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2. Smoking and alcohol by HPV status in head and neck cancer: a Mendelian randomization study

Author

Thakral, Abhinav, Lee, John JW., Hou, Tianzhichao, Hueniken, Katrina, Dudding, Tom, Gormley, Mark, Virani, Shama, Olshan, Andrew, Diergaarde, Brenda, Ness, Andrew R., Waterboer, Tim, Smith-Byrne, Karl, Brennan, Paul, Hayes, D. Neil, Sanderson, Eleanor, Brown, M. Catherine, Huang, Sophie, Bratman, Scott V., Spreafico, Anna, De Almeida, John, Davies, Joel C., Bierut, Laura, Macfarlane, Gary J., Lagiou, Pagona, Lagiou, Areti, Polesel, Jerry, Agudo, Antonio, Alemany, Laia, Ahrens, Wolfgang, Healy, Claire M., Conway, David I., Nygard, Mari, Canova, Cristina, Holcatova, Ivana, Richiardi, Lorenzo, Znaor, Ariana, Goldstein, David P., Hung, Rayjean J., Xu, Wei, Liu, Geoffrey, and Espin-Garcia, Osvaldo

Published
2024
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5. Selecting Valid Instrumental Variables in Linear Models with Multiple Exposure Variables: Adaptive Lasso and the Median-of-Medians Estimator

Author

Liang, Xiaoran, Sanderson, Eleanor, and Windmeijer, Frank

Subjects
Statistics - Methodology, Economics - Econometrics
Abstract

In a linear instrumental variables (IV) setting for estimating the causal effects of multiple confounded exposure/treatment variables on an outcome, we investigate the adaptive Lasso method for selecting valid instrumental variables from a set of available instruments that may contain invalid ones. An instrument is invalid if it fails the exclusion conditions and enters the model as an explanatory variable. We extend the results as developed in Windmeijer et al. (2019) for the single exposure model to the multiple exposures case. In particular we propose a median-of-medians estimator and show that the conditions on the minimum number of valid instruments under which this estimator is consistent for the causal effects are only moderately stronger than the simple majority rule that applies to the median estimator for the single exposure case. The adaptive Lasso method which uses the initial median-of-medians estimator for the penalty weights achieves consistent selection with oracle properties of the resulting IV estimator. This is confirmed by some Monte Carlo simulation results. We apply the method to estimate the causal effects of educational attainment and cognitive ability on body mass index (BMI) in a Mendelian Randomization setting.

Published
2022

7. DNA methylation at the suppressor of cytokine signaling 3 (SOCS3) gene influences height in childhood

Author

Issarapu, Prachand, Arumalla, Manisha, Elliott, Hannah R., Nongmaithem, Suraj S., Sankareswaran, Alagu, Betts, Modupeh, Sajjadi, Sara, Kessler, Noah J., Bayyana, Swati, Mansuri, Sohail R., Derakhshan, Maria, Krishnaveni, G. V., Shrestha, Smeeta, Kumaran, Kalyanaraman, Di Gravio, Chiara, Sahariah, Sirazul A., Sanderson, Eleanor, Relton, Caroline L., Ward, Kate A., Moore, Sophie E., Prentice, Andrew M., Lillycrop, Karen A., Fall, Caroline H. D., Silver, Matt J., and Chandak, Giriraj R.

Published
2023
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9. Separating the effects of early and later life adiposity on colorectal cancer risk: a Mendelian randomization study

Author

Papadimitriou, Nikos, Bull, Caroline J., Jenab, Mazda, Hughes, David J., Bell, Joshua A., Sanderson, Eleanor, Timpson, Nicholas J., Smith, George Davey, Albanes, Demetrius, Campbell, Peter T., Küry, Sébastien, Le Marchand, Loic, Ulrich, Cornelia M., Visvanathan, Kala, Figueiredo, Jane C., Newcomb, Polly A., Pai, Rish K., Peters, Ulrike, Tsilidis, Kostas K., Boer, Jolanda M. A., Vincent, Emma E., Mariosa, Daniela, Gunter, Marc J., Richardson, Tom G., and Murphy, Neil

