Comorbid Schizophrenia Research Articles

Comorbid ADHD and schizophrenia and the use of psychostimulants: a scoping review protocol

IntroductionSchizophrenia and attention deficit hyperactivity disorder (ADHD) are psychiatric disorders that have a profound impact on patients and healthcare systems globally. There is preliminary evidence suggesting a potential association between...

Quantifying the relative importance of genetics and environment on the comorbidity between mental and cardiometabolic disorders using 17 million Scandinavians

Mental disorders are leading causes of disability and premature death worldwide, partly due to high comorbidity with cardiometabolic disorders. Reasons for this comorbidity are still poorly understood. We leverage nation-wide health records and near-complete genealogies of Denmark and Sweden (n = 17 million) to reveal the genetic and environmental contributions underlying the observed comorbidity between six mental disorders and 15 cardiometabolic disorders. Genetic factors contributed about 50% to the comorbidity of schizophrenia, affective disorders, and autism spectrum disorder with cardiometabolic disorders, whereas the comorbidity of attention-deficit/hyperactivity disorder and anorexia with cardiometabolic disorders was mainly or fully driven by environmental factors. In this work we provide causal insight to guide clinical and scientific initiatives directed at achieving mechanistic understanding as well as preventing and alleviating the consequences of these disorders.

Parental mental disorders in patients with comorbid schizophrenia and obsessive-compulsive disorder: a nationwide family-link study.

Schizophrenia is highly comorbid with obsessive-compulsive disorder (OCD); both conditions share numerous pathophysiological etiologies. We, thus, examined the risk of mental disorders in the parents of probands with schizophrenia, OCD, or both conditions. Between 2001 and 2011, we enrolled a nationwide cohort of 69,813 patients with schizophrenia, OCD, or both. The control cohort included 698,130 individuals matched for demographics. Poisson regression models were employed to examine the risk of six mental disorders in their parents, including schizophrenia, bipolar disorder, depressive disorder, OCD, alcohol use disorder, and substance use disorder. We stratified patients into schizophrenia-only, OCD-only, and dual-diagnosis groups, and the dual-diagnosis group was further divided into schizophrenia-first, OCD-first, and simultaneously diagnosed groups. Compared with controls, the schizophrenia, OCD, and dual-diagnosis groups had higher risks for the six mental disorders in their parents (range of odds ratio [OR] 1.50-7.83). The sub-analysis of the dual-diagnosis group showed that the schizophrenia-first, OCD-first, and simultaneously diagnosed groups had higher odds for schizophrenia, bipolar disorder, depressive disorder, and OCD (range of OR 1.64-6.45) in their parents than the control group; the simultaneously diagnosed and OCD-first diagnosed groups had a higher odds of parental substance use disorder, while the schizophrenia-first diagnosed group had a higher odds of parental alcohol use disorder. The interrelationship between OCD and schizophrenia is linked to bipolar disorder, depressive disorder, alcohol use disorder, and substance use disorder. The results have implications for mental health policy and future research.

From brain to body: exploring the connection between altered reward processing and physical fitness in schizophrenia

Understanding the underlying mechanisms that link psychopathology and physical comorbidities in schizophrenia is crucial since decreased physical fitness and overweight pose major risk factors for cardio-vascular diseases and decrease the patients’ life expectancies. We hypothesize that altered reward anticipation plays an important role in this. We implemented the Monetary Incentive Delay task in a MR scanner and a fitness test battery to compare schizophrenia patients (SZ, n = 43) with sex- and age-matched healthy controls (HC, n = 36) as to reward processing and their physical fitness. We found differences in reward anticipation between SZs and HCs, whereby increased activity in HCs positively correlated with overall physical condition and negatively correlated with psychopathology. On the other handy, SZs revealed stronger activity in the posterior cingulate cortex and in cerebellar regions during reward anticipation, which could be linked to decreased overall physical fitness. These findings demonstrate that a dysregulated reward system is not only responsible for the symptomatology of schizophrenia, but might also be involved in physical comorbidities which could pave the way for future lifestyle therapy interventions.

