Genetic Obesity and the Risk of Atrial Fibrillation: Causal Estimates from Mendelian Randomization
Observational studies have identified an association between body mass index (BMI) and incident atrial fibrillation (AF). Inferring causality from observational studies, however, is subject to residual confounding, reverse causation, and bias. The primary objective of this study was to evaluate the...
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| Vydané v: | Circulation (New York, N.Y.) Ročník 135; číslo 8; s. 741 |
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| Hlavní autori: | , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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United States
21.02.2017
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| ISSN: | 1524-4539, 1524-4539 |
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| Abstract | Observational studies have identified an association between body mass index (BMI) and incident atrial fibrillation (AF). Inferring causality from observational studies, however, is subject to residual confounding, reverse causation, and bias. The primary objective of this study was to evaluate the causal association between BMI and AF by using genetic predictors of BMI.
We identified 51 646 individuals of European ancestry without AF at baseline from 7 prospective population-based cohorts initiated between 1987 and 2002 in the United States, Iceland, and the Netherlands with incident AF ascertained between 1987 and 2012. Cohort-specific mean follow-up ranged from 7.4 to 19.2 years, over which period there was a total of 4178 cases of incident AF. We performed a Mendelian randomization with instrumental variable analysis to estimate a cohort-specific causal hazard ratio for the association between BMI and AF. Two genetic instruments for BMI were used:
genotype (rs1558902) and a BMI gene score comprising 39 single-nucleotide polymorphisms identified by genome-wide association studies to be associated with BMI. Cohort-specific estimates were combined by random-effects, inverse variance-weighted meta-analysis.
In age- and sex-adjusted meta-analysis, both genetic instruments were significantly associated with BMI (
: 0.43 [95% confidence interval, 0.32-0.54] kg/m
per A-allele,
<0.001; BMI gene score: 1.05 [95% confidence interval, 0.90-1.20] kg/m
per 1-U increase,
<0.001) and incident AF (
, hazard ratio, 1.07 [1.02-1.11] per A-allele,
=0.004; BMI gene score, hazard ratio, 1.11 [1.05-1.18] per 1-U increase,
<0.001). Age- and sex-adjusted instrumental variable estimates for the causal association between BMI and incident AF were hazard ratio, 1.15 (1.04-1.26) per kg/m
,
=0.005 (
) and 1.11 (1.05-1.17) per kg/m
,
<0.001 (BMI gene score). Both of these estimates were consistent with the meta-analyzed estimate between observed BMI and AF (age- and sex-adjusted hazard ratio 1.05 [1.04-1.06] per kg/m
,
<0.001). Multivariable adjustment did not significantly change findings.
Our data are consistent with a causal relationship between BMI and incident AF. These data support the possibility that public health initiatives targeting primordial prevention of obesity may reduce the incidence of AF. |
|---|---|
| AbstractList | Observational studies have identified an association between body mass index (BMI) and incident atrial fibrillation (AF). Inferring causality from observational studies, however, is subject to residual confounding, reverse causation, and bias. The primary objective of this study was to evaluate the causal association between BMI and AF by using genetic predictors of BMI.
We identified 51 646 individuals of European ancestry without AF at baseline from 7 prospective population-based cohorts initiated between 1987 and 2002 in the United States, Iceland, and the Netherlands with incident AF ascertained between 1987 and 2012. Cohort-specific mean follow-up ranged from 7.4 to 19.2 years, over which period there was a total of 4178 cases of incident AF. We performed a Mendelian randomization with instrumental variable analysis to estimate a cohort-specific causal hazard ratio for the association between BMI and AF. Two genetic instruments for BMI were used:
genotype (rs1558902) and a BMI gene score comprising 39 single-nucleotide polymorphisms identified by genome-wide association studies to be associated with BMI. Cohort-specific estimates were combined by random-effects, inverse variance-weighted meta-analysis.
In age- and sex-adjusted meta-analysis, both genetic instruments were significantly associated with BMI (
: 0.43 [95% confidence interval, 0.32-0.54] kg/m
per A-allele,
<0.001; BMI gene score: 1.05 [95% confidence interval, 0.90-1.20] kg/m
per 1-U increase,
<0.001) and incident AF (
, hazard ratio, 1.07 [1.02-1.11] per A-allele,
=0.004; BMI gene score, hazard ratio, 1.11 [1.05-1.18] per 1-U increase,
<0.001). Age- and sex-adjusted instrumental variable estimates for the causal association between BMI and incident AF were hazard ratio, 1.15 (1.04-1.26) per kg/m
,
=0.005 (
) and 1.11 (1.05-1.17) per kg/m
,
<0.001 (BMI gene score). Both of these estimates were consistent with the meta-analyzed estimate between observed BMI and AF (age- and sex-adjusted hazard ratio 1.05 [1.04-1.06] per kg/m
,
<0.001). Multivariable adjustment did not significantly change findings.