Published
2023
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12. Investigation of the Interplay between Circulating Lipids and IGF-I and Relevance to Breast Cancer Risk: An Observational and Mendelian Randomization Study

Author

Tan, Vanessa Y, Bull, Caroline J, Biernacka, Kalina M, Teumer, Alexander, Richardson, Tom G, Sanderson, Eleanor, Corbin, Laura J, Dudding, Tom, Qi, Qibin, Kaplan, Robert C, Rotter, Jerome I, Friedrich, Nele, Völker, Uwe, Mayerle, Julia, Perks, Claire M, Holly, Jeff MP, and Timpson, Nicholas J

Subjects
Health Services and Systems, Biomedical and Clinical Sciences, Health Sciences, Oncology and Carcinogenesis, Clinical Research, Breast Cancer, Cardiovascular, Atherosclerosis, Cancer, Prevention, 2.1 Biological and endogenous factors, Aetiology, Breast Neoplasms, Causality, Cholesterol, HDL, Cholesterol, LDL, Cross-Sectional Studies, Female, Genome-Wide Association Study, Humans, Insulin-Like Growth Factor I, Mendelian Randomization Analysis, Triglycerides, Medical and Health Sciences, Epidemiology, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundCirculating lipids and insulin-like growth factor 1 (IGF-I) have been reliably associated with breast cancer. Observational studies suggest an interplay between lipids and IGF-I, however, whether these relationships are causal and if pathways from these phenotypes to breast cancer overlap is unclear.MethodsMendelian randomization (MR) was conducted to estimate the relationship between lipids or IGF-I and breast cancer risk using genetic summary statistics for lipids (low-density lipoprotein cholesterol, LDL-C; high-density lipoprotein cholesterol, HDL-C; triglycerides, TGs), IGF-I and breast cancer from GLGC/UKBB (N = 239,119), CHARGE/UKBB (N = 252,547), and Breast Cancer Association Consortium (N = 247,173), respectively. Cross-sectional observational and MR analyses were conducted to assess the bi-directional relationship between lipids and IGF-I in SHIP (N = 3,812) and UKBB (N = 422,389), and using genetic summary statistics from GLGC (N = 188,577) and CHARGE/UKBB (N = 469,872).ResultsIn multivariable MR (MVMR) analyses, the OR for breast cancer per 1-SD increase in HDL-C and TG was 1.08 [95% confidence interval (CI), 1.04-1.13] and 0.94 (95% CI, 0.89-0.98), respectively. The OR for breast cancer per 1-SD increase in IGF-I was 1.09 (95% CI, 1.04-1.15). MR analyses suggested a bi-directional TG-IGF-I relationship (TG-IGF-I β per 1-SD: -0.13; 95% CI, -0.23 to -0.04; and IGF-I-TG β per 1-SD: -0.11; 95% CI, -0.18 to -0.05). There was little evidence for a causal relationship between HDL-C and LDL-C with IGF-I. In MVMR analyses, associations of TG or IGF-I with breast cancer were robust to adjustment for IGF-I or TG, respectively.ConclusionsOur findings suggest a causal role of HDL-C, TG, and IGF-I in breast cancer. Observational and MR analyses support an interplay between IGF-I and TG; however, MVMR estimates suggest that TG and IGF-I may act independently to influence breast cancer.ImpactOur findings should be considered in the development of prevention strategies for breast cancer, where interventions are known to modify circulating lipids and IGF-I.

Published
2021

17. Applying Mendelian randomization to appraise causality in relationships between nutrition and cancer

Author

Wade, Kaitlin H., Yarmolinsky, James, Giovannucci, Edward, Lewis, Sarah J., Millwood, Iona Y., Munafò, Marcus R., Meddens, Fleur, Burrows, Kimberley, Bell, Joshua A., Davies, Neil M., Mariosa, Daniela, Kanerva, Noora, Vincent, Emma E., Smith-Byrne, Karl, Guida, Florence, Gunter, Marc J., Sanderson, Eleanor, Dudbridge, Frank, Burgess, Stephen, Cornelis, Marilyn C., Richardson, Tom G., Borges, Maria Carolina, Bowden, Jack, Hemani, Gibran, Cho, Yoonsu, Spiller, Wes, Richmond, Rebecca C., Carter, Alice R., Langdon, Ryan, Lawlor, Deborah A., Walters, Robin G., Vimaleswaran, Karani Santhanakrishnan, Anderson, Annie, Sandu, Meda R., Tilling, Kate, Davey Smith, George, Martin, Richard M., and Relton, Caroline L.

