Establishing causal relationships between sleep and adiposity traits using Mendelian randomization

Bryony Hayes; Marina Vabistsevits; Richard M Martin; Debbie A Lawlor; Rebecca Richmond; Tim Robinson

doi:10.1002/oby.23668

Establishing causal relationships between sleep and adiposity traits using Mendelian randomization

Bryony Hayes^*, Marina Vabistsevits, Richard M Martin, Debbie A Lawlor, Rebecca Richmond, Tim Robinson

^*Corresponding author for this work

Research output: Contribution to journal › Article (Academic Journal) › peer-review

11 Citations (Scopus)

Abstract

Objective
To systematically evaluate the direction of any potential causal effect between sleep and adiposity traits.

Methods
Two-sample Mendelian randomization (MR) was used to assess the association of genetically predicted sleep traits on adiposity and vice versa. Using data from UK Biobank and 23andme, the sleep traits explored were morning-preference (chronotype) (N=697,828), insomnia (N=1,331,010), sleep duration (N=446, 118), napping (N=452,633) and daytime-sleepiness (N=452,071). Using data from the GIANT and EGG consortia, the adiposity traits explored were adult BMI, hip circumference (HC), waist circumference (WC), waist-to-hip ratio (WHR) (N=322,154) and child-BMI (N=35,668).

Results
We found evidence that insomnia symptoms increased mean WC, BMI and WHR (difference in means WC=0.39 SD (95% CI=0.13, 0.64), BMI=0.47 SD (0.22, 0.73) and WHR=0.34 SD (0.16, 0.52)). Napping increased mean WHR (0.23 SD (0.08, 0.39). Higher HC, WC, and adult-BMI increased odds of daytime-sleepiness (HC=0.02 SD (0.01, 0.04), WC=0.04 SD (0.01, 0.06) and BMI 0.02 SD (0.00, 0.04), respectively). We also found that higher mean child-BMI resulted in lower odds of napping (-0.01 SD (0.02, 0.00).

Conclusions
The effects of insomnia on adiposity, and adiposity on daytime-sleepiness, suggest that poor sleep and weight gain may contribute to a feedback loop that could be detrimental to overall health.

Original language	English
Pages (from-to)	861-870
Number of pages	10
Journal	Obesity
Volume	31
Issue number	3
Early online date	15 Feb 2023
DOIs	https://doi.org/10.1002/oby.23668
Publication status	Published - 1 Mar 2023

Bibliographical note

Funding Information:
Above and Beyond, Grant/Award Number: ALB‐2019‐20‐06; British Heart Foundation, Grant/Award Numbers: AA/18/7/34219, CH/F/20/90003; Cancer Research UK, Grant/Award Number: C18281/A19169; Diabetes UK, Grant/Award Number: 17/0005700; Medical Research Council, Grant/Award Numbers: MC_UU_00011/1, MC_UU_00011/6; NIHR Bristol Biomedical Research Centre, Grant/Award Numbers: NF‐0616‐10102, NIHR302363 Funding information

Funding Information:
Bryony L. Hayes is funded by an Above & Beyond breast cancer legacy grant from University Hospitals Bristol National Health Service (NHS) Foundation Trust ( www.aboveandbeyond.org.uk ). Marina Vabistsevits is supported by the University of Bristol Alumni Fund (Professor Sir Eric Thomas Scholarship). Timothy Robinson is supported by a National Institute for Health Research (NIHR) Development and Skills Enhancement Award (NIHR302363). Rebecca C. Richmond is a de Pass Vice Chancellor's Research Fellow. Richard M. Martin is supported by a Cancer Research UK (C18281/A19169) programme grant (the Integrative Cancer Epidemiology Programme; www.cancerresearchuk.org/funding-for-researchers ). Bryony L. Hayes, Timothy Robinson, Richard M. Martin, Deborah A. Lawlor, and Rebecca C. Richmond work in the Medical Research Council Integrative Epidemiology Unit at the University of Bristol, supported by the Medical Research Council (MC_UU_00011/1 and MC_UU_00011/6 ( www.mrc.ukri.org ) and the University of Bristol. Richard M. Martin and Deborah A. Lawlor are also supported by the NIHR Bristol Biomedical Research Centre, which is funded by the NIHR ( www.nihr.ac.uk ) and is a partnership between University Hospitals Bristol and Weston NHS Foundation Trust and the University of Bristol. Deborah A. Lawlor is an NIHR Senior Investigator (NF‐0616‐10102) and is supported by the British Heart Foundation (CH/F/20/90003 and AA/18/7/34219) and Diabetes UK (17/0005700). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Funding Information:
Deborah A. Lawlor has received support from Roche Diagnostics and Medtronic plc for research unrelated to that presented here. Timothy Robinson has received grants from Daiichi‐Sankyo Company, Limited and Amgen Inc. to attend educational workshops. All other authors declared no conflict of interest.

