Tuesday, May 17, 2022

Small effect: Financial incentives can boost critical thinking skills

Revisiting the effect of incentivization on cognitive reflection: A meta-analysis. Eldad Yechiam, Dana Zeif. Journal of Behavioral Decision Making, May 17 2022. https://doi.org/10.1002/bdm.2286

Abstract: The effect of performance-based incentives on judgment biases is a controversial issue. A recent extensive meta-analysis of Brañas-Garza et al. (2019, https://doi.org/10.1016/j.socec.2019.101455) found no effect of incentives on performance in the cognitive reflection test (CRT), a test commonly used for assessing heuristic versus deliberative judgments. We conducted a meta-analysis of studies that directly compared an incentive versus no-incentive conditions (n = 2836) and found a small positive effect of incentivization (Cohen's d = .21) on CRT performance. In addition, we re-examined the Brañas-Garza et al. (2021) dataset (n = 39,385), taking into consideration not only whether incentivization was used but also the nominal and fiscal size of the incentive. The results show that surprisingly when including only studies that used monetary incentives, the effect of incentivization and incentive size are significant, even when taking into consideration other aspects of the studies. The results thus suggest a small but robust effect of incentives on judgment biases.

From 2019... Teams outperformed individuals in making accurate geopolitical predictions

From 2019... What Makes Foreign Policy Teams Tick: Explaining Variation in Group Performance at Geopolitical Forecasting. Michael Horowitz, Brandon M. Stewart, Dustin Tingley, Michael Bishop, Laura Resnick Samotin, Margaret Roberts, Welton Chang, Barbara Mellers and Philip Tetlock. The Journal of Politics, Vol. 81, No. 4, Oct 2019. https://www.journals.uchicago.edu/doi/abs/10.1086/704437

Abstract: When do groups—be they countries, administrations, or other organizations—more or less accurately understand the world around them and assess political choices? Some argue that group decision-making processes often fail due to biases induced by groupthink. Others argue that groups, by aggregating knowledge, are better at analyzing the foreign policy world. To advance knowledge about the intersection of politics and group decision making, this paper draws on evidence from a multiyear geopolitical forecasting tournament with thousands of participants sponsored by the US government. We find that teams outperformed individuals in making accurate geopolitical predictions, with regression discontinuity analysis demonstrating specific teamwork effects. Moreover, structural topic models show that more cooperative teams outperformed less cooperative teams. These results demonstrate that information sharing through groups, cultivating reasoning to hedge against cognitive biases, and ensuring all perspectives are heard can lead to greater success for groups at forecasting and understanding politics.

5 What Kinds of Teams Succeed? Modelling Team Communication

To test hypothesis 2 and hypothesis 3 concerning what explains variation in the ability of groups to forecast, we focus on the content of forecast explanations. In particular, we examine explanations given by individuals in the team conditions. By understanding how different kinds of teams (trained teams, untrained teams, and top teams) use explanations, we can begin unpacking what makes teams more or less effective. We find several patterns in the content of explanations that help to explain top team success. When making their predictions, participants —whether in the individual or team condition—could also choose to provide an explanation for their forecast. There was a comment box underneath the place where individuals entered their forecasts and participants were encouraged to leave a comment that included an explanation for their forecast. For participants in an individual experimental condition, only the researchers would see those explanations. For participants in a team experimental condition, however, their teammates would be able to see their explanation/comment. These explanations therefore potentially provide useful information to help identify what leads to forecasting accuracy, giving us a way to test hypotheses 2 and 3.

