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Peter Kraft - One of the best experts on this subject based on the ideXlab platform.
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Exploring genome-wide – dietary heme Iron Intake interactions and the risk of type 2 diabetes
Frontiers in genetics, 2013Co-Authors: Louis R. Pasquale, Stephanie Loomis, Hugues Aschard, Jae H. Kang, Marilyn C. Cornelis, Peter KraftAbstract:Aims/hypothesis: Genome-wide association studies have identified over 50 new genetic loci for type 2 diabetes (T2D). Several studies conclude that higher dietary heme Iron Intake increases the risk of T2D. Therefore we assessed whether the relation between genetic loci and type 2 diabetes is modified by dietary heme Iron Intake. Methods: We used Affymetrix Genome-Wide Human 6.0 array data (681,770 single nucleotide polymorphisms (SNPs)) and dietary information collected in the Health Professionals Follow-up Study (n=725 cases; n=1,273 controls) and the Nurses’ Health Study (n=1,081 cases; n=1,692 controls). We assessed whether genome-wide SNPs or Iron metabolism SNPs interacted with dietary heme Iron Intake in relation to T2D, testing for associations in each cohort separately and then meta-analyzing to pool the results. Finally, we created 1,000 synthetic pathways matched to an Iron metabolism pathway on number of genes, and number of SNPs in each gene. We compared the Iron metabolic pathway SNPs with these synthetic SNP assemblies in their relation to T2D to assess if the pathway as a whole interacts with dietary heme Iron Intake. Results: Using a genomic approach, we found no significant gene-envIronment interactions with dietary heme Iron Intake in relation to T2D (top SNP in pooled analysis: intergenic rs10980508; p=1.03E-06 > Bonferroni corrected p=7.33E-08). Furthermore, no SNP in the Iron metabolic pathway significantly interacted with dietary heme Iron Intake (top SNP in pooled analysis: rs1805313; p=1.14E-03 > Bonferroni corrected p=2.10E-04). Finally, neither the main genetic effects (pooled empirical p by SNP=0.41), nor gene – dietary heme-Iron interactions (pooled empirical p value for the interactions=0.72) were significant for the Iron metabolic pathway as a whole. Conclusions: We found no significant interactions between dietary heme Iron Intake and common SNPs in relation to T2D.
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exploring genome wide dietary heme Iron Intake interactions and the risk of type 2 diabetes
Frontiers in Genetics, 2013Co-Authors: Louis R. Pasquale, Stephanie Loomis, Hugues Aschard, Jae H. Kang, Marilyn C. Cornelis, Peter KraftAbstract:Aims/hypothesis: Genome-wide association studies have identified over 50 new genetic loci for type 2 diabetes (T2D). Several studies conclude that higher dietary heme Iron Intake increases the risk of T2D. Therefore we assessed whether the relation between genetic loci and type 2 diabetes is modified by dietary heme Iron Intake. Methods: We used Affymetrix Genome-Wide Human 6.0 array data (681,770 single nucleotide polymorphisms (SNPs)) and dietary information collected in the Health Professionals Follow-up Study (n=725 cases; n=1,273 controls) and the Nurses’ Health Study (n=1,081 cases; n=1,692 controls). We assessed whether genome-wide SNPs or Iron metabolism SNPs interacted with dietary heme Iron Intake in relation to T2D, testing for associations in each cohort separately and then meta-analyzing to pool the results. Finally, we created 1,000 synthetic pathways matched to an Iron metabolism pathway on number of genes, and number of SNPs in each gene. We compared the Iron metabolic pathway SNPs with these synthetic SNP assemblies in their relation to T2D to assess if the pathway as a whole interacts with dietary heme Iron Intake. Results: Using a genomic approach, we found no significant gene-envIronment interactions with dietary heme Iron Intake in relation to T2D (top SNP in pooled analysis: intergenic rs10980508; p=1.03E-06 > Bonferroni corrected p=7.33E-08). Furthermore, no SNP in the Iron metabolic pathway significantly interacted with dietary heme Iron Intake (top SNP in pooled analysis: rs1805313; p=1.14E-03 > Bonferroni corrected p=2.10E-04). Finally, neither the main genetic effects (pooled empirical p by SNP=0.41), nor gene – dietary heme-Iron interactions (pooled empirical p value for the interactions=0.72) were significant for the Iron metabolic pathway as a whole. Conclusions: We found no significant interactions between dietary heme Iron Intake and common SNPs in relation to T2D.
