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Type 2 diabetes, glucose, insulin, BMI, and ischemic stroke subtypes: Mendelian randomization study

Susanna C Larsson1, Robert A Scott2, Matthew Traylor2

  • 1From the Stroke Research Group (S.L.C., M.T., H.S.M.), Department of Clinical Neurosciences, and MRC Epidemiology Unit (R.A.S., C.C.L., N.J.W.), University of Cambridge, UK; Unit of Nutritional Epidemiology (S.C.L.), Institute of Environmental Medicine, Karolinska Institutet, Stockholm; Department of Clinical Sciences (G.H., O.M., M.O.-M.), Lund University, Malmö, Sweden; and Boston University School of Medicine (S.S.), MA. Susanna.Larsson@ki.se.

Neurology
|July 2, 2017
PubMed
Abstract

Insights

Type 2 diabetes mellitus (T2D) appears causally linked to large artery stroke, but not other stroke subtypes. This research used a Mendelian randomization approach to investigate genetic links between T2D and stroke.

Area of Science:

  • Genetics
  • Neurology
  • Metabolic Diseases

Background:

  • Type 2 diabetes mellitus (T2D) is a growing global health concern.
  • Ischemic stroke is a leading cause of disability and mortality worldwide.
  • Understanding the causal relationship between T2D and stroke subtypes is crucial for prevention and treatment.

Purpose of the Study:

  • To investigate the potential causal associations between T2D, fasting glucose, fasting insulin, and body mass index (BMI) with specific ischemic stroke subtypes using a Mendelian randomization (MR) approach.
  • To differentiate the effects of these risk factors on large artery stroke, small vessel stroke, and cardioembolic stroke.

Main Methods:

  • Employed a two-sample Mendelian randomization (MR) design.
  • Utilized summary statistics from large genome-wide association studies (GWAS) for T2D, fasting glucose, fasting insulin, BMI, and ischemic stroke subtypes.
  • Applied inverse-variance weighted (IVW) and weighted median methods for primary analysis, with MR-Egger regression to assess pleiotropy.

Main Results:

  • Genetically predicted T2D showed a significant causal association with large artery stroke (OR 1.28) and small vessel stroke (OR 1.21).
  • The association between T2D and large artery stroke remained consistent in sensitivity analyses.
  • No statistically significant causal associations were found for genetically predicted fasting glucose, fasting insulin, or BMI with any ischemic stroke subtype.

Conclusions:

  • This study provides robust evidence supporting a causal link between type 2 diabetes mellitus and large artery stroke.
  • The findings highlight the importance of T2D management in reducing the risk of specific ischemic stroke subtypes.

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