Publisher Copyright:
© 2023 The Authors. Obesity published by Wiley Periodicals LLC on behalf of The Obesity Society.

Research Groups and Themes

ICEP

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10.1002/oby.23668Licence: CC BY

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8074 (C18281/A29019) ICEP2 - Programme Award: Towards improved casual evidence and enhanced prediction of cancer risk and survival
Martin, R. M. (Principal Investigator)
1/10/20 → 30/09/25
Project: Research

Cite this

@article{3ec065a6648a4b63aaba31f62f097011,

title = "Establishing causal relationships between sleep and adiposity traits using Mendelian randomization",

abstract = "ObjectiveTo systematically evaluate the direction of any potential causal effect between sleep and adiposity traits. Methods Two-sample Mendelian randomization (MR) was used to assess the association of genetically predicted sleep traits on adiposity and vice versa. Using data from UK Biobank and 23andme, the sleep traits explored were morning-preference (chronotype) (N=697,828), insomnia (N=1,331,010), sleep duration (N=446, 118), napping (N=452,633) and daytime-sleepiness (N=452,071). Using data from the GIANT and EGG consortia, the adiposity traits explored were adult BMI, hip circumference (HC), waist circumference (WC), waist-to-hip ratio (WHR) (N=322,154) and child-BMI (N=35,668). Results We found evidence that insomnia symptoms increased mean WC, BMI and WHR (difference in means WC=0.39 SD (95% CI=0.13, 0.64), BMI=0.47 SD (0.22, 0.73) and WHR=0.34 SD (0.16, 0.52)). Napping increased mean WHR (0.23 SD (0.08, 0.39). Higher HC, WC, and adult-BMI increased odds of daytime-sleepiness (HC=0.02 SD (0.01, 0.04), WC=0.04 SD (0.01, 0.06) and BMI 0.02 SD (0.00, 0.04), respectively). We also found that higher mean child-BMI resulted in lower odds of napping (-0.01 SD (0.02, 0.00). Conclusions The effects of insomnia on adiposity, and adiposity on daytime-sleepiness, suggest that poor sleep and weight gain may contribute to a feedback loop that could be detrimental to overall health. ",

author = "Bryony Hayes and Marina Vabistsevits and Martin, {Richard M} and Lawlor, {Debbie A} and Rebecca Richmond and Tim Robinson",

