Causal relationship between obesity and vitamin D status: bi-directional Mendelian randomization analysis of multiple cohorts
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BACKGROUND: Obesity is associated with vitamin D deficiency, and both are areas of active public health concern. We explored the causality and direction of the relationship between body mass index (BMI) and 25-hydroxyvitamin D [25(OH)D] using genetic markers as instrumental variables (IVs) in bi-directional Mendelian randomization (MR) analysis. METHODS AND FINDINGS: We used information from 21 adult cohorts (up to 42,024 participants) with 12 BMI-related SNPs (combined in an allelic score) to produce an instrument for BMI and four SNPs associated with 25(OH)D (combined in two allelic scores, separately for genes encoding its synthesis or metabolism) as an instrument for vitamin D. Regression estimates for the IVs (allele scores) were generated within-study and pooled by meta-analysis to generate summary effects. Associations between vitamin D scores and BMI were confirmed in the Genetic Investigation of Anthropometric Traits (GIANT) consortium (n = 123,864). Each 1 kg/m(2) higher BMI was associated with 1.15% lower 25(OH)D (p = 6.52×10⁻²⁷). The BMI allele score was associated both with BMI (p = 6.30×10⁻⁶²) and 25(OH)D (-0.06% [95% CI -0.10 to -0.02], p = 0.004) in the cohorts that underwent meta-analysis. The two vitamin D allele scores were strongly associated with 25(OH)D (p≤8.07×10⁻⁵⁷ for both scores) but not with BMI (synthesis score, p = 0.88; metabolism score, p = 0.08) in the meta-analysis. A 10% higher genetically instrumented BMI was associated with 4.2% lower 25(OH)D concentrations (IV ratio: -4.2 [95% CI -7.1 to -1.3], p = 0.005). No association was seen for genetically instrumented 25(OH)D with BMI, a finding that was confirmed using data from the GIANT consortium (p≥0.57 for both vitamin D scores). CONCLUSIONS: On the basis of a bi-directional genetic approach that limits confounding, our study suggests that a higher BMI leads to lower 25(OH)D, while any effects of lower 25(OH)D increasing BMI are likely to be small. Population level interventions to reduce BMI are expected to decrease the prevalence of vitamin D deficiency.
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In the GIANT consortium (up to 104349 men), no significant evidence was found that any of the two autosomal testosterone SNPs were associated with BMI individually or combined as a genetic risk score.
“For the two autosomal SNPs it was possible to use the GIANT consortium, including up to 104349 men, to evaluate the causal effect of serum T on BMI in a larger setting. However, no significant evidence was found supporting that any of these T SNPs were associated with BMI individually, or when combined as a genetic risk score (S6 Table).”
From Causal relationship between obesity and serum testosterone status in men: A bi-directional mendelian randomization analysis (2017) · cites this paper as [28]
The MR approach enables the approximation of life-long differences in average concentrations, but genetic markers do not examine the influences arising from the extremes of non-linear distributions.
“While the MR approach enables the approximation of life-long differences in average concentrations, genetic markers do not examine the influences arising from the extremes of non-linear distributions [28, 50].”
From Causal relationship between obesity and serum testosterone status in men: A bi-directional mendelian randomization analysis (2017) · cites this paper as [28]
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- Authors
- Vimaleswaran, K. S., Berry, D. J., Lu, C., Tikkanen, E., Pilz, S., Hiraki, L. T., Cooper, J. D., Dastani, Z., Li, R., Houston, D. K., Wood, A. R., Michaëlsson, K., Vandenput, L., Zgaga, L., Yerges-Armstrong, L. M., McCarthy, M. I., Dupuis, J., Kaakinen, M., Kleber, M. E., Jameson, K., Arden, N., Raitakari, O., Viikari, J., Lohman, K. K., Ferrucci, L., Melhus, H., Ingelsson, E., Byberg, L., Lind, L., Lorentzon, M., Salomaa, V., Campbell, H., Dunlop, M., Mitchell, B. D., Herzig, K.-H., Pouta, A., Hartikainen, A.-L., the Genetic Investigation of Anthropometric Traits (GIANT) consortium, Streeten, E. A., Theodoratou, E., Jula, A., Wareham, N. J., Ohlsson, C., Frayling, T. M., Kritchevsky, S. B., Spector, T. D., Richards, J. B., Lehtimäki, T., Ouwehand, W. H., Kraft, P., Cooper, C., März, W., Power, C., Loos, R. J. F., Wang, T. J., Järvelin, M.-R., Whittaker, J. C., Hingorani, A. D., & Hyppönen, E.
