Neuroimaging and behavioral evidence that violent video games exert no negative effect on human empathy for pain and emotional reactivity to violence
- University of Vienna, Austria
- Karolinska Institute, Sweden
Abstract
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.
Data availability
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/.
Article and author information
Author details
Lukas Leopold Lengersdorff
Funding
Vienna Science and Technology Fund (WWTF VRG13-007)
- Claus Lamm
Hjärnfonden (FO2014-0189)
- Pedrag Petrovic
Karolinska Institutet (2-70/2014-97)
- Pedrag Petrovic
Knut och Alice Wallenbergs Stiftelse (KAW 2014.0237)
- Andreas Olsson
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
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.
Copyright
© 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.
Metrics
-
- 6,924
- views
-
- 599
- downloads
-
- 7
- citations
Views, downloads and citations are aggregated across all versions of this paper published by eLife.
Download links
A two-part list of links to download the article, or parts of the article, in various formats.
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
Neuroimaging and behavioral evidence that violent video games exert no negative effect on human empathy for pain and emotional reactivity to violence
eLife 12:e84951.
https://doi.org/10.7554/eLife.84951
Further reading
-
- Computational and Systems Biology
In eukaryotes, protein kinase signaling is regulated by a diverse array of post-translational modifications, including phosphorylation of Ser/Thr residues and oxidation of cysteine (Cys) residues. While regulation by activation segment phosphorylation of Ser/Thr residues is well understood, relatively little is known about how oxidation of cysteine residues modulate catalysis. In this study, we investigate redox regulation of the AMPK-related brain-selective kinases (BRSK) 1 and 2, and detail how broad catalytic activity is directly regulated through reversible oxidation and reduction of evolutionarily conserved Cys residues within the catalytic domain. We show that redox-dependent control of BRSKs is a dynamic and multilayered process involving oxidative modifications of several Cys residues, including the formation of intramolecular disulfide bonds involving a pair of Cys residues near the catalytic HRD motif and a highly conserved T-loop Cys with a BRSK-specific Cys within an unusual CPE motif at the end of the activation segment. Consistently, mutation of the CPE-Cys increases catalytic activity in vitro and drives phosphorylation of the BRSK substrate Tau in cells. Molecular modeling and molecular dynamics simulations indicate that oxidation of the CPE-Cys destabilizes a conserved salt bridge network critical for allosteric activation. The occurrence of spatially proximal Cys amino acids in diverse Ser/Thr protein kinase families suggests that disulfide-mediated control of catalytic activity may be a prevalent mechanism for regulation within the broader AMPK family.
-
- Computational and Systems Biology
- Genetics and Genomics
Obesity is a major risk factor for type 2 diabetes, dyslipidemia, cardiovascular disease, and hypertension. Intriguingly, there is a subset of metabolically healthy obese (MHO) individuals who are seemingly able to maintain a healthy metabolic profile free of metabolic syndrome. The molecular underpinnings of MHO, however, are not well understood. Here, we report that CTRP10/C1QL2-deficient mice represent a unique female model of MHO. CTRP10 modulates weight gain in a striking and sexually dimorphic manner. Female, but not male, mice lacking CTRP10 develop obesity with age on a low-fat diet while maintaining an otherwise healthy metabolic profile. When fed an obesogenic diet, female Ctrp10 knockout (KO) mice show rapid weight gain. Despite pronounced obesity, Ctrp10 KO female mice do not develop steatosis, dyslipidemia, glucose intolerance, insulin resistance, oxidative stress, or low-grade inflammation. Obesity is largely uncoupled from metabolic dysregulation in female KO mice. Multi-tissue transcriptomic analyses highlighted gene expression changes and pathways associated with insulin-sensitive obesity. Transcriptional correlation of the differentially expressed gene (DEG) orthologs in humans also shows sex differences in gene connectivity within and across metabolic tissues, underscoring the conserved sex-dependent function of CTRP10. Collectively, our findings suggest that CTRP10 negatively regulates body weight in females, and that loss of CTRP10 results in benign obesity with largely preserved insulin sensitivity and metabolic health. This female MHO mouse model is valuable for understanding sex-biased mechanisms that uncouple obesity from metabolic dysfunction.
