Estimated and projected burden of multiple sclerosis attributable to smoking and childhood and adolescent high body-mass index: a comparative risk assessment.


Journal

International journal of epidemiology
ISSN: 1464-3685
Titre abrégé: Int J Epidemiol
Pays: England
ID NLM: 7802871

Informations de publication

Date de publication:
23 01 2021
Historique:
accepted: 24 07 2020
pubmed: 28 8 2020
medline: 3 6 2021
entrez: 27 8 2020
Statut: ppublish

Résumé

Smoking and childhood and adolescent high body-mass index (BMI) are leading lifestyle-related risk factors of global premature morbidity and mortality, and have been associated with an increased risk of developing multiple sclerosis (MS). This study aims to estimate and project the proportion of MS incidence that could be prevented with elimination of these risk factors. Prevalence estimates of high BMI during childhood/adolescence and smoking in early adulthood, and relative risks of MS, were obtained from published literature. A time-lag of 10 years was assumed between smoking in early adulthood and MS incidence, and a time-lag of 20 years was assumed between childhood/adolescent high BMI and MS incidence. The MS population attributable fractions (PAFs) of smoking and high BMI were estimated as individual and combined risk factors, by age, country and sex in 2015, 2025 and 2035 where feasible. The combined estimated PAFs for smoking and high BMI in 2015 were 14, 11, 12 and 12% for the UK, USA, Russia and Australia in a conservative estimate, and 21, 20, 19 and 16% in an independent estimate, respectively. Estimates for smoking are declining over time, whereas estimates for high early life BMI are rising. The PAF for high early life BMI is highest in the USA and is estimated to increase to 14% by 2035. Assuming causality, there is the potential to substantially reduce MS incidence with the elimination of lifestyle-related modifiable risk factors, which are the target of global public health prevention strategies.

Sections du résumé

BACKGROUND
Smoking and childhood and adolescent high body-mass index (BMI) are leading lifestyle-related risk factors of global premature morbidity and mortality, and have been associated with an increased risk of developing multiple sclerosis (MS). This study aims to estimate and project the proportion of MS incidence that could be prevented with elimination of these risk factors.
METHODS
Prevalence estimates of high BMI during childhood/adolescence and smoking in early adulthood, and relative risks of MS, were obtained from published literature. A time-lag of 10 years was assumed between smoking in early adulthood and MS incidence, and a time-lag of 20 years was assumed between childhood/adolescent high BMI and MS incidence. The MS population attributable fractions (PAFs) of smoking and high BMI were estimated as individual and combined risk factors, by age, country and sex in 2015, 2025 and 2035 where feasible.
RESULTS
The combined estimated PAFs for smoking and high BMI in 2015 were 14, 11, 12 and 12% for the UK, USA, Russia and Australia in a conservative estimate, and 21, 20, 19 and 16% in an independent estimate, respectively. Estimates for smoking are declining over time, whereas estimates for high early life BMI are rising. The PAF for high early life BMI is highest in the USA and is estimated to increase to 14% by 2035.
CONCLUSIONS
Assuming causality, there is the potential to substantially reduce MS incidence with the elimination of lifestyle-related modifiable risk factors, which are the target of global public health prevention strategies.

Identifiants

pubmed: 32844186
pii: 5897122
doi: 10.1093/ije/dyaa151
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2051-2057

Informations de copyright

© The Author(s) 2020; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.

Auteurs

Julia Pakpoor (J)

Medical Sciences Division, Oxford University Clinical Academic Graduate School, University of Oxford, Oxford, UK.

Klaus Schmierer (K)

Blizard Institute (Centre for Neuroscience, Surgery & Trauma), Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Department of Neurology, The Royal London Hospital, Barts Health NHS Trust, London, UK.

Jack Cuzick (J)

Wolfson Institute of Preventive Medicine, Queen Mary University of London, London, UK.

Gavin Giovannoni (G)

Blizard Institute (Centre for Neuroscience, Surgery & Trauma), Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Department of Neurology, The Royal London Hospital, Barts Health NHS Trust, London, UK.
Wolfson Institute of Preventive Medicine, Queen Mary University of London, London, UK.

Ruth Dobson (R)

Department of Neurology, The Royal London Hospital, Barts Health NHS Trust, London, UK.
Wolfson Institute of Preventive Medicine, Queen Mary University of London, London, UK.

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