- Affiliations
- University College London (GB)
- Boston University (US)
- University of Helsinki (FI)
- Medical University of Graz (AT)
- Harvard University (US)
- University of Cambridge (GB)
- Jewish General Hospital (CA)
- Wake Forest University Health Sciences (US)
- University of Exeter (GB)
- Uppsala University (SE)
- University of Gothenburg (SE)
- University of Zagreb (HR)
- University of Maryland, Baltimore (US)
- Centre for Human Genetics (GB)
- University of Oulu (FI)
- Heidelberg University (DE)
- MRC Lifecourse Epidemiology Unit (GB)
- University of Turku (FI)
- Wake Forest University (US)
- MedStar Harbor Hospital (US)
- Karolinska Institutet (SE)
- Finnish Institute for Health and Welfare (FI)
- University of Edinburgh (GB)
- Western General Hospital (GB)
- Kuopio University Hospital (FI)
- Addenbrooke's Hospital (GB)
- King's College London (GB)
- Tampere University Hospital (FI)
- NHS Blood and Transplant (GB)
- Massachusetts General Hospital (US)
- GlaxoSmithKline (United Kingdom) (GB)
- Corresponding author
- Hyppönen, Elina
- ORCID
- Vimaleswaran, Karani S.
- Lu, Chen
- Tikkanen, Emmi
- Pilz, Stefan
- Hiraki, Linda T.
- Cooper, Jason D.
- Li, Rui
- Houston, Denise K.
- Wood, Andrew R.
- Michaëlsson, Karl
- Vandenput, Liesbeth
- Zgaga, Lina
- Yerges-Armstrong, Laura M.
- McCarthy, Mark I.
- Dupuis, Josée
- Kaakinen, Marika
- Kleber, Marcus E.
- Arden, Nigel
- Raitakari, Olli
- Ferrucci, Luigi
- Ingelsson, Erik
- Byberg, Liisa
- Lind, Lars
- Lorentzon, Mattias
- Salomaa, Veikko
- Dunlop, Malcolm
- Mitchell, Braxton D.
- Herzig, Karl-Heinz
- Streeten, Elizabeth A.
- Jula, Antti
- Wareham, Nicholas J.
- Ohlsson, Claes
- Frayling, Timothy M.
- Kritchevsky, Stephen B.
- Richards, J. Brent
- Lehtimäki, Terho
- Ouwehand, Willem H.
- Kraft, Peter
- Cooper, Cyrus
- März, Winfried
- Power, Chris
- Loos, Ruth J. F.
- Wang, Thomas J.
- Järvelin, Marjo-Riitta
- Whittaker, John C.
- Hingorani, Aroon D.
- Hyppönen, Elina
- Venue
- PLoS Medicine
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-02-05
- Volume
- 10
- Issue
- 2
- Pages
- e1001383
- ISSN
- 1549-1277 (ISSN-L)
- 1549-1676
- PMC
- PMC3564800
- OpenAlex
- W2117706634
- Cited by
- 1,046
- References
- 54
- Citations by year
- 2026: 28 · 2025: 47 · 2024: 50 · 2023: 62 · 2022: 70 · 2021: 88 · 2020: 80 · 2019: 97 · 2018: 104 · 2017: 101 · 2016: 100 · 2015: 104 · 2014: 77 · 2013: 38
- FWCI
- 79.51
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS Medicine (publishedVersion, cc-by)
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- Funders
- Amgen
- Eli Lilly and Company
- GlaxoSmithKline
- London School of Hygiene and Tropical Medicine
- Wellcome Trust (090532, 096964/Z/11/Z)
- Cancer Research UK (14136, 12076)
- National Institute for Health and Care Research (NF-SI-0611-10136, NF-SI-0508-10082, NF-SI-0611-10099, NF-SI-0512-10114, NF-SI-0611-10219)
- British Heart Foundation (FS05/125, PG/09/023/26806, PG/09/023)
- University College London
- Great Ormond Street Hospital for Children
- Novo Nordisk Fonden (NNF13OC0005785, #NNF10OC1013354, NNF11OC1014660)
- Servier
- Versus Arthritis (17413, 13181, 13157, 13147, 16349, 17265, 16095, 13230, 13085)
- Canadian Institutes of Health Research
- Medical Research Council (G0601653, MC_UU_12011/1, MC_UU_12015/1)
- National Institute on Alcohol Abuse and Alcoholism (K05AA017688)
- National Institute on Aging (K01AG030506, P30AG021332)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Vitamin D Research Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Nutrition, Genetics, and Disease
- Keywords
- obesity, vitamin D deficiency, 25-hydroxyvitamin D, body mass index, bidirectional causality, genetic instruments, vitamin D status, confounding adjustment
- MeSH terms
- Adult, Aged, Aged, 80 and over, Europe, Female, Humans, Male, Middle Aged, North America, Obesity, Phenotype, Risk Factors, Vitamin D, Vitamin D Deficiency, Biomarkers, Body Mass Index, Multivariate Analysis, Linear Models, Risk Assessment, Evidence-Based Medicine, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, White People, Mendelian Randomization Analysis
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