible to unmeasured confounding or reverse causality. Using genetic risk variants as instrumental variables, we investigated the causal relationship between genetically elevated CRP concentration and CRC risk, using a Mendelian randomization approach.Methods: Individual-level data from 30 480 CRC cases and 22 844 controls from 33 participating studies in three international consortia were used: the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), the Colorectal Transdisciplinary Study (CORECT) and the Colon Cancer Family Registry (CCFR). As instrumental variables, we included 19 single nucleotide polymorphisms (SNPs) previously associated with CRP concentration. The SNP-CRC associations were estimated using a logistic regression model adjusted for age, sex, principal components and genotyping phases. An inverse-variance weighted method was applied to estimate the causal effect of CRP on CRC risk.Results: Among the 19 CRP-associated SNPs, rs1260326 and rs6734238 were significantly associated with CRC risk (P = 7.5 × 10-4, and P = 0.003, respectively). A genetically predicted one-unit increase in the log-transformed CRP concentrations (mg/l) was not associated with increased risk of CRC [odds ratio (OR) = 1.04; 95% confidence interval (CI): 0.97, 1.12; P = 0.256). No evidence of association was observed in subgroup analyses stratified by other risk factors.Conclusions: In spite of adequate statistical power to detect moderate association, we found genetically elevated CRP concentration was not associated with increased risk of CRC among individuals of European ancestry. Our findings suggested that circulating CRP is unlikely to be a causal factor in CRC development.
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