5.1 The Conversational Norms Of Successful Geopolitical Forecasting Groups

An obvious starting point is to ask whether, on average, individuals differ in how extensively they made explanations (i.e., how many comments per IFP) and how intensively (i.e., how long were the comments). Both of these metrics give us a sense of forecaster engagement - since those that explain their predictions are likely more engaged than those that do not. We do this by contrasting behavior by whether a forecaster was on a team or not, whether they were on a team that got training, or not, and whether they were on a top team. Below, we switch from focusing on the extent of engagement to the intensity of engagement, when it occurs.
To calculate the degree of extensive engagement, for each individual we first calculated the total number of explanations made per IFP for which the individual made at least one explanation. Then for each individual we calculated their average number of comments per IFP, averaging over all of the forecasting questions they answered. Thus, for any person we know the average number of explanations they will give for an prediction task.
Figure 3 plots the resulting distribution of this value for each group (individuals, untrained teams, trained teams, and top teams). The x-axis is scaled along a base 10 log for each individual’s score because this distribution is heavily skewed. The log transformation reduces the presentational influence of extreme outliers in this distribution. Each group is presented as a different density plot, with the height of the plot giving a relative estimate of how many observations were at the particular value of the x-axis.15 We observe that both individuals and untrained teams have relatively low levels of average responses per IFP. Trained teams and particularly top teams have considerably higher average responses per IFP.
Next we calculate how intensively individuals engage with explaining their prediction. For each individual we calculated the median length of their first explanation of an IFP. We use the first explanation for a variety of reasons. First, as seen in Figure 3, individuals that were not on a team, or were in untrained teams, rarely made more than one explanation per IFP. Second, we are most interested in individuals providing information and analysis to others on their team. Someone’s first explanation is an important first step in doing this. Figure 4 shows the distribution for the four conditions. We see that individuals who are in top teams are clearly engaging in more intensive explanation compared to individuals in other conditions.
Next, we combine Figures 3 and 4 and plot each individual’s value of their extensive engagement and intensive engagement in Figure 5. Here we separate out the plots by each of our groups and overlay a contour plot to give a sense of the distribution of data in this space. As expected, we observe that top teams tend to have more individuals who are engaging both more extensively per IFP and more intensively. On the other hand, while people not on teams on occasion would provide multiple explanations per IFP, most did not. Teams with and without training had individuals who provided more lengthy explanations, but these teams do not have individuals who both supplied multiple responses to an IFP and began their engagement with an IFP with a lengthy explanation (which could then be read by other participants on their team).
We also examined other metrics of intensive engagement. Figure 6 plots the fraction of total words in explanations that came after the first response.16 The plot shows a low proportion of total words coming after the very first explanation from individuals. Teams did better, with more intensive engagement after the first explanation by trained teams and top teams.
Figure 7 investigates the degree to which explanations are generated by a single member of a team or a broader discussion amongst multiple participants. To measure this we calculate for each IFP, in each team, the total number of explanations of the most prolific responder. We then divided this by the average number of responses within the team to that IFP to generate a score for each team/IFP combination. We then plot the distribution of these scores by condition in Figure 7. This shows a distinct pattern illustrating strong effects for one particular type of team - top teams. Prolific posters for top teams posted four times as much as the team average. But for non-top teams, the relative contribution of the most prolific posters was significantly higher. Essentially, in non-top teams, a single person often completely dominates the conversation while top teams featured broader conversations among more team members.

Rolf Degen summarizing... Everyday sadism, the dispositional tendency to take pleasure in others' suffering, finds its natural playing field in the online world

A systematic review and meta-analysis examining the relationship between everyday sadism and aggression: Can subclinical sadistic traits predict aggressive behaviour within the general population? Leah Thomas, Vincent Egan. Aggression and Violent Behavior, May 16 2022, 101750. https://doi.org/10.1016/j.avb.2022.101750


• The aim of this systematic review and meta-analysis was to investigate the relationship between everyday sadism and aggressive behaviour.

• The synthesized evidence suggests that everyday sadism, a trait that resides within the general population, was consistently correlated with dispositional aggression and a range of aggressive behaviour.

• A moderate effect size was found for the relationship between sadism aggressive behaviour perpetrated online.

• Meta-analyses were completed to examine the relationship between subclinical sadism and sexual aggression.

• This review emphasises the importance of dark personality research, and the risks associated with subclinical sadism residing in the general population.


Background: Everyday sadism is unique among the dark personality traits that form the Dark Tetrad. Whilst it shares the Dark Core of Personality with psychopathy, narcissism, and Machiavellianism, it is theoretically distinct from the other members in that involves an appetite for cruelty.

Objective: Given mounting evidence of everyday sadism being associated with socially aversive behaviour, and its potential utility in predicting harmful behaviour within the general population; the current review examined the relationship between sadism and aggressive behaviour.

Data sources: Seven well-established electronic bibliographic databases and two other sources were systematically searched. Supplementary searches were employed.