Published
2022
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18. Mendelian randomization

Author

Sanderson, Eleanor, Glymour, M. Maria, Holmes, Michael V., Kang, Hyunseung, Morrison, Jean, Munafò, Marcus R., Palmer, Tom, Schooling, C. Mary, Wallace, Chris, Zhao, Qingyuan, and Davey Smith, George

Published
2022
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28. Methodological approaches, challenges, and opportunities in the application of Mendelian randomisation to lifecourse epidemiology: A systematic literature review

Author

Power, Grace M., primary, Sanderson, Eleanor, additional, Pagoni, Panagiota, additional, Fraser, Abigail, additional, Morris, Tim, additional, Prince, Claire, additional, Frayling, Timothy M., additional, Heron, Jon, additional, Richardson, Tom G., additional, Richmond, Rebecca, additional, Tyrrell, Jessica, additional, Warrington, Nicole, additional, Davey Smith, George, additional, Howe, Laura D., additional, and Tilling, Kate M., additional

Published
2023
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29. Estimation of time-varying causal effects with multivariable Mendelian randomization: the importance of model specification.

Author

Sanderson, Eleanor and Tilling, Kate

Subjects
*SINGLE nucleotide polymorphisms, *GENETIC correlations, *FIX-point estimation, *GENE expression, *GENETIC variation
Abstract

The article discusses the importance of model specification when estimating the effects of the same exposure at different time points using multivariable Mendelian randomization (MVMR). The authors compare MVMR estimates with the direct effect of each exposure time point and highlight that any misspecification of the MVMR model can lead to misleading estimates of the causal effect. They provide simulation results to support their claims. The article emphasizes the need to consider biologically plausible relationships between exposures and how exposure-outcome effects might change over time when using MVMR. [Extracted from the article]

Published
2024
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30. Associations between insomnia and pregnancy and perinatal outcomes: Evidence from mendelian randomization and multivariable regression analyses

Author

Yang, Qian, Borges, Maria Carolina, Sanderson, Eleanor, Magnus, Maria C., Kilpi, Fanny, Collings, Paul J., Soares, Ana Luiza, West, Jane, Magnus, Per, Wright, John, Håberg, Siri E., Tilling, Kate, and Lawlor, Deborah A.

Subjects
Miscarriage -- Risk factors, Insomnia -- Complications and side effects, Birth weight, Low -- Risk factors, Multivariate analysis -- Methods, Biological sciences
Abstract

Background Insomnia is common and associated with adverse pregnancy and perinatal outcomes in observational studies. However, those associations could be vulnerable to residual confounding or reverse causality. Our aim was to estimate the association of insomnia with stillbirth, miscarriage, gestational diabetes (GD), hypertensive disorders of pregnancy (HDP), perinatal depression, preterm birth (PTB), and low/high offspring birthweight (LBW/HBW). Methods and findings We used 2-sample mendelian randomization (MR) with 81 single-nucleotide polymorphisms (SNPs) instrumenting for a lifelong predisposition to insomnia. Our outcomes included ever experiencing stillbirth, ever experiencing miscarriage, GD, HDP, perinatal depression, PTB (gestational age Conclusions In this study, we observed some evidence in support of a possible causal relationship between genetically predicted insomnia and miscarriage, perinatal depression, and LBW. Our study also found observational evidence in support of an association between insomnia in pregnancy and perinatal depression, with no clear multivariable evidence of an association with LBW. Our findings highlight the importance of healthy sleep in women of reproductive age, though replication in larger studies, including with genetic instruments specific to insomnia in pregnancy are important., Author(s): Qian Yang 1,2,*, Maria Carolina Borges 1,2, Eleanor Sanderson 1,2, Maria C. Magnus 1,2,3, Fanny Kilpi 1,2, Paul J. Collings 4, Ana Luiza Soares 1,2, Jane West 4, Per [...]

