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2015 ; 71
(1
): 1-14
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Causal mediation analysis with multiple mediators
#MMPMID25351114
Daniel RM
; De Stavola BL
; Cousens SN
; Vansteelandt S
Biometrics
2015[Mar]; 71
(1
): 1-14
PMID25351114
show ga
In diverse fields of empirical research-including many in the biological
sciences-attempts are made to decompose the effect of an exposure on an outcome
into its effects via a number of different pathways. For example, we may wish to
separate the effect of heavy alcohol consumption on systolic blood pressure (SBP)
into effects via body mass index (BMI), via gamma-glutamyl transpeptidase (GGT),
and via other pathways. Much progress has been made, mainly due to contributions
from the field of causal inference, in understanding the precise nature of
statistical estimands that capture such intuitive effects, the assumptions under
which they can be identified, and statistical methods for doing so. These
contributions have focused almost entirely on settings with a single mediator, or
a set of mediators considered en bloc; in many applications, however, researchers
attempt a much more ambitious decomposition into numerous path-specific effects
through many mediators. In this article, we give counterfactual definitions of
such path-specific estimands in settings with multiple mediators, when earlier
mediators may affect later ones, showing that there are many ways in which
decomposition can be done. We discuss the strong assumptions under which the
effects are identified, suggesting a sensitivity analysis approach when a
particular subset of the assumptions cannot be justified. These ideas are
illustrated using data on alcohol consumption, SBP, BMI, and GGT from the Izhevsk
Family Study. We aim to bridge the gap from "single mediator theory" to "multiple
mediator practice," highlighting the ambitious nature of this endeavor and giving
practical suggestions on how to proceed.