note = "Funding Information: Above and Beyond, Grant/Award Number: ALB‐2019‐20‐06; British Heart Foundation, Grant/Award Numbers: AA/18/7/34219, CH/F/20/90003; Cancer Research UK, Grant/Award Number: C18281/A19169; Diabetes UK, Grant/Award Number: 17/0005700; Medical Research Council, Grant/Award Numbers: MC_UU_00011/1, MC_UU_00011/6; NIHR Bristol Biomedical Research Centre, Grant/Award Numbers: NF‐0616‐10102, NIHR302363 Funding information Funding Information: Bryony L. Hayes is funded by an Above & Beyond breast cancer legacy grant from University Hospitals Bristol National Health Service (NHS) Foundation Trust ( www.aboveandbeyond.org.uk ). Marina Vabistsevits is supported by the University of Bristol Alumni Fund (Professor Sir Eric Thomas Scholarship). Timothy Robinson is supported by a National Institute for Health Research (NIHR) Development and Skills Enhancement Award (NIHR302363). Rebecca C. Richmond is a de Pass Vice Chancellor's Research Fellow. Richard M. Martin is supported by a Cancer Research UK (C18281/A19169) programme grant (the Integrative Cancer Epidemiology Programme; www.cancerresearchuk.org/funding-for-researchers ). Bryony L. Hayes, Timothy Robinson, Richard M. Martin, Deborah A. Lawlor, and Rebecca C. Richmond work in the Medical Research Council Integrative Epidemiology Unit at the University of Bristol, supported by the Medical Research Council (MC_UU_00011/1 and MC_UU_00011/6 ( www.mrc.ukri.org ) and the University of Bristol. Richard M. Martin and Deborah A. Lawlor are also supported by the NIHR Bristol Biomedical Research Centre, which is funded by the NIHR ( www.nihr.ac.uk ) and is a partnership between University Hospitals Bristol and Weston NHS Foundation Trust and the University of Bristol. Deborah A. Lawlor is an NIHR Senior Investigator (NF‐0616‐10102) and is supported by the British Heart Foundation (CH/F/20/90003 and AA/18/7/34219) and Diabetes UK (17/0005700). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Funding Information: Deborah A. Lawlor has received support from Roche Diagnostics and Medtronic plc for research unrelated to that presented here. Timothy Robinson has received grants from Daiichi‐Sankyo Company, Limited and Amgen Inc. to attend educational workshops. All other authors declared no conflict of interest. Publisher Copyright: {\textcopyright} 2023 The Authors. Obesity published by Wiley Periodicals LLC on behalf of The Obesity Society.",

year = "2023",

month = mar,

day = "1",

doi = "10.1002/oby.23668",

language = "English",

volume = "31",

pages = "861--870",

journal = "Obesity",

issn = "1930-7381",

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number = "3",

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TY - JOUR

T1 - Establishing causal relationships between sleep and adiposity traits using Mendelian randomization

AU - Hayes, Bryony

AU - Vabistsevits, Marina

AU - Martin, Richard M

AU - Lawlor, Debbie A

AU - Richmond, Rebecca

AU - Robinson, Tim

N1 - Funding Information: Above and Beyond, Grant/Award Number: ALB‐2019‐20‐06; British Heart Foundation, Grant/Award Numbers: AA/18/7/34219, CH/F/20/90003; Cancer Research UK, Grant/Award Number: C18281/A19169; Diabetes UK, Grant/Award Number: 17/0005700; Medical Research Council, Grant/Award Numbers: MC_UU_00011/1, MC_UU_00011/6; NIHR Bristol Biomedical Research Centre, Grant/Award Numbers: NF‐0616‐10102, NIHR302363 Funding information Funding Information: Bryony L. Hayes is funded by an Above & Beyond breast cancer legacy grant from University Hospitals Bristol National Health Service (NHS) Foundation Trust ( www.aboveandbeyond.org.uk ). Marina Vabistsevits is supported by the University of Bristol Alumni Fund (Professor Sir Eric Thomas Scholarship). Timothy Robinson is supported by a National Institute for Health Research (NIHR) Development and Skills Enhancement Award (NIHR302363). Rebecca C. Richmond is a de Pass Vice Chancellor's Research Fellow. Richard M. Martin is supported by a Cancer Research UK (C18281/A19169) programme grant (the Integrative Cancer Epidemiology Programme; www.cancerresearchuk.org/funding-for-researchers ). Bryony L. Hayes, Timothy Robinson, Richard M. Martin, Deborah A. Lawlor, and Rebecca C. Richmond work in the Medical Research Council Integrative Epidemiology Unit at the University of Bristol, supported by the Medical Research Council (MC_UU_00011/1 and MC_UU_00011/6 ( www.mrc.ukri.org ) and the University of Bristol. Richard M. Martin and Deborah A. Lawlor are also supported by the NIHR Bristol Biomedical Research Centre, which is funded by the NIHR ( www.nihr.ac.uk ) and is a partnership between University Hospitals Bristol and Weston NHS Foundation Trust and the University of Bristol. Deborah A. Lawlor is an NIHR Senior Investigator (NF‐0616‐10102) and is supported by the British Heart Foundation (CH/F/20/90003 and AA/18/7/34219) and Diabetes UK (17/0005700). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Funding Information: Deborah A. Lawlor has received support from Roche Diagnostics and Medtronic plc for research unrelated to that presented here. Timothy Robinson has received grants from Daiichi‐Sankyo Company, Limited and Amgen Inc. to attend educational workshops. All other authors declared no conflict of interest. Publisher Copyright: © 2023 The Authors. Obesity published by Wiley Periodicals LLC on behalf of The Obesity Society.