Our data are consistent with a causal relationship between BMI and incident AF. These data support the possibility that public health initiatives targeting primordial prevention of obesity may reduce the incidence of AF. Observational studies have identified an association between body mass index (BMI) and incident atrial fibrillation (AF). Inferring causality from observational studies, however, is subject to residual confounding, reverse causation, and bias. The primary objective of this study was to evaluate the causal association between BMI and AF by using genetic predictors of BMI.BACKGROUNDObservational studies have identified an association between body mass index (BMI) and incident atrial fibrillation (AF). Inferring causality from observational studies, however, is subject to residual confounding, reverse causation, and bias. The primary objective of this study was to evaluate the causal association between BMI and AF by using genetic predictors of BMI.We identified 51 646 individuals of European ancestry without AF at baseline from 7 prospective population-based cohorts initiated between 1987 and 2002 in the United States, Iceland, and the Netherlands with incident AF ascertained between 1987 and 2012. Cohort-specific mean follow-up ranged from 7.4 to 19.2 years, over which period there was a total of 4178 cases of incident AF. We performed a Mendelian randomization with instrumental variable analysis to estimate a cohort-specific causal hazard ratio for the association between BMI and AF. Two genetic instruments for BMI were used: FTO genotype (rs1558902) and a BMI gene score comprising 39 single-nucleotide polymorphisms identified by genome-wide association studies to be associated with BMI. Cohort-specific estimates were combined by random-effects, inverse variance-weighted meta-analysis.METHODSWe identified 51 646 individuals of European ancestry without AF at baseline from 7 prospective population-based cohorts initiated between 1987 and 2002 in the United States, Iceland, and the Netherlands with incident AF ascertained between 1987 and 2012. Cohort-specific mean follow-up ranged from 7.4 to 19.2 years, over which period there was a total of 4178 cases of incident AF. We performed a Mendelian randomization with instrumental variable analysis to estimate a cohort-specific causal hazard ratio for the association between BMI and AF. Two genetic instruments for BMI were used: FTO genotype (rs1558902) and a BMI gene score comprising 39 single-nucleotide polymorphisms identified by genome-wide association studies to be associated with BMI. Cohort-specific estimates were combined by random-effects, inverse variance-weighted meta-analysis.In age- and sex-adjusted meta-analysis, both genetic instruments were significantly associated with BMI (FTO: 0.43 [95% confidence interval, 0.32-0.54] kg/m2 per A-allele, P<0.001; BMI gene score: 1.05 [95% confidence interval, 0.90-1.20] kg/m2 per 1-U increase, P<0.001) and incident AF (FTO, hazard ratio, 1.07 [1.02-1.11] per A-allele, P=0.004; BMI gene score, hazard ratio, 1.11 [1.05-1.18] per 1-U increase, P<0.001). Age- and sex-adjusted instrumental variable estimates for the causal association between BMI and incident AF were hazard ratio, 1.15 (1.04-1.26) per kg/m2, P=0.005 (FTO) and 1.11 (1.05-1.17) per kg/m2, P<0.001 (BMI gene score). Both of these estimates were consistent with the meta-analyzed estimate between observed BMI and AF (age- and sex-adjusted hazard ratio 1.05 [1.04-1.06] per kg/m2, P<0.001). Multivariable adjustment did not significantly change findings.RESULTSIn age- and sex-adjusted meta-analysis, both genetic instruments were significantly associated with BMI (FTO: 0.43 [95% confidence interval, 0.32-0.54] kg/m2 per A-allele, P<0.001; BMI gene score: 1.05 [95% confidence interval, 0.90-1.20] kg/m2 per 1-U increase, P<0.001) and incident AF (FTO, hazard ratio, 1.07 [1.02-1.11] per A-allele, P=0.004; BMI gene score, hazard ratio, 1.11 [1.05-1.18] per 1-U increase, P<0.001). Age- and sex-adjusted instrumental variable estimates for the causal association between BMI and incident AF were hazard ratio, 1.15 (1.04-1.26) per kg/m2, P=0.005 (FTO) and 1.11 (1.05-1.17) per kg/m2, P<0.001 (BMI gene score). Both of these estimates were consistent with the meta-analyzed estimate between observed BMI and AF (age- and sex-adjusted hazard ratio 1.05 [1.04-1.06] per kg/m2, P<0.001). Multivariable adjustment did not significantly change findings.Our data are consistent with a causal relationship between BMI and incident AF. These data support the possibility that public health initiatives targeting primordial prevention of obesity may reduce the incidence of AF.CONCLUSIONSOur data are consistent with a causal relationship between BMI and incident AF. These data support the possibility that public health initiatives targeting primordial prevention of obesity may reduce the incidence of AF. |
| Author | Lin, Honghuang Albert, Christine M Verweij, Niek Rose, Lynda M Niemeijer, Maartje N Arking, Dan E Benjamin, Emelia J Ellinor, Patrick T Smith, Albert V Gudnason, Vilmundur Heeringa, Jan Van Der Harst, Pim Geelhoed, Bastiaan Rienstra, Michiel Chatterjee, Neal A Soliman, Elsayed Z Alonso, Alvaro Lunetta, Kathryn L Lubitz, Steven A Stricker, Bruno H C Giulianini, Franco Misialek, Jeffrey R Chasman, Daniel I |