Psychotherapeutic Approach to the Treatment of a Youth with Schizophrenia and OCD: A Case Report

Schizophrenia and obsessive-compulsive disorder (OCD), which are often first detected during adolescence, commonly co-occur. Individually, they are some of the most complex and challenging psychiatric disorders to manage. This article reports on a case of an adolescent with co-morbid schizophrenia and OCD and the use of exposure and response prevention (ERP) for the treatment of OCD in the context of management of his schizophrenia and addressing developmental issues. This contributed to the overall stabilization of the youth’s condition.

Longitudinal study of insomnia, suicidal ideation, and psychopathology in schizophrenia

ObjectiveInsomnia is a common comorbidity in schizophrenia. Increasing cross-sectional evidence suggests an association between insomnia and suicidal ideation (SI) and symptom severity in schizophrenia. We investigated longitudinal associations over 3 months between insomnia, suicidal ideation, and symptom severity in a group of patients with chronic schizophrenia. MethodWe performed a secondary analysis of data from n = 305 participants from the Preventing Relapse Oral Antipsychotics Compared to Injectables Evaluating Efficacy (PROACTIVE) schizophrenia trial using regression models. ResultsThe prevalence of moderate-to-severe insomnia was 17.7 % at baseline and 13.6 % at 3 months, respectively. The prevalence of SI was 22 % at baseline and 22.5 % at 3 months. After controlling for potential confounders, improved SI from baseline to 3 months was associated with both baseline moderate-to-severe insomnia (OR = 3.81, 95 % CI 1.11–13.12, p = 0.034) and improvement in insomnia (OR = 3.50, 95 % CI 1.23–9.92, p = 0.013). Worsening SI from baseline to 3 months was associated with worsening insomnia (OR = 3.50, 95 % CI 1.23–9.92, p = 0.013), but not baseline insomnia. Improvement in BPRS total score from baseline to 3 months was associated with improvement in insomnia (β = 0.17, p = 0.029), but not baseline insomnia. ConclusionInsomnia is common in patients with chronic schizophrenia and insomnia showed significant associations with SI and psychopathology. Clinicians should consider insomnia when assessing suicide risk in patients with schizophrenia.

Medication-Induced Hepatitis caused by Antipsychotic Drugs as a Revelation of Wilson's disease

Wilson's disease is an autosomal recessive genetic disorder that results from a mutation in the gene for a heavy metal transporter. This leads to a decrease or absence of copper transport in the bile and its accumulation in organs, particularly the brain. Affected patients have hepatic, neurological or psychiatric forms, and the diagnosis is based on clinical, biological, radiological and presumptive phenotypic arguments, as well as on associated molecular anomalies. Wilson's disease can result in behavioral disorders, depression, and psychosis: schizophrenia or manic depression. The diagnosis can be made if there is a combination of low ceruloplasmin, high cupremia, high cupruria, and a Kayser-Fleisher ring. In case of hemolysis, the cupremia may be elevated. On MRI, signal abnormalities of the basal ganglia, white matter and trunk are indicative of Wilson's disease. Genetic study is performed in case of family history. We present a clinical case of drug-induced hepatitis under antipsychotic drugs in the context of schizophrenia which was revealing of wilson's disease. Although rare, the onset of Wilson's disease can take the form of a late-onset adult psychosis, and is important to address in psychiatry. Is this a comorbidity of schizophrenia and wilson's disease, or is the psychiatric picture merely a consequence of neurological involvement with the disease?

Nicotine Exposure in a Phencyclidine-Induced Mice Model of Schizophrenia: Sex-Selective Medial Prefrontal Cortex Protein Markers of the Combined Insults in Adolescent Mice.

