Neuroscientific evidence is increasingly utilized in criminal legal proceedings, prompting discussions about how such evidence might influence legal decisions. The effect of neuroscientific testimony on legal decisions remains uncertain, with some studies finding no effect, others reporting that neuroscience has a mitigating impact, and some indicating neuroscience evidence has an aggravating effect. The present study attempts to explain these divergent findings by showing that the effect of neuroscience evidence on sentencing interacts with beliefs about the goals of the criminal legal system. Using a between-subjects design, participants (N = 784) were asked to assume different rationales for imprisonment, before receiving neuroscientific evidence about antisocial behavior and its potential relation to the defendant. Participants recommended a sentence for the defendant prior to and after reading the neuroscientific evidence. Participants who were given the rationale of retribution as the primary goal of imprisonment significantly decreased their sentencing recommendations. When the goal of imprisonment was to protect the public from dangerous people, participants provided longer post-testimony sentences. Lastly, when the goal was to rehabilitate wrongdoers, participants also increased sentences from pre to post. Thus, the impact of neuroscientific evidence is not monolithic, but can lead to either mitigated or aggravated sentences by interacting with penal philosophy.

Most consumers of genetic testing for health conditions test negative, yet the psychological perils of this are hardly known. In three experiments (N = 2103) participants discounted repercussions of alcohol use disorder (AUD), after learning or imagining that they were not genetically predisposed to AUD. Such discounting can lead people to avoid treatment and to feel safe to continue or even increase their drinking, ironically turning the negative genetic feedback into a risk factor for AUD. Concerningly, the debriefing currently used by a direct-to-consumer genetic testing company failed to counteract this discounting among those already engaging in problematic drinking in all three studies. It was hypothesized that this discounting derives from not understanding the Causal Markov condition; once AUD symptoms are present, their ramifications remain the same regardless of whether genes or environmental factors caused the symptoms. Educating participants about this principle successfully mitigated the irrational discounting of threats of AUD.

Most consumers of genetic testing for health conditions test negative, yet the psychological perils of this are hardly known. In three experiments (N=2,103) participants discounted repercussions of Alcohol Use Disorder (AUD), after learning or imagining that they were not genetically predisposed to AUD. Such discounting can lead people to avoid treatment and to feel safe to continue or even increase their drinking, ironically turning the negative genetic feedback into a risk factor for AUD. This misconception derives from not understanding the Causal Markov condition as applied to this case; once AUD symptoms are present, their ramifications remain the same regardless of whether genes or environments caused the symptoms. Educating participants about this principle mitigated the irrational discounting of threats of AUD, even among Individuals already engaging in problematic drinking, for whom the debriefing currently used by a direct-to-consumer genetic testing company was found to be ineffective in the current study.

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Genomic research is rapidly advancing, and personalized genetic risk information about various mental disorders is likely to become readily available for many individuals. Although genetic profiling is intended to improve individually tailored treatments, knowing one’s genetic risks or lack thereof can have unintended consequences. Upon learning that they have elevated genetic risks for a mental disorder (e.g., depression), people may become more pessimistic about their prognosis and misremember their symptoms as being more serious because they misconceive genes as immutable and defining of their identity. Upon learning that they are not genetically predisposed to a mental disorder (e.g., alcohol use disorder), people may underplay the downstream ramifications of the symptoms even when they are currently experiencing those symptoms. Possible interventions to counteract these problems and suggestions for future research are also discussed.