Literature DB >> 31975536

Mendelian Randomization Study of Obesity and Cerebrovascular Disease.

Sandro Marini1,2, Jordi Merino1,3,4,5, Bailey E Montgomery1, Rainer Malik6, Catherine L Sudlow7, Martin Dichgans6,8,9, Jose C Florez1,3,4,10, Jonathan Rosand1,10,11,12, Dipender Gill13, Christopher D Anderson1,10,11,12.   

Abstract

OBJECTIVE: To systematically investigate causal relationships between obesity and cerebrovascular disease and the extent to which hypertension and hyperglycemia mediate the effect of obesity on cerebrovascular disease.
METHODS: We used summary statistics from genome-wide association studies for body mass index (BMI), waist-to-hip ratio (WHR), and multiple cerebrovascular disease phenotypes. We explored causal associations with 2-sample Mendelian randomization (MR) accounting for genetic covariation between BMI and WHR, and we assessed what proportion of the association between obesity and cerebrovascular disease was mediated by systolic blood pressure (SBP) and blood glucose levels, respectively.
RESULTS: Genetic predisposition to higher BMI did not increase the risk of cerebrovascular disease. In contrast, for each 10% increase in WHR there was a 75% increase (95% confidence interval [CI] = 44-113%) in risk for large artery ischemic stroke, a 57% (95% CI = 29-91%) increase in risk for small vessel ischemic stroke, a 197% increase (95% CI = 59-457%) in risk of intracerebral hemorrhage, and an increase in white matter hyperintensity volume (β = 0.11, 95% CI = 0.01-0.21). These WHR associations persisted after adjusting for genetic determinants of BMI. Approximately one-tenth of the observed effect of WHR was mediated by SBP for ischemic stroke (proportion mediated: 12%, 95% CI = 4-20%), but no evidence of mediation was found for average blood glucose.
INTERPRETATION: Abdominal adiposity may trigger causal pathological processes, partially independent from blood pressure and totally independent from glucose levels, that lead to cerebrovascular disease. Potential targets of these pathological processes could represent novel therapeutic opportunities for stroke. ANN NEUROL 2020;87:516-524.
© 2020 American Neurological Association.

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Year:  2020        PMID: 31975536      PMCID: PMC7392199          DOI: 10.1002/ana.25686

Source DB:  PubMed          Journal:  Ann Neurol        ISSN: 0364-5134            Impact factor:   10.422


  49 in total

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Review 2.  Overweight and Obesity in Young Adulthood and the Risk of Stroke: a Meta-analysis.

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4.  Measuring adiposity in patients: the utility of body mass index (BMI), percent body fat, and leptin.

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5.  Mendelian randomization analysis with multiple genetic variants using summarized data.

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6.  Network Mendelian randomization: using genetic variants as instrumental variables to investigate mediation in causal pathways.

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