Walter C. Willett - One of the best experts on this subject based on the ideXlab platform.
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Iron Intake and risk of ovulatory infertility.
Obstetrics and gynecology, 2006Co-Authors: Jorge E. Chavarro, Janet W. Rich-edwards, Bernard Rosner, Walter C. WillettAbstract:Objective To evaluate whether Iron supplement use or greater Intake of total, heme and nonheme Iron is associated with lower risk of ovulatory infertility. Methods We conducted a prospective cohort study among 18,555 married, premenopausal women without a history of infertility who attempted a pregnancy or became pregnant between 1991 and 1999 (mean baseline age+/-standard deviation 32.6+/-3.6). Diet was assessed twice during follow-up and prospectively related to the incidence of infertility due to ovulatory disorder. Results During the 8 years of follow-up, 438 women reported infertility due to ovulatory disorder. Women who consumed Iron supplements had a significantly lower risk of ovulatory infertility than women who did not use Iron supplements (relative risk 0.60, 95% confidence interval 0.39-0.92), after adjusting for potential confounders. Total nonheme Iron Intake, primarily consumed as multivitamins and Iron supplements, was inversely associated with the risk of infertility (relative risk Quintile 1 compared with 5, 95% confidence interval 0.39-0.92; P, trend .005.) Heme Iron Intake was unrelated to ovulatory infertility in multivariable adjusted analyses. Conclusion Consumption of Iron supplements and nonheme Iron from other sources may decrease the risk of ovulatory infertility. Level of evidence II-2.
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Dietary Iron Intake and blood donations in relation to risk of type 2 diabetes in men: a prospective cohort study.
The American journal of clinical nutrition, 2004Co-Authors: Rui Jiang, Alberto Ascherio, Meir J. Stampfer, Walter C. WillettAbstract:Background: Excessive Iron stores may promote insulin resistance and lead to the development of type 2 diabetes. However, prospective data relating Iron Intake and blood donations (determinants of body Iron stores) to diabetes incidence are limited. Objective: We examined Iron Intake and blood donations in relation to the incidence of type 2 diabetes. Design: We followed men aged 40–75 y who participated in the Health Professionals’ Follow-up Study; were free of diabetes, cardiovascular disease, and cancer in 1986; and provided dietary data (n 38 394). Of those participants, 33 541 also provided a history of blood donation during the past 30 y in 1992. Results: During 12 y of follow-up, we ascertained 1168 new cases of type 2 diabetes. After adjustment for age, body mass index, and other diabetes risk factors, total Iron Intake was not associated with the risk of type 2 diabetes. Intakes of total heme Iron [multivariate relative risk (RR) for extreme quintiles: 1.28; 95% CI: 1.02, 1.61; P for trend 0.045] and of heme Iron from red meat (RR: 1.63; 1.26, 2.10; P for trend 0.001) were associated with an increased risk. However, heme-Iron Intake from sources other than red meat was not associated with diabetes risk (RR: 0.99; 0.81, 1.22). No significant associations were found between blood donation and the risk of type 2 diabetes. Conclusions: Heme-Iron Intake from red meat sources is positively associated with the risk of type 2 diabetes. Total Iron Intake, heme-Iron Intake from non–red meat sources, and blood donations are not related to the risk of type 2 diabetes. Am J Clin Nutr 2004;79:70–5.
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Dietary Iron Intake and risk of coronary disease among men.
Circulation, 1994Co-Authors: Alberto Ascherio, Edward Giovannucci, Walter C. Willett, Eric B. Rimm, Meir J. StampferAbstract:BACKGROUNDWe prospectively studied Iron Intake in relation to the incidence of coronary disease in a 4-year follow-up of 44,933 men (with no previous history of cardiovascular disease) aged 40 to 75 years in 1986 who completed a food frequency questionnaire at baseline.METHODS AND RESULTSWe documented 844 incident cases of coronary disease (249 nonfatal myocardial infarctions, 137 coronary disease fatalities, and 458 bypass operations or angioplasties). After adjustment for established risk factors, there was no significant association between total Iron Intake and risk of coronary heart disease. Men in the highest quintile of total Intake (median, 37 mg/d) had a relative risk (RR) of fatal coronary disease or nonfatal myocardial infarction of 0.73 (95% confidence intervals [CI], 0.51, 1.06) compared with men in the lowest quintile of Intake (median, 11 mg/d). Dietary Intake of heme Iron--mainly from red meat--also was not significantly associated with risk of coronary heart disease. However, incidence of...
