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Updated: Nov 12, 2025

Candidate Gene Testing in Clinical Cohort Studies with Multiplexed Genotyping and Mass Spectrometry
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Childhood obesity and multiple sclerosis: A Mendelian randomization study

Adil Harroud1, Ruth E Mitchell2, Tom G Richardson2

  • 1Department of Neurology, University of California San Francisco, San Francisco, CA, USA/Weill Institute for Neurosciences, University of California San Francisco, San Francisco, CA, USA/Centre for Clinical Epidemiology, Department of Epidemiology, Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC, Canada.

Multiple Sclerosis (Houndmills, Basingstoke, England)
|March 22, 2021
PubMed
Abstract

Insights

Childhood obesity increases multiple sclerosis (MS) risk, with this effect primarily driven by obesity persisting into adulthood. Pubertal timing does not appear to influence this association.

Area of Science:

  • Epidemiology
  • Genetics
  • Neurology

Background:

  • Higher childhood body mass index (BMI) is linked to increased multiple sclerosis (MS) risk.
  • Investigating the causal relationship between childhood BMI and MS is crucial for understanding disease etiology.

Purpose of the Study:

  • To determine if childhood BMI causally influences MS risk.
  • To assess if this effect is independent of adult obesity and pubertal timing.

Main Methods:

  • Mendelian randomization (MR) analysis using genetic data from MS cases and controls.
  • Genome-wide association studies (GWAS) for childhood and adult BMI.
  • Multivariable MR and replication in UK Biobank data.

Main Results:

  • Genetically predicted childhood BMI was associated with higher MS odds (OR=1.26 per SD).
  • This association diminished after adjusting for adult BMI, suggesting mediation by adult obesity.
  • Adult BMI independently predicted MS risk (OR=1.43), irrespective of childhood BMI.

Conclusions:

  • Genetic evidence supports a link between childhood obesity and MS susceptibility.
  • The effect is mediated by the persistence of obesity into early adulthood.
  • Pubertal timing does not significantly modify the association between BMI and MS risk.
Keywords:
Mendelian randomizationMultiple sclerosisgenetic epidemiologyobesity

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