Individuals with bipolar disorder often experience reduced quality of life (QoL). Transcranial direct current stimulation (tDCS) is a promising non-invasive treatment for bipolar depression that is portable, safe, and suitable for use at home. We developed a home-based tDCS protocol with real-time remote supervision and examined its effect on QoL in bipolar depression. In an open‐label design, 44 participants (31 women) with bipolar depression of at least a moderate severity received 21 sessions of home‐based tDCS (2 mA, 30 min, F3 anode/F4 cathode) over 6 weeks, with a follow-up visit conducted 5 months from baseline. QoL was assessed using the quality of life enjoyment and satisfaction questionnaire (Q-LES-Q) at baseline, week 2, end of treatment, and follow-up session. Baseline and post treatment scores were compared with healthy control participants (28 adults; 17 women). At baseline and at the end of treatment, bipolar participants showed a significantly lower Q-LES-Q score than healthy controls (p < 0.001). Within the bipolar group, there was a significant improvement in total Q-LES-Q scores (p < 0.001) and across multiple domains by week 6 and remained elevated at follow-up. Changes in Q-LES-Q were no longer significant after adjustment for depressive symptoms. A 6-week course of supervised home-based tDCS was associated with significant QoL improvements in bipolar depression, which appeared to be closely linked to reduction in depressive symptoms. Randomized, sham‐controlled trials are warranted to clarify the specific contribution of tDCS to improve QoL in bipolar depression.

Background Bipolar disorder is an episodic mental illness, often requiring complex pharmacological management. Lithium is a first-line treatment, while antidepressant monotherapy can precipitate mania symptoms in some patients. Aims To (a) describe patterns of antidepressant, antipsychotic and mood stabiliser prescribing in the 12-month periods before and after first-recorded bipolar diagnosis; (b) describe treatment trajectories in the year post-diagnosis; and (c) investigate associations between sociodemographic and treatment-related characteristics of (i) antidepressant monotherapy and (ii) lithium prescription post-diagnosis. Method A longitudinal cohort study of patients with a first-recorded diagnosis of bipolar disorder between 2000 and 2022 derived from Clinical Practice Research Datalink. Prescriptions for antidepressants, antipsychotics and mood stabilisers were examined in the 12 months before and after diagnosis. Logistic regression models tested associations between sociodemographic and treatment-related characteristics and prescribing outcomes. A web application ( https://dop-mhds.shinyapps.io/bpd-prescribing-uk-shiny/ ) was developed to visualise treatment trajectories over the year following diagnosis. Results We included 40 965 patients with a first-recorded diagnosis of bipolar disorder between 2000 and 2022 (median age at diagnosis 43 years, 60.9% female, 11.1% ethnic minority). Of these, 32 460 (79.2%) were prescribed a relevant medication in the year prior to diagnosis compared with 37 208 (90.8%) in the year after. Antidepressant monotherapy was the most common pre-diagnosis treatment (48.4%), but was also prescribed to 28.9% during at least 1 month in the year after diagnosis. Antipsychotic monotherapy was the most common post-diagnosis treatment (36.0%). Lithium was prescribed to 18.5% within 1 year of diagnosis, with 4.0% receiving it as first-line monotherapy. Almost half (46.0%) switched medication at least once within 1 year. Males, ethnic minorities and patients residing in the most deprived areas had lower odds of receiving either lithium or antidepressant monotherapy. Conclusions Prescribing patterns for bipolar disorder in the UK are highly variable and often outside of guideline recommendations, with persistent use of antidepressant monotherapy and potential under-utilisation of lithium.

