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Investigating causal relationships between Body Mass Index and risk of atopic dermatitis: a Mendelian randomization analysis
Population studies suggest that atopic dermatitis (AD) is associated with an increased risk of obesity, however a causal relationship between these two conditions remains to be established. We therefore use Mendelian randomization (MR) to evaluate whether obesity and AD are causally interlinked. We...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7498603/ https://www.ncbi.nlm.nih.gov/pubmed/32943721 http://dx.doi.org/10.1038/s41598-020-72301-2 |
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author | Yew, Yik Weng Loh, Marie Thng, Steven Tien Guan Chambers, John C. |
author_facet | Yew, Yik Weng Loh, Marie Thng, Steven Tien Guan Chambers, John C. |
author_sort | Yew, Yik Weng |
collection | PubMed |
description | Population studies suggest that atopic dermatitis (AD) is associated with an increased risk of obesity, however a causal relationship between these two conditions remains to be established. We therefore use Mendelian randomization (MR) to evaluate whether obesity and AD are causally interlinked. We used summary statistics extracted from genome wide association studies of Body Mass Index (BMI) and AD. MR analysis was performed in both directions to establish the direction of causality between BMI and AD. We find that genetically determined increase in adiposity is associated with increased risk of AD (odds ratio of AD 1.08 [95% CI 1.01 to 1.14; p = 0.015] per unit increase in BMI). Conversely, genetically determined increased risk of AD is not associated with a higher BMI (change in BMI attributable to AD based on genetic information: 0.00; 95% CI − 0.02 to 0.02; p = 0.862). There was no evidence for confounding of these genetic analyses by horizontal pleiotropy. Our results indicate that the association of AD with obesity is likely to reflect a causal role for adiposity in the development of AD. Our findings enhance understanding of the etiology of AD, and the basis for experimental studies to evaluate the mechanistic pathways by which adiposity promotes AD. |
format | Online Article Text |
id | pubmed-7498603 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-74986032020-09-18 Investigating causal relationships between Body Mass Index and risk of atopic dermatitis: a Mendelian randomization analysis Yew, Yik Weng Loh, Marie Thng, Steven Tien Guan Chambers, John C. Sci Rep Article Population studies suggest that atopic dermatitis (AD) is associated with an increased risk of obesity, however a causal relationship between these two conditions remains to be established. We therefore use Mendelian randomization (MR) to evaluate whether obesity and AD are causally interlinked. We used summary statistics extracted from genome wide association studies of Body Mass Index (BMI) and AD. MR analysis was performed in both directions to establish the direction of causality between BMI and AD. We find that genetically determined increase in adiposity is associated with increased risk of AD (odds ratio of AD 1.08 [95% CI 1.01 to 1.14; p = 0.015] per unit increase in BMI). Conversely, genetically determined increased risk of AD is not associated with a higher BMI (change in BMI attributable to AD based on genetic information: 0.00; 95% CI − 0.02 to 0.02; p = 0.862). There was no evidence for confounding of these genetic analyses by horizontal pleiotropy. Our results indicate that the association of AD with obesity is likely to reflect a causal role for adiposity in the development of AD. Our findings enhance understanding of the etiology of AD, and the basis for experimental studies to evaluate the mechanistic pathways by which adiposity promotes AD. Nature Publishing Group UK 2020-09-17 /pmc/articles/PMC7498603/ /pubmed/32943721 http://dx.doi.org/10.1038/s41598-020-72301-2 Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Yew, Yik Weng Loh, Marie Thng, Steven Tien Guan Chambers, John C. Investigating causal relationships between Body Mass Index and risk of atopic dermatitis: a Mendelian randomization analysis |
title | Investigating causal relationships between Body Mass Index and risk of atopic dermatitis: a Mendelian randomization analysis |
title_full | Investigating causal relationships between Body Mass Index and risk of atopic dermatitis: a Mendelian randomization analysis |
title_fullStr | Investigating causal relationships between Body Mass Index and risk of atopic dermatitis: a Mendelian randomization analysis |
title_full_unstemmed | Investigating causal relationships between Body Mass Index and risk of atopic dermatitis: a Mendelian randomization analysis |
title_short | Investigating causal relationships between Body Mass Index and risk of atopic dermatitis: a Mendelian randomization analysis |
title_sort | investigating causal relationships between body mass index and risk of atopic dermatitis: a mendelian randomization analysis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7498603/ https://www.ncbi.nlm.nih.gov/pubmed/32943721 http://dx.doi.org/10.1038/s41598-020-72301-2 |
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