Psychological Medicine最新文献

Background: Parental prenatal mood and anxiety disorders (PMADs) are linked to child neurodevelopmental disorders (NDDs), but evaluations of the magnitude and mechanisms of this association are limited. This study estimates the strength of the association and whether it is impacted by genetic and environmental factors.

Methods: A systematic search of PubMed, CENTRAL, PsycINFO, OVID, and Google Scholar was performed for articles published from January 1988 to September 2025. Of 2,420 articles screened, 74 met the inclusion criteria. Meta-analyses were conducted on 21 studies, and 53 were included in the narrative synthesis. We conducted random-effects meta-analyses, along with tests for heterogeneity (I²) and publication bias (Egger's test). The review followed PRISMA and MOOSE guidelines.

Results: Maternal PMADs were associated with a significantly increased risk of attention-deficit/hyperactivity disorder (ADHD; odds ratio [OR] 1.91, 95% confidence interval [CI] 1.45-2.52) and autism spectrum disorder (ASD; OR 1.75, 95% CI 1.43-2.14) in children. Paternal PMADs were also associated with the risk of NDDs, with combined odds for ASD and ADHD (OR = 1.23, 95% CI 1.14-1.33). Several studies suggested that the link between parental PMADs and offspring NDDs might be impacted by both genetic and environmental factors, including the impact of ongoing parental depression on child behavior.

Conclusions: Parental PMADs are associated with increased risk of NDDs in children. These findings likely reflect a combination of inherited liability and environmental processes; clarifying mechanisms will require genetically informed designs. Regardless of mechanism, offering optional, family-centered developmental support may help promote child well-being in families where a parent is experiencing PMADs.

Loneliness is a major psychological challenge in older adulthood, contributing to increased risks of depression, anxiety, and mortality. Conversational agents - technologies that interact with users via natural language - have emerged as potential tools to support psychological well-being in later life. This systematic review and meta-analysis evaluated the effects of autonomous conversational agents, including robotic and nonrobotic systems, on loneliness, as well as social isolation, depression, and anxiety in older people without cognitive impairment. Seventeen studies with pre-post intervention data were included. Nine used physically embodied robots and eight employed nonrobotic agents, such as personal voice assistants, chatbots, or screen-based embodied agents. Due to the limited number of high-quality comparison studies, all meta-analyses were based on within-group pre-post comparisons. Meta-analytic results showed mild to moderate improvements in loneliness (standardized mean changes using change score [SMCC] = 0.350, 95% confidence interval [CI]: 0.180-0.520) and depression (SMCC = 0.464, 95% CI: 0.327-0.602), with no study reporting symptom worsening. No study included validated measures of social isolation, and only one assessed anxiety. These findings indicate that conversational agents may offer scalable support for older adults' mental health, with potential especially for reducing loneliness and depression. Nonetheless, methodological limitations, including lack of blinded outcome assessment, inconsistent reporting, and heterogeneous intervention designs, underscore the need for more rigorous research. Advances in large language models may further enhance the responsiveness and relevance of these technologies for supporting psychological well-being in aging populations.

Background: Hypochondriasis, or health anxiety disorder, is associated with increased mortality, mainly from potentially preventable causes. Substance misuse is a well-known contributor to premature death, yet its relationship with hypochondriasis remains unclear. We assessed the risk of broadly defined substance-related problems in individuals diagnosed with hypochondriasis.

Methods: This Swedish register-based matched cohort study included 4,129 individuals diagnosed with hypochondriasis in specialist services between 1997 and 2020 and 41,290 demographically matched unexposed individuals. Stratified Cox proportional hazards models were fitted to estimate hazard ratios (HRs) for the association between hypochondriasis and substance-related problems - defined as alcohol and drug use disorders, dispensed medications for alcohol dependence and opioid use disorders, and alcohol- and drug-related accidental poisonings, deaths, and suspected criminal offenses. Models were adjusted for sociodemographic variables, parental substance-related problems, and personal psychiatric history.

Results: Substance-related problems were identified in 504 (12.2%) individuals with hypochondriasis and 1,924 (4.7%) matched unexposed individuals. After adjustment for sociodemographic and parental covariates, hypochondriasis was significantly associated with an increased risk of substance-related problems (HR, 2.55; 95% confidence interval [CI], 2.30-2.84). Similar results were observed in individuals without preexisting substance-related problems (HR, 2.85; 95% CI, 2.48-3.27). Further adjustment for psychiatric comorbidity, particularly anxiety and depression, reduced the risk estimates, but the associations remained statistically significant. In an additional analysis including primary care diagnoses of hypochondriasis (presumably reflecting less complex cases), the risk of substance-related problems remained elevated (HR, 1.61; 95% CI, 1.39-1.86).

Conclusion: Improved recognition of, and clinical awareness of substance misuse may help reduce long-term adverse outcomes in individuals with hypochondriasis.

