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تسجيل مستخدم جديدMediation Analysis in Online Experiments at Booking.com: Disentangling Direct and Indirect Effects
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Online experimentation is at the core of Booking.coms customer-centric product development. While randomised controlled trials are a powerful tool for estimating the overall effects of product changes on business metrics, they often fall short in explaining the mechanism of change. This becomes problematic when decision-making depends on being able to distinguish between the direct effect of a treatment on some outcome variable and its indirect effect via a mediator variable. In this paper, we demonstrate the need for mediation analyses in online experimentation, and use simulated data to show how these methods help identify and estimate direct causal effect. Failing to take into account all confounders can lead to biased estimates, so we include sensitivity analyses to help gauge the robustness of estimates to missing causal factors.
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There is an extensive literature about online controlled experiments, both on the statistical methods available to analyze experiment results as well as on the infrastructure built by several large scale Internet companies but also on the organizatio
nal challenges of embracing online experiments to inform product development. At Booking.com we have been conducting evidenced based product development using online experiments for more than ten years. Our methods and infrastructure were designed from their inception to reflect Booking.com culture, that is, with democratization and decentralization of experimentation and decision making in mind. In this paper we explain how building a central repository of successes and failures to allow for knowledge sharing, having a generic and extensible code library which enforces a loose coupling between experimentation and business logic, monitoring closely and transparently the quality and the reliability of the data gathering pipelines to build trust in the experimentation infrastructure, and putting in place safeguards to enable anyone to have end to end ownership of their experiments have allowed such a large organization as Booking.com to truly and successfully democratize experimentation.
Causal mediation analysis aims to characterize an exposures effect on an outcome and quantify the indirect effect that acts through a given mediator or a group of mediators of interest. With the increasing availability of measurements on a large numb
er of potential mediators, like the epigenome or the microbiome, new statistical methods are needed to simultaneously accommodate high-dimensional mediators while directly target penalization of the natural indirect effect (NIE) for active mediator identification. Here, we develop two novel prior models for identification of active mediators in high-dimensional mediation analysis through penalizing NIEs in a Bayesian paradigm. Both methods specify a joint prior distribution on the exposure-mediator effect and mediator-outcome effect with either (a) a four-component Gaussian mixture prior or (b) a product threshold Gaussian prior. By jointly modeling the two parameters that contribute to the NIE, the proposed methods enable penalization on their product in a targeted way. Resultant inference can take into account the four-component composite structure underlying the NIE. We show through simulations that the proposed methods improve both selection and estimation accuracy compared to other competing methods. We applied our methods for an in-depth analysis of two ongoing epidemiologic studies: the Multi-Ethnic Study of Atherosclerosis (MESA) and the LIFECODES birth cohort. The identified active mediators in both studies reveal important biological pathways for understanding disease mechanisms.
Causal mediation analysis has historically been limited in two important ways: (i) a focus has traditionally been placed on binary treatments and static interventions, and (ii) direct and indirect effect decompositions have been pursued that are only
identifiable in the absence of intermediate confounders affected by treatment. We present a theoretical study of an (in)direct effect decomposition of the population intervention effect, defined by stochastic interventions jointly applied to the treatment and mediators. In contrast to existing proposals, our causal effects can be evaluated regardless of whether a treatment is categorical or continuous and remain well-defined even in the presence of intermediate confounders affected by treatment. Our (in)direct effects are identifiable without a restrictive assumption on cross-world counterfactual independencies, allowing for substantive conclusions drawn from them to be validated in randomized controlled trials. Beyond the novel effects introduced, we provide a careful study of nonparametric efficiency theory relevant for the construction of flexible, multiply robust estimators of our (in)direct effects, while avoiding undue restrictions induced by assuming parametric models of nuisance parameter functionals. To complement our nonparametric estimation strategy, we introduce inferential techniques for constructing confidence intervals and hypothesis tests, and discuss open source software implementing the proposed methodology.
To estimate direct and indirect effects of an exposure on an outcome from observed data strong assumptions about unconfoundedness are required. Since these assumptions cannot be tested using the observed data, a mediation analysis should always be ac
companied by a sensitivity analysis of the resulting estimates. In this article we propose a sensitivity analysis method for parametric estimation of direct and indirect effects when the exposure, mediator and outcome are all binary. The sensitivity parameters consist of the correlation between the error terms of the mediator and outcome models, the correlation between the error terms of the mediator model and the model for the exposure assignment mechanism, and the correlation between the error terms of the exposure assignment and outcome models. These correlations are incorporated into the estimation of the model parameters and identification sets are then obtained for the direct and indirect effects for a range of plausible correlation values. We take the sampling variability into account through the construction of uncertainty intervals. The proposed method is able to assess sensitivity to both mediator-outcome confounding and confounding involving the exposure. To illustrate the method we apply it to a mediation study based on data from the Swedish Stroke Register (Riksstroke).
We discuss causal mediation analyses for survival data and propose a new approach based on the additive hazards model. The emphasis is on a dynamic point of view, that is, understanding how the direct and indirect effects develop over time. Hence, im
portantly, we allow for a time varying mediator. To define direct and indirect effects in such a longitudinal survival setting we take an interventional approach (Didelez (2018)) where treatment is separated into one aspect affecting the mediator and a different aspect affecting survival. In general, this leads to a version of the non-parametric g-formula (Robins (1986)). In the present paper, we demonstrate that combining the g-formula with the additive hazards model and a sequential linear model for the mediator process results in simple and interpretable expressions for direct and indirect effects in terms of relative survival as well as cumulative hazards. Our results generalise and formalise the method of dynamic path analysis (Fosen et al. (2006), Strohmaier et al. (2015)). An application to data from a clinical trial on blood pressure medication is given.
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