Summary Background Major depressive disorder (MDD), a leading cause of disability worldwide, exhibits substantial heterogeneity in treatment outcomes. Patients who do not respond to standard antidepressant therapy account for the majority of MDD’s disease burden. Risk factors have been implicated in treatment response, including genes impacting on how antidepressants are metabolised. Yet, despite its clinical importance, risk factors for treatment-resistant depression (TRD) remain unexplored in low- and middle-income countries (LMIC). We used data from the DIVERGE study on MDD to investigate the risk factors of TRD in Pakistan. Methods DIVERGE is a genetic epidemiological study that recruited adult MDD patients (≥18 years) between Sep 27,2021 to Jun 30, 2025, from psychiatric care facilities across Pakistan. Detailed phenotypic information was collected by trained interviewers and blood samples taken. Infinium Global Diversity Array with Enhanced PGx-8 from Illumina was used for genotyping followed by DRAGEN calling to infer metaboliser phenotypes for Cytochrome P450 (CYP) enzyme genes. We defined TRD as minimal to no improvement after ≥12 weeks of adherent antidepressant therapy. We conducted multi-level logistic regression to test the association of demographic, clinical and pharmacogenetic variables with TRD. Findings Among 3,677 eligible patients, polypharmacy was rampant; 86% were prescribed another psychotropic drug along with an antidepressant. Psychological therapies were uncommon (6%) while 49% of patients had previously visited to a religious leader/faith healer in relation to their mental health problems. TRD was experienced by 34% (95%CI: 32-36%) patients. The TRD group was characterised by more psychotic symptoms and suicidal behaviour (OR=1.39, 95%CI=1.04-1.84, p=0.02; OR=1.03, 95%CI=1.01-1.05, p=0.005). Social support (OR=0.55, 95%CI=0.44-0.69, p=1.4x10 -7 ) and parents being first cousins (OR=0.81, 95%CI=0.69-0.96, p=0.01) were associated with lower odds of TRD. In 1,085 patients with CYP enzyme data, poor (OR=1.85, 95%CI=1.11-3.07, p=0.01) and ultra-rapid (OR=3.11, 95%CI=1.59-6.12, p=0.0009) metabolizers for CYP2C19 had increased risk of TRD compared with normal metabolisers. Interpretation There was an excessive use of polypharmacy in the treatment of depression while psychological therapies were uncommon highlighting the need for more evidence-based practice. This first large study of MDD from Pakistan uncovered the importance of culture-specific forms of social support in preventing TRD, highlighting opportunities for interventions in low-income settings. Pharmacogenetic markers can be leveraged to predict TRD.

Most genetic variants associated with complex heritability phenotypes lie in non-coding regions and are thought to influence disease risk by regulating gene expression. However, most transcriptome-wide association approaches primarily model local (cis) genetic effects, leaving much of gene regulation unexplained. Here, we show that incorporating distal (trans) regulatory effects improves the prediction of gene expression and the identification of disease-associated genes. Using RNA sequencing data from six human post-mortem brain regions, we developed INGENE and MODULE, two models capturing the combined influence of candidate trans-acting variants within gene coexpression networks. Integrating these models with conventional cis-based predictors improved gene expression imputation (maximum likelihood estimation, α = 0.05) for 18,744 genes across regions. Applying this framework to Psychiatric Genomics Consortium wave 3 genotypes identified 766 genes associated with schizophrenia (PFDR < 0.01), including 641 not previously reported by transcriptome-wide analyses. These findings highlight the contribution of distal regulatory mechanisms and gene network interactions to schizophrenia risk.

