scholarly journals Multi-Cause Effect Estimation with Disentangled Confounder Representation

Author(s):  
Jing Ma ◽  
Ruocheng Guo ◽  
Aidong Zhang ◽  
Jundong Li

One fundamental problem in causality learning is to estimate the causal effects of one or multiple treatments (e.g., medicines in the prescription) on an important outcome (e.g., cure of a disease). One major challenge of causal effect estimation is the existence of unobserved confounders -- the unobserved variables that affect both the treatments and the outcome. Recent studies have shown that by modeling how instances are assigned with different treatments together, the patterns of unobserved confounders can be captured through their learned latent representations. However, the interpretability of the representations in these works is limited. In this paper, we focus on the multi-cause effect estimation problem from a new perspective by learning disentangled representations of confounders. The disentangled representations not only facilitate the treatment effect estimation but also strengthen the understanding of causality learning process. Experimental results on both synthetic and real-world datasets show the superiority of our proposed framework from different aspects.

Author(s):  
Negar Hassanpour

To identify the appropriate action to take, an intelligent agent must infer the causal effects of every possible action choices. A prominent example is precision medicine that attempts to identify which medical procedure will benefit each individual patient the most. This requires answering counterfactual questions such as: ""Would this patient have lived longer, had she received an alternative treatment?"". In my PhD, I attempt to explore ways to address the challenges associated with causal effect estimation; with a focus on devising methods that enhance performance according to the individual-based measures (as opposed to population-based measures).


2021 ◽  
Vol 12 ◽  
Author(s):  
Yixin Gao ◽  
Jinhui Zhang ◽  
Huashuo Zhao ◽  
Fengjun Guan ◽  
Ping Zeng

BackgroundIn two-sample Mendelian randomization (MR) studies, sex instrumental heterogeneity is an important problem needed to address carefully, which however is often overlooked and may lead to misleading causal inference.MethodsWe first employed cross-trait linkage disequilibrium score regression (LDSC), Pearson’s correlation analysis, and the Cochran’s Q test to examine sex genetic similarity and heterogeneity in instrumental variables (IVs) of exposures. Simulation was further performed to explore the influence of sex instrumental heterogeneity on causal effect estimation in sex-specific two-sample MR analyses. Furthermore, we chose breast/prostate cancer as outcome and four anthropometric traits as exposures as an illustrative example to illustrate the importance of taking sex heterogeneity of instruments into account in MR studies.ResultsThe simulation definitively demonstrated that sex-combined IVs can lead to biased causal effect estimates in sex-specific two-sample MR studies. In our real applications, both LDSC and Pearson’s correlation analyses showed high genetic correlation between sex-combined and sex-specific IVs of the four anthropometric traits, while nearly all the correlation coefficients were larger than zero but less than one. The Cochran’s Q test also displayed sex heterogeneity for some instruments. When applying sex-specific instruments, significant discrepancies in the magnitude of estimated causal effects were detected for body mass index (BMI) on breast cancer (P = 1.63E-6), for hip circumference (HIP) on breast cancer (P = 1.25E-20), and for waist circumference (WC) on prostate cancer (P = 0.007) compared with those generated with sex-combined instruments.ConclusionOur study reveals that the sex instrumental heterogeneity has non-ignorable impact on sex-specific two-sample MR studies and the causal effects of anthropometric traits on breast/prostate cancer would be biased if sex-combined IVs are incorrectly employed.


Author(s):  
Liuyi Yao ◽  
Sheng Li ◽  
Yaliang Li ◽  
Hongfei Xue ◽  
Jing Gao ◽  
...  

Estimating the treatment effect benefits decision making in various domains as it can provide the potential outcomes of different choices. Existing work mainly focuses on covariates with numerical values, while how to handle covariates with textual information for treatment effect estimation is still an open question. One major challenge is how to filter out the nearly instrumental variables which are the variables more predictive to the treatment than the outcome. Conditioning on those variables to estimate the treatment effect would amplify the estimation bias. To address this challenge, we propose a conditional treatment-adversarial learning based matching method (CTAM). CTAM incorporates the treatment-adversarial learning to filter out the information related to nearly instrumental variables when learning the representations, and then it performs matching among the learned representations to estimate the treatment effects. The conditional treatment-adversarial learning helps reduce the bias of treatment effect estimation, which is demonstrated by our experimental results on both semi-synthetic and real-world datasets.