Tobacco misuse as a comorbidity of schizophrenia is frequently established during adolescence. However, comorbidity markers are still missing. Here, the method of label-free proteomics was used to identify deregulated proteins in the medial prefrontal cortex (prelimbic and infralimbic) of male and female mice modelled to schizophrenia with a history of nicotine exposure during adolescence. Phencyclidine (PCP), used to model schizophrenia (SCHZ), was combined with an established model of nicotine minipump infusions (NIC). The combined insults led to worse outcomes than each insult separately when considering the absolute number of deregulated proteins and that of exclusively deregulated ones. Partially shared Reactome pathways between sexes and between PCP, NIC and PCPNIC groups indicate functional overlaps. Distinctively, proteins differentially expressed exclusively in PCPNIC mice reveal unique effects associated with the comorbidity model. Interactome maps of these proteins identified sex-selective subnetworks, within which some proteins stood out: for females, peptidyl-prolyl cis-trans isomerase (Fkbp1a) and heat shock 70 kDa protein 1B (Hspa1b), both components of the oxidative stress subnetwork, and gamma-enolase (Eno2), a component of the energy metabolism subnetwork; and for males, amphiphysin (Amph), a component of the synaptic transmission subnetwork. These are proposed to be further investigated and validated as markers of the combined insult during adolescence.

Comorbidity of schizophrenia and diabetes mellitus at the present stage of development of an interdisciplinary approach to treatment and diagnosis

The article presents an overview of the current problem of comorbidity of schizophrenia and type 2 diabetes mellitus, the diseases that considerably limit the quality of life of patients and cause significant difficulties in patient management. We seek to clarify the current understanding of the factors contributing to the coexistence of these diseases, highlighting the potential role of genetic, epigenetic, and environmental factors in this regard. Particular attention is paid to the effect of antipsychotic drugs on glucose metabolism and the development of insulin resistance, which may contribute to the development of type 2 diabetes in patients with schizophrenia. Data from the most relevant studies on this issue are presented, and possible strategies for managing patients with these conditions are discussed. The purpose of this article is not only to collect and systematize the existing information on the comorbidity of schizophrenia and type 2 diabetes, but also to stimulate further research in this area to develop effective approaches to the diagnosis, treatment, and management of patients with these comorbid pathologies.

Comorbidity of schizophrenia and alcoholism in the modern paradigm of outpatient psychiatric care

The comorbidity of alcohol disorder and schizophrenia or schizoaffective disorder is a complex and multifaceted problem that has a significant impact on the quality of life of patients and the complexity of medical care. This article discusses the common neurobiological mechanisms that explain the high rates of co-occurrence of these disorders, as well as the consequences of such comorbidity for patients and the healthcare system. Additionally, potential ways to optimize the treatment of these patients are being considered.

Predictive model, miRNA-TF network, related subgroup identification and drug prediction of ischemic stroke complicated with mental disorders based on genes related to gut microbiome.