Published
2022
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31. Testing for weak instruments in two-stage least squares estimation of linear instrumental variable models

Author

Sanderson, Eleanor

Subjects
330
Abstract

Instrumental Variable (IV) methods are widely used in the analysis of economic data when the explanatory variable of interest is endogenous and so OLS estimation of the model is biased. However, if the instruments used do not strongly predict the endogenous variable being instrumented then the IV estimator will also give biased results. Weak Instrument Asymptotic theory can be used to model the strength of the instruments in Two-Stage Least Squares (2SLS) IV models and critical values have been developed to test for Weak Instruments in models with one time period. In the first part of this thesis I extend Weak Instrument Asymptotics to a model with multiple endogenous variables where the instruments available can strongly predict each of the endogenous variables separately but correlation between the endogenous variables means that they cannot be jointly predicted and so the overall strength of the instruments in the model is weak. I develop a partial F-statistic to test for 'Weak Instruments of this form and show that this test has the correct size using currently existing critical values for testing for Weak Instruments. I then extend the Weak Instrument Asymptotics to Panel Data models with multiple time periods, and one endogenous variable. I show that it is no longer possible to use the F -statistic to test for Weak Instruments but it is possible to use the Effective F-statistic developed by Olea and Pflueger (2013) with appropriately clustered standard errors to test for 'Weak Instruments in Pallel Data models. Finally, I extend this analysis to look a AR(l) panel data models and show that it is possible to control the strcngth of the instruments asymptotically by changing the persistence of the autoregressive process. I also show the Effective F-statistic has the correct size in these AR(l) models.

Published
2014

32. Estimating the health impact of nicotine exposure by dissecting the effects of nicotine versus non-nicotine constituents of tobacco smoke: A multivariable Mendelian randomisation study.

Author

Khouja, Jasmine N., Sanderson, Eleanor, Wootton, Robyn E., Taylor, Amy E., Church, Billy A., Richmond, Rebecca C., and Munafò, Marcus R.

Subjects
*NICOTINE, *TOBACCO smoke, *SMOKING, *COTININE, *CHRONIC obstructive pulmonary disease, *GENOME-wide association studies
Abstract

The detrimental health effects of smoking are well-known, but the impact of regular nicotine use without exposure to the other constituents of tobacco is less clear. Given the increasing daily use of alternative nicotine delivery systems, such as e-cigarettes, it is increasingly important to understand and separate the effects of nicotine use from the impact of tobacco smoke exposure. Using a multivariable Mendelian randomisation framework, we explored the direct effects of nicotine compared with the non-nicotine constituents of tobacco smoke on health outcomes (lung cancer, chronic obstructive pulmonary disease [COPD], forced expiratory volume in one second [FEV-1], forced vital capacity [FVC], coronary heart disease [CHD], and heart rate [HR]). We used Genome-Wide Association Study (GWAS) summary statistics from Buchwald and colleagues, the GWAS and Sequencing Consortium of Alcohol and Nicotine, the International Lung Cancer Consortium, and UK Biobank. Increased nicotine metabolism increased the risk of COPD, lung cancer, and lung function in the univariable analysis. However, when accounting for smoking heaviness in the multivariable analysis, we found that increased nicotine metabolite ratio (indicative of decreased nicotine exposure per cigarette smoked) decreases heart rate (b = -0.30, 95% CI -0.50 to -0.10) and lung function (b = -33.33, 95% CI -41.76 to -24.90). There was no clear evidence of an effect on the remaining outcomes. The results suggest that these smoking-related outcomes are not due to nicotine exposure but are caused by the other components of tobacco smoke; however, there are multiple potential sources of bias, and the results should be triangulated using evidence from a range of methodologies. Author summary: Although we know that smoking tobacco negatively impacts health, we know relatively little about whether nicotine plays a role in causing poor health outcomes. When used for short periods of time, nicotine appears to have little impact on health. However, until recently, nicotine has rarely been used for long periods without accompanying exposure to tobacco smoke, so it is hard to disentangle the effects of regular nicotine use from the effects of tobacco smoke exposure. In this study, we aimed to dissect the effects of nicotine versus non-nicotine constituents of tobacco smoke on heart and lung health using multivariable Mendelian randomisation and data from a range of sources (including UK Biobank). We found that nicotine does not appear to be an independent cause of poor lung function, lung cancer, chronic obstructive pulmonary disease, or coronary heart disease, but does increase heart rate. These results support previous evidence which suggests that nicotine on its own does not directly cause poor health outcomes, with the exception of increasing heart rate. [ABSTRACT FROM AUTHOR]

