Bias formulas for sensitivity analysis for direct and indirect effects

A key question in many studies is how to divide the total effect of an exposure into a component that acts directly on the outcome and a component that acts indirectly, ie, through some intermediate. For example, one might be interested in the extent to which the effect of diet on blood pressure is...

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Vydáno v:Epidemiology (Cambridge, Mass.) Ročník 21; číslo 4; s. 540
Hlavní autor: VanderWeele, Tyler J
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 01.07.2010
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ISSN:1531-5487, 1531-5487
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Abstract A key question in many studies is how to divide the total effect of an exposure into a component that acts directly on the outcome and a component that acts indirectly, ie, through some intermediate. For example, one might be interested in the extent to which the effect of diet on blood pressure is mediated through sodium intake and the extent to which it operates through other pathways. In the context of such mediation analysis, even if the effect of the exposure on the outcome is unconfounded, estimates of direct and indirect effects will be biased if control is not made for confounders of the mediator-outcome relationship. Often data are not collected on such mediator-outcome confounding variables; the results in this paper allow researchers to assess the sensitivity of their estimates of direct and indirect effects to the biases from such confounding. Specifically, the paper provides formulas for the bias in estimates of direct and indirect effects due to confounding of the exposure-mediator relationship and of the mediator-outcome relationship. Under some simplifying assumptions, the formulas are particularly easy to use in sensitivity analysis. The bias formulas are illustrated by examples in the literature concerning direct and indirect effects in which mediator-outcome confounding may be present.
AbstractList A key question in many studies is how to divide the total effect of an exposure into a component that acts directly on the outcome and a component that acts indirectly, ie, through some intermediate. For example, one might be interested in the extent to which the effect of diet on blood pressure is mediated through sodium intake and the extent to which it operates through other pathways. In the context of such mediation analysis, even if the effect of the exposure on the outcome is unconfounded, estimates of direct and indirect effects will be biased if control is not made for confounders of the mediator-outcome relationship. Often data are not collected on such mediator-outcome confounding variables; the results in this paper allow researchers to assess the sensitivity of their estimates of direct and indirect effects to the biases from such confounding. Specifically, the paper provides formulas for the bias in estimates of direct and indirect effects due to confounding of the exposure-mediator relationship and of the mediator-outcome relationship. Under some simplifying assumptions, the formulas are particularly easy to use in sensitivity analysis. The bias formulas are illustrated by examples in the literature concerning direct and indirect effects in which mediator-outcome confounding may be present.
A key question in many studies is how to divide the total effect of an exposure into a component that acts directly on the outcome and a component that acts indirectly, ie, through some intermediate. For example, one might be interested in the extent to which the effect of diet on blood pressure is mediated through sodium intake and the extent to which it operates through other pathways. In the context of such mediation analysis, even if the effect of the exposure on the outcome is unconfounded, estimates of direct and indirect effects will be biased if control is not made for confounders of the mediator-outcome relationship. Often data are not collected on such mediator-outcome confounding variables; the results in this paper allow researchers to assess the sensitivity of their estimates of direct and indirect effects to the biases from such confounding. Specifically, the paper provides formulas for the bias in estimates of direct and indirect effects due to confounding of the exposure-mediator relationship and of the mediator-outcome relationship. Under some simplifying assumptions, the formulas are particularly easy to use in sensitivity analysis. The bias formulas are illustrated by examples in the literature concerning direct and indirect effects in which mediator-outcome confounding may be present.A key question in many studies is how to divide the total effect of an exposure into a component that acts directly on the outcome and a component that acts indirectly, ie, through some intermediate. For example, one might be interested in the extent to which the effect of diet on blood pressure is mediated through sodium intake and the extent to which it operates through other pathways. In the context of such mediation analysis, even if the effect of the exposure on the outcome is unconfounded, estimates of direct and indirect effects will be biased if control is not made for confounders of the mediator-outcome relationship. Often data are not collected on such mediator-outcome confounding variables; the results in this paper allow researchers to assess the sensitivity of their estimates of direct and indirect effects to the biases from such confounding. Specifically, the paper provides formulas for the bias in estimates of direct and indirect effects due to confounding of the exposure-mediator relationship and of the mediator-outcome relationship. Under some simplifying assumptions, the formulas are particularly easy to use in sensitivity analysis. The bias formulas are illustrated by examples in the literature concerning direct and indirect effects in which mediator-outcome confounding may be present.
