gms | German Medical Science

MAINZ//2011: 56. GMDS-Jahrestagung und 6. DGEpi-Jahrestagung

Deutsche Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie e. V.
Deutsche Gesellschaft für Epidemiologie e. V.

26. - 29.09.2011 in Mainz

Mendelian randomization study does not support a role for hepatic steatosis influencing hypertension

Meeting Abstract

  • Sebastian Baumeister - University of Greifswald, Greifswald
  • Carsten Schmidt - University of Greifswald, Greifswald
  • Katharina Lau - University of Greifswald, Greifswald
  • Alexander Teumer - University of Greifswald, Greifswald
  • Wolfgang Lieb - University of Greifswald, Greifswald
  • Henri Wallaschofski - University of Greifswald, Greifswald
  • Marcus Dörr - University of Greifswald, Greifswald
  • Marcello Markus - University of Greifswald, Greifswald
  • Henry Völzke - University of Greifswald, Greifswald

Mainz//2011. 56. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds), 6. Jahrestagung der Deutschen Gesellschaft für Epidemiologie (DGEpi). Mainz, 26.-29.09.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. Doc11gmds333

doi: 10.3205/11gmds333, urn:nbn:de:0183-11gmds3331

Published: September 20, 2011

© 2011 Baumeister et al.
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Outline

Text

Findings from observational studies suggest that hepatic steatosis is associated with blood pressure and hypertension. Whether this association is causal or subject to confounding is unknown. We used a Mendelian randomization approach to further elucidate the causative nature of the correlation between hepatic steatosis and blood pressure traits. We performed our analyses within the Study of Health in Pomerania (SHIP), a population-based study in the north-eastern part of Germany. The study population comprised 3,997 individuals aged 20-81 years. Hepatic steatosis was defined as the presence of a hyperechogenic ultrasound pattern of the liver and increased serum alanine transferase (ALT) levels. Mendelian randomization was implemented using treatment effects and bivariate probit regression, with the single-nucleotide polymorphisms (SNPs) rs738409 and rs214357 as instruments. The standard regression models revealed consistent associations of hepatic steatosis with systolic blood pressure (ß coefficient: 2.5, 95% confidence interval (CI): 0.9-4.2) and hypertension (risk difference: 0.07, 95% CI: 0.03-0.11) after adjustment for sex, age, smoking, alcohol consumption, body mass index, waist-to-height ratio, physical activity, antihypertensive medication, total : HDL cholesterol ratio, C-reactive protein, fibrinogen, hemoglobin A1c, and diabetes. By contrast, findings from the Mendelian randomization experiment provided no evidence for a direct causal effect of hepatic steatosis on blood pressure traits. These data suggest that hepatic steatosis does not lead to elevated blood pressure.