Background: Confidence exhibits systematic individual differences across mental health, gender, and age. However, it remains unknown whether these distinct sources of metacognitive bias have common or distinct computational origins.

Methods: To address this question, we developed a novel dynamic computational model of metacognition to study the temporal evolution of underconfidence associated with individual differences in transdiagnostic anxiety symptoms and gender in samples of online participants (total N = 1,447).

Results: We found that underconfidence associated with anxiety symptoms became more prominent the longer individuals took to make metacognitive judgments - suggesting that it is exacerbated by additional time for introspection. In contrast, gender-related underconfidence decreased with greater metacognitive judgment time - suggesting that additional time for introspection is able to remediate prepotent biases. Our computational model of confidence explained these effects - while both gender and anxiety symptoms involved shifts in confidence criteria, only anxiety symptoms involved a temporal accumulation of negatively biased evidence about one's ability.

Conclusions: Our study reveals multiple computational pathways to the formation of underconfidence, in turn highlighting specific potential mechanisms for its remediation.

Background: Cognitive fatigue is a prevalent and disabling symptom in neurological and post-viral conditions, including multiple sclerosis (MS) and Long COVID. Assessment relies largely on self-report, and no validated objective biomarker exists, limiting reliable diagnosis and treatment monitoring. The aperiodic exponent of the Electroencephalogram (EEG) power spectrum, reflecting the excitation/inhibition (E/I) balance, is a promising candidate biomarker. We examined whether aperiodic exponent values can objectively identify pathological fatigue and assessed their classification accuracy.

Methods: We conducted a cross-sectional study, including 119 participants: 36 healthy controls, 33 with Long COVID-related fatigue (LCOF), and 50 with MS (23 fatigued and 27 nonfatigued). Resting-state EEGs were analyzed, and associations with fatigue ratings and group differences were assessed. Logistic mixed-effects regression models evaluated classification accuracy for fatigue status.

Results: Lower frontal aperiodic exponents were associated with higher cognitive fatigue across participants. Fatigued individuals, regardless of diagnosis, showed reduced frontal exponent values compared with nonfatigued groups, while no differences emerged in occipital regions. Logistic regression confirmed that frontal exponent values significantly predicted fatigue status, improving classification accuracy beyond age and depression, with good sensitivity and specificity.

Conclusions: The frontal aperiodic exponent is a regionally specific biomarker of cognitive fatigue across MS and LCOF. Mechanistic interpretation suggests an altered prefrontal E/I balance, which could inform the development of targeted interventions to alleviate cognitive fatigue. It offers a clinically accessible tool to complement self-report, support trial stratification, and enable objective treatment monitoring. Importantly, its presence across distinct disorders highlights its value as a transdiagnostic marker of fatigue.

Background: Substance use is sustained partly through implicit associations toward drugs - i.e. automatic positive attitudes and motivational responses toward drug-related cues. Such implicit associations may be inferred by behavioral measures that capture the relative ease, speed, or priming of those associations. However, implicit opioid associations in patients with opioid use disorder (OUD) remain underexplored, and it is unknown whether mindfulness-based interventions such as Mindfulness-Oriented Recovery Enhancement (MORE) can modify implicit associations to support recovery.

Methods: We conducted secondary analyses of data from a clinical trial of adults with OUD (N = 154), randomized to either methadone treatment as usual (TAU) or TAU plus MORE. Participants completed an opioid implicit association test (IAT) at baseline. Days of opioid use were tracked over 16 weeks. Data were analyzed using logistic and zero-inflated negative binomial (ZINB) regressions to examine the impact of baseline IAT scores on future opioid use and MORE's moderating effect.

Results: In the TAU group, each 1-unit increase in IAT D score was associated with a 216% increase in the odds of opioid use (OR = 3.16, p = 0.049). However, in the MORE group, IAT scores were not significantly associated with future opioid use (OR = 0.58, p = 0.57). ZINB analysis revealed that each 1-unit increase in IAT D score predicted 0.96 fewer days of use in MORE relative to TAU (B = -1.25; SE = 0.58; p = 0.030).

Conclusions: Implicit attitudes toward opioids predicted higher opioid use among individuals receiving methadone. However, MORE attenuated this relationship and may counteract automatic cognitive biases that sustain opioid use.

While the concept of futility has been used widely in somatic medicine, to date, there has been limited consideration of its relevance to psychiatry. We summarize the findings of an international, multidisciplinary workshop involving clinicians, ethicists, philosophers, patient advocates, and persons with lived experience, which was focused on describing futility in psychiatry and developing ethical guidelines for making futility judgments. We outline three leading concepts of futility as they have been used in somatic medicine: physiological futility, quantitative futility, and qualitative futility. We examine the application of these concepts to the care of persons with mental illness, finding that the notion of qualitative futility is most likely to be fruitful. We consider how the concept of qualitative futility in psychiatry could relate to other ethically salient concepts such as terminal mental illness and recovery. We consider (1) who should have authority to make futility judgments in psychiatry (i.e. patients, providers, others), (2) what the process for introducing and evaluating futility judgments should be, and (3) how futility assessments should respond to patients' goals and values. We identify potential risks of futility assessments, including psychological harms and premature treatment discontinuation, as well as potential benefits, such as reductions in harmful treatments and helpful reevaluation of the goals of care. Workshop participants regarded the concept of psychiatric futility as potentially useful. They identified how the concept could be applied to psychiatric care, as well as ethical limits on doing so.

Background: Subjective cognitive complaints are poor predictors of neurodegenerative disease and future dementia. Errors in metacognition, positive or negative differences between actual and perceived performance, may partially explain this. We aimed to assess whether hypothesized indicators of underlying neurodegenerative factors (e.g. hippocampal atrophy) in mild cognitive impairment (MCI) were associated with overestimation of actual cognitive performance, and hypothesized non-degenerative factors (e.g. depression) were associated with underestimation of performance.

Methods: Metacognitive error was estimated from paired subjective and objective cognitive assessments using the Multifactorial Memory Questionnaire and Addenbrooke's Cognitive Examination - Revised, respectively. A normative model was developed with cognitively healthy older adults (n = 36), and applied to individuals with suspected MCI due to Alzheimer's disease (AD) or MCI with Lewy bodies (total n = 88). Theorized predictors of subjective overestimation or underestimation of performance (metacognitive error) were assessed, including demographics, AD biomarkers, and mental and physical ill health. Metacognitive error was also assessed as a predictor of conversion to dementia.

Results: Underestimation of cognitive function was associated with depressive symptoms, anxiety, and self-reported autonomic symptoms. Overestimation of cognitive function was associated with age, hippocampal atrophy, plasma glial fibrillary acidic protein, and subsequent dementia conversion.

Conclusions: Underestimation of cognitive function may reflect functional cognitive changes linked to mental and physical ill health, while overestimation of function may be a marker of neurodegenerative changes. Quantifying metacognitive error may provide a noninvasive screening tool for progressive MCI, requiring investigation in an independent sample.

Background: Anhedonia and rumination, a form of repetitive negative thinking (RNT), are key features of depression associated with poor treatment outcomes, chronic disease progression, and an increased risk of suicidality. Although their interaction is thought to sustain depressive states, the state-level mechanisms linking these symptoms remain poorly understood.

Methods: In this multilevel, randomized within-subjects study, 62 individuals (n = 38 females) with varying levels of depressive symptoms completed the Probabilistic Reward Task (PRT) under two conditions: experimentally induced RNT and an active control. Concurrent electroencephalography was employed to assess electroencephalographic markers of reward functioning.

Results: RNT significantly attenuated both reward response bias and feedback-related positivity (FRP) amplitudes, with the most pronounced effects in individuals with more severe depressive symptoms. These effects were not attributable to differences in task difficulty or perceptual cortical processing of PRT stimuli, supporting the specificity of RNT's impact on reward-related processes.

Conclusions: RNT may transiently disrupt behavioral and neural indicators of reward functioning. These findings suggest that cognitive states such as RNT can exacerbate or reveal the latent reward-processing deficits typically observed in individuals with anhedonia. This state-dependent sensitivity highlights the potential utility of targeting RNT to restore reward processing in depression.

Background: Parenthood is consistently identified as a protective factor for suicidal behavior. However, it remains unclear whether this relationship varies as a function of sex, age, time since birth, number of children, and other risk/protective factors.

Methods: We used Cox proportional hazards models to describe the relationship between the birth of up to four children and suicide attempt (SA) risk in Swedish individuals born between 1960 and 1980. Models were stratified by sex and controlled for a range of covariates. We tested whether the relationship between parenthood and SA risk varies based on age at first birth and explored whether SA risk differed based on education, genetic liability, cohabitation with one's co-parent, and geographic proximity to one's mother (the child's grandmother).

Results: The first year following childbirth was associated with reduced SA risk in mothers (hazard ratios [HRs] = 0.34-0.64) and fathers (HRs = 0.60-0.86). However, later time periods following the birth of one's third and fourth children were associated with elevated risk (HRs = 1.02-1.26). Moreover, age at first birth moderated the association between parenthood and SA: individuals who became parents at age 15 exhibited increased risk for SA (HRs = 2.81-5.30), while individuals with an older age at first birth (30+ years) experienced a reduction in risk (HRs = 0.31-0.92). The effect of parenthood also varied based on cohabitation and proximity to one's mother.

Conclusions: These findings underscore the complexity of the relationship between parenthood and SA, indicating that there are some subgroups for whom the transition to parenthood is not protective. Clinical outreach may be warranted as a preventative measure.