Louis R. Pasquale - One of the best experts on this subject based on the ideXlab platform.
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Exploring genome-wide – dietary heme Iron Intake interactions and the risk of type 2 diabetes
Frontiers in genetics, 2013Co-Authors: Louis R. Pasquale, Stephanie Loomis, Hugues Aschard, Jae H. Kang, Marilyn C. Cornelis, Peter KraftAbstract:Aims/hypothesis: Genome-wide association studies have identified over 50 new genetic loci for type 2 diabetes (T2D). Several studies conclude that higher dietary heme Iron Intake increases the risk of T2D. Therefore we assessed whether the relation between genetic loci and type 2 diabetes is modified by dietary heme Iron Intake. Methods: We used Affymetrix Genome-Wide Human 6.0 array data (681,770 single nucleotide polymorphisms (SNPs)) and dietary information collected in the Health Professionals Follow-up Study (n=725 cases; n=1,273 controls) and the Nurses’ Health Study (n=1,081 cases; n=1,692 controls). We assessed whether genome-wide SNPs or Iron metabolism SNPs interacted with dietary heme Iron Intake in relation to T2D, testing for associations in each cohort separately and then meta-analyzing to pool the results. Finally, we created 1,000 synthetic pathways matched to an Iron metabolism pathway on number of genes, and number of SNPs in each gene. We compared the Iron metabolic pathway SNPs with these synthetic SNP assemblies in their relation to T2D to assess if the pathway as a whole interacts with dietary heme Iron Intake. Results: Using a genomic approach, we found no significant gene-envIronment interactions with dietary heme Iron Intake in relation to T2D (top SNP in pooled analysis: intergenic rs10980508; p=1.03E-06 > Bonferroni corrected p=7.33E-08). Furthermore, no SNP in the Iron metabolic pathway significantly interacted with dietary heme Iron Intake (top SNP in pooled analysis: rs1805313; p=1.14E-03 > Bonferroni corrected p=2.10E-04). Finally, neither the main genetic effects (pooled empirical p by SNP=0.41), nor gene – dietary heme-Iron interactions (pooled empirical p value for the interactions=0.72) were significant for the Iron metabolic pathway as a whole. Conclusions: We found no significant interactions between dietary heme Iron Intake and common SNPs in relation to T2D.
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exploring genome wide dietary heme Iron Intake interactions and the risk of type 2 diabetes
Frontiers in Genetics, 2013Co-Authors: Louis R. Pasquale, Stephanie Loomis, Hugues Aschard, Jae H. Kang, Marilyn C. Cornelis, Peter KraftAbstract:Aims/hypothesis: Genome-wide association studies have identified over 50 new genetic loci for type 2 diabetes (T2D). Several studies conclude that higher dietary heme Iron Intake increases the risk of T2D. Therefore we assessed whether the relation between genetic loci and type 2 diabetes is modified by dietary heme Iron Intake. Methods: We used Affymetrix Genome-Wide Human 6.0 array data (681,770 single nucleotide polymorphisms (SNPs)) and dietary information collected in the Health Professionals Follow-up Study (n=725 cases; n=1,273 controls) and the Nurses’ Health Study (n=1,081 cases; n=1,692 controls). We assessed whether genome-wide SNPs or Iron metabolism SNPs interacted with dietary heme Iron Intake in relation to T2D, testing for associations in each cohort separately and then meta-analyzing to pool the results. Finally, we created 1,000 synthetic pathways matched to an Iron metabolism pathway on number of genes, and number of SNPs in each gene. We compared the Iron metabolic pathway SNPs with these synthetic SNP assemblies in their relation to T2D to assess if the pathway as a whole interacts with dietary heme Iron Intake. Results: Using a genomic approach, we found no significant gene-envIronment interactions with dietary heme Iron Intake in relation to T2D (top SNP in pooled analysis: intergenic rs10980508; p=1.03E-06 > Bonferroni corrected p=7.33E-08). Furthermore, no SNP in the Iron metabolic pathway significantly interacted with dietary heme Iron Intake (top SNP in pooled analysis: rs1805313; p=1.14E-03 > Bonferroni corrected p=2.10E-04). Finally, neither the main genetic effects (pooled empirical p by SNP=0.41), nor gene – dietary heme-Iron interactions (pooled empirical p value for the interactions=0.72) were significant for the Iron metabolic pathway as a whole. Conclusions: We found no significant interactions between dietary heme Iron Intake and common SNPs in relation to T2D.