Aims: Various antipsychotics and antidepressants have pharmacogenomic guidelines available from international sources, recommending dose adjustments and/or alternative drug selection based on a patient’s genetic profile. However, pharmacogenomic implementation remains limited in UK healthcare. Methods: Genetics and Environment in Mental Health Study (GEMS) is a prospective study of pharmacogenomic testing in psychosis; the first in the UK. Adults taking an antipsychotic medication have been recruited across England. Participants provided a DNA sample for genotyping on a multi-gene panel, selected from evidence-based pharmacogenomic guidelines. Pharmacogenomic reports, displaying the participants’ genetic profile and any alterations to usual prescribing guidelines were delivered to the prescribing clinician. Any changes to the participants’ prescription were at the discretion of the clinician. Results: A diverse sample of 584 people taking an antipsychotic medication has been recruited so far, consisting of participants aged 18-82 years, with an even split of male and female participants, and 32.5% of the sample from Black, Asian, and Minority Ethnic (BAME) backgrounds. Across the four genes with pharmacogenomic guidelines in psychiatry ( CYP2D6 , CYP2C19 , CYP2B6 , and CYP3A4 ), 90.4% of the sample carried at least one actionable variant. At the time of recruitment, 20.9% of participants carried a pharmacogenomic variant that (based on current guidelines) was actionable for the antipsychotic and/or antidepressant they were currently prescribed. By medication class, 6.8% were taking an antipsychotic and 15.1% were taking an antidepressant for which they had a pharmacogenomic recommendation. A further 69.5% of the sample would have a recommendation for at least one antipsychotic or antidepressant medication. Based on the estimated population prevalence of pharmacogenomic actionable variants and prescription data in England, approximately 45% of people would be expected to carry an actionable variant for antipsychotic medications and at least 61% would be expected to carry an actionable variant for antidepressants. This equates to approximately 285,000 people currently taking an antipsychotic medication that could have a pharmacogenomic recommendation and at least 4.2 million people taking an antidepressant with a pharmacogenomic recommendation in England. Conclusion: Pharmacogenomics has the potential to personalise medication prescriptions and improve patient outcomes. Workforce training and implementation barriers present a challenge. However, in line with the NHS 10 Year Plan goal of 50% of healthcare interventions being genomics-informed by 2035, psychiatry is one of the most promising areas for the implementation of pharmacogenomic-guided prescribing.

Clozapine is the most effective therapy for treatment-resistant schizophrenia, although it can cause neutropenia. In many countries, neutrophil count monitoring is mandatory for people taking clozapine, who must remain above a minimum threshold to start and continue treatment. Some people have low neutrophil counts without increased infection risk, caused by a homozygous variant in ACKR1 and termed ACKR1/DARC-associated neutropenia (ADAN). When ADAN is confirmed, reduced neutrophil count thresholds are applied to allow people to start and continue clozapine. However, ADAN diagnoses are often missed, resulting in reduced access to clozapine and unnecessary discontinuation. We review the evidence for ACKR1 genetic testing to rapidly identify ADAN in people taking clozapine. With multidisciplinary input, we recommend internationally relevant test eligibility criteria, comprising pre-emptive and reactive testing strategies, and we conduct a health economic analysis, estimating total cost savings between £42,732 and £727,990 for the UK healthcare system during the first year of testing. Finally, we propose how to integrate these criteria into clinical practice to enable equitable access to clozapine. This Perspective considers the addition of ACKR1 genetic testing for identifying ACKR1/DARC-associated neutropenia in patients receiving clozapine, recommending eligibility criteria and testing strategies while estimating substantial cost savings for the UK healthcare system and enhancing equitable treatment access.

A survey was conducted to determine attitudes, knowledge, and educational needs of mental health professionals regarding pharmacogenomics. We recruited 128 clinicians working in mental health in England, and we assessed their experiences using an adapted version of the "U-PGx Clinician's Questionnaire". Responding clinicians had positive attitudes towards pharmacogenomics testing, although they lacked confidence in ordering and interpreting tests, for which most had never received any formal training. Only 6% of clinicians answered all 4 knowledge testing questions correctly, and barriers to clinical implementation included lack of familiarity and knowledge for several pharmacogenomics concepts, such as drug metabolism and genetics, as well as needing support from their working institution. Looking ahead, we found that accredited workshops and patient cases were preferred learning formats, and we suggest tailored education programmes to enable mental health professionals to apply pharmacogenomics in clinical practice.

