Past studies indicate daily increases in estrogen across the menstrual cycle protect against binge-eating (BE) phenotypes (e.g. emotional eating), whereas increases in progesterone enhance risk. Two previous studies from our laboratory suggest these associations could be due to differential genomic effects of estrogen and progesterone. However, these prior studies were unable to directly model effects of daily changes in hormones on etiologic risk, instead relying on menstrual cycle phase or mean hormone levels. The current study used newly modified twin models to examine, for the first time, the effects of daily changes in estradiol and progesterone on genetic/environmental influences on emotional eating in our archival twin sample assessed across 45 consecutive days.

Participants included 468 female twins from the Michigan State University Twin Registry. Daily emotional eating was assessed with the Dutch Eating Behavior Questionnaire, and daily saliva samples were assayed for ovarian hormone levels. Modified genotype × environment interaction models examined daily changes in genetic/environmental effects across hormone levels.

Findings revealed differential effects of daily changes in hormones on etiologic risk, with increasing genetic influences across progesterone levels, and increasing shared environmental influences at the highest estradiol levels. Results were consistent across primary analyses examining all study days and sensitivity analyses within menstrual cycle phases.

Findings are significant in being the first to identify changes in etiologic risk for BE symptoms across daily hormone levels and highlighting novel mechanisms (e.g. hormone threshold effects, regulation of conserved genes) that may contribute to the etiology of BE.

Achieving equitable healthcare access is a global challenge. Improving whole-population mental health and reducing the global burden of mental disorders is a key recommendation of the 2018 Lancet Global Mental Health Commission, which proposed monitoring national indicators, including the proportion of people with severe mental disorders who are service-users. This study aims to derive an equity indicator from national datasets integrating need, service utilisation and socioeconomic status, and demonstrate its utility in identifying gaps in mental health service use amongst those with the greatest need, thereby guiding equitable healthcare delivery.

We present a case study of a universal health insurance scheme (Medicare) in Australia. We developed the equity indicator using three national datasets. Geographic areas were linked to an area-based socioeconomic deprivation quintile (Census 2016). Per geographic area, we estimated the number with a mental healthcare need using scores ≥30 on the Kessler-10 (Australian National Health Surveys 2015 and 2018), and obtained the number of services used, defined as mental health-related contacts with general practitioners and mental health professionals (Medicare administrative data 2015–2019). We divided the number of services by the population with an estimated mental healthcare need and averaged these use-rates across each socioeconomic deprivation quintile. The equity indicator is the ratio of the use-rates in the least versus most deprived quintiles.

Those estimated to have the greatest need for mental healthcare in 2019 ranged between 8.2% in the most disadvantaged area quintile (Q1) and 2.4% in the least (Q5), corresponding to a proportional increase of 27.7% in Q1 and 19.5% in Q5 since 2015. Equity-indicator-adjusted service rates of 4.2 (3.8–4.6) and 23.9 (22.4–25.4) showed that individuals with the highest need for care residing in Q1 areas received a stark 6 times fewer services compared to their Q5 counterparts, producing an equity indicator of 6.

As the global prevalence of common mental disorders may be increasing, it is crucial to calculate robust indicators evaluating the equity of mental health service use. In this Australian case study, we developed an equity indicator enabling the direct comparison of geographic areas with different need profiles. The results revealed striking inequities that persisted despite publicly-funded universal healthcare, recent service reforms and being a high-income country. This study demonstrates the importance and feasibility of generating such an indicator to inform and empower communities, healthcare providers and policymakers to pursue equitable service provision.

To evaluate the motor proficiency, identify risk factors for abnormal motor scores, and examine the relationship between motor proficiency and health-related quality of life in school-aged patients with CHD.

