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Träfflista för sökning "WFRF:(Huerta Jose M.) ;srt2:(2018)"

Sökning: WFRF:(Huerta Jose M.) > (2018)

  • Resultat 11-15 av 15
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11.
  • Li, Sherly X., et al. (författare)
  • Interplay between genetic predisposition, macronutrient intake and type 2 diabetes incidence analysis within EPIC-InterAct across eight European countries
  • 2018
  • Ingår i: Diabetologia. - Springer. - 0012-186X .- 1432-0428. ; 61:6, s. 1325-1332
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Aims/hypothesis: Gene-macronutrient interactions may contribute to the development of type 2 diabetes but research evidence to date is inconclusive. We aimed to increase our understanding of the aetiology of type 2 diabetes by investigating potential interactions between genes and macronutrient intake and their association with the incidence of type 2 diabetes.</p><p>Methods: We investigated the influence of interactions between genetic risk scores (GRSs) for type 2 diabetes, insulin resistance and BMI and macronutrient intake on the development of type 2 diabetes in the European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct, a prospective case-cohort study across eight European countries (N = 21,900 with 9742 incident type 2 diabetes cases). Macronutrient intake was estimated from diets reported in questionnaires, including proportion of energy derived from total carbohydrate, protein, fat, plant and animal protein, saturated, monounsaturated and polyunsaturated fat and dietary fibre. Using multivariable-adjusted Cox regression, we estimated country-specific interaction results on the multiplicative scale, using random-effects meta-analysis. Secondary analysis used isocaloric macronutrient substitution.</p><p>Results: No interactions were identified between any of the three GRSs and any macronutrient intake, with low-to-moderate heterogeneity between countries (I-2 range 0-51.6%). Results were similar using isocaloric macronutrient substitution analyses and when weighted and unweighted GRSs and individual SNPs were examined.</p><p>Conclusions/interpretation: Genetic susceptibility to type 2 diabetes, insulin resistance and BMI did not modify the association between macronutrient intake and incident type 2 diabetes. This suggests that macronutrient intake recommendations to prevent type 2 diabetes do not need to account for differences in genetic predisposition to these three metabolic conditions.</p>
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12.
  • Murphy, Neil, et al. (författare)
  • A prospective evaluation of plasma polyphenol levels and colon cancer risk
  • 2018
  • Ingår i: International Journal of Cancer. - John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 143:7, s. 1620-1631
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Polyphenols have been shown to exert biological activity in experimental models of colon cancer; however, human data linking specific polyphenols to colon cancer is limited. We assessed the relationship between pre-diagnostic plasma polyphenols and colon cancer risk in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition study. Using high pressure liquid chromatography coupled to tandem mass spectrometry, we measured concentrations of 35 polyphenols in plasma from 809 incident colon cancer cases and 809 matched controls. We used multivariable adjusted conditional logistic regression models that included established colon cancer risk factors. The false discovery rate (q<sub>values</sub> ) was computed to control for multiple comparisons. All statistical tests were two-sided. After false discovery rate correction and in continuous log<sub>2</sub> -transformed multivariable models, equol (odds ratio [OR] per log<sub>2</sub> -value, 0.86, 95% confidence interval [95% CI] = 0.79-0.93; q<sub>value</sub>  = 0.01) and homovanillic acid (OR per log<sub>2</sub> -value, 1.46, 95% CI = 1.16-1.84; q<sub>value</sub>  = 0.02) were associated with colon cancer risk. Comparing extreme fifths, equol concentrations were inversely associated with colon cancer risk (OR = 0.61, 95% CI = 0.41-0.91, p<sub>trend</sub>  = 0.003), while homovanillic acid concentrations were positively associated with colon cancer development (OR = 1.72, 95% CI = 1.17-2.53, p<sub>trend</sub>  &lt; 0.0001). No heterogeneity for these associations was observed by sex and across other colon cancer risk factors. The remaining polyphenols were not associated with colon cancer risk. Higher equol concentrations were associated with lower risk, and higher homovanillic acid concentrations were associated with greater risk of colon cancer. These findings support a potential role for specific polyphenols in colon tumorigenesis.</p>
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13.