Non-coding genetic variants statistically associated with complex heritability phenotypes are thought to act primarily through transcriptome regulatory mechanisms. Predictions of gene expression in tissue like the human brain traditionally rely primarily on cis -eQTLs. Here, we introduce INGENE and MODULE, trans -eQTLs models designed to enhance the prediction of gene expression by capturing the collective impact of candidate trans -eQTLs acting within co-expression networks. Exploiting RNA-seq data in six post-mortem brain regions (amygdala, caudate nucleus, dorsal/subgenual anterior cingulate cortex, dorsolateral prefrontal cortex, and hippocampus), we validate our models on two testing datasets, demonstrating increased gene predictability compared to both an original cis -based model and to EpiXcan, the leading benchmark in cis -model performance. Integration of cis - and trans -predictions significantly improves gene-level expression imputation (MLE α= 0.05) for 18,744 genes across the six brain regions considered. Applying cis and trans models to PGC wave 3 genotypes identifies 766 SCZ-associated genes across brain regions (pFDR < .01), emphasizing the complementary nature of cis and trans predictions in trait association discovery. Of these genes, 641 represent novel transcriptome-wide associations with schizophrenia, highlighting the role of trans -heritability and genetic interactions underlying risk for this disorder, in addition to further supporting 125 previous candidates. ### Competing Interest Statement A. Bertolino received consulting fees from Biogen and lecture fees from Otsuka, Janssen, and Lundbeck. D. Weinberger serves on the scientific advisory boards of Sage Therapeutics and Pasithea Therapeutics. G. Pergola and G. C. Kikidis received lecture fees from Lundbeck. A. K. Malhotra is a consultant to Genomind, InformedDNA and Concert Pharmaceuticals. M. C. O Donovan, M. J. Owen, and J. T. R. Walters are supported by collaborative research grants from Takeda Pharmaceuticals. O. A. Andreassen is a consultant for HealthLytix and received speaker s honoraria from Lundbeck. C. Arango has been a consultant to or has received honoraria or grants from Acadia, Angelini, Gedeon Richter, Janssen Cilag, Lundbeck, Minerva, Otsuka, Roche, Sage, Servier, Shire, Schering Plough, Sumitomo Dainippon Pharma, Sunovion and Takeda. Research Projects of National Relevance 2020 (PRIN 2020; 2020WSCSLZ) Research Projects of National Relevance 2022 (PRIN 2022; 2022KXJYJA) Research Projects Of National Relevance PNRR 2022 (P2022HNBJX) The LIBD funded the collection and analysis of postmortem brain tissue

Carbamazepine is licensed in the United Kingdom for the treatment of epilepsy, bipolar disorder and trigeminal neuralgia. The related compounds oxcarbazepine and eslicarbazepine are licensed for the treatment of epilepsy. These drugs can cause immune-mediated hypersensitivity reactions, which typically affect the skin, and can be of variable severity. The liver and other organ systems can also be affected. The HLA alleles, HLA-B*15:02, HLA-B*15:11 and HLA-A*31:01, are known predisposing factors for these hypersensitivity reactions. Any treatment-naïve patient, regardless of ancestry or indication for treatment, who is about to be prescribed carbamazepine, oxcarbazepine or eslicarbazepine, or has been on these drugs for less than 3 months, should undergo pharmacogenetic testing to identify all clinically relevant HLA alleles to reduce the risk of hypersensitivity reactions. Carbamazepine, oxcarbazepine and eslicarbazepine should be avoided in HLA-B*15:02-positive patients. These drugs should also be avoided in patients positive for HLA-A*31:01 or HLA-B*15:11 if an alternative is possible. Where it is not possible to use an alternative, treatment should only be commenced after careful consideration of the benefits and risks, with increased monitoring and advising patients on appropriate action to take if a skin rash occurs. Our guideline is compatible with other international pharmacogenetics prescribing guidelines. This guideline is grounded in the latest evidence but cannot account for all individual factors relevant to patient care. Therefore, prescribers must conduct a thorough assessment of each patient's risk-benefit profile, ensuring that therapy is optimised to maximise benefits whilst minimising potential harms.