Vicky C Chang - One of the best experts on this subject based on the ideXlab platform.
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Iron Intake oxidative stress related genes and breast cancer risk
International Journal of Cancer, 2020Co-Authors: Vicky C Chang, Michelle Cotterchio, Susan J Bondy, Joanne KotsopoulosAbstract:Iron has been suggested to contribute to breast cancer development through oxidative stress generation. Our study investigated associations between Iron Intake and breast cancer risk, overall and by menopausal and estrogen receptor/progesterone receptor (ER/PR) status, and modification by oxidative stress-related genetic polymorphisms (MnSOD, GSTM1 and GSTT1). A population-based case-control study (3,030 cases and 3,402 controls) was conducted in Ontario, Canada. Iron Intake (total, dietary, supplemental, heme, nonheme) was assessed using a validated food frequency questionnaire. Odds ratios (OR) and 95% confidence intervals (CI) were estimated from multivariable logistic regression models. Interactions between Iron Intake and genotypes were assessed among 1,696 cases and 1,761 controls providing DNA. Overall, no associations were observed between Iron Intake and breast cancer risk. Among premenopausal women, total, dietary and dietary nonheme Iron were positively associated with ER-/PR- breast cancer risk (all ptrend 18 vs. 0 mg/day = 0.68, 95% CI: 0.51-0.91), and dietary heme Iron was associated with an increased risk, particularly the ER-/PR- subtype (ORhighest vs. lowest quintile = 1.69, 95% CI: 1.16-2.47; ptrend = 0.02). Furthermore, GSTT1 and combined GSTM1/GSTT1 polymorphisms modified some of the associations. For example, higher dietary Iron was most strongly associated with increased breast cancer risk among women with GSTT1 deletion or GSTM1/GSTT1 double deletions (pinteraction < 0.05). Findings suggest that Iron Intake may have different effects on breast cancer risk according to menopausal and hormone receptor status, as well as genotypes affecting antioxidant capacity.
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Iron Intake, oxidative stress‐related genes and breast cancer risk
International journal of cancer, 2020Co-Authors: Vicky C Chang, Michelle Cotterchio, Susan J Bondy, Joanne KotsopoulosAbstract:Iron has been suggested to contribute to breast cancer development through oxidative stress generation. Our study investigated associations between Iron Intake and breast cancer risk, overall and by menopausal and estrogen receptor/progesterone receptor (ER/PR) status, and modification by oxidative stress-related genetic polymorphisms (MnSOD, GSTM1 and GSTT1). A population-based case-control study (3,030 cases and 3,402 controls) was conducted in Ontario, Canada. Iron Intake (total, dietary, supplemental, heme, nonheme) was assessed using a validated food frequency questionnaire. Odds ratios (OR) and 95% confidence intervals (CI) were estimated from multivariable logistic regression models. Interactions between Iron Intake and genotypes were assessed among 1,696 cases and 1,761 controls providing DNA. Overall, no associations were observed between Iron Intake and breast cancer risk. Among premenopausal women, total, dietary and dietary nonheme Iron were positively associated with ER-/PR- breast cancer risk (all ptrend 18 vs. 0 mg/day = 0.68, 95% CI: 0.51-0.91), and dietary heme Iron was associated with an increased risk, particularly the ER-/PR- subtype (ORhighest vs. lowest quintile = 1.69, 95% CI: 1.16-2.47; ptrend = 0.02). Furthermore, GSTT1 and combined GSTM1/GSTT1 polymorphisms modified some of the associations. For example, higher dietary Iron was most strongly associated with increased breast cancer risk among women with GSTT1 deletion or GSTM1/GSTT1 double deletions (pinteraction
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Iron Intake, body Iron status, and risk of breast cancer: a systematic review and meta-analysis.