Author VanderWeele, Tyler J
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  givenname: Tyler J
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  email: tvanderw@hsph.harvard.edu
  organization: Department of Epidemiology, Harvard School of Public Health, Harvard University, Boston, MA 02115, USA. tvanderw@hsph.harvard.edu
BackLink https://www.ncbi.nlm.nih.gov/pubmed/20479643$$D View this record in MEDLINE/PubMed
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References_xml – reference: 17825022 - Biometrics. 2007 Sep;63(3):926-34
– reference: 22462121 - Int J Biostat. 2008;4(1):Article 23
– reference: 11071492 - Neurology. 2000 Oct 24;55(8):1144-50
– reference: 19330454 - Eur J Epidemiol. 2009;24(5):217-24
– reference: 20954780 - Psychol Methods. 2010 Dec;15(4):309-34
– reference: 15507130 - Epidemiol Perspect Innov. 2004 Oct 08;1(1):4
– reference: 1576220 - Epidemiology. 1992 Mar;3(2):143-55
– reference: 11821313 - Int J Epidemiol. 2001 Dec;30(6):1233-41
– reference: 15308962 - Epidemiology. 2004 Sep;15(5):615-25
– reference: 19689488 - Paediatr Perinat Epidemiol. 2009 Sep;23(5):394-402
– reference: - Epidemiology. 2011 Jan;22(1):134
– reference: 18482060 - Biometrics. 2008 Jun;64(2):645-9
– reference: 19829187 - Epidemiology. 2009 Nov;20(6):880-3
– reference: 21052008 - Epidemiology. 2011 Jan;22(1):42-52
– reference: 20502339 - Epidemiology. 2011 Nov;22(6):753-64
– reference: 17702973 - Am J Epidemiol. 2007 Nov 1;166(9):1096-104
– reference: 19234398 - Epidemiology. 2009 Jan;20(1):18-26
– reference: 16617276 - Epidemiology. 2006 May;17(3):276-84
– reference: 19806060 - Epidemiology. 2009 Nov;20(6):851-60
– reference: 19184975 - Stat Med. 2009 Mar 30;28(7):1108-30
– reference: 18079133 - Am J Epidemiol. 2008 Feb 15;167(4):429-37
– reference: 3806354 - J Pers Soc Psychol. 1986 Dec;51(6):1173-82
– reference: 16717205 - Neurology. 2006 May 23;66(10):1476-84
– reference: 19261660 - Int J Epidemiol. 2009 Jun;38(3):838-45
– reference: 18759834 - Biometrics. 2009 Jun;65(2):514-20
– reference: 11914315 - Int J Epidemiol. 2002 Feb;31(1):166-7
– reference: 16931543 - Am J Epidemiol. 2006 Dec 1;164(11):1115-20
– reference: 25473138 - Sociol Methods Res. 2010 May 1;38(4):515-544
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Snippet A key question in many studies is how to divide the total effect of an exposure into a component that acts directly on the outcome and a component that acts...
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SubjectTerms Bias
Brain - anatomy & histology
Brain - drug effects
Cognition Disorders - chemically induced
Humans
Lead Poisoning - complications
Models, Statistical
Organ Size - drug effects
Regression Analysis
Risk Factors
Sensitivity and Specificity
Statistics as Topic
Title Bias formulas for sensitivity analysis for direct and indirect effects
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