Zheng, Yan and Huang, Tao and Wang, Tiange and Mei, Zhendong and Sun, Zhonghan and Zhang, Tao and Ellervik, Christina and Chai, Jin-Fang and Sim, Xueling and van Dam, Rob M. and Tai, E-Shyong and Koh, Woon-Puay and Dorajoo, Rajkumar and Saw, Seang-Mei and Sabanayagam, Charumathi and Wong, Tien Yin and Gupta, Preeti and Rossing, Peter and Ahluwalia, Tarunveer S. and Vinding, Rebecca K. and Bisgaard, Hans and Bonnelykke, Klaus and Wang, Yujie and Graff, Mariaelisa and Voortman, Trudy and van Rooij, Frank J. A. and Hofman, Albert and van Heemst, Diana and Noordam, Raymond and Estampador, Angela C. and Varga, Tibor V. and Enzenbach, Cornelia and Scholz, Markus and Thiery, Joachim and Burkhardt, Ralph and Orho-Melander, Marju and Schulz, Christina-Alexandra and Ericson, Ulrika and Sonestedt, Emily and Kubo, Michiaki and Akiyama, Masato and Zhou, Ang and Kilpelainen, Tuomas O. and Hansen, Torben and Kleber, Marcus E. and Delgado, Graciela and McCarthy, Mark and Lemaitre, Rozenn N. and Felix, Janine F. and Jaddoe, Vincent W. V. and Wu, Ying and Mohlke, Karen L. and Lehtimaki, Terho and Wang, Carol A. and Pennell, Craig E. and Schunkert, Heribert and Kessler, Thorsten and Zeng, Lingyao and Willenborg, Christina and Peters, Annette and Lieb, Wolfgang and Grote, Veit and Rzehak, Peter and Koletzko, Berthold and Erdmann, Jeanette and Munz, Matthias and Wu, Tangchun and He, Meian and Yu, Caizheng and Lecoeur, Cecile and Froguel, Philippe and Corella, Dolores and Moreno, Luis A. and Lai, Chao-Qiang and Pitkanen, Niina and Boreham, Colin A. and Ridker, Paul M. and Rosendaal, Frits R. and de Mutsert, Renee and Power, Chris and Paternoster, Lavinia and Sorensen, Thorkild I. A. and Tjonneland, Anne and Overvad, Kim and Djousse, Luc and Rivadeneira, Fernando and Lee, Nanette R. and Raitakari, Olli T. and Kahonen, Mika and Viikari, Jorma and Langhendries, Jean-Paul and Escribano, Joaquin and Verduci, Elvira and Dedoussis, George and Koenig, Inke and Balkau, Beverley and Coltell, Oscar and Dallongeville, Jean and Meirhaeghe, Aline and Amouyel, Philippe and Gottrand, Frederic and Pahkala, Katja and Niinikoski, Harri and Hypponen, Elina and Maerz, Winfried and Mackey, David A. and Gruszfeld, Dariusz and Tucker, Katherine L. and Fumeron, Frederic and Estruch, Ramon and Ordovas, Jose M. and Arnett, Donna K. and Mook-Kanamori, Dennis O. and Mozaffarian, Dariush and Psaty, Bruce M. and North, Kari E. and Chasman, Daniel and Qi, Lu (2020) Mendelian randomization analysis does not support causal associations of birth weight with hypertension risk and blood pressure in adulthood. EUROPEAN JOURNAL OF EPIDEMIOLOGY, 35 (7). pp. 685-697. ISSN 0393-2990, 1573-7284
Full text not available from this repository. (Request a copy)Abstract
Epidemiology studies suggested that low birthweight was associated with a higher risk of hypertension in later life. However, little is known about the causality of such associations. In our study, we evaluated the causal association of low birthweight with adulthood hypertension following a standard analytic protocol using the study-level data of 183,433 participants from 60 studies (CHARGE-BIG consortium), as well as that with blood pressure using publicly available summary-level genome-wide association data from EGG consortium of 153,781 participants, ICBP consortium and UK Biobank cohort together of 757,601 participants. We used seven SNPs as the instrumental variable in the study-level analysis and 47 SNPs in the summary-level analysis. In the study-level analyses, decreased birthweight was associated with a higher risk of hypertension in adults (the odds ratio per 1 standard deviation (SD) lower birthweight, 1.22; 95% CI 1.16 to 1.28), while no association was found between genetically instrumented birthweight and hypertension risk (instrumental odds ratio for causal effect per 1 SD lower birthweight, 0.97; 95% CI 0.68 to 1.41). Such results were consistent with that from the summary-level analyses, where the genetically determined low birthweight was not associated with blood pressure measurements either. One SD lower genetically determined birthweight was not associated with systolic blood pressure (beta = - 0.76, 95% CI - 2.45 to 1.08 mmHg), 0.06 mmHg lower diastolic blood pressure (beta = - 0.06, 95% CI - 0.93 to 0.87 mmHg), or pulse pressure (beta = - 0.65, 95% CI - 1.38 to 0.69 mmHg, all p > 0.05). Our findings suggest that the inverse association of birthweight with hypertension risk from observational studies was not supported by large Mendelian randomization analyses.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | GENOME-WIDE ASSOCIATION; GENETIC-VARIANTS; CHINESE FAMINE; EARLY-LIFE; INSTRUMENTS; LOCI; BIAS; HETEROGENEITY; EXPOSURE; DISEASE; Birthweight; Hypertension; Blood pressure; Mendelian randomization; Causal association |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Klinische Chemie und Laboratoriumsmedizin |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 24 Mar 2021 10:09 |
| Last Modified: | 24 Mar 2021 10:09 |
| URI: | https://pred.uni-regensburg.de/id/eprint/44594 |
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