Patients with comorbid schizophrenia, depression, drug use, and multiple psychiatric diagnoses have a greater risk of carotid revascularization following stroke. The gut microbiome (GM) plays a crucial role in the attack of mental illness and IS, which may become an index for the diagnosis of IS. A genomic study of the genetic commonalities between SC and IS, as well as its mediated pathways and immune infiltration, will be conducted to determine how schizophrenia contributes to the high prevalence of IS. According to our study, this could be an indicator of ischemic stroke development. We selected two datasets of IS from the Gene Expression Omnibus (GEO), one for training and the other for the verification group. Five genes related to mental disorders and GM were extracted from Gene cards and other databases. Linear models for microarray data (Limma) analysis was utilized to identify differentially expressed genes (DEGs) and perform functional enrichment analysis. It was also used to conduct machine learning exercises such as random forest and regression to identify the best candidate for immune-related central genes. Protein-protein interaction (PPI) network and artificial neural network (ANN) were established for verification. The receiver operating characteristic (ROC) curve was drawn for the diagnosis of IS, and the diagnostic model was verified by qRT-PCR. Further immune cell infiltration analysis was performed to study the IS immune cell imbalance. We also performed consensus clustering (CC) to analyze the expression of candidate models under different subtypes. Finally, miRNA, transcription factors (TFs), and drugs related to candidate genes were collected through the Network analyst online platform. Through comprehensive analysis, a diagnostic prediction model with good effect was obtained. Both the training group (AUC 0.82, CI 0.93-0.71) and the verification group (AUC 0.81, CI 0.90-0.72) had a good phenotype in the qRT-PCR test. And in verification group 2 we validated between the two groups with and without carotid-related ischemic cerebrovascular events (AUC 0.87, CI 1-0.64). Furthermore, we investigated cytokines in both GSEA and immune infiltration and verified cytokine-related responses by flow cytometry, particularly IL-6, which played an important role in IS occurrence and progression. Therefore, we speculate that mental illness may affect the development of IS in B cells and IL-6 in T cells. MiRNA (hsa-mir-129-2-3p, has-mir-335-5p, and has-mir-16-5p) and TFs (CREB1, FOXL1), which may be related to IS, were obtained. Through comprehensive analysis, a diagnostic prediction model with good effect was obtained. Both the training group (AUC 0.82, CI 0.93-0.71) and the verification group (AUC 0.81, CI 0.90-0.72) had a good phenotype in the qRT-PCR test. And in verification group 2 we validated between the two groups with and without carotid-related ischemic cerebrovascular events (AUC 0.87, CI 1-0.64). MiRNA (hsa-mir-129-2-3p, has-mir-335-5p, and has-mir-16-5p) and TFs (CREB1, FOXL1), which may be related to IS, were obtained.

Investigating the shared genetic architecture between schizophrenia and body mass index.

Evidence for reciprocal comorbidity of schizophrenia (SCZ) and body mass index (BMI) has grown in recent years. However, little is known regarding the shared genetic architecture or causality underlying the phenotypic association between SCZ and BMI. Leveraging summary statistics from the hitherto largest genome-wide association study (GWAS) on each trait, we investigated the genetic overlap and causal associations of SCZ with BMI. Our study demonstrated a genetic correlation between SCZ and BMI, and the correlation was more evident in local genomic regions. The cross-trait meta-analysis identified 27 significant SNPs shared between SCZ and BMI, most of which had the same direction of influence on both diseases. Mendelian randomization analysis showed the causal association of SCZ with BMI, but not vice versa. Combining the gene expression information, we found that the genetic correlation between SCZ and BMI is enriched in six regions of brain, led by the brain frontal cortex. Additionally, 34 functional genes and 18 specific cell types were found to have an impact on both SCZ and BMI within these regions. Taken together, our comprehensive genome-wide cross-trait analysis suggests a shared genetic basis including pleiotropic loci, tissue enrichment, and shared function genes between SCZ and BMI. This work provides novel insights into the intrinsic genetic overlap of SCZ and BMI, and highlights new opportunities and avenues for future investigation.

Cell Adhesion Molecules in Schizophrenia Patients with Metabolic Syndrome.

Metabolic syndrome (MetS) is a common comorbidity of schizophrenia and significantly shortens life expectancy of the patients. Intercellular (ICAM), vascular (VCAM), and neural (NCAM) cell adhesion molecules (CAMs) mediate neuroinflammatory processes, and their soluble forms (e.g., sICAM) in plasma are present in parallel with their cell-bound forms. In this study, their serum levels were examined in 211 white Siberian patients with paranoid schizophrenia (82 patients with and 129 without MetS according to the 2005 International Diabetes Federation criteria). Serum levels of CAMs were determined with Magpix and Luminex 200 (Luminex, Austin, TX, USA) using xMAP Technology. The level of sICAM-1 was significantly higher and that of sVCAM-1 significantly lower in patients with MetS compared to patients without MetS. Levels of NCAM did not differ between the groups. More pronounced Spearman's correlations between CAMs, age, duration of schizophrenia, and body-mass index were observed among patients without MetS than among patients with MetS. Our results are consistent with MetS's being associated with endothelial dysfunction along with other components of inflammation. Through these endothelial components of peripheral inflammatory processes, MetS might induce intracerebral neuroinflammatory changes, but further investigation is needed to confirm this.

