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Thyroid function and ischemic heart disease: a Mendelian randomization study.

Jie V Zhao1, C Mary Schooling2,3

  • 1School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, SAR, China.

Scientific Reports
|August 19, 2017
PubMed
Summary
This summary is machine-generated.

Thyroid function, including thyroid stimulating hormone (TSH) and free thyroxine (FT4), does not appear to significantly impact ischemic heart disease (IHD) risk. This Mendelian randomization study found no strong genetic link between thyroid markers and IHD development.

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Area of Science:

  • Endocrinology and Cardiology
  • Genetic Epidemiology
  • Metabolic Disease Research

Background:

  • The relationship between thyroid function and ischemic heart disease (IHD) remains incompletely understood.
  • Thyroid hormones influence cardiovascular physiology, but their direct role in IHD pathogenesis requires clarification.
  • Genetic prediction offers a method to assess long-term effects of thyroid function on IHD.

Purpose of the Study:

  • To investigate the causal role of genetically predicted thyroid stimulating hormone (TSH), free thyroxine (FT4), and thyroid peroxidase antibody (TPOAb) positivity in ischemic heart disease (IHD).
  • To assess the association between genetically predicted thyroid function and major IHD risk factors, including lipids, diabetes, and adiposity.

Main Methods:

  • Utilized Mendelian randomization analysis with genetic instruments in a large case-control study (CARDIoGRAMplusC4D).
  • Assessed associations with lipids, diabetes, and adiposity using large-scale genetic consortia (Global Lipids Genetics Consortium, DIAbetes Genetics Replication And Meta-analysis, Genetic Investigation of ANthropometric Traits).
  • Employed sensitivity analyses, including weighted median and MR Egger methods, to ensure robustness of findings.

Main Results:

  • Genetically predicted TSH, FT4, and TPOAb positivity were not significantly associated with IHD risk.
  • No significant associations were found between genetically predicted thyroid function and IHD risk factors after Bonferroni correction.
  • An inverse association was observed between genetically predicted FT4 and low-density lipoprotein-cholesterol levels.

Conclusions:

  • This study provides limited evidence that genetically determined TSH, FT4, or TPOAb positivity causally influences ischemic heart disease risk.
  • While thyroid function may affect certain risk factors like LDL-cholesterol, its direct impact on IHD appears minimal.
  • Further research may explore nuanced interactions or specific subpopulations.