BMC cancer, 2019Co-Authors: Vicky C Chang, Michelle Cotterchio, Edwin KhooAbstract:Iron has been shown to promote breast carcinogenesis in animal models through generation of oxidative stress and interaction with estrogen. Heme Iron, which is found exclusively in animal-sourced foods, is suggested to have a more detrimental effect. Epidemiological evidence of the association between Iron and breast cancer risk remains inconclusive and has not been comprehensively summarized. This systematic review and meta-analysis evaluated associations between both Iron Intake and body Iron status and breast cancer risk. Four electronic databases (MEDLINE, EMBASE, CINAHL, and Scopus) were searched up to December 2018 for studies assessing Iron Intake and/or biomarkers of Iron status in relation to breast cancer risk. Using random-effects meta-analyses, pooled relative risks (RRs) and 95% confidence intervals (CIs) were calculated comparing the highest vs. lowest category of each Iron measure. Dose-response meta-analyses were also performed to investigate linear and nonlinear associations. A total of 27 studies were included in the review, of which 23 were eligible for meta-analysis of one or more Iron Intake/status measures. Comparing the highest vs. lowest category, heme Iron Intake was significantly associated with increased breast cancer risk, with a pooled RR of 1.12 (95% CI: 1.04–1.22), whereas no associations were found for dietary (1.01, 95% CI: 0.89–1.15), supplemental (1.02, 95% CI: 0.91–1.13), or total (0.97, 95% CI: 0.82–1.14) Iron Intake. Associations of Iron status indicators with breast cancer risk were generally in the positive direction; however, a significant pooled RR was found only for serum/plasma levels (highest vs. lowest) of Iron (1.22, 95% CI: 1.01–1.47), but not for ferritin (1.13, 95% CI: 0.78–1.62), transferrin saturation (1.16, 95% CI: 0.91–1.47), or total Iron-binding capacity (1.10, 95% CI: 0.97–1.25). In addition, a nonlinear dose-response was observed for heme Iron Intake and serum Iron (both Pnonlinearity
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Iron Intake body Iron status and risk of breast cancer a systematic review and meta analysis
BMC Cancer, 2019Co-Authors: Vicky C Chang, Michelle Cotterchio, Edwin KhooAbstract:Iron has been shown to promote breast carcinogenesis in animal models through generation of oxidative stress and interaction with estrogen. Heme Iron, which is found exclusively in animal-sourced foods, is suggested to have a more detrimental effect. Epidemiological evidence of the association between Iron and breast cancer risk remains inconclusive and has not been comprehensively summarized. This systematic review and meta-analysis evaluated associations between both Iron Intake and body Iron status and breast cancer risk. Four electronic databases (MEDLINE, EMBASE, CINAHL, and Scopus) were searched up to December 2018 for studies assessing Iron Intake and/or biomarkers of Iron status in relation to breast cancer risk. Using random-effects meta-analyses, pooled relative risks (RRs) and 95% confidence intervals (CIs) were calculated comparing the highest vs. lowest category of each Iron measure. Dose-response meta-analyses were also performed to investigate linear and nonlinear associations. A total of 27 studies were included in the review, of which 23 were eligible for meta-analysis of one or more Iron Intake/status measures. Comparing the highest vs. lowest category, heme Iron Intake was significantly associated with increased breast cancer risk, with a pooled RR of 1.12 (95% CI: 1.04–1.22), whereas no associations were found for dietary (1.01, 95% CI: 0.89–1.15), supplemental (1.02, 95% CI: 0.91–1.13), or total (0.97, 95% CI: 0.82–1.14) Iron Intake. Associations of Iron status indicators with breast cancer risk were generally in the positive direction; however, a significant pooled RR was found only for serum/plasma levels (highest vs. lowest) of Iron (1.22, 95% CI: 1.01–1.47), but not for ferritin (1.13, 95% CI: 0.78–1.62), transferrin saturation (1.16, 95% CI: 0.91–1.47), or total Iron-binding capacity (1.10, 95% CI: 0.97–1.25). In addition, a nonlinear dose-response was observed for heme Iron Intake and serum Iron (both Pnonlinearity < 0.05). Heme Iron Intake and serum Iron levels may be positively associated with breast cancer risk. Although associations were modest, these findings may have public health implications given the widespread consumption of (heme) Iron-rich foods. In light of methodological and research gaps identified, further research is warranted to better elucidate the relationship between Iron and breast cancer risk.
Marilyn C. Cornelis - One of the best experts on this subject based on the ideXlab platform.