Management of comorbid schizophrenia with prolactinome (about a case)

IntroductionProlactin adenoma, called “prolactinoma” is a benign neoplasm, it is the most common secreting pituitary tumor, and represents up to 40% of all pituitary adenomas. More than 90% are small intrasellar tumors which rarely increase in size.Objectivesthe problem of management lies in how to stabilize the patient on a psychiatric level without increasing the level of prolactin.MethodsWe report the case of a young woman who presented a comorbid schizophrenia with a prolactinoma. We will try through this clinical vignette to study the different pillars of management of such pathologies.At the same time, we did a literature review. The main search engines used were Pubmed, medline, and Science Direct. The keywords Prolatinoma schizophrenia olanzapineResultsThis is Mrs. N. Q., 39 years old She is single, an engineer but currently without a profession, from an average socio-economic level of a teacher father and a housewife mother. She is the 3rd of his siblings of 6 . She is currently hospitalized at Ar-razi Tanger hospital for treatment of decompensation of her chronic psychotic disorder. The patient would have been born following a premature delivery of 34 weeks. For her antecedent, she was followed for asthma since her childhood. Her mother and her maternal grandfather would have been psychotic. The history of the disease dates back to 2017. The patient suffered from headaches resistant to any treatment. The patient would have consulted a neurologist. Magnetic resonance brain imaging would have been requested, which objectified at the left latero-pituitary level a lesional process of 7 mm discretely intense in T2, hypo-intense in T1 and not enhanced by Gd reflecting a pituitary micro adenoma. The patient was put on Cabergoline (Dostinex®). So the psychiatric symptomatology dates back to the end of 2019, by behavioral problems, social withdrawal, she will have stopped all professional activity. At the same time, she will have stopped all medication (Cabergoline). In 2020, the patient would have been hospitalized for the first time at the Ar-razi Tangier psychiatric hospital. The diagnosis of schizophrenia was retained according to the DSM 5 criteria. After a stay of 5 weeks, the patient would be stabilized on olanzapine 20mg/d. Currently, and following non-compliance with treatment (because of adverse effects such as amenorrhea and galactorrhea), the patient has returned, suffering from a relapse, justifying her second hospitalization. During his stay, a check-up would have been requested to show hyperprolactinemia 3 times normal. We therefore switched to Aripiprazole.ConclusionsWe have proposed an approach to the management of patients with comorbid schizophrenia and prolactinoma, an approach that balances the benefits and risks of managing the psychiatric stability of the patient on antipsychotics with the management of prolactinoma and symptoms. of hyperprolactinemia.Disclosure of InterestNone Declared

Network Analysis of the Structure of the Core Symptoms and Clinical Correlates in Comorbid Schizophrenia and Gambling Disorder

Few studies have analyzed the clinical profile of treatment-seeking patients with the comorbid presence of schizophrenia (SCZ) and gambling disorder (GD), which warrants new research to assess the network structure of this complex mental condition. The aim of this study was to explore the organization of the symptoms and other clinical correlates of SCZ with GD. Network analysis was applied to a sample of N = 179 SCZ patients (age range: 19–70 years, mean=39.5, SD=9.9) who met clinical criteria for gambling disorder-related problems. Variables included in the network were the core GD symptoms according to the DSM-5, psychotic and paranoid ideation levels, global psychological distress, GD severity measures (debts and illegal behavior related with gambling), substances (tobacco, alcohol, and illegal drugs), and personality profile. The nodes with the highest authority in the network (variables of highest relevance) were personality traits and psychological distress. Four empirical modules/clusters were identified, and linkage analysis identified the nodes with the highest closeness (bridge nodes) to be novelty seeking and reward dependence (these traits facilitate the transition between the modules). Identification of the variables with the highest centrality/linkage can be particularly useful for developing precise management plans to prevent and treat SCZ with GD.