Clozapine is licenced for treatment-resistant schizophrenia and psychosis in Parkinson's disease. In the United Kingdom, there is a mandatory requirement for absolute neutrophil count (ANC) and white blood cell count (WBC) monitoring to safeguard against agranulocytosis. Some people have naturally low ANCs without increased infection risk, caused by a homozygous T > C variant in ACKR1, commonly called the Duffy-null genotype. This condition is known as ADAN (ACKR1/DARC-associated neutropenia) and synonyms include DANC (Duffy-null associated neutrophil count) and BEN (benign ethnic neutropenia). It is usual UK practice to lower WBC/ANC thresholds for people confirmed to have ADAN. However, ADAN often remains undetected, resulting in unnecessary discontinuation and exclusion from clozapine. This CERSI-PGx guideline provides a framework to offer ACKR1 genotype testing within the existing clinical pathway. We recommend three eligibility criteria, including pre-emptive testing for all people starting clozapine, testing for people registered in the Central Non-Rechallenge Database and reactive testing following a below-threshold blood result (defined as 'amber' or 'red'). We recommend that people with the Duffy-null genotype should be monitored using revised WBC/ANC thresholds for ADAN. Regardless of ACKR1 genotype, haematology input is required for people returning a WBC < 2.0 × 109/L and/or ANC < 1.0 × 109/L who present with a key clinical feature, such as sustained temperature ≥38°C. Finally, we summarize health economic evidence, estimating in the first year of testing, 129 people with the Duffy-null genotype could be identified, resulting in savings ranging from £42 732 to £727 990. We propose ACKR1 testing as a cost-effective approach for facilitating access to clozapine, the optimal therapy for treatment-resistant schizophrenia.

Cognitive impairment is an important but often under-researched symptom in psychosis. Both psychosis and cognition are highly heritable and there is evidence of a genetic effect on the relationship between them. Using samples of adults (N = 4 506) and children (N = 10 981), we investigated the effect of schizophrenia and bipolar disorder polygenic scores on cognitive performance, and intelligence and educational attainment polygenic scores on psychosis presentation. Schizophrenia polygenic score was negatively associated with visuospatial processing in adults (beta: −0.0569; 95% confidence interval [CI]: −0.0926, −0.0212) and working memory (beta: −0.0432; 95% CI: −0.0697, −0.0168), processing speed (beta: −0.0491; 95% CI: −0.0760, −0.0223), episodic memory (betas: −0.0581 to −0.0430; 95% CIs: −0.0847, −0.0162), executive functioning (beta: −0.0423; 95% CI: −0.0692, −0.0155), fluid intelligence (beta: −0.0583; 95% CI: −0.0847, −0.0320), and total intelligence (beta: −0.0458; 95% CI: −0.0709, −0.0206) in children. Bipolar disorder polygenic score was not associated with any cognitive domains studied. Lower polygenic scores for intelligence were associated with greater odds of psychosis in adults (odds ratio [OR]: 0.886; 95% CI: 0.811–0.968). In children, lower polygenic scores for both intelligence (OR: 0.829; 95% CI: 0.777–0.884) and educational attainment (OR: 0.771; 95% CI: 0.724–0.821) were associated with greater odds of psychotic-like experiences. Our findings suggest that polygenic scores for both cognitive phenotypes and psychosis phenotypes are implicated in the relationship between psychosis and cognitive performance. Further research is needed to determine the direction of this effect and the mechanisms by which it occurs.

