Influential accounts claim that violent video games (VVG) decrease players' emotional empathy by desensitizing them to both virtual and real-life violence. However, scientific evidence for this claim is inconclusive and controversially debated. To assess the causal effect of VVGs on the behavioral and neural correlates of empathy and emotional reactivity to violence, we conducted a prospective experimental study using functional magnetic resonance imaging (fMRI). We recruited eighty-nine male participants without prior VVG experience. Over the course of two weeks, participants played either a highly violent video game, or a non-violent version of the same game. Before and after this period, participants completed an fMRI experiment with paradigms measuring their empathy for pain and emotional reactivity to violent images. Applying a Bayesian analysis approach throughout enabled us to find substantial evidence for the absence of an effect of VVGs on the behavioral and neural correlates of empathy. Moreover, participants in the VVG group were not desensitized to images of real-world violence. These results imply that short and controlled exposure to VVGs does not numb empathy nor the responses to real-world violence. We discuss the implications of our findings regarding the potential and limitations of experimental research on the causal effects of VVGs. While VVGs might not have a discernible effect on the investigated subpopulation within our carefully controlled experimental setting, our results cannot preclude that effects could be found in settings with higher ecological validity, in vulnerable subpopulations, or after more extensive VVG play.
Behavioral data, fMRI signal timecourses extracted from our regions of interest, task event timings, custom STAN code, and game images used in the emotional reactivity task are accessible at https://osf.io/yx423/. Unthresholded statistical maps are accessible at https://identifiers.org/neurovault.collection:13395. These include statistical maps from the analyses underlying the definition of our regions of interest, as well as the statistical maps from the frequentist analyses presented in Appendix 5. Full fMRI datasets from all participants are accessible at https://doi.org/10.5281/zenodo.10057633
Grand Theft Empathy: Effects of Violent Video Games on Empathy and Emotional ReactivityOpen Science Framework, https://osf.io/yx423/.
- Claus Lamm
- Pedrag Petrovic
- Pedrag Petrovic
- Andreas Olsson
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Human subjects: The study was approved by the ethics committee of the Medical University of Vienna (decision number 1258/2017). All participants gave informed consent prior to the start of the first experimental session. The confederate depicted in Figure 1A has given informed consent that his photograph may be used for this publication.
- Clare Press, Birkbeck, University of London, United Kingdom
- Received: November 16, 2022
- Accepted: November 17, 2023
- Accepted Manuscript published: November 17, 2023 (version 1)
© 2023, Lengersdorff et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
A deep analysis of multiple genomic datasets reveals which genetic pathways associated with atherosclerosis and coronary artery disease are shared between mice and humans.
Mouse models have been used extensively to study human coronary artery disease (CAD) or atherosclerosis and to test therapeutic targets. However, whether mouse and human share similar genetic factors and pathogenic mechanisms of atherosclerosis has not been thoroughly investigated in a data-driven manner. We conducted a cross-species comparison study to better understand atherosclerosis pathogenesis between species by leveraging multiomics data. Specifically, we compared genetically driven and thus CAD-causal gene networks and pathways, by using human GWAS of CAD from the CARDIoGRAMplusC4D consortium and mouse GWAS of atherosclerosis from the Hybrid Mouse Diversity Panel (HMDP) followed by integration with functional multiomics human (STARNET and GTEx) and mouse (HMDP) databases. We found that mouse and human shared >75% of CAD causal pathways. Based on network topology, we then predicted key regulatory genes for both the shared pathways and species-specific pathways, which were further validated through the use of single cell data and the latest CAD GWAS. In sum, our results should serve as a much-needed guidance for which human CAD-causal pathways can or cannot be further evaluated for novel CAD therapies using mouse models.