Cannabis Abuse among Patients with Schizophrenia

Background: Cannabis is the most frequently used substance among patients of schizophrenia. Past deliberate surveys have reported a strong association between cannabis abuse and schizophrenia. However; the whole frequency of cannabis abuse among schizophrenia patients remains ambiguous, as do the variables influencing this rate. Because cannabis abuse in schizophrenia is presently an active area of research, so there is a requirement for a fresh review particularly in our culture where studies are lacking on this topic. Objective: The current study explores the frequency of cannabis abuse among patients suffering from schizophrenia presenting in a tertiary care hospital of Lahore. Methods: Cross-sectional prospective research design was used. Sample of 381 diagnosed patients of schizophrenia using cannabis for at least one year was selected from Sir Ganga Ram Hospital, by convenient sampling technique. Drug Abuse
 Screening Test was applied for the frequency of cannabis abuse. The data were stored and analysed in SPSS version 20. Results: The results revealed that cannabis abuse was present among 42.3% of the patients with schizophrenia. Chi-square analysis showed that there were significant differences among the frequencies of cannabis abuse regarding various age groups, where young age group had significantly higher ratio of cannabis abuse (p=.04). On using independent sample t-test for marital status and duration of the schizophrenia, it was found that cannabis abuse was significantly higher among unmarried patients (t=-4.24, p=.001), however, no significant differences were found for duration of schizophrenia (t=-1.50, p=0.43). Conclusion: The study highlights cannabis abuse is more prevalent in the males as compared to the females. Young age group of patients is more prone to cannabis. These findings can help to decrease the comorbidity of schizophrenia associated with cannabis abuse.

Attention-Deficit Hyperactivity Disorder and Comorbid Mental Health Conditions Associated with Increased Risk of Injury.

Background To describe the influence of attention-deficit hyperactivity disorder (ADHD) and comorbid mental health conditions on the risk of selected injuries. Methods A retrospective cohort study design was employed using medical claim data from the Deseret Mutual Benefit Administrators (DMBA). Mental health conditions, injury, medication, and demographic data were extracted from claim files for ages 4-64, years 2016-2020. Results Approximately 51.8% of individuals with ADHD had one or more comorbid mental health conditions (anxiety [37.0%], depression [29.9%], autism spectrum disorder (ASD) [3.6%], bipolar disorder [4.7%], obsessive compulsive disorder (OCD) [2.4%], schizophrenia [0.9%], and manic disorder [0.2%]). The rate of injury was 1.33 (95% CI 1.27–1.39) for ADHD only versus no ADHD and 1.62 (95% CI 1.56–1.68) for ADHD and comorbid mental health conditions versus no ADHD, after adjusting for age, sex, salary, and year. Cases with ADHD but no comorbid mental health conditions versus no ADHD were at increased risk of each of 12 types of injury. The increased risk was noticeably more pronounced for ADHD cases with one or more comorbid mental health conditions versus no ADHD. The greatest increased risk of injury was among ADHD cases with comorbid schizophrenia, followed by bipolar disorder and OCD. Comorbid autism disorder does not increase the risk of injury, but lowers it. Finally, the number of comorbid mental health conditions among ADHD cases was positively associated with increased injury rates (6% for one, 30% for two, 65% for three, and 129% for four). Conclusions ADHD is positively associated with an increased risk of injury. Comorbid mental health conditions further increase the risk of injury among those with ADHD.

Mendelian Randomization and GWAS Meta Analysis Revealed the Risk-Increasing Effect of Schizophrenia on Cancers.

