DNA methylation and body-mass index: a genome-wide analysis
Open accessAbstract
Background Obesity is a major health problem that is determined by interactions between lifestyle and environmental and genetic factors. Although associations between several genetic variants and body-mass index (BMI) have been identified, little is known about epigenetic changes related to BMI. We undertook a genome-wide analysis of methylation at CpG sites in relation to BMI.Methods 479 individuals of European origin recruited by the Cardiogenics Consortium formed our discovery cohort. We typed their whole-blood DNA with the Infinium HumanMethylation450 array. After quality control, methylation levels were tested for association with BMI. Methylation sites showing an association with BMI at a false discovery rate q value of 0·05 or less were taken forward for replication in a cohort of 339 unrelated white patients of northern European origin from the MARTHA cohort. Sites that remained significant in this primary replication cohort were tested in a second replication cohort of 1789 white patients of European origin from the KORA cohort. We examined whether methylation levels at identified sites also showed an association with BMI in DNA from adipose tissue (n=635) and skin (n=395) obtained from white female individuals participating in the MuTHER study. Finally, we examined the association of methylation at BMI-associated sites with genetic variants and with gene expression.Findings 20 individuals from the discovery cohort were excluded from analyses after quality-control checks, leaving 459 participants. After adjustment for covariates, we identified an association (q value ≤0·05) between methylation at five probes across three different genes and BMI. The associations with three of these probes--cg22891070, cg27146050, and cg16672562, all of which are in intron 1 of HIF3A--were confirmed in both the primary and second replication cohorts. For every 0·1 increase in methylation β value at cg22891070, BMI was 3·6% (95% CI 2·4-4·9) higher in the discovery cohort, 2·7% (1·2-4·2) higher in the primary replication cohort, and 0·8% (0·2-1·4) higher in the second replication cohort. For the MuTHER cohort, methylation at cg22891070 was associated with BMI in adipose tissue (p=1·72 × 10(-5)) but not in skin (p=0·882). We observed a significant inverse correlation (p=0·005) between methylation at cg22891070 and expression of one HIF3A gene-expression probe in adipose tissue. Two single nucleotide polymorphisms--rs8102595 and rs3826795--had independent associations with methylation at cg22891070 in all cohorts. However, these single nucleotide polymorphisms were not significantly associated with BMI.Interpretation Increased BMI in adults of European origin is associated with increased methylation at the HIF3A locus in blood cells and in adipose tissue. Our findings suggest that perturbation of hypoxia inducible transcription factor pathways could have an important role in the response to increased weight in people.Funding The European Commission, National Institute for Health Research, British Heart Foundation, and Wellcome Trust.
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EWAS identified DNA methylation sites with much larger effect sizes compared to a typical GWAS of the same trait.
“Using hundreds to thousands of subjects, these EWAS identified DNAm sites with much larger effect sizes compared to a typical GWAS of the same trait (Demerath et al., 2015; Dick et al., 2014).”
From Integrative Analysis of Multi-omics Data for Discovery and Functional Studies of Complex Human Diseases (2016) · cites this paper as Dick et al., 2014
Numerous EWAS have identified leukocyte-based DNA methylation markers associated with disease traits.
“numerous studies have successfully identified leukocyte-based DNAm markers associated with disease traits (Demerath et al., 2015; Dick et al., 2014; Hidalgo et al., 2014; Irvin et al., 2014; Liang et al., 2015; Liu, Aryee, et al., 2013).”
From Integrative Analysis of Multi-omics Data for Discovery and Functional Studies of Complex Human Diseases (2016) · cites this paper as Dick et al., 2014
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- Authors
- Dick, K. J., Nelson, C. P., Tsaprouni, L., Sandling, J. K., Aïssi, D., Wahl, S., Meduri, E., Morange, P.-E., Gagnon, F., Grallert, H., Waldenberger, M., Peters, A., Erdmann, J., Hengstenberg, C., Cambien, F., Goodall, A. H., Ouwehand, W. H., Schunkert, H., Thompson, J. R., Spector, T. D., Gieger, C., Trégouët, D.-A., Deloukas, P., & Samani, N. J.
- Affiliations
- University of Leicester (GB)
- University of Bedfordshire (GB)
- Uppsala University (SE)
- Inserm (FR)
- Helmholtz Munich (DE)
- Wellcome Sanger Institute (GB)
- University of Toronto (CA)
- Institute for Integrative and Experimental Genomics (DE)
- German Centre for Cardiovascular Research (DE)
- National Health Service (GB)
- King's College London (GB)
- Queen Mary University of London (GB)
- Corresponding author
- Samani, Nilesh J
- ORCID
- Nelson, Christopher P
- Tsaprouni, Loukia
- Sandling, Johanna K
- Aïssi, Dylan
- Meduri, Eshwar
- Morange, Pierre-Emmanuel
- Grallert, Harald
- Peters, Annette
- Erdmann, Jeanette
- Goodall, Alison H
- Ouwehand, Willem H
- Schunkert, Heribert
- Thompson, John R
- Spector, Tim D
- Gieger, Christian
- Trégouët, David-Alexandre
- Deloukas, Panos
- Samani, Nilesh J
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2014-06
- Volume
- 383
- Issue
- 9933
- Pages
- 1990-1998
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- OpenAlex
- W2099562966
- Cited by
- 778
- References
- 45
- Citations by year
- 2026: 15 · 2025: 24 · 2024: 39 · 2023: 47 · 2022: 43 · 2021: 53 · 2020: 63 · 2019: 84 · 2018: 73 · 2017: 102 · 2016: 96 · 2015: 86 · 2014: 53
- FWCI
- 46.04
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- The Lancet (publishedVersion)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
- Site cant be reached (submittedVersion)
- University of Bedfordshire Repository (University of Bedfordshire) (submittedVersion)
- BCU Open Access Repository (Birmingham City University) (submittedVersion)
- Funders
- European Union (LSHM-CT 2006–037593)
- Canadian Institutes of Health Research (grant MOP 86466)
- Heart and Stroke Foundation of Canada (grant T6484)
- Wellcome Trust (081917/Z/07/Z)
- NJS collaborate under a Fondation Leducq Grant (12CVD02)
- Wellcome Trust core grant to the Wellcome Trust Sanger Institute (098051)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Keywords
- DNA methylation, body mass index, obesity, HIF-3α, epigenetics, CpG sites, adipose tissue, skin, gene expression, genetic variants, epigenetic regulation, whole blood DNA, KORA cohort
- MeSH terms
- Chromosomes, Human, Pair 15, Chromosomes, Human, Pair 19, Female, Humans, Male, Middle Aged, Obesity, Repressor Proteins, Body Mass Index, DNA Methylation, Polymorphism, Single Nucleotide, Apoptosis Regulatory Proteins, Basic Helix-Loop-Helix Proteins, Genome-Wide Association Study
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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