Statistical disclosure control for numeric microdata via sequential joint probability preserving data shuffling

Traditional perturbative statistical disclosure control (SDC) approaches such as microaggregation, noise addition, rank swapping, etc, perturb the data in an ``ad-hoc" way in the sense that while they manage to preserve some particular aspects of the data, they end up modifying others. Synthetic data approaches based on the fully conditional specification data synthesis paradigm, on the other hand, aim to generate new datasets that follow the same joint probability distribution as the original data. These synthetic data approaches, however, rely either on parametric statistical models, or non-parametric machine learning models, which need to fit well the original data in order to generate credible and useful synthetic data. Another important drawback is that they tend to perform better when the variables are synthesized in the correct causal order (i.e., in the same order as the true data generating process), which is often unknown in practice. To circumvent these issues, we propose a fully non-parametric and model free perturbative SDC approach that approximates the joint distribution of the original data via sequential applications of restricted permutations to the numerical microdata (where the restricted permutations are guided by the joint distribution of a discretized version of the data). Empirical comparisons against popular SDC approaches, using both real and simulated datasets, suggest that the proposed approach is competitive in terms of the trade-off between confidentiality and data utility.Comment: 25 page, 12 figure

Causal graphical models in systems genetics: A unified framework for joint inference of causal network and genetic architecture for correlated phenotypes

Causal inference approaches in systems genetics exploit quantitative trait loci (QTL) genotypes to infer causal relationships among phenotypes. The genetic architecture of each phenotype may be complex, and poorly estimated genetic architectures may compromise the inference of causal relationships among phenotypes. Existing methods assume QTLs are known or inferred without regard to the phenotype network structure. In this paper we develop a QTL-driven phenotype network method (QTLnet) to jointly infer a causal phenotype network and associated genetic architecture for sets of correlated phenotypes. Randomization of alleles during meiosis and the unidirectional influence of genotype on phenotype allow the inference of QTLs causal to phenotypes. Causal relationships among phenotypes can be inferred using these QTL nodes, enabling us to distinguish among phenotype networks that would otherwise be distribution equivalent. We jointly model phenotypes and QTLs using homogeneous conditional Gaussian regression models, and we derive a graphical criterion for distribution equivalence. We validate the QTLnet approach in a simulation study. Finally, we illustrate with simulated data and a real example how QTLnet can be used to infer both direct and indirect effects of QTLs and phenotypes that co-map to a genomic region.Comment: Published in at http://dx.doi.org/10.1214/09-AOAS288 the Annals of Applied Statistics (http://www.imstat.org/aoas/) by the Institute of Mathematical Statistics (http://www.imstat.org