Estimating the causal effect of BMI on mortality risk in people with heart disease, diabetes and cancer using Mendelian randomization.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
01 05 2021
Historique:
received: 12 08 2020
revised: 02 02 2021
accepted: 11 02 2021
pubmed: 17 2 2021
medline: 29 5 2021
entrez: 16 2 2021
Statut: ppublish

Résumé

Observational data have reported that being overweight or obese, compared to being normal weight, is associated with a lower risk for death - the "obesity paradox". We used Mendelian randomization (MR) to estimate causal effects of body mass index (BMI) on mortality risks in people with coronary heart disease (CHD), type 2 diabetes mellitus (T2DM) or malignancy in whom this paradox has been often reported. We studied 457,746 White British UK Biobank participants including three subgroups with T2DM (n = 19,737), CHD (n = 21,925) or cancer (n = 42,612) at baseline and used multivariable-adjusted Cox models and MR approaches to describe relationships between BMI and mortality risk. Observational Cox models showed J-shaped relationships between BMI and mortality risk including within disease subgroups in which the BMI values associated with minimum mortality risk were within overweight/obese ranges (26.5-32.5 kg/m These data support the idea that population efforts to promote intentional weight loss towards the normal BMI range would reduce, not enhance, mortality risk in the general population including, importantly, individuals with CHD.

Sections du résumé

BACKGROUND
Observational data have reported that being overweight or obese, compared to being normal weight, is associated with a lower risk for death - the "obesity paradox". We used Mendelian randomization (MR) to estimate causal effects of body mass index (BMI) on mortality risks in people with coronary heart disease (CHD), type 2 diabetes mellitus (T2DM) or malignancy in whom this paradox has been often reported.
METHODS
We studied 457,746 White British UK Biobank participants including three subgroups with T2DM (n = 19,737), CHD (n = 21,925) or cancer (n = 42,612) at baseline and used multivariable-adjusted Cox models and MR approaches to describe relationships between BMI and mortality risk.
RESULTS
Observational Cox models showed J-shaped relationships between BMI and mortality risk including within disease subgroups in which the BMI values associated with minimum mortality risk were within overweight/obese ranges (26.5-32.5 kg/m
CONCLUSION
These data support the idea that population efforts to promote intentional weight loss towards the normal BMI range would reduce, not enhance, mortality risk in the general population including, importantly, individuals with CHD.

Identifiants

pubmed: 33592239
pii: S0167-5273(21)00280-1
doi: 10.1016/j.ijcard.2021.02.027
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

214-220

Subventions

Organisme : Wellcome Trust
ID : 202802/Z/16/Z
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_00011/2
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/K006665/1
Pays : United Kingdom

Informations de copyright

Copyright © 2021. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of Competing Interest MKR reports speaker fees from Novo Nordisk and modest stock ownership in GSK. NS has consulted for Astrazeneca, Boehringer Ingelheim, Eli-Lilly, Napp, Novo Nordisk, Pfizer and Sanofi. The remaining authors have nothing to disclose.

Auteurs

David A Jenkins (DA)

NIHR Greater Manchester Patient Safety Translational Research Centre, The University of Manchester, Manchester, UK; School of Health Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Oxford Road, Manchester M13 9PL, UK. Electronic address: david.jenkins-5@manchester.ac.uk.

Kaitlin H Wade (KH)

MRC Integrative Epidemiology Unit, Population Health Sciences, Oakfield House, Oakfield Grove, University of Bristol, Bristol BS8 2BN, UK.

David Carslake (D)

MRC Integrative Epidemiology Unit, Population Health Sciences, Oakfield House, Oakfield Grove, University of Bristol, Bristol BS8 2BN, UK.

Jack Bowden (J)

MRC Integrative Epidemiology Unit, Population Health Sciences, Oakfield House, Oakfield Grove, University of Bristol, Bristol BS8 2BN, UK; Exeter Diabetes Group (ExCEED), College of Medicine and Health, University of Exeter, Exeter, UK.

Naveed Sattar (N)

Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.

Ruth J F Loos (RJF)

The Charles Bronfman Institute for Personalized Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; The Mindich Child Health Development Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.

Nicholas J Timpson (NJ)

MRC Integrative Epidemiology Unit, Population Health Sciences, Oakfield House, Oakfield Grove, University of Bristol, Bristol BS8 2BN, UK.

Matthew Sperrin (M)

School of Health Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Oxford Road, Manchester M13 9PL, UK.

Martin K Rutter (MK)

Division of Endocrinology, Diabetes & Gastroenterology, School of Medical Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Oxford Rd, Manchester M13 9PL, UK; Diabetes, Endocrinology and Metabolism Centre, Peter Mount Building, Manchester Royal Infirmary, Manchester University NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester M13 0HY, UK.

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