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Background There is amassing evidence that risky decision-making in bipolar disorder is related to reward-based differences in frontostriatal regions. However, the roles of early attentional and later cognitive processes remain unclear, limiting theoretical understanding and development of targeted interventions. Methods Twenty euthymic bipolar disorder and 19 matched control participants played a Roulette task in which they won and lost money. Event-related potentials and source analysis were used to quantify predominantly sensory-attentional (N1), motivational salience (feedback-related negativities [FRN]), and cognitive appraisal (P300) stages of processing. We predicted that the bipolar disorder group would show increased N1, consistent with increased attentional orienting, and reduced FRN, consistent with a bias to perceive outcomes more favorably. Results As predicted, the bipolar disorder group showed increased N1 and reduced FRN but no differences in P300. N1 amplitude was additionally associated with real-life risk taking, and N1 source activity was reduced in visual cortex but increased activity in precuneus, frontopolar, and premotor cortex, compared to those of controls. Conclusions These findings demonstrate an early attentional bias to reward that potentially drives risk taking by priming approach behavior and elevating reward salience in the frontostriatal pathway. Although later cognitive appraisals of these inputs may be relatively intact in remission, interventions targeting attention orienting may also be effective in long-term reduction of relapse. [ABSTRACT FROM AUTHOR]

Bipolar disorder is characterized by impaired decision-making captured in impulsivity and risk-taking. We sought to determine whether this is driven by a failure to effectively weight the lower-order goal of obtaining a strongly desired reward in relation to higher-order goals, and how this relates to trait impulsivity and risk-taking. We hypothesized that in bipolar disorder the weighting of valuation signals converging on ventromedial prefrontal cortex are more heavily weighted towards ventral striatum inputs (lower-order), with less weighting of dorsolateral prefrontal cortex inputs (higher-order). Twenty euthymic patients with bipolar disorder not in receipt of antipsychotic medication and 20 case-matched controls performed a roulette task during functional magnetic resonance imaging. Activity in response to high-probability (‘safe’) and low-probability (‘risky’) prospects was measured during both anticipation, and outcome. In control subjects, anticipatory and outcome-locked activity in dorsolateral prefrontal cortex was greater for safe than risky reward prospects. The bipolar disorder group showed the opposite pattern with preferential response to risky rewards. This group also showed increased anticipatory and outcome-locked activity in ventral striatum in response to rewards. In control subjects, however, ventromedial prefrontal activation was positively associated with both ventral striatum and dorsolateral prefrontal activity; patients evidenced a strong positive association with ventral striatum, but a negative association with dorsolateral prefrontal cortex. Response to high-probability rewards in dorsolateral prefrontal cortex was inversely associated with trait impulsivity and risk-taking in the bipolar disorder group. Our findings suggest that clinically impulsive and risky decision-making are related to subjective valuation that is biased towards lower-order preference, with diminished integration of higher-order goals. The findings extend a functional neuroanatomical account of disorders characterized by clinically impulsive decision-making, and provide targets for evaluating interventions that foster self-control. [ABSTRACT FROM AUTHOR]

Background: The primary objective of this randomized controlled trial (RCT) is to establish the effectiveness of time-restricted eating (TRE) compared with the Mediterranean diet for people with bipolar disorder (BD) who have symptoms of sleep disorders or circadian rhythm sleep–wake disruption. This work builds on the growing evidence that TRE has benefits for improving circadian rhythms. TRE and Mediterranean diet guidance will be offered remotely using self-help materials and an app, with coaching support. Methods: This study is an international RCT to compare the effectiveness of TRE and the Mediterranean diet. Three hundred participants will be recruited primarily via social media. Main inclusion criteria are: receiving treatment for a diagnosis of BD I or II (confirmed via DIAMOND structured diagnostic interview), endorsement of sleep or circadian problems, self-reported eating window of ≥ 12 h, and no current mood episode, acute suicidality, eating disorder, psychosis, alcohol or substance use disorder, or other health conditions that would interfere with or limit the safety of following the dietary guidance. Participants will be asked to complete baseline daily food logging for two weeks and then will be randomly allocated to follow TRE or the Mediterranean diet for 8 weeks, during which time, they will continue to complete daily food logging. Intervention content will be delivered via an app. Symptom severity interviews will be conducted at baseline; mid-intervention (4 weeks after the intervention begins); end of intervention; and at 6, 9, and 15 months post-baseline by phone or videoconference. Self-rated symptom severity and quality of life data will be gathered at those timepoints, as well as at 16 weeks post baseline. To provide a more refined index of whether TRE successfully decreases emotional lability and improves sleep, participants will be asked to complete a sleep diary (core CSD) each morning and complete six mood assessments per day for eight days at baseline and again at mid-intervention. Discussion: The planned research will provide novel and important information on whether TRE is more beneficial than the Mediterranean diet for reducing mood symptoms and improving quality of life in individuals with BD who also experience sleep or circadian problems. Trial registration: ClinicalTrials.gov ID NCT06188754. [ABSTRACT FROM AUTHOR]