Patients ≥ 4 years old referred to the cardiac neurodevelopmental program between June 2017 and April 2020 were included. Motor skills were evaluated by therapist-administered Bruininks-Oseretsky Test of Motor Proficiency Second-Edition Short Form and parent-reported Adaptive Behavior Assessment System and Patient-Reported Outcomes Measurement Inventory System Physical Functioning questionnaires. Neuropsychological status and health-related quality of life were assessed using a battery of validated questionnaires. Demographic, clinical, and educational variables were collected from electronic medical records. General linear modelling was used for multivariable analysis.

The median motor proficiency score was the 10th percentile, and the cohort (n = 272; mean age: 9.1 years) scored well below normative values on all administered neuropsychological questionnaires. In the final multivariable model, worse motor proficiency score was associated with family income, presence of a genetic syndrome, developmental delay recognised in infancy, abnormal neuroimaging, history of heart transplant, and executive dysfunction, and presence of an individualised education plan (p < 0.03 for all predictors). Worse motor proficiency correlated with reduced health-related quality of life. Parent-reported adaptive behaviour (p < 0.001) and physical functioning (p < 0.001) had a strong association with motor proficiency scores.

This study highlights the need for continued motor screening for school-aged patients with CHD. Clinical factors, neuropsychological screening results, and health-related quality of life were associated with worse motor proficiency.

Educational attainment (EduA) is correlated with life outcomes, and EduA itself is influenced by both cognitive and non-cognitive factors. A recent study performed a ‘genome-wide association study (GWAS) by subtraction,’ subtracting genetic effects for cognitive performance from an educational attainment GWAS to create orthogonal ‘cognitive’ and ‘non-cognitive’ factors. These cognitive and non-cognitive factors showed associations with behavioral health outcomes in adults; however, whether these correlations are present during childhood is unclear.

Using data from up to 5517 youth (ages 9–11) of European ancestry from the ongoing Adolescent Brain Cognitive DevelopmentSM Study, we examined associations between polygenic scores (PGS) for cognitive and non-cognitive factors and cognition, risk tolerance, decision-making & personality, substance initiation, psychopathology, and brain structure (e.g. volume, fractional anisotropy [FA]). Within-sibling analyses estimated whether observed genetic associations may be consistent with direct genetic effects.

Both PGSs were associated with greater cognition and lower impulsivity, drive, and severity of psychotic-like experiences. The cognitive PGS was also associated with greater risk tolerance, increased odds of choosing delayed reward, and decreased likelihood of ADHD and bipolar disorder; the non-cognitive PGS was associated with lack of perseverance and reward responsiveness. Cognitive PGS were more strongly associated with larger regional cortical volumes; non-cognitive PGS were more strongly associated with higher FA. All associations were characterized by small effects.

While the small sizes of these associations suggest that they are not effective for prediction within individuals, cognitive and non-cognitive PGS show unique associations with phenotypes in childhood at the population level.

Clinical research is critical for healthcare advancement, but participant recruitment remains challenging. Clinical research professionals (CRPs; e.g., clinical research coordinator, research assistant) perform eligibility prescreening, ensuring adherence to study criteria while upholding scientific and ethical standards. This study investigates the key information CRP prioritizes during eligibility prescreening, providing insights to optimize data standardization, and recruitment approaches.

We conducted a freelisting survey targeting 150 CRPs from diverse domains (i.e., neurological disorders, rare diseases, and other diseases) where they listed essential information they look for from medical records, participant/caregiver inquiries, and discussions with principal investigators to determine a potential participant’s research eligibility. We calculated the salience scores of listed items using Anthropac, followed by a two-level analytic procedure to classify and thematically categorize the data.

The majority of participants were female (81%), identified as White (44%) and as non-Hispanic (64.5%). The first-level analysis universally emphasized age, medication list, and medical history across all domains. The second-level analysis illuminated domain-specific approaches in information retrieval: for instance, history of present illness was notably significant in neurological disorders during participant and principal investigator inquiries, while research participation was distinctly salient in potential participant inquiries within the rare disease domain.

