Publication

Blood Eosinophil Count and Metabolic, Cardiac and Pulmonary Outcomes: A Mendelian Randomization Study

Amini, M., Vonk, J. M., Abbasi, A., Prins, B. P., Bruinenberg, M., Franke, L., van der Harst, P., Navis, G., Koppelman, G. H., Wolffenbuttel, B. H. R., Boezen, H. M., Snieder, H., Chasman, D. I. & Alizadeh, B. Z., Apr-2018, In : Twin research and human genetics. 21, 2, p. 89-100 12 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Amini, M., Vonk, J. M., Abbasi, A., Prins, B. P., Bruinenberg, M., Franke, L., ... Alizadeh, B. Z. (2018). Blood Eosinophil Count and Metabolic, Cardiac and Pulmonary Outcomes: A Mendelian Randomization Study. Twin research and human genetics, 21(2), 89-100. https://doi.org/10.1017/thg.2018.6

Author

Amini, Marzyeh ; Vonk, Judith M ; Abbasi, Ali ; Prins, Bram P ; Bruinenberg, Marcel ; Franke, Lude ; van der Harst, Pim ; Navis, Gerjan ; Koppelman, Gerard H ; Wolffenbuttel, Bruce H R ; Boezen, H Marike ; Snieder, Harold ; Chasman, Daniel I ; Alizadeh, Behrooz Z. / Blood Eosinophil Count and Metabolic, Cardiac and Pulmonary Outcomes : A Mendelian Randomization Study. In: Twin research and human genetics. 2018 ; Vol. 21, No. 2. pp. 89-100.

Harvard

Amini, M, Vonk, JM, Abbasi, A, Prins, BP, Bruinenberg, M, Franke, L, van der Harst, P, Navis, G, Koppelman, GH, Wolffenbuttel, BHR, Boezen, HM, Snieder, H, Chasman, DI & Alizadeh, BZ 2018, 'Blood Eosinophil Count and Metabolic, Cardiac and Pulmonary Outcomes: A Mendelian Randomization Study', Twin research and human genetics, vol. 21, no. 2, pp. 89-100. https://doi.org/10.1017/thg.2018.6

Standard

Blood Eosinophil Count and Metabolic, Cardiac and Pulmonary Outcomes : A Mendelian Randomization Study. / Amini, Marzyeh; Vonk, Judith M; Abbasi, Ali; Prins, Bram P; Bruinenberg, Marcel; Franke, Lude; van der Harst, Pim; Navis, Gerjan; Koppelman, Gerard H; Wolffenbuttel, Bruce H R; Boezen, H Marike; Snieder, Harold; Chasman, Daniel I; Alizadeh, Behrooz Z.

In: Twin research and human genetics, Vol. 21, No. 2, 04.2018, p. 89-100.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Amini M, Vonk JM, Abbasi A, Prins BP, Bruinenberg M, Franke L et al. Blood Eosinophil Count and Metabolic, Cardiac and Pulmonary Outcomes: A Mendelian Randomization Study. Twin research and human genetics. 2018 Apr;21(2):89-100. https://doi.org/10.1017/thg.2018.6


BibTeX

@article{a382fc4427be4079a004f019c0d34909,
title = "Blood Eosinophil Count and Metabolic, Cardiac and Pulmonary Outcomes: A Mendelian Randomization Study",
abstract = "Blood eosinophil count is associated with a variety of common complex outcomes in epidemiological observation. The aim of this study was to explore the causal association between determined blood eosinophil count and 20 common complex outcomes (10 metabolic, 6 cardiac, and 4 pulmonary). Through Mendelian randomization, we investigated genetic evidence for the genetically determined eosinophil in association with each outcomes using individual-level LifeLines cohort data (n = 13,301), where a weighted eosinophil genetic risk score comprising five eosinophil associated variants was created. We further examined the associations of the genetically determined eosinophil with those outcomes using summary statistics obtained from genome-wide association study consortia (6 consortia and 14 outcomes). Blood eosinophil count, by a 1-SD genetically increased, was not statistically associated with common complex outcomes in the LifeLines. Using the summary statistics, we showed that a higher genetically determined eosinophil count had a significant association with lower odds of obesity (odds ratio (OR) 0.81, 95{\%} confidence interval (CI) [0.74, 0.89]) but not with the other traits and diseases. To conclude, an elevated eosinophil count is unlikely to be causally associated to higher risk of metabolic, cardiac, and pulmonary outcomes. Further studies with a stronger genetic risk score for eosinophil count may support these results.",
keywords = "eosinophil count, genetic risk score, Mendelian randomization, instrumental variable, complex diseases, metabolic diseases, cardiovascular diseases, pulmonary diseases, GENOME-WIDE ASSOCIATION, CORONARY-ARTERY-DISEASE, TYPE-2 DIABETES RISK, GENETIC ARCHITECTURE, GLUCOSE-HOMEOSTASIS, PROVIDES INSIGHTS, CONTROLLED-TRIAL, LOCI, METAANALYSIS, CELL",
author = "Marzyeh Amini and Vonk, {Judith M} and Ali Abbasi and Prins, {Bram P} and Marcel Bruinenberg and Lude Franke and {van der Harst}, Pim and Gerjan Navis and Koppelman, {Gerard H} and Wolffenbuttel, {Bruce H R} and Boezen, {H Marike} and Harold Snieder and Chasman, {Daniel I} and Alizadeh, {Behrooz Z}",
year = "2018",
month = "4",
doi = "10.1017/thg.2018.6",
language = "English",
volume = "21",
pages = "89--100",
journal = "Twin research and human genetics",
issn = "1832-4274",
publisher = "Cambridge University Press",
number = "2",