Simple SummaryThe relationship between schizophrenia and tumors has sparked much interest and controversy. On the one hand, the health of patients with schizophrenia is affected by a variety of risk factors associated with cancer development, such as smoking, alcohol, and drug abuse. On the other hand, early investigations have found that patients with schizophrenia have a lower cancer incidence than the overall population. This phenomenon has prompted new theories on the processes underlying the protective effect. To explore the connection between schizophrenia and tumors, we used two-sample Mendelian randomization and GWAS meta-analysis methods on the GWAS summary data to assess potential genetic links between schizophrenia and 13 cancers. It was revealed that schizophrenia may lead to an increased risk of breast, ovarian, and thyroid cancers. Furthermore, the thyroid-stimulating hormone level is impacted by schizophrenia, which may further affect the estrogen and thyroid hormone levels. Meanwhile, based on our results, AS3MT, SFXN2, and PCCB may be potential biomarkers for preventing breast and thyroid cancers in patients diagnosed with schizophrenia. Therefore, we suggest that patients with schizophrenia should pay close attention to early risk warnings for breast, ovarian, and thyroid cancers.The causal relationship between cancer and Schizophrenia (SCZ) remains controversial. Some researchers have found that SCZ is a cancer-preventive factor in cohort studies or meta-analyses, whereas others have found the opposite. To understand more about this issue, we used two-sample Mendelian randomization (2SMR) on available GWAS summary results to evaluate potential genetic connections between SCZ and 13 cancers. We discovered that the genetic susceptibility to schizophrenia lead to an increasing risk of breast cancer (odds ratio [OR] per log-odds increase in schizophrenia risk: 1.049, 95% confidence interval [CI]:1.023–1.075; p = 0.00012; FDR = 0.0017), ovarian cancer (OR, 1.326; 95% CI, 1.267–1.387; p = 0.0007; FDR = 0.0045), and thyroid cancer (OR, 1.575; 95% CI, 1.048–2.365; p = 0.0285; FDR = 0.123). Secondly, we performed a meta-analysis based on the GWAS summary statistics of SCZ and the three significant cancers. Next, we associated genetic variants to genes using two gene mapping strategies: (a) positional mapping based on genomic proximity and (b) expression quantitative trait loci (eQTL) mapping based on gene expression linkage across multiple tissues. As a result, we identified 114 shared loci and 437 shared genes in three groups, respectively. Functional enrichment analysis shows that the most enriched biological pathways are related to epigenetic modification. In addition, we noticed that SCZ would affect the level of thyroid-stimulating hormone (OR, 1.095; 95% CI, 1.006–1.191; p = 0.0354; FDR = 0.177), which may further affect the level of estrogen and the risk of the above three cancers. In conclusion, our findings under the 2SMR assumption provide crucial insights into the risk-increasing effect of SCZ on three cancers’ risk. Furthermore, these results may provide insights into understanding the genetic predisposition and underlying biological pathways of comorbid SCZ and cancers.

Visual phenomenology in schizophrenia and post-traumatic stress disorder: an exploratory study.

Visual experiences such as hallucinations are commonly reported by people with psychosis, psychological trauma and dissociative states, although questions remain about their similarities and differences. For diagnostic and therapeutic purposes, clinical research must better delineate and compare the characteristics of these experiences in post-traumatic stress disorder (PTSD) and in schizophrenia. To compare visual phenomena and dissociation in participants with a primary psychotic illness and those with a trauma diagnosis. A quantitative group design study comparing visual phenomena in three participant groups who also have a history of hearing voices: schizophrenia and no trauma history (n = 19), PTSD with dissociation (n = 17) and comorbid schizophrenia and PTSD (n = 20). Validated clinical measures included the North-East Visual Hallucination Interview, PTSD Symptoms Scale Interview, Clinician Administered Dissociative States Scale, Psychotic Symptoms Rating Scales and Positive and Negative Syndrome Scale. There was a remarkable similarity in visual experiences, including rates of complex visual hallucinations, between the three diagnostic groups. There were no significant differences in the severity or components of distress surrounding the visual experiences. Dissociation predicted visual hallucination severity for the comorbid schizophrenia and PTSD group, but not for PTSD or schizophrenia alone. Visual experiences in PTSD can include visual hallucinations that are indistinguishable from those experienced in schizophrenia. Multimodal hallucinations are frequently observed in both schizophrenia and PTSD. A model for visual hallucinations in PTSD is suggested, following two separate neurobiological pathways based on distinct responses to trauma.

