Rebuilding trust in psychotherapy for biologically explained depression: A two-part experimental study examining the durability of an online psychoeducational intervention.

Biological explanations of mental disorders, which are gaining prominence, can decrease trust in psychotherapy. To rebuild trust, this experimental study tests a psychoeducational intervention targeting misconceptions that (1) psychotherapy cannot change the brain; (2) people rarely have agency over biology while psychotherapy requires agency; (3) psychosocial causes, addressed in psychotherapy, are less probable given biological causes. U.S. adults (N = 602) rated psychotherapy's effectiveness for depression before and after learning about depression's biological causes. Absent any intervention, control-condition participants rated psychotherapy to be less effective post biological-causes-information. However, participants who viewed an intervention video explaining why the misconceptions are flawed judged psychotherapy as more effective even after learning about depression's biological causes. Active-control-condition participants, who viewed a video about psychotherapy's effectiveness, without directly addressing the misconceptions, also increased psychotherapy ratings, albeit significantly less than the intervention group. Approximately four weeks later, intervention-condition participants maintained their enhanced trust, without any reminder of the video, whereas the two control conditions showed reduced trust. The study offers a practical tool for broader public use with a lasting effect.

Explaining How Psychotherapy Affects the Brain Can Increase the Perceived Effectiveness of Psychotherapy: A Randomized Controlled Trial.

Past studies repeatedly found that biological explanations of mental disorders cause laypeople and clinicians to doubt the effectiveness of psychotherapy. This could be clinically detrimental, as combined pharmacotherapy and psychotherapy is often optimal. The distrust of psychotherapy is theorized to stem from dualistic reasoning that psychotherapy, perceived as occurring in the mind, does not necessarily affect the brain. The current study aims to mitigate this belief in a randomized controlled trial. Participants (individuals with symptoms of depression (n = 262), the general public (n = 374), and mental health clinicians (n = 607)) rated the efficacy of psychotherapy for a depression case before and after learning that the case was biologically caused. Participants also received either an intervention passage describing how psychotherapy results in brain-level changes, an active control passage emphasizing the effectiveness of psychotherapy without explaining the underlying biological mechanisms, or no intervention. Unlike the active control and no-intervention control conditions, the intervention caused participants to judge psychotherapy as significantly more effective than at baseline even though they learned that depression was biologically caused. An intervention counteracting dualism can mitigate the belief that psychotherapy is less effective for biologically caused depression. Future research should examine the durability of this intervention in clinical settings.

The effect of neuroscientific evidence on sentencing depends on how one conceives of reasons for incarceration.

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.

The symptom discounting effect: what to do when negative genetic test results become risk factors for alcohol use disorder.

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.