Background/objectivesMedications to treat psychosis (i.e., antipsychotics) have common and sometimes serious adverse drug reactions and can require several trials before finding a suitable drug and dose. To address this, there is increasing focus on personalizing medicine. Pharmacogenetics investigates how genetic variation influences drug metabolism and response, with recent clinical trials suggesting pharmacogenetic testing can improve remission and reduce adverse drug reactions. Therefore, understanding stakeholder perspectives on acceptability is critical.MethodsThis pilot study is part of ‘GEMS’ (Genetics and Environment in Mental Health Study), which investigates pharmacogenetic testing for psychosis. A participant survey, co-created with patients, was completed by 22 patient-participants, and semi-structured interviews were conducted with 11 clinician-participants who had used pharmacogenetic test reports with patients.ResultsBoth patients and clinicians were generally positive about pharmacogenetics, although clinicians saw this as just one component in the multifactorial process of individualized prescribing. Clinicians and patients both suggested a more user-friendly format of the pharmacogenetic report to enhance patient understanding. Some described the reports as promoting more collaborative care, but this was not universal. Clinicians highlighted both retrospective and prospective value in pharmacogenetics providing more certainty through reducing ‘trial-and-error’ prescribing. However, accessibility, understanding, and logistics were identified as potential barriers to implementation.ConclusionAmong patients and clinicians who have experienced pharmacogenetic testing to inform antipsychotic prescribing, acceptability is good. There is potential for pharmacogenetics to enhance personalized prescribing, but barriers to widespread implementation remain.

Background Physical health checks in primary care for people with severe mental illness ((SMI) defined as schizophrenia, bipolar disorders and non-organic psychosis) aim to reduce health inequalities. Patients who decline or are deemed unsuitable for screening are removed from the denominator used to calculate incentivisation, termed exception reporting. Aims To describe the prevalence of, and patient characteristics associated with, exception reporting in patients with SMI. Method We identified adult patients with SMI from the UK Clinical Practice Research Datalink (CPRD), registered with a general practice between 2004 and 2018. We calculated the annual prevalence of exception reporting and investigated patient characteristics associated with exception reporting, using logistic regression. Results Of 193 850 patients with SMI, 27.7% were exception reported from physical health checks at least once. Exception reporting owing to non-response or declining screening increased over the study period. Patients of Asian or Black ethnicity (Asian: odds ratio 0.72, 95% CI 0.65–0.80; Black: odds ratio 0.86, 95% CI 0.76–0.97; compared with White) and women (odds ratio 0.90, 95% CI 0.88–0.92) had a reduced odds of being exception reported, whereas patients diagnosed with ‘other psychoses’ (odds ratio 1.19, 95% CI 1.15–1.23; compared with bipolar disorder) had increased odds. Younger patients and those diagnosed with schizophrenia were more likely to be exception reported owing to informed dissent. Conclusions Exception reporting was common in people with SMI. Interventions are required to improve accessibility and uptake of physical health checks to improve physical health in people with SMI.

Rare copy number variants (CNVs) are a key component of the genetic basis of psychiatric conditions, but have not been well characterized for most. We conducted a genome-wide CNV analysis across six diagnostic categories (N = 574,965): autism (ASD), ADHD, bipolar disorder (BD), major depressive disorder (MDD), PTSD, and schizophrenia (SCZ). We identified 35 genome-wide significant associations at 18 loci, including novel associations in SCZ ( SMYD3, USP7 - HAPSTR1 ) and in the combined cross-disorder analysis ( ASTN2 ). Rare CNVs accounted for 1-3% of heritability across diagnoses. In ASD, associations were uniformly positive, consistent with autism having diverse etiologies and clinical presentations. By contrast, CNVs showed a dose-dependent relationship for other diagnoses, including SCZ and PTSD, with reciprocal deletions and duplications having inversely correlated effects and distinct genotype-phenotype relationships. Our findings suggest that genes have effects that are both dose-dependent and pleiotropic, such that a positive influence on one dimension of psychopathology may be accompanied by positive or negative effects on others.

