Bias from self selection and loss to follow-up in prospective cohort studies
Self-selection into prospective cohort studies and loss to follow-up can cause biased exposure-outcome association estimates. Previous investigations illustrated that such biases can be small in large prospective cohort studies. The structural approach to selection bias shows that general statements...
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Published in | European journal of epidemiology Vol. 34; no. 10; pp. 927 - 938 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Dordrecht
Springer Science + Business Media
01.10.2019
Springer Netherlands Springer Nature B.V |
Subjects | |
Online Access | Get full text |
ISSN | 0393-2990 1573-7284 1573-7284 |
DOI | 10.1007/s10654-019-00550-1 |
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Abstract | Self-selection into prospective cohort studies and loss to follow-up can cause biased exposure-outcome association estimates. Previous investigations illustrated that such biases can be small in large prospective cohort studies. The structural approach to selection bias shows that general statements about bias are not possible for studies that investigate multiple exposures and outcomes, and that inverse probability of participation weighting (IPPW) but not adjustment for participation predictors generally reduces bias from self-selection and loss to follow-up. We propose to substantiate assumptions in structural models of selection bias through calculation of genetic correlations coefficients between participation predictors, outcome, and exposure, and to estimate a lower bound for bias due to self-selection and loss to follow-up by comparing effect estimates from IPP weighted and unweighted analyses. This study used data from the Norwegian Mother and Child Cohort Study and the Medical Birth Registry of Norway. Using the example of risk factors for ADHD, we find that genetic correlations between participation predictors, exposures, and outcome suggest the presence of bias. The comparison of exposure-outcome associations from regressions with and without IPPW revealed meaningful deviations. Assessment of selection bias for entire multi-exposure multi-outcome cohort studies is not possible. Instead, it has to be assessed and controlled on a case-by-case basis. |
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AbstractList | Self-selection into prospective cohort studies and loss to follow-up can cause biased exposure-outcome association estimates. Previous investigations illustrated that such biases can be small in large prospective cohort studies. The structural approach to selection bias shows that general statements about bias are not possible for studies that investigate multiple exposures and outcomes, and that inverse probability of participation weighting (IPPW) but not adjustment for participation predictors generally reduces bias from self-selection and loss to follow-up. We propose to substantiate assumptions in structural models of selection bias through calculation of genetic correlations coefficients between participation predictors, outcome, and exposure, and to estimate a lower bound for bias due to self-selection and loss to follow-up by comparing effect estimates from IPP weighted and unweighted analyses. This study used data from the Norwegian Mother and Child Cohort Study and the Medical Birth Registry of Norway. Using the example of risk factors for ADHD, we find that genetic correlations between participation predictors, exposures, and outcome suggest the presence of bias. The comparison of exposure-outcome associations from regressions with and without IPPW revealed meaningful deviations. Assessment of selection bias for entire multi-exposure multi-outcome cohort studies is not possible. Instead, it has to be assessed and controlled on a case-by-case basis. Self-selection into prospective cohort studies and loss to follow-up can cause biased exposure-outcome association estimates. Previous investigations illustrated that such biases can be small in large prospective cohort studies. The structural approach to selection bias shows that general statements about bias are not possible for studies that investigate multiple exposures and outcomes, and that inverse probability of participation weighting (IPPW) but not adjustment for participation predictors generally reduces bias from self-selection and loss to follow-up. We propose to substantiate assumptions in structural models of selection bias through calculation of genetic correlations coefficients between participation predictors, outcome, and exposure, and to estimate a lower bound for bias due to self-selection and loss to follow-up by comparing effect estimates from IPP weighted and unweighted analyses. This study used data from the Norwegian Mother and Child Cohort Study and the Medical Birth Registry of Norway. Using the example of risk factors for ADHD, we find that genetic correlations between participation predictors, exposures, and outcome suggest the presence of bias. The comparison of exposure-outcome associations from regressions with and without IPPW revealed meaningful deviations. Assessment of selection bias for entire multi-exposure multi-outcome cohort studies is not possible. Instead, it has to be assessed and controlled on a case-by-case basis.Self-selection into prospective cohort studies and loss to follow-up can cause biased exposure-outcome association estimates. Previous investigations illustrated that such biases can be small in large prospective cohort studies. The structural approach to selection bias shows that general statements about bias are not possible for studies that investigate multiple exposures and outcomes, and that inverse probability of participation weighting (IPPW) but not adjustment for participation predictors generally reduces bias from self-selection and loss to follow-up. We propose to substantiate assumptions in structural models of selection bias through calculation of genetic correlations coefficients between participation predictors, outcome, and exposure, and to estimate a lower bound for bias due to self-selection and loss to follow-up by comparing effect estimates from IPP weighted and unweighted analyses. This study used data from the Norwegian Mother and Child Cohort Study and the Medical Birth Registry of Norway. Using the example of risk factors for ADHD, we find that genetic correlations between participation predictors, exposures, and outcome suggest the presence of bias. The comparison of exposure-outcome associations from regressions with and without IPPW revealed meaningful deviations. Assessment of selection bias for entire multi-exposure multi-outcome cohort studies is not possible. Instead, it has to be assessed and controlled on a case-by-case basis. |
Author | Magnus, Per Minor Reichborn-Kjennerud, Ted Gustavson, Kristin Nilsen, Roy Miodini Aase, Heidi Biele, Guido Czajkowski, Nikolai Olavi Stoltenberg, Camilla |
Author_xml | – sequence: 1 givenname: Guido surname: Biele fullname: Biele, Guido – sequence: 2 givenname: Kristin surname: Gustavson fullname: Gustavson, Kristin – sequence: 3 givenname: Nikolai Olavi surname: Czajkowski fullname: Czajkowski, Nikolai Olavi – sequence: 4 givenname: Roy Miodini surname: Nilsen fullname: Nilsen, Roy Miodini – sequence: 5 givenname: Ted surname: Reichborn-Kjennerud fullname: Reichborn-Kjennerud, Ted – sequence: 6 givenname: Per Minor surname: Magnus fullname: Magnus, Per Minor – sequence: 7 givenname: Camilla surname: Stoltenberg fullname: Stoltenberg, Camilla – sequence: 8 givenname: Heidi surname: Aase fullname: Aase, Heidi |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31451995$$D View this record in MEDLINE/PubMed |
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Copyright | Springer Nature B.V. 2019 European Journal of Epidemiology is a copyright of Springer, (2019). All Rights Reserved. |
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Keywords | ADHD Bayesian estimation Bias Cohort study Directed acyclic graphs Inverse probability weighting Self selection Loss to follow up |
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Title | Bias from self selection and loss to follow-up in prospective cohort studies |
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