Pathogenic KCNQ2 variants are the most common genetic cause of neonatal-onset epilepsies, with phenotypes ranging from self-limited (familial) neonatal epilepsy (SeL(F)NE) to severe developmental and epileptic encephalopathy (KCNQ2-DEE). Sodium channel blockers (SCBs) have shown promise for seizure control in these disorders, but their impact on neurodevelopmental outcomes and possible relationship with timing of initiation remain incompletely understood. We leveraged a large, multicentre international cohort comprising 282 individuals with pathogenic KCNQ2 variants to retrospectively assess the effectiveness of antiseizure medications (ASMs), particularly SCBs, on seizure control and neurodevelopment. Individuals were grouped according to the predicted variant-specific functional effects: loss-of-function (LOF) variants known to be associated with SeL(F)NE or DEE respectively, and gain-of-function (GOF) variants. Epilepsy course, ASM effectiveness, and neurodevelopmental milestones were systematically collected and analysed, including time-to-event and adjusted outcome analyses. SCBs, especially carbamazepine (CBZ) and oxcarbazepine (OXC), emerged as the most effective ASMs in both LOF groups. In LOF KCNQ2-DEE, time-to-event analyses showed that early SCB initiation (≤1 month) was associated with earlier seizure offset. Early SCB initiation was also associated with significantly more favourable neurodevelopmental outcomes, including higher rates of attaining major motor milestones. This association remained significant after adjustment for seizure control by 1 month and total ASM burden. Considerable phenotypic variability persisted, with some individuals experiencing severe impairment despite early seizure control and SCB initiation, suggesting that variant severity and additional genetic or biological modifiers contribute to outcome heterogeneity.Our results support the use of SCBs, particularly CBZ and OXC, as first-line therapy in (LOF) KCNQ2-DEE and SeL(F)NE. Earlier SCB initiation was associated with earlier seizure offset and more favourable developmental outcomes, underscoring the importance of early genetic diagnosis and timely SCB therapy. We however emphasise that early treatment is not universally transformative and further prospective work, including exploration of targeted therapies and standardised neurodevelopmental assessments, is needed to optimise long-term outcomes in this heterogeneous population.

Disordered eating is a subclinical constellation of symptoms-including uncontrolled eating, emotional eating, and cognitive restraint-that constitutes an important risk factor for eating disorders. We examined the associations between childhood maltreatment and disordered eating symptoms and whether food reward drive is a mediator in this relationship. Domain-general anticipatory pleasure was examined as an alternative mediator.

Blue-space exposure has been studied in relation to mental health, but studies have often labeled non-equivalent outcomes-including depression-focused symptoms, psychological distress, mental-health functioning, diagnostic disorders, and binary self-reports-as "depression." This systematic review examined how depression-related outcomes were operationalized in studies of adult blue-space exposure and whether the available evidence supported quantitative synthesis. The review was reported in accordance with the PRISMA 2020 reporting guideline. Six databases were searched for studies published between January 2000 and March 2026, and the protocol was prospectively registered in PROSPERO. Eight observational studies involving 35,797 adults were included. Blue-space exposure definitions, exposure contrasts, outcome constructs, covariate adjustment, and effect metrics varied substantially. One study using the 15-item Geriatric Depression Scale reported an inverse adjusted association between street-view blue space and geriatric depressive symptoms, but its exposure contrast, outcome scale, population, and setting were not directly comparable with those of the other studies. Because the available estimates could not be transparently expressed on a common effect scale, no meta-analysis was performed; findings were synthesized as structured study-level evidence. Current evidence does not establish whether associations between blue-space exposure and depression-related outcomes differ by outcome-measurement category. Future studies should prespecify the target construct, select measures aligned with the proposed mechanism and study population, and report sufficient domain- or item-level information to support transparent evidence synthesis.

Chronic liver diseases and periodontitis are prevalent inflammatory disorders that impose substantial global health and economic burdens. Increasing evidence supports an oral-hepatic axis through which periodontal dysbiosis and chronic oral inflammation may influence hepatic homeostasis and disease progression. Epidemiologic studies have linked periodontitis with metabolic dysfunction-associated steatotic liver disease (MASLD), nonalcoholic fatty liver disease (NAFLD), viral hepatitis, cirrhosis, and hepatocellular carcinoma. Although many associations persist after adjustment for shared risk factors, including obesity, diabetes, smoking, nutritional status, and socioeconomic factors, the independent contribution of periodontitis to liver disease remains unclear. Experimental and translational studies indicate that periodontal pathogens and their virulence factors promote systemic inflammation, endotoxemia, microbial translocation, immune dysregulation, and alterations in gut microbial ecology. Nutritional factors may further influence these interactions through their effects on host immunity, inflammation, and microbial communities. Together, these mechanisms converge along the oral-gut-liver axis to activate hepatic inflammatory, oxidative stress and profibrotic pathways that contribute to steatosis, immune activation, and fibrogenesis. Emerging evidence suggests that trained immunity, driven by metabolic and epigenetic reprogramming, may represent an additional mechanism linking periodontitis and liver disease warranting future studies. Preliminary studies indicate that periodontal therapy may reduce systemic inflammatory burden and improve hepatic biomarkers; however, evidence for an effect on liver disease progression or clinical outcomes remains limited. Similarly, hepatic dysfunction may exacerbate immune dysregulation and periodontal breakdown, reinforcing an inflammatory loop. However, overall causal relationships remain to be established. This review summarizes current epidemiological, clinical, and mechanistic evidence linking periodontitis and chronic liver diseases, highlighting the oral-gut-liver axis, shared immunometabolic and nutritional pathways. Understanding these interactions shows the significance of integrated dental-medical care and opens new avenues for prevention and adjunctive therapy to sustain oral and hepatic health.