Disrupted leptin-fatty acid biosynthesis is an early manifestation of metabolic abnormalities in schizophrenia.

BACKGROUNDInsulin resistance (IR) and impaired energy expenditure (IEE) are irreparable metabolic comorbidities in schizophrenia. Although mechanism(s) underlying IR and IEE remains unclear, leptin and fatty acid signaling, which has profound influence on insulin secretion/sensitivity, glucose metabolism and energy expenditure, could be disrupted. However, no association of plasma leptin with erythrocyte membrane fatty acids, body mass index (BMI), and psychotic symptoms in the same cohort of untreated patients with first-episode psychosis (FEP) or medicated patients with chronic schizophrenia (CSZ) is presented before. These studies are crucial for deciphering the role of leptin and fatty acids in the development of IR and IEE in schizophrenia.AIMTo determine the association between plasma leptin, erythrocyte membrane fatty acids, particularly, saturated fatty acids (SFAs), BMI and psychotic symptoms in patients with FEP and CSZ.METHODSIn this study, twenty-two drug naive patients with FEP, twenty-one CSZ patients treated with atypical antipsychotic drugs, and fourteen healthy control (CNT) subjects were analyzed. Plasma leptin was measured using sandwich mode enzyme-linked immunosorbent assay. Erythrocyte membrane SFAs were measured using ultrathin capillary gas chromatography. BMI was calculated by using the formula: weight (kg)/height (m2). Psychiatric symptoms were evaluated at baseline using brief psychiatric rating scale (BPRS), and positive and negative syndrome scale (PANSS). The total BPRS scores, positive and negative symptom scores (PANSS-PSS and PANSS-NSS, respectively) were recorded. Pearson correlation coefficient (r) analyses were performed to find the nature and strength of association between plasma leptin, PANSS scores, BMI and SFAs, particularly, palmitic acid (PA). RESULTSIn patients with FEP, plasma leptin not BMI was significantly lower (P = 0.034), whereas, erythrocyte membrane SFAs were significantly higher (P < 0.005) compared to the CNT subjects. Further, plasma leptin showed negative correlation with erythrocyte membrane SFAs-PA (r = −0.4972, P = 0.001), PANSS-PSS (r = −0.4034, P = 0.028), and PANSS-NSS (r = −0.3487, P = 0.048). However, erythrocyte membrane SFAs-PA showed positive correlation with PANSS-PSS (r = 0.5844, P = 0.0034) and PANSS-NSS (r = 0.5380, P = 0.008). In CSZ patients, plasma leptin, BMI, and erythrocyte membrane SFAs, all were significantly higher (P < 0.05) compared to the CNT subjects. Plasma leptin showed positive correlation with BMI (r = 0.312, P = 0.032) but not with PANSS scores or erythrocyte membrane SFAs-PA. However, erythrocyte membrane SFAs-PA showed positive correlation with PANSS-NSS only (r = 0.4729, P = 0.031). Similar changes in the plasma leptin and erythrocyte membrane SFAs have also been reported in individuals at ultra-high risk of developing psychosis; therefore, the above findings suggest that leptin-fatty acid biosynthesis could be disrupted before the onset of psychosis in schizophrenia.CONCLUSIONDisrupted leptin-fatty acid biosynthesis/signaling could be an early manifestation of metabolic comorbidities in schizophrenia. Large-scale studies are warranted to validate the above findings.