The Effect of Iron Status on Risk of Coronary Artery Disease: A Mendelian Randomization Study—Brief Report
Abstract
Objective— Iron status is a modifiable trait that has been implicated in cardiovascular disease. This study uses the Mendelian randomization technique to investigate whether there is any causal effect of iron status on risk of coronary artery disease (CAD). Approach and Results— A 2-sample Mendelian randomization approach is used to estimate the effect of iron status on CAD risk. Three loci (rs1800562 and rs1799945 in the HFE gene and rs855791 in TMPRSS6 ) that are each associated with serum iron, transferrin saturation, ferritin, and transferrin in a pattern suggestive of an association with systemic iron status are used as instruments. SNP (single-nucleotide polymorphism)-iron status association estimates are based on a genome-wide association study meta-analysis of 48 972 individuals. SNP-CAD estimates are derived by combining the results of a genome-wide association study meta-analysis of 60 801 CAD cases and 123 504 controls with those of a meta-analysis of 63 746 CAD cases and 130 681 controls obtained from Metabochip and genome-wide association studies. Combined Mendelian randomization estimates are obtained for each marker by pooling results across the 3 instruments. We find evidence of a protective effect of higher iron status on CAD risk (iron odds ratio, 0.94 per SD unit increase; 95% confidence interval, 0.88–1.00; P =0.039; transferrin saturation odds ratio, 0.95 per SD unit increase; 95% confidence interval, 0.91–0.99; P =0.027; log-transformed ferritin odds ratio, 0.85 per SD unit increase; 95% confidence interval, 0.73–0.98; P =0.024; and transferrin odds ratio, 1.08 per SD unit increase; 95% confidence interval, 1.01–1.16; P =0.034). Conclusions— This Mendelian randomization study supports the hypothesis that higher iron status reduces CAD risk. These findings may highlight a therapeutic target.
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The Genetics of Iron Status Consortium GWAS on 48,972 European subjects identified the 3 SNPs rs1800562, rs1799945, and rs855791.
“A genome-wide association study (GWAS) performed by the Genetics of Iron Status Consortium on 48,972 European subjects (combined Discovery [N = 23,986] and Replication [N = 24,986] cohorts, 55% female) identified 3 such single-nucleotide polymorphisms (SNPs): rs1800562 and rs1799945 in the hemochromatosis (HFE) gene and rs855791 in the transmembrane protease serine 6 (TMPRSS6) gene [2,8,10].”
From Associations of genetically determined iron status across the phenome: A mendelian randomization study (2019) · cites this paper as [8]
The Abstract reports a GWAS meta-analysis of 48,972 individuals and names all three SNPs with their HFE and TMPRSS6 genes; Table 1 also lists the three SNPs. Our copy does not substantiate the sentence’s European ancestry, discovery/replication cohort sizes, or 55% female figure. (LLM, conf=0.87)
Experimental — accuracy not yet measuredAll three SNPs are strong instruments for MR as measured by F-statistics > 10.
“All three of these SNPs have previously been shown to be strong instruments for MR analysis as measured by F-statistics > 10 [8,18]”
From Associations of genetically determined iron status across the phenome: A mendelian randomization study (2019) · cites this paper as [8]
The three SNPs collectively explain approximately 3.8% of the variation in serum iron.
“collectively explain approximately 3.8% of the variation in serum iron [2,8].”
From Associations of genetically determined iron status across the phenome: A mendelian randomization study (2019) · cites this paper as [8]
Three genetic variants (rs1800562 and rs1799945 in HFE and rs855791 in TMPRSS6) associate with increased serum iron, ferritin, and transferrin saturation and decreased transferrin levels, serving as instruments for systemic iron status.
“3 genetic variants (rs1800562 and rs1799945 in the hemochromatosis gene [HFE] and rs855791 in the transmembrane protease serine 6 gene [TMPRSS6]) that associate with increased serum iron, ferritin, and transferrin saturation and decreased transferrin levels, thus serving as instruments for systemic iron status.”
From Associations of genetically determined iron status across the phenome: A mendelian randomization study (2019) · cites this paper as [8]
Using strong instruments associated with serum iron, ferritin, transferrin, and transferrin saturation in a pattern consistent with their effect on systemic iron status aims to reflect the effects of varying iron exposure per se rather than that of some other associated traits.
“by using strong instruments associated with serum iron, ferritin, transferrin, and transferrin saturation in a pattern consistent with their effect on systemic iron status, our analysis aims to reflect the effects of varying iron exposure per se rather than that of some other associated traits [8,10].”
From Associations of genetically determined iron status across the phenome: A mendelian randomization study (2019) · cites this paper as [8]
The previously described MR effects of iron status on risk of Parkinson's disease and coronary artery disease were not statistically significant after correcting for multiple testing in the current analysis.
“The previously described MR effects of iron status on risk of Parkinson’s disease and coronary artery disease (coronary atherosclerosis) were not statistically significant after correcting for multiple testing in our current analysis, although the directions of effect were consistent with previous work (S5 Table) [8,9].”
From Associations of genetically determined iron status across the phenome: A mendelian randomization study (2019) · cites this paper as [8]
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- Authors
- Gill, D., Del Greco M., F., Walker, A. P., Srai, S. K. S., Laffan, M. A., & Minelli, C.
- Affiliations
- Eurac Research (IT)
- From the Imperial College Healthcare NHS Trust, London, United Kingdom (D.G., M.A.L.); Department of Clinical Pharmacology and Therapeutics (D.G.), Department of Haematology (M.A.L.), and Department of Population Health and Occupational Disease (C.M.), Imperial College London, United Kingdom; Institute for Biomedicine, Eurac Research, Bolzano, Italy (F.D.G.M.); and Centre for Cardiovascular Genetics (A.P.W.), and Division of Biosciences (S.K.S.S.), University College London, United Kingdom.
- Venue
- Arteriosclerosis Thrombosis and Vascular Biology
- Published
- 2017-09
- Volume
- 37
- Issue
- 9
- Pages
- 1788-1792
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2733617698
- Cited by
- 95
- References
- 43
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 14 · 2023: 10 · 2022: 10 · 2021: 12 · 2020: 14 · 2019: 13 · 2018: 9
- FWCI
- 7.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Spiral (Imperial College London) (submittedVersion)
- Open Research (University of Surrey) (submittedVersion)
- Funders
- National Institute for Health and Care Research (ACF-2013-21-018)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Keywords
- iron status, coronary artery disease, serum iron, transferrin saturation, ferritin, transferrin, HFE gene, TMPRSS6, genetic instruments, cardiovascular risk
- MeSH terms
- Hemochromatosis Protein, Coronary Artery Disease, Ferritins, Humans, Iron, Membrane Proteins, Phenotype, Risk Factors, Serine Endopeptidases, Transferrin, Odds Ratio, Case-Control Studies, Risk Assessment, Iron Metabolism Disorders, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Databases, Genetic, Genetic Association Studies, Mendelian Randomization Analysis, Protective Factors
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