Published
2024
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33. The mediating role of mammographic density in the protective effect of early-life adiposity on breast cancer risk: a multivariable Mendelian randomization study

Author

Vabistsevits, Marina, primary, Davey Smith, George, additional, Richardson, Tom G, additional, Richmond, Rebecca C, additional, Sieh, Weiva, additional, Rothstein, Joseph H, additional, Habel, Laurel A, additional, Alexeeff, Stacey E, additional, Lloyd-Lewis, Bethan, additional, and Sanderson, Eleanor, additional

Published
2023
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37. Adiposity, metabolites, and colorectal cancer risk: Mendelian randomization study

Author

Bull, Caroline J., Bell, Joshua A., Murphy, Neil, Sanderson, Eleanor, Davey Smith, George, Timpson, Nicholas J., Banbury, Barbara L., Albanes, Demetrius, Berndt, Sonja I., Bézieau, Stéphane, Bishop, D. Timothy, Brenner, Hermann, Buchanan, Daniel D., Burnett-Hartman, Andrea, Casey, Graham, Castellví-Bel, Sergi, Chan, Andrew T., Chang-Claude, Jenny, Cross, Amanda J., de la Chapelle, Albert, Figueiredo, Jane C., Gallinger, Steven J., Gapstur, Susan M., Giles, Graham G., Gruber, Stephen B., Gsur, Andrea, Hampe, Jochen, Hampel, Heather, Harrison, Tabitha A., Hoffmeister, Michael, Hsu, Li, Huang, Wen-Yi, Huyghe, Jeroen R., Jenkins, Mark A., Joshu, Corinne E., Keku, Temitope O., Kühn, Tilman, Kweon, Sun-Seog, Le Marchand, Loic, Li, Christopher I., Li, Li, Lindblom, Annika, Martín, Vicente, May, Anne M., Milne, Roger L., Moreno, Victor, Newcomb, Polly A., Offit, Kenneth, Ogino, Shuji, Phipps, Amanda I., Platz, Elizabeth A., Potter, John D., Qu, Conghui, Quirós, J. Ramón, Rennert, Gad, Riboli, Elio, Sakoda, Lori C., Schafmayer, Clemens, Schoen, Robert E., Slattery, Martha L., Tangen, Catherine M., Tsilidis, Kostas K., Ulrich, Cornelia M., van Duijnhoven, Fränzel J. B., van Guelpen, Bethany, Visvanathan, Kala, Vodicka, Pavel, Vodickova, Ludmila, Wang, Hansong, White, Emily, Wolk, Alicja, Woods, Michael O., Wu, Anna H., Campbell, Peter T., Zheng, Wei, Peters, Ulrike, Vincent, Emma E., and Gunter, Marc J.

Published
2020
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39. Evaluating causal associations of chronotype with pregnancy and perinatal outcomes and its interactions with insomnia and sleep duration: a Mendelian randomization study

Author

Yang, Qian, primary, Magnus, Maria C, additional, Kilpi, Fanny, additional, Santorelli, Gillian, additional, Goncalves Soares, Ana Luiza, additional, West, Jane, additional, Magnus, Per, additional, Haberg, Siri E, additional, Tilling, Kate, additional, Lawlor, Deborah A, additional, Borges, Maria Carolina, additional, and Sanderson, Eleanor, additional

Published
2023
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40. A systematic literature review of methodological approaches, challenges, and opportunities in the application of Mendelian randomisation to lifecourse epidemiology.