| Author_xml | – sequence: 1 givenname: Neal A surname: Chatterjee fullname: Chatterjee, Neal A organization: Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA – sequence: 2 givenname: Franco surname: Giulianini fullname: Giulianini, Franco organization: Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA – sequence: 3 givenname: Bastiaan surname: Geelhoed fullname: Geelhoed, Bastiaan organization: Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands – sequence: 4 givenname: Kathryn L surname: Lunetta fullname: Lunetta, Kathryn L organization: The Framingham Heart Study, Framingham, MA, USA; Cardiology and Preventive Medicine Sections, Boston University School of Medicine, Epidemiology Department, Boston University School of Public Health, Boston, MA, USA – sequence: 5 givenname: Jeffrey R surname: Misialek fullname: Misialek, Jeffrey R organization: Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, USA – sequence: 6 givenname: Maartje N surname: Niemeijer fullname: Niemeijer, Maartje N organization: Department of Epidemiology, Erasmus Medical Center-University Medical Center, Rotterdam, The Netherlands – sequence: 7 givenname: Michiel surname: Rienstra fullname: Rienstra, Michiel organization: Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands – sequence: 8 givenname: Lynda M surname: Rose fullname: Rose, Lynda M organization: Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA – sequence: 9 givenname: Albert V surname: Smith fullname: Smith, Albert V organization: Icelandic Heart Association, Research Institute, Kpoavogur, Iceland and University of Iceland, Reykjavik, Iceland – sequence: 10 givenname: Dan E surname: Arking fullname: Arking, Dan E organization: McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA – sequence: 11 givenname: Patrick T surname: Ellinor fullname: Ellinor, Patrick T organization: Cardiovascular Research Center and Cardiac Arrhythmia Service, Massachusetts General Hospital, Boston, MA, USA and Program in Medical and Population Genetics, The Broad Institute of Harvard and MIT, Cambridge, MA, USA – sequence: 12 givenname: Jan surname: Heeringa fullname: Heeringa, Jan organization: Department of Epidemiology, Erasmus Medical Center-University Medical Center, Rotterdam, The Netherlands – sequence: 13 givenname: Honghuang surname: Lin fullname: Lin, Honghuang organization: Computational Biomedicine Section, Boston University School of Medicine, Boston, MA, USA – sequence: 14 givenname: Steven A surname: Lubitz fullname: Lubitz, Steven A organization: Cardiovascular Research Center and Cardiac Arrhythmia Service, Massachusetts General Hospital, Boston, MA, USA and Program in Medical and Population Genetics, The Broad Institute of Harvard and MIT, Cambridge, MA, USA – sequence: 15 givenname: Elsayed Z surname: Soliman fullname: Soliman, Elsayed Z organization: Epidemiological Cardiology Research Center (EPICARE), Wake Forest School of Medicine, Winston Salem, NC, USA – sequence: 16 givenname: Niek surname: Verweij fullname: Verweij, Niek organization: Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands – sequence: 17 givenname: Alvaro surname: Alonso fullname: Alonso, Alvaro organization: Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA – sequence: 18 givenname: Emelia J surname: Benjamin fullname: Benjamin, Emelia J organization: The Framingham Heart Study, Framingham, MA, USA; Cardiology and Preventive Medicine Sections, Boston University School of Medicine, Epidemiology Department, Boston University School of Public Health, Boston, MA, USA – sequence: 19 givenname: Vilmundur surname: Gudnason fullname: Gudnason, Vilmundur organization: Icelandic Heart Association, Research Institute, Kpoavogur, Iceland and University of Iceland, Reykjavik, Iceland – sequence: 20 givenname: Bruno H C surname: Stricker fullname: Stricker, Bruno H C organization: Department of Epidemiology, Erasmus Medical Center-University Medical Center, Rotterdam, The Netherlands – sequence: 21 givenname: Pim surname: Van Der Harst fullname: Van Der Harst, Pim organization: Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands – sequence: 22 givenname: Daniel I surname: Chasman fullname: Chasman, Daniel I organization: Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA – sequence: 23 givenname: Christine M surname: Albert fullname: Albert, Christine M organization: Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27974350$$D View this record in MEDLINE/PubMed |
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| Copyright | 2016 American Heart Association, Inc. |
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| SubjectTerms | Aged Alleles Alpha-Ketoglutarate-Dependent Dioxygenase FTO - genetics Atrial Fibrillation - epidemiology Atrial Fibrillation - etiology Body Mass Index Cohort Studies Female Genotype Humans Incidence Male Middle Aged Obesity - genetics Obesity - pathology Polymorphism, Single Nucleotide Proportional Hazards Models Prospective Studies Random Allocation Risk Factors |
| Title | Genetic Obesity and the Risk of Atrial Fibrillation: Causal Estimates from Mendelian Randomization |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/27974350 https://www.proquest.com/docview/1852686021 |
| Volume | 135 |
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