Study selection: The initial search identified 627 full-text articles. Following application of inclusion and exclusion criteria, 39 full-text articles inclusive of 52 studies were subject to quality assessment. Data was extracted from 52 studies, with 48 studies eligible for quantitative synthesis.

Data synthesis: Correlational analyses were the most common method of examining sadism and aggression. A multi-method approach was employed to standardize effect sizes into a common metric (correlation coefficient). A meta-analysis was conducted using 57 effect sizes from 48 studies with 22,179 participants, revealing a pooled correlation coefficient of 0.35 (95% CI = 0.29, 0.40). Significant heterogeneity was observed which warranted sensitivity and subgroup analyses.

Conclusions: Overall, a moderate relationship was found between subclinical sadism and aggressive behaviour, as defined by acts ranging from verbal to physical, and sexual aggression and violence. A stronger, moderate relationship was found between sadism and perpetration of aggressive behaviour online, indicating that anonymity may unleash the darker side of personality within the general population. The implications of this finding are considered.

Keywords: Everyday sadismDark tetradAggressive behaviourPersonalityIndividual differencesSystematic reviewmeta-analysis

Potential gene-editing treatment for anxiety and alcohol use disorder in adult rats who were exposed to binge drinking in their adolescence

Targeted epigenomic editing ameliorates adult anxiety and excessive drinking after adolescent alcohol exposure. John Peyton Bohnsack, Huaibo Zhang, Gabriela M. Wandling, Donghong He, Evan J. Kyzar, Amy W. Lasek and Subhash C. Pandey. Science Advances, May 4 2022. DOI: 10.1126/sciadv.abn2748

Abstract: Adolescent binge drinking is a major risk factor for psychiatric disorders later in life including alcohol use disorder. Adolescent alcohol exposure induces epigenetic reprogramming at the enhancer region of the activity-regulated cytoskeleton-associated protein (Arc) immediate-early gene, known as synaptic activity response element (SARE), and decreases Arc expression in the amygdala of both rodents and humans. The causal role of amygdalar epigenomic regulation at Arc SARE in adult anxiety and drinking after adolescent alcohol exposure is unknown. Here, we show that dCas9-P300 increases histone acetylation at the Arc SARE and normalizes deficits in Arc expression, leading to attenuation of adult anxiety and excessive alcohol drinking in a rat model of adolescent alcohol exposure. Conversely, dCas9-KRAB increases repressive histone methylation at the Arc SARE, decreases Arc expression, and produces anxiety and alcohol drinking in control rats. These results demonstrate that epigenomic editing in the amygdala can ameliorate adult psychopathology after adolescent alcohol exposure.

Popular version: A study by researchers from the University of Illinois Chicago has found a potential gene-editing treatment for anxiety and alcohol use disorder in adults who were exposed to binge drinking in their adolescence. Binge drinking in adolescence alters brain chemistry in the enhancer region of the Arc gene and reduces Arc expression in the amygdala for both rodents and humans. This contributes to a predisposition to alcohol use disorder in adulthood. Rats that had been exposed to alcohol during adolescence showed fewer indicators of anxiety and lower alcohol consumption when Arc gene expression was increased using CRISPR technology. Normal rats showed more indicators of anxiety and increased their alcohol consumption when Arc gene expression was decreased.