Author(s):  
Hao Wang ◽  
Huawei Shen ◽  
Wentao Ouyang ◽  
Xueqi Cheng

Point-of-interest (POI) recommendation, i.e., recommending unvisited POIs for users, is a fundamental problem for location-based social networks. POI recommendation distinguishes itself from traditional item recommendation, e.g., movie recommendation, via geographical influence among POIs. Existing methods model the geographical influence between two POIs as the probability or propensity that the two POIs are co-visited by the same user given their physical distance. These methods assume that geographical influence between POIs is determined by their physical distance, failing to capture the asymmetry of geographical influence and the high variation of geographical influence across POIs. In this paper, we exploit POI-specific geographical influence to improve POI recommendation. We model the geographical influence between two POIs using three factors: the geo-influence of POI, the geo-susceptibility of POI, and their physical distance. Geo-influence captures POI?s capacity at exerting geographical influence to other POIs, and geo-susceptibility reflects POI?s propensity of being geographically influenced by other POIs. Experimental results on two real-world datasets demonstrate that POI-specific geographical influence significantly improves the performance of POI recommendation.


Author(s):  
Zhao Wang ◽  
Aron Culotta

Studies across many disciplines have shown that lexical choice can affect audience perception. For example, how users describe themselves in a social media profile can affect their perceived socio-economic status. However, we lack general methods for estimating the causal effect of lexical choice on the perception of a specific sentence. While randomized controlled trials may provide good estimates, they do not scale to the potentially millions of comparisons necessary to consider all lexical choices. Instead, in this paper, we first offer two classes of methods to estimate the effect on perception of changing one word to another in a given sentence. The first class of algorithms builds upon quasi-experimental designs to estimate individual treatment effects from observational data. The second class treats treatment effect estimation as a classification problem. We conduct experiments with three data sources (Yelp, Twitter, and Airbnb), finding that the algorithmic estimates align well with those produced by randomized-control trials. Additionally, we find that it is possible to transfer treatment effect classifiers across domains and still maintain high accuracy.


2021 ◽  
pp. 1-21
Author(s):  
Keith A. Markus

Abstract Rubin and Pearl offered approaches to causal effect estimation and Lewis and Pearl offered theories of counterfactual conditionals. Arguments offered by Pearl and his collaborators support a weak form of equivalence such that notation from the rival theory can be re-purposed to express Pearl’s theory in a way that is equivalent to Pearl’s theory expressed in its native notation. Nonetheless, the many fundamental differences between the theories rule out any stronger form of equivalence. A renewed emphasis on comparative research can help to guide applications, further develop each theory, and better understand their relative strengths and weaknesses.


Author(s):  
Jing Wang ◽  
Xin Geng

Although Label Distribution Learning (LDL) has found wide applications in varieties of classification problems, it may face the challenge of objective mismatch -- LDL neglects the optimal label for the sake of learning the whole label distribution, which leads to performance deterioration. To improve classification performance and solve the objective mismatch, we propose a new LDL algorithm called LDL-HR. LDL-HR provides a new perspective of label distribution, \textit{i.e.}, a combination of the \textbf{highest label} and the \textbf{rest label description degrees}. It works as follows. First, we learn the highest label by fitting the degenerated label distribution and large margin. Second, we learn the rest label description degrees to exploit generalization. Theoretical analysis shows the generalization of LDL-HR. Besides, the experimental results on 18 real-world datasets validate the statistical superiority of our method.