This study unveils the intricacies of eligibility prescreening, with both universal and domain-specific methods observed. Variations in data use across domains suggest the need for tailored prescreening in clinical research. Incorporating these insights into CRP training and refining prescreening tools, combined with an ethical, participant-focused approach, can advance eligibility prescreening practices.

Major depressive disorder (MDD) is a tremendous global disease burden and the leading cause of disability worldwide. Unfortunately, individuals diagnosed with MDD typically experience a delayed response to traditional antidepressants and many do not adequately respond to pharmacotherapy, even after multiple trials. The critical need for novel antidepressant treatments has led to a recent resurgence in the clinical application of psychedelics, and intravenous ketamine, which has been investigated as a rapid-acting treatment for treatment resistant depression (TRD) as well acute suicidal ideation and behavior. However, variations in the type and quality of experimental design as well as a range of treatment outcomes in clinical trials of ketamine make interpretation of this large body of literature challenging.

This umbrella review aims to advance our understanding of the effectiveness of intravenous ketamine as a pharmacotherapy for TRD by providing a systematic, quantitative, large-scale synthesis of the empirical literature.

We performed a comprehensive PubMed search for peer-reviewed meta-analyses of primary studies of intravenous ketamine used in the treatment of TRD. Meta-analysis and primary studies were then screened by two independent coding teams according to pre-established inclusion criteria as well as PRISMA and METRICS guidelines. We then employed metaumbrella, a statistical package developed in R, to perform effect size calculations and conversions as well as statistical tests.

In a large-scale analysis of 1,182 participants across 51 primary studies, repeated-dose administration of intravenous ketamine demonstrated statistically significant effects (p<0.05) compared to placebo-controlled as well as other experimental conditions in patients with TRD, as measured by standardized clinician-administered and self-report depression symptom severity scales.

This study provides large-scale, quantitative support for the effectiveness of intravenous, repeated-dose ketamine as a therapy for TRD and a report of the relative effectiveness of several treatment parameters across a large and rapidly growing literature. Future investigations should use similar analytic tools to examine evidence-stratified conditions and the comparative effectiveness of other routes of administration and treatment schedules as well as the moderating influence of other clinical and demographic variables on the effectiveness of ketamine on TRD and suicidal ideation and behavior.

None Declared

There has been rapidly growing interest in understanding the pharmaceutical and clinical properties of psychedelic and dissociative drugs, with a particular focus on ketamine. This compound, long known for its anesthetic and dissociative properties, has garnered attention due to its potential to rapidly alleviate symptoms of depression, especially in individuals with treatment-resistant depression (TRD) or acute suicidal ideation or behavior. However, while ketamine’s psychopharmacological effects are increasingly well-documented, the specific patterns of its neural impact remain a subject of exploration and basic questions remain about its effects on functional activation in both clinical and healthy populations.

This meta-analysis seeks to contribute to the evolving landscape of neuroscience research on dissociative drugs such as ketamine by comprehensively examining the effects of acute ketamine administration on neural activation, as measured by functional magnetic resonance imaging (fMRI), in healthy participants.

We conducted a meta-analysis of existing fMRI activation studies of ketamine using multilevel kernel density analysis (MKDA). Following a comprehensive PubMed search, we quantitatively synthesized all published primary fMRI whole-brain activation studies of the effects of ketamine in healthy subjects with no overlapping samples (N=18). This approach also incorporated ensemble thresholding (α=0.05-0.0001) to minimize cluster-size detection bias and Monte Carlo simulations to correct for multiple comparisons.

Our meta-analysis revealed statistically significant (p<0.05-0.0001; FWE-corrected) alterations in neural activation in multiple cortical and subcortical regions following the administration of ketamine to healthy participants (N=306).

These results offer valuable insights into the functional neuroanatomical effects caused by acute ketamine administration. These findings may also inform development of therapeutic applications of ketamine for various psychiatric and neurological conditions. Future studies should investigate the neural effects of ketamine administration, including both short-term and long-term effects, in clinical populations and their relation to clinical and functional improvements.

None Declared