Our results indicate that targeted epigenomic editing at the Arc SARE can bidirectionally modulate behavioral changes caused by adolescent alcohol exposure (Fig. 5). Furthermore, we demonstrate that these changes are largely due to an epigenetic circuit involving transcription of eRNAs from the Arc SARE, which causes epigenetic remodeling at the Arc promoter by looping of the chromatin to allow localized release of NELF. In addition, our results indicate that activating the Arc SARE site through histone acetylation using dCas9-P300 facilitates Arc eRNA transcription and long-range promoter-enhancer interactions and modulates transcription factor binding, which is consistent with other findings (253940). Conversely, dCas9-KRAB–mediated epigenetic suppression at Arc SARE decreases eRNA transcription and increases NELF binding at the promoter without changing enhancer and promoter interactions and promotes anxiety and excessive drinking (Fig. 5). This contrasts with other studies in which KRAB is involved in heterochromatin spreading and transcriptional repression via alternative mechanisms (41). Here, we demonstrate that dCas9-KRAB increases repressive H3K27me3, which has previously been shown to be involved in repressing eRNA transcription (35). We observed no change in H3K9me3 occupancy at the Arc SARE site after dCas9-KRAB manipulations. Other studies have shown that targeting dCas9-KRAB to specific genomic loci increases H3K9me3, but these changes have been shown to be transitory and not sufficient for transcriptional repression (3842). While it is likely that increased H3K27me3 at the Arc SARE contributes to repressed Arc eRNA and mRNA expression and subsequent behavioral correlates, the current study did not investigate other repressive mechanisms induced by dCas9-KRAB.
Fig. 5. Model showing that adolescent alcohol exposure produces epigenetic reprogramming in the CeA as well as anxiety and excessive alcohol intake in adulthood.
dCas9-P300 infusion in the CeA was able to increase H3K27ac at Arc SARE, increase Arc eRNA and mRNA expression, and ameliorate anxiety and excessive alcohol intake induced by AIE exposure in adulthood. On the other hand, dCas9-KRAB increased repressive epigenetic marks, H3K27me3 at Arc SARE, leading to decreased Arc eRNA and mRNA expression and development of anxiety and alcohol drinking behaviors in control adult rats. These data causally link epigenetic modifications at an enhancer region of synaptic gene Arc to adult AUD and anxiety after adolescent alcohol exposure.
Preclinical and clinical data clearly suggest that adolescent alcohol consumption can increase the susceptibility of an individual to anxiety and AUD (47910). Several studies in the field have shown that various biological mechanisms, including epigenetic changes, may be involved in the persistence of the effects of adolescent alcohol exposure into adulthood (91043). It has been shown that epigenetic drugs such as histone deacetylase (HDAC) and DNA methyltransferase (DNMT) inhibitors can attenuate adolescent alcohol exposure–induced anxiety-like and alcohol drinking behaviors in adult rats (2844). Similar to what was found in the current study using dCas9-P300, treatment with either a systemic HDAC inhibitor or DNMT inhibitor did not result in anxiolysis or reduce alcohol intake in AIS adult rats (2844). Here, there was a trend toward an increase in Arc expression and histone acetylation after dCas9-P300 treatment, but this was not statistically significant. Conversely, acute ethanol challenge in AIS adult rats increased Arc expression and produced anxiolysis that was associated with increased KDM6B/CBP, decreased H3K27me3, and increased H3K27ac occupancy at the Arc SARE site in the amygdala. These epigenetic modifications were associated with a significant increase in Arc expression in the amygdala of AIS rats (11). We therefore suggest that the dCas9-P300 manipulation did not reach the set point or biological threshold of Arc expression to induce anxiolysis, and this may be a possible explanation for the lack of observed effects of dCas9-P300 on anxiety and alcohol intake in AIS control rats.
The Arc gene is one of the most interactive genes in the altered synaptic gene network in the adult amygdala after adolescent alcohol exposure in rats (11). Arc interacts with a brain-derived neurotrophic factor (BDNF), and both are down-regulated via epigenetic mechanisms in the amygdala of rodents and humans in adulthood after adolescent alcohol consumption (111230). Arc protein expression is lower in the CeA of alcohol-preferring rats as compared with alcohol nonpreferring rats, and this is most likely the result of increased HDAC2-mediated deficits in histone acetylation of Arc gene. Inhibition of HDAC2 expression in the CeA of preferring rats attenuated anxiety-like behaviors and excessive drinking and increased histone acetylation and Arc protein expression in the CeA (45). Furthermore, HDAC and DNMT inhibitors are also effective in preventing excessive drinking and alcohol self-administration in other animal models of AUD (4648). These studies suggest that Arc expression is regulated via histone acetylation mechanisms and that pharmacological epigenetic agents are effective in attenuating anxiety and alcohol intake in several models of AUD. However, these studies do not establish the specific epigenetically regulated genomic regions implicated in these effects. Here, we used epigenomic editing (2527) to modulate histone acetylation/methylation levels at a specific genomic locus regulating anxiety and excessive drinking.