2021 ◽  
Vol 9 (1) ◽  
pp. 211-218
Author(s):  
Sergio Garrido ◽  
Stanislav Borysov ◽  
Jeppe Rich ◽  
Francisco Pereira

Abstract The estimation of causal effects is fundamental in situations where the underlying system will be subject to active interventions. Part of building a causal inference engine is defining how variables relate to each other, that is, defining the functional relationship between variables entailed by the graph conditional dependencies. In this article, we deviate from the common assumption of linear relationships in causal models by making use of neural autoregressive density estimators and use them to estimate causal effects within Pearl’s do-calculus framework. Using synthetic data, we show that the approach can retrieve causal effects from non-linear systems without explicitly modeling the interactions between the variables and include confidence bands using the non-parametric bootstrap. We also explore scenarios that deviate from the ideal causal effect estimation setting such as poor data support or unobserved confounders.


2020 ◽  
Vol 34 (04) ◽  
pp. 5395-5402
Author(s):  
Johan Pensar ◽  
Topi Talvitie ◽  
Antti Hyttinen ◽  
Mikko Koivisto

We present a novel Bayesian method for the challenging task of estimating causal effects from passively observed data when the underlying causal DAG structure is unknown. To rigorously capture the inherent uncertainty associated with the estimate, our method builds a Bayesian posterior distribution of the linear causal effect, by integrating Bayesian linear regression and averaging over DAGs. For computing the exact posterior for all cause-effect variable pairs, we give an algorithm that runs in time O(3d d) for d variables, being feasible up to 20 variables. We also give a variant that computes the posterior probabilities of all pairwise ancestor relations within the same time complexity, significantly improving the fastest previous algorithm. In simulations, our Bayesian method outperforms previous methods in estimation accuracy, especially for small sample sizes. We further show that our method for effect estimation is well-adapted for detecting strong causal effects markedly deviating from zero, while our variant for computing posteriors of ancestor relations is the method of choice for detecting the mere existence of a causal relation. Finally, we apply our method on observational flow cytometry data, detecting several causal relations that concur with previous findings from experimental data.


2020 ◽  
Vol 20 (1) ◽  
Author(s):  
E. Caitlin Lloyd ◽  
Hannah M. Sallis ◽  
Bas Verplanken ◽  
Anne M. Haase ◽  
Marcus R. Munafò

Abstract Background Evidence from observational studies suggests an association between anxiety disorders and anorexia nervosa (AN), but causal inference is complicated by the potential for confounding in these studies. We triangulate evidence across a longitudinal study and a Mendelian randomization (MR) study, to evaluate whether there is support for anxiety disorder phenotypes exerting a causal effect on AN risk. Methods Study One assessed longitudinal associations of childhood worry and anxiety disorders with lifetime AN in the Avon Longitudinal Study of Parents and Children cohort. Study Two used two-sample MR to evaluate: causal effects of worry, and genetic liability to anxiety disorders, on AN risk; causal effects of genetic liability to AN on anxiety outcomes; and the causal influence of worry on anxiety disorder development. The independence of effects of worry, relative to depressed affect, on AN and anxiety disorder outcomes, was explored using multivariable MR. Analyses were completed using summary statistics from recent genome-wide association studies. Results Study One did not support an association between worry and subsequent AN, but there was strong evidence for anxiety disorders predicting increased risk of AN. Study Two outcomes supported worry causally increasing AN risk, but did not support a causal effect of anxiety disorders on AN development, or of AN on anxiety disorders/worry. Findings also indicated that worry causally influences anxiety disorder development. Multivariable analysis estimates suggested the influence of worry on both AN and anxiety disorders was independent of depressed affect. Conclusions Overall our results provide mixed evidence regarding the causal role of anxiety exposures in AN aetiology. The inconsistency between outcomes of Studies One and Two may be explained by limitations surrounding worry assessment in Study One, confounding of the anxiety disorder and AN association in observational research, and low power in MR analyses probing causal effects of genetic liability to anxiety disorders. The evidence for worry acting as a causal risk factor for anxiety disorders and AN supports targeting worry for prevention of both outcomes. Further research should clarify how a tendency to worry translates into AN risk, and whether anxiety disorder pathology exerts any causal effect on AN.


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