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Exploring genome-wide – dietary heme Iron Intake interactions and the risk of type 2 diabetes
Frontiers in genetics, 2013Co-Authors: Louis R. Pasquale, Stephanie Loomis, Hugues Aschard, Jae H. Kang, Marilyn C. Cornelis, Peter KraftAbstract:Aims/hypothesis: Genome-wide association studies have identified over 50 new genetic loci for type 2 diabetes (T2D). Several studies conclude that higher dietary heme Iron Intake increases the risk of T2D. Therefore we assessed whether the relation between genetic loci and type 2 diabetes is modified by dietary heme Iron Intake. Methods: We used Affymetrix Genome-Wide Human 6.0 array data (681,770 single nucleotide polymorphisms (SNPs)) and dietary information collected in the Health Professionals Follow-up Study (n=725 cases; n=1,273 controls) and the Nurses’ Health Study (n=1,081 cases; n=1,692 controls). We assessed whether genome-wide SNPs or Iron metabolism SNPs interacted with dietary heme Iron Intake in relation to T2D, testing for associations in each cohort separately and then meta-analyzing to pool the results. Finally, we created 1,000 synthetic pathways matched to an Iron metabolism pathway on number of genes, and number of SNPs in each gene. We compared the Iron metabolic pathway SNPs with these synthetic SNP assemblies in their relation to T2D to assess if the pathway as a whole interacts with dietary heme Iron Intake. Results: Using a genomic approach, we found no significant gene-envIronment interactions with dietary heme Iron Intake in relation to T2D (top SNP in pooled analysis: intergenic rs10980508; p=1.03E-06 > Bonferroni corrected p=7.33E-08). Furthermore, no SNP in the Iron metabolic pathway significantly interacted with dietary heme Iron Intake (top SNP in pooled analysis: rs1805313; p=1.14E-03 > Bonferroni corrected p=2.10E-04). Finally, neither the main genetic effects (pooled empirical p by SNP=0.41), nor gene – dietary heme-Iron interactions (pooled empirical p value for the interactions=0.72) were significant for the Iron metabolic pathway as a whole. Conclusions: We found no significant interactions between dietary heme Iron Intake and common SNPs in relation to T2D.
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exploring genome wide dietary heme Iron Intake interactions and the risk of type 2 diabetes
Frontiers in Genetics, 2013Co-Authors: Louis R. Pasquale, Stephanie Loomis, Hugues Aschard, Jae H. Kang, Marilyn C. Cornelis, Peter KraftAbstract:Aims/hypothesis: Genome-wide association studies have identified over 50 new genetic loci for type 2 diabetes (T2D). Several studies conclude that higher dietary heme Iron Intake increases the risk of T2D. Therefore we assessed whether the relation between genetic loci and type 2 diabetes is modified by dietary heme Iron Intake. Methods: We used Affymetrix Genome-Wide Human 6.0 array data (681,770 single nucleotide polymorphisms (SNPs)) and dietary information collected in the Health Professionals Follow-up Study (n=725 cases; n=1,273 controls) and the Nurses’ Health Study (n=1,081 cases; n=1,692 controls). We assessed whether genome-wide SNPs or Iron metabolism SNPs interacted with dietary heme Iron Intake in relation to T2D, testing for associations in each cohort separately and then meta-analyzing to pool the results. Finally, we created 1,000 synthetic pathways matched to an Iron metabolism pathway on number of genes, and number of SNPs in each gene. We compared the Iron metabolic pathway SNPs with these synthetic SNP assemblies in their relation to T2D to assess if the pathway as a whole interacts with dietary heme Iron Intake. Results: Using a genomic approach, we found no significant gene-envIronment interactions with dietary heme Iron Intake in relation to T2D (top SNP in pooled analysis: intergenic rs10980508; p=1.03E-06 > Bonferroni corrected p=7.33E-08). Furthermore, no SNP in the Iron metabolic pathway significantly interacted with dietary heme Iron Intake (top SNP in pooled analysis: rs1805313; p=1.14E-03 > Bonferroni corrected p=2.10E-04). Finally, neither the main genetic effects (pooled empirical p by SNP=0.41), nor gene – dietary heme-Iron interactions (pooled empirical p value for the interactions=0.72) were significant for the Iron metabolic pathway as a whole. Conclusions: We found no significant interactions between dietary heme Iron Intake and common SNPs in relation to T2D.