AIE is associated with diminished synaptic events that are characterized by decreased mRNA and protein levels of Arc and decreased dendritic spines and synapses in the CeA in adulthood (1128). Our previous studies showed that up-regulation of EZH2 and down-regulation of KDM6B and CBP after AIE initiate repression of the Arc gene through increases in H3K27me3 and decreases in H3K27ac occupancy at the Arc SARE, providing an endogenous mechanism for epigenetic reprogramming in the amygdala of rodents (11) and AUD subjects with early age of onset (12). All these studies are correlative in nature, and we now causally demonstrate in detail how epigenetic activation and repression at the Arc SARE site can drive adult excessive drinking and anxiety induced by adolescent alcohol exposure. Our results further indicate that epigenetic editing using dCas9-P300 at the Arc SARE is sufficient for enhancer-mediated activation of Arc expression and can drive increased H3K27ac at the promoter site, most likely via chromatin looping (3439). There are few caveats to the present study. One caveat is that it was only performed in male animals, and since sex-specific effects of ethanol have been shown in the literature (49), a future study in female animals needs to be conducted. Another caveat is that we chose to mechanistically interrogate only the CeA, whereas previous studies have shown similar changes in Arc expression in the medial nucleus of amygdala (MeA) after AIE in adulthood (28). While the results of current study imply that epigenomic editing of Arc SARE in the CeA is sufficient to modulate anxiety-like and alcohol drinking behaviors, we cannot rule out the involvement of other brain regions that are implicated in these behaviors and addiction (250).
Previous reports have indicated that the use of dCas9-induced epigenetic modulation at promoter regions can modulate behavior (5153) as well as CRISPR-mediated chromosomal looping (54). Here, we demonstrate that this technology can also be used to investigate the role of noncoding RNAs, such as eRNAs, in regulating the interplay between three-dimensional chromatin structure, genetic regulatory elements, transcription factor binding, and RNA to influence adult anxiety and drinking after adolescent alcohol exposure. The current study focused on reversing epigenetic and behavioral changes in adulthood that were induced by adolescent alcohol exposure. However, we have previously observed that histone acetylation and behavioral changes also occur immediately after the AIE paradigm in adolescence and persist into adulthood (28). While the current study only focused on the long-term changes that persist until adulthood to better model what is seen in humans (47), the findings support the idea that activating the Arc SARE with dCas9-P300 could be applied as an intervention in adolescence. Our previous study showed that KDM6B siRNA infusion into the CeA of control adult rats produced anxiety-like behaviors, decreases in KDM6B, and increases in H3K27me3 occupancy at the Arc SARE site and suppressed Arc eRNA and mRNA expression in the amygdala (11). In addition, inhibition of Arc eRNA (−) levels in the CeA increased NELF binding, decreased Arc expression, and provoked anxiety-like behaviors in control adult rats (11). Here, we demonstrate that dCas9-KRAB infusion into CeA produces an increase in repressive H3K27me3 at the Arc SARE, decreases eRNA levels, increases NELF binding at the promoter, down-regulates Arc expression, and increases anxiety-like behavior and alcohol intake in control adult rats. Together, this suggests that epigenetic regulation at the Arc SARE site in the CeA is involved in modulating anxiety and alcohol intake. Thus, both developmental alcohol exposure–induced suppression of Arc expression and direct suppression of Arc expression in adulthood in the CeA appear to be crucial in anxiety and AUD.
Our findings regarding epigenomic editing allow for the analysis of gene- and amygdala nuclei–specific epigenetic changes that occur after adolescent alcohol exposure and persist until adulthood, driving complex behavior. The Cas9 system is easier to use and more modular than previous iterations [e.g., transcription activator–like effector nucleases (TALENs)] designed to alter precise epigenetic marks (55). In addition, the use of dCas9 to modulate gene expression, in lieu of a Cas9 enzyme with active endonuclease activity, could confer additional therapeutic and research benefit. Considerable effort has gone into reducing “off-target” double-stranded breaks that result in genome instability (56). The use of the dCas9 system avoids many of these off-target effects since DNA is not cut and not subject to error-prone nonhomologous end joining or spontaneous recombination events. The use of a dCas9 system is especially useful in the context of epigenetic regulation, and it has broad applications in the interrogation of long-lasting epigenetic changes that drive AUD and anxiety after adolescent alcohol exposure and the identification of tractable targets for the treatment of AUD and comorbid anxiety.