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Systolic Blood Pressure and Risk of Type 2 Diabetes: A Mendelian Randomization Study.

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Citation: Diabetes. 66(2):543-550, 2017 FebPMID: 27702834Institution: MedStar Health Research InstituteForm of publication: Journal ArticleMedline article type(s): Journal ArticleSubject headings: *Blood Pressure/ge [Genetics] | *Diabetes Mellitus, Type 2/ge [Genetics] | Case-Control Studies | Causality | Diabetes Mellitus, Type 2/ep [Epidemiology] | European Continental Ancestry Group | Genetic Variation | Humans | Mendelian Randomization Analysis | Odds Ratio | Polymorphism, Single Nucleotide | Regression Analysis | Risk Factors | SystoleYear: 2017 Local holdings: Available online from MWHC library: 1995 - present (after 3 months), Available in print through MWHC library: 1999 - 2006ISSN:

0012-1797

Name of journal: DiabetesAbstract: Copyright � 2017 by the American Diabetes Association.Observational studies have shown that elevated systolic blood pressure (SBP) is associated with future onset of type 2 diabetes, but whether this association is causal is not known. We applied the Mendelian randomization framework to evaluate the causal hypothesis that elevated SBP increases risk for type 2 diabetes. We used 28 genetic variants associated with SBP and evaluated their impact on type 2 diabetes using a European-centric meta-analysis comprising 37,293 case and 125,686 control subjects. We found that elevation of SBP levels by 1 mmHg due to our genetic score was associated with a 2% increase in risk of type 2 diabetes (odds ratio 1.02, 95% CI 1.01-1.03, P = 9.05 x 10-5). To limit confounding, we constructed a second score based on 13 variants exclusively associated with SBP and found a similar increase in type 2 diabetes risk per 1 mmHg of genetic elevation in SBP (odds ratio 1.02, 95% CI 1.01-1.03, P = 1.48 x 10-3). Sensitivity analyses using multiple, alternative causal inference measures and simulation studies demonstrated consistent association, suggesting robustness of our primary observation. In line with previous reports from observational studies, we found that genetically elevated SBP was associated with increased risk for type 2 diabetes. Further work will be required to elucidate the biological mechanism and translational implications.All authors: Aikens RC, Epstein SE, Reilly MP, Saleheen D, Salomaa V, Tikkanen E, Voight BF, Zhao WFiscal year: FY2017Digital Object Identifier:

https://dx.doi.org/10.2337/db16-0868

Date added to catalog: 2017-05-06

Holdings ( 1 )
Title notes ( 4 )

Holdings
Item type	Current library	Collection	Call number	Status	Date due	Barcode
Journal Article	MedStar Authors Catalog	Article	27702834	Available		27702834

Available online from MWHC library: 1995 - present (after 3 months), Available in print through MWHC library: 1999 - 2006

Observational studies have shown that elevated systolic blood pressure (SBP) is associated with future onset of type 2 diabetes, but whether this association is causal is not known. We applied the Mendelian randomization framework to evaluate the causal hypothesis that elevated SBP increases risk for type 2 diabetes. We used 28 genetic variants associated with SBP and evaluated their impact on type 2 diabetes using a European-centric meta-analysis comprising 37,293 case and 125,686 control subjects. We found that elevation of SBP levels by 1 mmHg due to our genetic score was associated with a 2% increase in risk of type 2 diabetes (odds ratio 1.02, 95% CI 1.01-1.03, P = 9.05 x 10-5). To limit confounding, we constructed a second score based on 13 variants exclusively associated with SBP and found a similar increase in type 2 diabetes risk per 1 mmHg of genetic elevation in SBP (odds ratio 1.02, 95% CI 1.01-1.03, P = 1.48 x 10-3). Sensitivity analyses using multiple, alternative causal inference measures and simulation studies demonstrated consistent association, suggesting robustness of our primary observation. In line with previous reports from observational studies, we found that genetically elevated SBP was associated with increased risk for type 2 diabetes. Further work will be required to elucidate the biological mechanism and translational implications.

English