}

RIS

TY - JOUR

T1 - Blood Eosinophil Count and Metabolic, Cardiac and Pulmonary Outcomes

T2 - A Mendelian Randomization Study

AU - Amini, Marzyeh

AU - Vonk, Judith M

AU - Abbasi, Ali

AU - Prins, Bram P

AU - Bruinenberg, Marcel

AU - Franke, Lude

AU - van der Harst, Pim

AU - Navis, Gerjan

AU - Koppelman, Gerard H

AU - Wolffenbuttel, Bruce H R

AU - Boezen, H Marike

AU - Snieder, Harold

AU - Chasman, Daniel I

AU - Alizadeh, Behrooz Z

PY - 2018/4

Y1 - 2018/4

N2 - Blood eosinophil count is associated with a variety of common complex outcomes in epidemiological observation. The aim of this study was to explore the causal association between determined blood eosinophil count and 20 common complex outcomes (10 metabolic, 6 cardiac, and 4 pulmonary). Through Mendelian randomization, we investigated genetic evidence for the genetically determined eosinophil in association with each outcomes using individual-level LifeLines cohort data (n = 13,301), where a weighted eosinophil genetic risk score comprising five eosinophil associated variants was created. We further examined the associations of the genetically determined eosinophil with those outcomes using summary statistics obtained from genome-wide association study consortia (6 consortia and 14 outcomes). Blood eosinophil count, by a 1-SD genetically increased, was not statistically associated with common complex outcomes in the LifeLines. Using the summary statistics, we showed that a higher genetically determined eosinophil count had a significant association with lower odds of obesity (odds ratio (OR) 0.81, 95% confidence interval (CI) [0.74, 0.89]) but not with the other traits and diseases. To conclude, an elevated eosinophil count is unlikely to be causally associated to higher risk of metabolic, cardiac, and pulmonary outcomes. Further studies with a stronger genetic risk score for eosinophil count may support these results.

AB - Blood eosinophil count is associated with a variety of common complex outcomes in epidemiological observation. The aim of this study was to explore the causal association between determined blood eosinophil count and 20 common complex outcomes (10 metabolic, 6 cardiac, and 4 pulmonary). Through Mendelian randomization, we investigated genetic evidence for the genetically determined eosinophil in association with each outcomes using individual-level LifeLines cohort data (n = 13,301), where a weighted eosinophil genetic risk score comprising five eosinophil associated variants was created. We further examined the associations of the genetically determined eosinophil with those outcomes using summary statistics obtained from genome-wide association study consortia (6 consortia and 14 outcomes). Blood eosinophil count, by a 1-SD genetically increased, was not statistically associated with common complex outcomes in the LifeLines. Using the summary statistics, we showed that a higher genetically determined eosinophil count had a significant association with lower odds of obesity (odds ratio (OR) 0.81, 95% confidence interval (CI) [0.74, 0.89]) but not with the other traits and diseases. To conclude, an elevated eosinophil count is unlikely to be causally associated to higher risk of metabolic, cardiac, and pulmonary outcomes. Further studies with a stronger genetic risk score for eosinophil count may support these results.

KW - eosinophil count

KW - genetic risk score

KW - Mendelian randomization

KW - instrumental variable

KW - complex diseases

KW - metabolic diseases

KW - cardiovascular diseases

KW - pulmonary diseases

KW - GENOME-WIDE ASSOCIATION

KW - CORONARY-ARTERY-DISEASE

KW - TYPE-2 DIABETES RISK

KW - GENETIC ARCHITECTURE

KW - GLUCOSE-HOMEOSTASIS

KW - PROVIDES INSIGHTS

KW - CONTROLLED-TRIAL

KW - LOCI

KW - METAANALYSIS

KW - CELL

U2 - 10.1017/thg.2018.6

DO - 10.1017/thg.2018.6

M3 - Article

VL - 21

SP - 89

EP - 100

JO - Twin research and human genetics

JF - Twin research and human genetics

SN - 1832-4274

IS - 2

ER -

ID: 55476822