  • Ward, Heather A., et al. (författare)
  • Meat and haem iron intake in relation to glioma in the European Prospective Investigation into Cancer and Nutrition study
  • 2018
  • Ingår i: European Journal of Cancer Prevention. - Lippincott Williams & Wilkins. - 0959-8278 .- 1473-5709. ; 27:4, s. 379-383
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Diets high in red or processed meat have been associated positively with some cancers, and several possible underlying mechanisms have been proposed, including iron-related pathways. However, the role of meat intake in adult glioma risk has yielded conflicting findings because of small sample sizes and heterogeneous tumour classifications. The aim of this study was to examine red meat, processed meat and iron intake in relation to glioma risk in the European Prospective Investigation into Cancer and Nutrition study. In this prospective cohort study, 408751 individuals from nine European countries completed demographic and dietary questionnaires at recruitment. Multivariable Cox proportional hazards models were used to examine intake of red meat, processed meat, total dietary iron and haem iron in relation to incident glioma. During an average follow-up of 14.1 years, 688 incident glioma cases were diagnosed. There was no evidence that any of the meat variables (red, processed meat or subtypes of meat) or iron (total or haem) were associated with glioma; results were unchanged when the first 2 years of follow-up were excluded. This study suggests that there is no association between meat or iron intake and adult glioma. This is the largest prospective analysis of meat and iron in relation to glioma and as such provides a substantial contribution to a limited and inconsistent literature.</p>
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14.
  • Meidtner, Karina, et al. (författare)
  • Interaction of dietary and genetic factors influencing body iron status and risk of type 2 diabetes within the EPIC-InterAct study
  • 2018
  • Ingår i: Diabetes Care. - American Diabetes Association. - 0149-5992. ; 41:2, s. 277-285
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE Meat intake has been consistently shown to be positively associated with incident type 2 diabetes. Part of that association may be mediated by body iron status, which is influenced by genetic factors. We aimed to test for interactions of genetic and dietary factors influencing body iron status in relation to the risk of incident type 2 diabetes. RESEARCH DESIGN AND METHODS The case-cohort comprised 9,347 case subjects and 12,301 subcohort participants from eight European countries. Single nucleotide polymorphisms (SNPs) were selected from genome-wide association studies on iron status biomarkers and candidate gene studies. A ferritin-related gene score was constructed. Multiplicative and additive interactions of heme iron and SNPs as well as the gene score were evaluated using Cox proportional hazards regression. RESULTS Higher heme iron intake (per 1 SD) was associated with higher ferritin levels (b = 0.113 [95% CI 0.082; 0.144]), but not with transferrin (20.019 [20.043; 0.006]) or transferrin saturation (0.016 [20.006; 0.037]). Five SNPs located in four genes (rs1799945 [HFE H63D], rs1800562 [HFE C282Y], rs236918 [PCK7], rs744653 [SLC40A1], and rs855791 [TMPRSS6 V736A]) were associated with ferritin. We did not detect an interaction of heme iron and the gene score on the risk of diabetes in the overall study population (Padd = 0.16, Pmult = 0.21) but did detect a trend toward a negative interaction in men (Padd = 0.04, Pmult = 0.03). CONCLUSIONS We found no convincing evidence that the interplay of dietary and genetic factors related to body iron status associates with type 2 diabetes risk above the level expected from the sum or product of the two individual exposures.
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15.
  • Meidtner, Karina, et al. (författare)
  • Interaction of Dietary and Genetic Factors Influencing Body Iron Status and Risk of Type 2 Diabetes Within the EPIC-InterAct Study
  • 2018
  • Ingår i: Diabetes Care. - 0149-5992 .- 1935-5548. ; 41:2, s. 277-285
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>OBJECTIVE:</strong> Meat intake has been consistently shown to be positively associated with incident type 2 diabetes. Part of that association may be mediated by body iron status, which is influenced by genetic factors. We aimed to test for interactions of genetic and dietary factors influencing body iron status in relation to the risk of incident type 2 diabetes.</p><p><strong>RESEARCH DESIGN AND METHODS:</strong> The case-cohort comprised 9,347 case subjects and 12,301 subcohort participants from eight European countries. Single nucleotide polymorphisms (SNPs) were selected from genome-wide association studies on iron status biomarkers and candidate gene studies. A ferritin-related gene score was constructed. Multiplicative and additive interactions of heme iron and SNPs as well as the gene score were evaluated using Cox proportional hazards regression.</p><p><strong>RESULTS:</strong> Higher heme iron intake (per 1 SD) was associated with higher ferritin levels (β = 0.113 [95% CI 0.082; 0.144]), but not with transferrin (−0.019 [−0.043; 0.006]) or transferrin saturation (0.016 [−0.006; 0.037]). Five SNPs located in four genes (rs1799945 [<em>HFE</em> H63D], rs1800562 [<em>HFE</em> C282Y], rs236918 [<em>PCK7</em>], rs744653 [<em>SLC40A1</em>], and rs855791 [<em>TMPRSS6</em>V736A]) were associated with ferritin. We did not detect an interaction of heme iron and the gene score on the risk of diabetes in the overall study population (<em>P</em>add = 0.16, <em>P</em>mult = 0.21) but did detect a trend toward a negative interaction in men (<em>P</em>add = 0.04, <em>P</em>mult = 0.03).</p><p><strong>CONCLUSIONS:</strong> We found no convincing evidence that the interplay of dietary and genetic factors related to body iron status associates with type 2 diabetes risk above the level expected from the sum or product of the two individual exposures.</p>
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