Dataset Information

Conceptual framework for investigating causal effects from observational data in livestock.

ABSTRACT: Understanding causal mechanisms among variables is critical to efficient management of complex biological systems such as animal agriculture production. The increasing availability of data from commercial livestock operations offers unique opportunities for attaining causal insight, despite the inherently observational nature of these data. Causal claims based on observational data are substantiated by recent theoretical and methodological developments in the rapidly evolving field of causal inference. Thus, the objectives of this review are as follows: 1) to introduce a unifying conceptual framework for investigating causal effects from observational data in livestock, 2) to illustrate its implementation in the context of the animal sciences, and 3) to discuss opportunities and challenges associated with this framework. Foundational to the proposed conceptual framework are graphical objects known as directed acyclic graphs (DAGs). As mathematical constructs and practical tools, DAGs encode putative structural mechanisms underlying causal models together with their probabilistic implications. The process of DAG elicitation and causal identification is central to any causal claims based on observational data. We further discuss necessary causal assumptions and associated limitations to causal inference. Last, we provide practical recommendations to facilitate implementation of causal inference from observational data in the context of the animal sciences.

SUBMITTER: Bello NM

PROVIDER: S-EPMC6162585 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Conceptual framework for investigating causal effects from observational data in livestock.

Bello Nora M NM Ferreira Vera C VC Gianola Daniel D Rosa Guilherme J M GJM

Journal of animal science 20180901 10

Understanding causal mechanisms among variables is critical to efficient management of complex biological systems such as animal agriculture production. The increasing availability of data from commercial livestock operations offers unique opportunities for attaining causal insight, despite the inherently observational nature of these data. Causal claims based on observational data are substantiated by recent theoretical and methodological developments in the rapidly evolving field of causal inf ...[more]

PMID: 30107524

Similar Datasets

Project description:BACKGROUND: In recent years, there has been great interest in using transcriptomic data to infer gene regulatory networks. For the time being, methodological development in this area has primarily made use of graphical Gaussian models for observational wild-type data, resulting in undirected graphs that are not able to accurately highlight causal relationships among genes. In the present work, we seek to improve the estimation of causal effects among genes by jointly modeling observational transcriptomic data with arbitrarily complex intervention data obtained by performing partial, single, or multiple gene knock-outs or knock-downs. RESULTS: Using the framework of causal Gaussian Bayesian networks, we propose a Markov chain Monte Carlo algorithm with a Mallows proposal model and analytical likelihood maximization to sample from the posterior distribution of causal node orderings, and in turn, to estimate causal effects. The main advantage of the proposed algorithm over previously proposed methods is its flexibility to accommodate any kind of intervention design, including partial or multiple knock-out experiments. Using simulated data as well as data from the Dialogue for Reverse Engineering Assessments and Methods (DREAM) 2007 challenge, the proposed method was compared to two alternative approaches: one requiring a complete, single knock-out design, and one able to model only observational data. CONCLUSIONS: The proposed algorithm was found to perform as well as, and in most cases better, than the alternative methods in terms of accuracy for the estimation of causal effects. In addition, multiple knock-outs proved to contribute valuable additional information compared to single knock-outs. Finally, the simulation study confirmed that it is not possible to estimate the causal ordering of genes from observational data alone. In all cases, we found that the inclusion of intervention experiments enabled more accurate estimation of causal regulatory relationships than the use of wild-type data alone.

Project description:Observationally, higher caffeine consumption is associated with poorer sleep and insomnia. We investigated whether these associations are a result of shared genetic risk factors and/or (possibly bidirectional) causal effects. Summary-level data were available from genome-wide association studies on caffeine intake (n = 91 462), plasma caffeine and caffeine metabolic rate (n = 9876), sleep duration and chronotype (being a "morning" versus an "evening" person) (n = 128 266), and insomnia complaints (n = 113 006). First, genetic correlations were calculated, reflecting the extent to which genetic variants influencing caffeine consumption and those influencing sleep overlap. Next, causal effects were estimated with bidirectional, two-sample Mendelian randomization. This approach utilizes the genetic variants most robustly associated with an exposure variable as an "instrument" to test causal effects. Estimates from individual variants were combined using inverse-variance weighted meta-analysis, weighted median regression and MR-Egger regression. We found no clear evidence for a genetic correlation between caffeine intake and sleep duration (rg = 0.000, p = .998), chronotype (rg = 0.086, p = .192) or insomnia complaints (rg = -0.034, p = .700). For plasma caffeine and caffeine metabolic rate, genetic correlations could not be calculated because of the small sample size. Mendelian randomization did not support causal effects of caffeine intake on sleep, or vice versa. There was weak evidence that higher plasma caffeine levels causally decrease the odds of being a morning person. Although caffeine may acutely affect sleep when taken shortly before bedtime, our findings suggest that a sustained pattern of high caffeine consumption is more likely to be associated with poorer sleep through shared environmental factors. Future research should identify such environments, which could aid the development of interventions to improve sleep.

Dataset Information

Conceptual framework for investigating causal effects from observational data in livestock.

Publications

Conceptual framework for investigating causal effects from observational data in livestock.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure