Psychological Medicine最新文献

Background: Drug use disorder (DUD) clusters in families due partly to shared environment, including sibling influences. Low academic achievement (AA) in adolescence increases DUD risk. This study examined whether low AA in an older sibling causally increases DUD risk in younger siblings.

Methods: We studied all Swedish full sibling pairs (n = 309,666) born 1972-1985 and ≤ 5 years apart. Older sibling AA was assessed at age 16. Using Month-of-Birth (MoB) as an instrument, we conducted instrumental variable (IV) analyses and propensity score (PS) models to evaluate the causal impact of older sibling AA on younger sibling DUD risk, assessed by DUD registration in national medical, criminal, or pharmacy registries.

Results: Older sibling AA significantly predicted younger sibling DUD risk across models. Beta coefficients (±95% CI) were 2.04 (1.97-2.12) in raw analysis, 1.88 (0.74-3.02) in IV, and 1.26 (1.17-1.34) in PS models. Together with the strong first-stage association, the IV estimates remain positive under small departures from the ideal identifying assumptions. Effect sizes declined with increasing sibling age differences (p = 0.036 for IV; p < 0.0001 for PS) and were strongest in male-male pairs (IV: 4.01 [1.42-6.61]; PS: 1.74 [1.55-1.93]). Mediation by older sibling DUD was modest.

Conclusions: Findings from two causal inference approaches support a largely causal link between low AA in an older sibling and increased DUD risk in younger siblings. Stronger effects in close-aged and male-male pairs further support this conclusion. Interventions to improve AA in older siblings may yield indirect preventive benefits for younger siblings.

Background: Childhood trauma is common in functional motor disorder (FMD), but it is unclear whether specific trauma dimensions are differentially linked to symptom burden, and whether depression, anxiety, or multimorbidity can mediate these associations.

Methods: We conducted a cross-sectional case-control study including 322 patients with clinically definite FMD and 215 neurologically healthy controls, balanced with respect to age and sex. Six outcomes - motor symptom severity, cognitive complaints, depression, anxiety, fatigue, and pain - were jointly modeled using Bayesian multivariate regression with Childhood Trauma Questionnaire subscales as predictors. Bayesian structural equation modeling tested mediation by depression, anxiety, and multimorbidity.

Results: In FMD, emotional abuse was the most consistent trauma correlate, associated with higher depression (β = 0.37, 95% CrI 0.22-0.51), anxiety (β = 0.32, 95% CrI 0.16-0.47), cognitive complaints (β = 0.27, 95% CrI 0.11-0.42), fatigue (β = 0.17, 95% CrI 0.03-0.32), and motor symptom severity (β = 0.15, 95% CrI 0.04-0.25). Mediation analyses indicated that affective symptoms fully accounted for trauma-symptom associations (indirect effect β = 0.42, 95% CrI 0.27-0.56). Multimorbidity was associated with more severe affective symptoms (β = 0.24, 95% CrI 0.12-0.37) and FMD symptoms (β = 0.24, 95% CrI 0.07-0.42) but did not mediate trauma-symptom relationships.

Conclusions: Emotional abuse is a key developmental risk factor for FMD, with its effects on symptom severity mediated by depression and anxiety. Multimorbidity increases symptom burden but is not a primary pathway linking trauma to FMD. Findings support routine trauma and affective symptom screening in FMD and targeted psychotherapeutic interventions.

Background: Depression as a mental illness is commonly observed to co-occur with various somatic diseases, such as gastrointestinal diseases. However, previous studies have primarily focused on the risk of mental disorders following physical illnesses. Our study took depression as a risk factor, attempting to explore its relationship with gastrointestinal diseases.

Methods: A total of 457,940 participants (aged 37-73 years) in the UK Biobank were included. The Cox proportional hazards model was used to assess the relationship between depression and gastrointestinal diseases. Mendelian randomization assessed the causal link between depression and gastrointestinal disorders, and seven machine learning algorithms (including LightGBM, XGBoost, and Random Forest) were trained in the total population to develop predictive models for incident gastrointestinal diseases, with model performance evaluated using the area under the receiver operating characteristic curve (AUC).