Bipolar depression is commonly accompanied by cognitive impairments. Transcranial direct current stimulation (tDCS) is emerging as a novel non-invasive treatment for bipolar depression. Given the portability and safety of tDCS, we developed a home-based protocol with real-time supervision. Our aim was to assess the cognitive effects of a course of tDCS treatment in bipolar depression. 44 participants (31 women, mean age 47.27 years, SD 12.89) with bipolar depression of at least a moderate severity received 21 sessions of home-based tDCS over 6 weeks in an open-label design. The stimulation protocol involved 2 mA in a bilateral frontal montage (F3 anode, F4 cathode) for 30 min per session. Cognitive assessments were conducted at baseline and after the course of treatment: Rey Auditory Verbal Learning Test (RAVLT) to assess verbal learning and memory and Symbol Digit Modalities Test (SDMT) to assess psychomotor processing speed and visuospatial attention. 93.18% (n = 41) completed RAVLT and 59.09% of participants (n = 26) completed SDMT. A significant improvement was observed in RAVLT verbal learning score post-treatment ( p = 0.002), which was not maintained following adjustment for improvement in depressive symptoms. In summary, a course of home-based tDCS in bipolar depression was associated with an improvement in verbal learning, which appeared to be related to improvement in depressive symptoms. These findings suggest potential benefits of tDCS for addressing cognitive impairments in bipolar depression, which can be investigated further in a sham-controlled design.

Initiating aripiprazole as antipsychotic monotherapy rather than olanzapine, quetiapine, or risperidone, might prevent/delay major adverse cardiovascular events (MACEs) over the long-term in people diagnosed with severe mental illness. Using Clinical Practice Research Datalink data, we emulated a trial of aripiprazole versus olanzapine, quetiapine, and risperidone in 20,404 patients 2005–2014. Primary outcome was five-year MACE risk (composite of hospitalisation for acute myocardial infarction or stroke and cardiovascular death). Here we show that patients initiating aripiprazole had a similar five-year MACE risk as those initiating olanzapine (risk ratio: 1.03, 95

Background People with severe mental illness (SMI) are at increased risk of cardiovascular disease (CVD), and initiatives for CVD risk factor screening in the UK have not reduced disparities.Objectives To describe the annual screening prevalence for CVD risk factors in people with SMI from April 2000 to March 2018, and to identify factors associated with receiving no screening and regular screening.Methods We identified adults with a diagnosis of SMI (schizophrenia, bipolar disorder or ‘other psychosis’) from UK primary care records in Clinical Practice Research Datalink. We calculated the annual prevalence of screening for blood pressure, cholesterol, glucose, body mass index, alcohol consumption and smoking status using multinomial logistic regression to identify factors associated with receiving no screening and complete screening.Results Of 216 136 patients with SMI, 55% received screening for all six CVD risk factors at least once during follow-up and 35% received all six within a 1-month period. Our findings suggest that patient characteristics and financial incentivisation influence screening prevalence of individual CVD risk factors, the likelihood of receiving screening for all six CVD risk factors annually and risk of receiving no screening.Conclusions The low proportion of people with SMI receiving regular comprehensive CVD risk factor screening is concerning. Screening needs to be embedded as part of broad physical health checks to ensure the health needs of people with SMI are being met. If we are to improve cardiovascular health, interventions are needed where risk of receiving no screening or not receiving regular screening is highest.

Bipolar disorder is characterized by marked changes in mood and activity levels and is a leading cause of disability worldwide. We sought to investigate the application of deep learning methods to electroencephalogram (EEG) signals to predict clinical remission after 6 weeks of home-based transcranial direct current stimulation (tDCS) treatment. Pre-treatment resting-state EEG acquired from 21 bipolar participants was used for this work. A hybrid 1DCNN and GRU model, with input from power spectral density values of theta, beta and gamma frequency bands of the AF7 and TP10 electrodes, achieved a treatment remission prediction accuracy of 78.5% (sensitivity 81.4%, specificity 74.64%).