PY - 2023/3/1

Y1 - 2023/3/1

N2 - ObjectiveTo systematically evaluate the direction of any potential causal effect between sleep and adiposity traits. Methods Two-sample Mendelian randomization (MR) was used to assess the association of genetically predicted sleep traits on adiposity and vice versa. Using data from UK Biobank and 23andme, the sleep traits explored were morning-preference (chronotype) (N=697,828), insomnia (N=1,331,010), sleep duration (N=446, 118), napping (N=452,633) and daytime-sleepiness (N=452,071). Using data from the GIANT and EGG consortia, the adiposity traits explored were adult BMI, hip circumference (HC), waist circumference (WC), waist-to-hip ratio (WHR) (N=322,154) and child-BMI (N=35,668). Results We found evidence that insomnia symptoms increased mean WC, BMI and WHR (difference in means WC=0.39 SD (95% CI=0.13, 0.64), BMI=0.47 SD (0.22, 0.73) and WHR=0.34 SD (0.16, 0.52)). Napping increased mean WHR (0.23 SD (0.08, 0.39). Higher HC, WC, and adult-BMI increased odds of daytime-sleepiness (HC=0.02 SD (0.01, 0.04), WC=0.04 SD (0.01, 0.06) and BMI 0.02 SD (0.00, 0.04), respectively). We also found that higher mean child-BMI resulted in lower odds of napping (-0.01 SD (0.02, 0.00). Conclusions The effects of insomnia on adiposity, and adiposity on daytime-sleepiness, suggest that poor sleep and weight gain may contribute to a feedback loop that could be detrimental to overall health.

AB - ObjectiveTo systematically evaluate the direction of any potential causal effect between sleep and adiposity traits. Methods Two-sample Mendelian randomization (MR) was used to assess the association of genetically predicted sleep traits on adiposity and vice versa. Using data from UK Biobank and 23andme, the sleep traits explored were morning-preference (chronotype) (N=697,828), insomnia (N=1,331,010), sleep duration (N=446, 118), napping (N=452,633) and daytime-sleepiness (N=452,071). Using data from the GIANT and EGG consortia, the adiposity traits explored were adult BMI, hip circumference (HC), waist circumference (WC), waist-to-hip ratio (WHR) (N=322,154) and child-BMI (N=35,668). Results We found evidence that insomnia symptoms increased mean WC, BMI and WHR (difference in means WC=0.39 SD (95% CI=0.13, 0.64), BMI=0.47 SD (0.22, 0.73) and WHR=0.34 SD (0.16, 0.52)). Napping increased mean WHR (0.23 SD (0.08, 0.39). Higher HC, WC, and adult-BMI increased odds of daytime-sleepiness (HC=0.02 SD (0.01, 0.04), WC=0.04 SD (0.01, 0.06) and BMI 0.02 SD (0.00, 0.04), respectively). We also found that higher mean child-BMI resulted in lower odds of napping (-0.01 SD (0.02, 0.00). Conclusions The effects of insomnia on adiposity, and adiposity on daytime-sleepiness, suggest that poor sleep and weight gain may contribute to a feedback loop that could be detrimental to overall health.

U2 - 10.1002/oby.23668

DO - 10.1002/oby.23668

M3 - Article (Academic Journal)

C2 - 36790827

SN - 1930-7381

VL - 31

SP - 861

EP - 870

JO - Obesity

JF - Obesity

IS - 3

ER -

Establishing causal relationships between sleep and adiposity traits using Mendelian randomization

Abstract

Bibliographical note

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Projects

8074 (C18281/A29019) ICEP2 - Programme Award: Towards improved casual evidence and enhanced prediction of cancer risk and survival

Cite this