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Tyler J. VanderWeele

Publications and source records attributed to Tyler J. VanderWeele.

26 records · Page 2Linked to original sources
arXiv2015

Interference and Sensitivity Analysis

Causal inference with interference is a rapidly growing area. The literature has begun to relax the "no-interference" assumption that the treatment received by one individual does not affect the outcomes of other individuals. In this paper we briefly review the literature on causal inference in the presence of interference when treatments have been randomized. We then consider settings in which causal effects in the presence of interference are not identified, either because randomization alone does not suffice for identification or because treatment is not randomized and there may be unmeasured confounders of the treatment-outcome relationship. We develop sensitivity analysis techniques for these settings. We describe several sensitivity analysis techniques for the infectiousness effect which, in a vaccine trial, captures the effect of the vaccine of one person on protecting a second person from infection even if the first is infected. We also develop two sensitivity analysis techniques for causal effects under interference in the presence of unmeasured confounding which generalize analogous techniques when interference is absent. These two techniques for unmeasured confounding are compared and contrasted.

stat.ME↗
arXiv2014

Generalized Cornfield conditions for the risk difference

A central question in causal inference with observational studies is the sensitivity of conclusions to unmeasured confounding. The classical Cornfield condition allows us to assess whether an unmeasured binary confounder can explain away the observed relative risk of the exposure on the outcome. It states that for an unmeasured confounder to explain away an observed relative risk, the association between the unmeasured confounder and the exposure, and also that between the unmeasured confounder and the outcome, must both be larger than the observed relative risk. In this paper, we extend the classical Cornfield condition in three directions. First, we consider analogous conditions for the risk difference, and allow for a categorical, not just a binary, unmeasured confounder. Second, we provide more stringent thresholds which the maximum of the above-mentioned associations must satisfy, rather than simply weaker conditions that both must satisfy. Third, we show that all previous results on Cornfield conditions hold under weaker assumptions than previously used. We illustrate their potential applications by real examples, where our new conditions give more information than the classical ones.

stat.AP↗
arXiv2014

Joint analysis of SNP and gene expression data in genetic association studies of complex diseases

Genetic association studies have been a popular approach for assessing the association between common Single Nucleotide Polymorphisms (SNPs) and complex diseases. However, other genomic data involved in the mechanism from SNPs to disease, for example, gene expressions, are usually neglected in these association studies. In this paper, we propose to exploit gene expression information to more powerfully test the association between SNPs and diseases by jointly modeling the relations among SNPs, gene expressions and diseases. We propose a variance component test for the total effect of SNPs and a gene expression on disease risk. We cast the test within the causal mediation analysis framework with the gene expression as a potential mediator. For eQTL SNPs, the use of gene expression information can enhance power to test for the total effect of a SNP-set, which is the combined direct and indirect effects of the SNPs mediated through the gene expression, on disease risk. We show that the test statistic under the null hypothesis follows a mixture of $χ^2$ distributions, which can be evaluated analytically or empirically using the resampling-based perturbation method. We construct tests for each of three disease models that are determined by SNPs only, SNPs and gene expression, or include also their interactions. As the true disease model is unknown in practice, we further propose an omnibus test to accommodate different underlying disease models. We evaluate the finite sample performance of the proposed methods using simulation studies, and show that our proposed test performs well and the omnibus test can almost reach the optimal power where the disease model is known and correctly specified. We apply our method to reanalyze the overall effect of the SNP-set and expression of the ORMDL3 gene on the risk of asthma.

stat.AP↗
arXiv2014

Vaccines, Contagion, and Social Networks

Consider the causal effect that one individual's treatment may have on another individual's outcome when the outcome is contagious, with specific application to the effect of vaccination on an infectious disease outcome. The effect of one individual's vaccination on another's outcome can be decomposed into two different causal effects, called the "infectiousness" and "contagion" effects. We present identifying assumptions and estimation or testing procedures for infectiousness and contagion effects in two different settings: (1) using data sampled from independent groups of observations, and (2) using data collected from a single interdependent social network. The methods that we propose for social network data require fitting generalized linear models (GLMs). GLMs and other statistical models that require independence across subjects have been used widely to estimate causal effects in social network data, but, because the subjects in networks are presumably not independent, the use of such models is generally invalid, resulting in inference that is expected to be anticonservative. We introduce a way to ensure that GLM residuals are uncorrelated across subjects despite the fact that outcomes are non-independent. This simultaneously demonstrates the possibility of using GLMs and related statistical models for network data and highlights their limitations.

stat.ME↗
arXiv2013

On the definition of a confounder

The causal inference literature has provided a clear formal definition of confounding expressed in terms of counterfactual independence. The literature has not, however, come to any consensus on a formal definition of a confounder, as it has given priority to the concept of confounding over that of a confounder. We consider a number of candidate definitions arising from various more informal statements made in the literature. We consider the properties satisfied by each candidate definition, principally focusing on (i) whether under the candidate definition control for all "confounders" suffices to control for "confounding" and (ii) whether each confounder in some context helps eliminate or reduce confounding bias. Several of the candidate definitions do not have these two properties. Only one candidate definition of those considered satisfies both properties. We propose that a "confounder" be defined as a pre-exposure covariate C for which there exists a set of other covariates X such that effect of the exposure on the outcome is unconfounded conditional on (X,C) but such that for no proper subset of (X,C) is the effect of the exposure on the outcome unconfounded given the subset. We also provide a conditional analogue of the above definition; and we propose a variable that helps reduce bias but not eliminate bias be referred to as a "surrogate confounder." These definitions are closely related to those given by Robins and Morgenstern [Comput. Math. Appl. 14 (1987) 869-916]. The implications that hold among the various candidate definitions are discussed.

stat.ME↗
arXiv2013

General theory for interactions in sufficient cause models with dichotomous exposures

The sufficient-component cause framework assumes the existence of sets of sufficient causes that bring about an event. For a binary outcome and an arbitrary number of binary causes any set of potential outcomes can be replicated by positing a set of sufficient causes; typically this representation is not unique. A sufficient cause interaction is said to be present if within all representations there exists a sufficient cause in which two or more particular causes are all present. A singular interaction is said to be present if for some subset of individuals there is a unique minimal sufficient cause. Empirical and counterfactual conditions are given for sufficient cause interactions and singular interactions between an arbitrary number of causes. Conditions are given for cases in which none, some or all of a given set of causes affect the outcome monotonically. The relations between these results, interactions in linear statistical models and Pearl's probability of causation are discussed.

math.ST↗
arXiv2009

Minimal sufficient causation and directed acyclic graphs

Notions of minimal sufficient causation are incorporated within the directed acyclic graph causal framework. Doing so allows for the graphical representation of sufficient causes and minimal sufficient causes on causal directed acyclic graphs while maintaining all of the properties of causal directed acyclic graphs. This in turn provides a clear theoretical link between two major conceptualizations of causality: one counterfactual-based and the other based on a more mechanistic understanding of causation. The theory developed can be used to draw conclusions about the sign of the conditional covariances among variables.

math.ST↗