Author

Power, Grace Marion, primary, Sanderson, Eleanor, additional, Pagoni, Panagiota, additional, Fraser, Abigail, additional, Morris, Tim T, additional, Prince, Claire L, additional, Frayling, Timothy, additional, Heron, Jon, additional, Richardson, Tom G, additional, Richmond, Rebecca, additional, Tyrrell, Jess, additional, Davey Smith, George, additional, Howe, Laura D, additional, and Tilling, Kate, additional

Published
2023
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43. Evaluating causal associations of chronotype with pregnancy and perinatal outcomes and its interactions with insomnia and sleep duration: a Mendelian randomization study

Author

Yang, Qian, Magnus, Maria C, Kilpi, Fanny, Santorelli, Gillian, Soares, Ana Goncalves, West, Jane, Magnus, Per, Håberg, Siri E., Tilling, Kate, Lawlor, Deborah A, Borges, M Carolina, and Sanderson, Eleanor

Subjects
Article
Abstract

IMPORTANCE: Observational studies suggest that chronotype is associated with pregnancy and perinatal outcomes. Whether these associations are causal is unclear. OBJECTIVE: To explore associations of a lifetime genetic predisposition to an evening preference chronotype with pregnancy and perinatal outcomes, and explore differences in associations of insomnia and sleep duration with those outcomes between chronotype. DESIGN, SETTING, AND PARTICIPANTS: We conducted two-sample Mendelian randomization (MR) using 105 genetic variants reported in a genome-wide association study (N=248 100) to instrument for lifelong predisposition to evening-versus morning-preference chronotypes. We generated variant-outcome associations in European ancestry women from UK Biobank (UKB, N=176 897), Avon Longitudinal Study of Parents and Children (ALSPAC, N=6826), Born in Bradford (BiB, N=2940) and Norwegian Mother, Father and Child Cohort Study (MoBa, with linked data from the Medical Birth Registry of Norway (MBRN), N=57 430), and extracted equivalent associations from FinnGen (N=190 879). We used inverse variance weighted (IVW) as main analysis, with weighted median and MR-Egger as sensitivity analyses. We also conducted IVW analyses of insomnia and sleep duration on the outcomes stratified by genetically predicted chronotype. EXPOSURES: Self-reported and genetically predicted chronotype, insomnia and sleep duration. MAIN OUTCOMES AND MEASURES: Stillbirth, miscarriage, preterm birth, gestational diabetes, hypertensive disorders of pregnancy, perinatal depression, low birthweight and macrosomia. RESULTS: In IVW and sensitivity analyses we did not find robust evidence of effects of chronotype on the outcomes. Insomnia was associated with a higher risk of preterm birth among evening preference women (odds ratio 1.61, 95% confidence interval: 1.17, 2.21), but not among morning preference women (odds ratio 0.87, 95% confidence interval: 0.64, 1.18), with an interaction P-value=0.01. There was no evidence of interactions between insomnia and chronotype on other outcomes, or between sleep duration and chronotype on any outcomes. CONCLUSIONS AND RELEVANCE: This study raises the possibility of a higher risk of preterm birth among women with insomnia who also have an evening preference chronotype. Our findings warrant replications due to imprecision of the estimates. KEY POINTS: QUESTION: Does an evening preference chronotype adversely affect pregnancy and perinatal outcomes? Is there an interaction between chronotype and either insomnia or sleep duration in relation to those outcomes? FINDINGS: There was no evidence that evening preference was associated with pregnancy or perinatal outcomes. Women with a genetically predicted insomnia had a higher risk of preterm birth, if they also had a genetically predicted preference for evening chronotype. MEANING: The suggestive interaction between insomnia and evening preference on preterm birth, if replicated, supports targeting insomnia prevention in women of reproductive age with an evening chronotype.

Published
2023

48. Intergenerational effects of parental educational attainment on parenting and childhood educational outcomes: Evidence from MoBa using within-family Mendelian randomization

Author

Havdahl, Alexandra, primary, Hughes, Amanda, additional, Sanderson, Eleanor, additional, Ask, Helga, additional, Cheesman, Rosa, additional, Reichborn-Kjennerud, Ted, additional, Andreassen, Ole, additional, Corfield, Elizabeth, additional, Hannigan, Laurie, additional, Magnus, Per, additional, Njolstad, Pal R, additional, Stoltenberg,, Camilla, additional, Ask Torvik, Fartein, additional, Brandlistuen, Ragnhild, additional, Davey Smith, George, additional, Ystrom, Eivind, additional, and Davies, Neil M, additional

Published
2023
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