Results: During a median follow-up period of 13.7 years, 9563 esophagitis events, 36,420 gastroesophageal reflux disease events, 5469 gastric ulcer events, 3096 duodenal ulcer events, 37,225 gastritis and duodenitis events, and 9153 dyspepsia events were recorded. After adjusting for covariates, depression was associated with increased risk of all six diseases. Two-sample MR analysis supported a causal association. Machine learning models demonstrated good discrimination, with the highest predictive accuracy observed for duodenal ulcer (AUC = 0.76) and gastric ulcer (AUC = 0.75).

Conclusions: Addressing depression as a modifiable risk factor may reduce gastrointestinal disease risk, especially in disadvantaged populations, by integrating mental health care into primary care and using predictive models for early intervention.

Individuals at clinical high risk (CHR) for psychosis exhibit both baseline and progressive brain structural abnormalities. However, the extent to which these changes reflect neurobiological trajectories of illness progression versus iatrogenic effects of antipsychotic (AP) treatment remains unresolved. A total of 148 AP-naïve CHRs and 65 healthy controls (HCs) underwent baseline structural magnetic resonance imaging (MRI) scans. One hundred thirty CHRs received second-generation AP treatment and completed 2-month follow-up scans. HCs also completed the follow-up scans. We compared baseline and longitudinal brain volume changes between CHRs and HCs and explored the relationship between AP treatment and brain structural changes in CHR. At baseline, CHRs showed enlarged third and inferior lateral ventricles compared to HCs. Within CHRs, larger ventricular, as well as smaller hippocampus and amygdala volumes, were associated with more severe symptoms and poorer functioning. No cortical volume differences were observed between groups at baseline, nor were cortical volumes related to clinical symptoms. After 2-month AP treatment, CHRs exhibited continued ventricular enlargement, reduced accumbens volume, and widespread cortical volume loss relative to HCs. Notably, cortical volume reductions were dose-dependent, with higher AP dose correlating with more pronounced cortical reductions. Additionally, cortical volume changes were linked to treatment response, with high-dose responders showing more significant HC-referenced changes compared to high-dose non-responders, low-dose responders, and low-dose non-responders. Our findings underscore the complex, region-specific, and clinically relevant neuroanatomical changes in CHR individuals, emphasizing the critical need to account for AP exposure in CHR neuroimaging studies.

Background: The impact of combat injury on the development of chronic pain and mental health concerns in combat-exposed populations is unknown. This study examined associations of combat injury and injury-related pain with pain-related factors and mental health outcomes, and potential mediation of the relation between combat injury and mental health outcomes by pain-related factors.

Methods: Pain interference, pain catastrophizing, pain intensity, post-traumatic stress disorder (PTSD), and major depressive episode (MDE) were assessed in (1) a probability sample of US Army soldiers and veterans cross-sectionally and (2) US Army soldiers before and 1, 3, and 9 months after deployment to Afghanistan. Associations among these variables were modeled using logistic regression and multiple mediation analyses.

Results: Among 5003 service members with cross-sectional data, combat injury-related pain was associated with increased odds of clinically significant pain intensity (OR=2.69), pain interference (OR=3.69), MDE (OR=2.17), and PTSD (OR=3.96) relative to pain from other injuries and conditions. Among 4645 service members assessed pre- and post-deployment, combat injury was associated with increased odds of new-onset pain interference (OR=2.78), pain catastrophizing (OR=2.75), PTSD (OR=4.06), and MDE (OR=2.56) 3 months post-deployment, and PTSD (OR=2.86) and MDE (OR=1.74) 9 months post-deployment. Pain-related factors mediated the relations of combat injury with post-deployment PTSD and MDE.

Conclusions: Combat injury is associated with greater odds of pain interference, pain catastrophizing, PTSD, and MDE compared to other sources of pain in a cohort of US service members. Efforts to address pain-related factors following combat injury may mitigate the risk of subsequent chronic pain and mental health disorders.