Krill oil protects dopaminergic neurons from age-related degeneration through temporal transcriptome rewiring and suppression of several hallmarks of aging.

There is accumulating evidence that interfering with the basic aging mechanisms can enhance healthy longevity. The interventional/therapeutic strategies targeting multiple aging hallmarks could be more effective than targeting one hallmark. While health-promoting qualities of marine oils have been extensively studied, the underlying molecular mechanisms are not fully understood. Lipid extracts from Antarctic krill are rich in long-chain omega-3 fatty acids choline, and astaxanthin. Here, we used C. elegans and human cells to investigate whether krill oil promotes healthy aging. In a C. elegans model of Parkinson´s disease, we show that krill oil protects dopaminergic neurons from aging-related degeneration, decreases alpha-synuclein aggregation, and improves dopamine-dependent behavior and cognition. Krill oil rewires distinct gene expression programs that contribute to attenuating several aging hallmarks, including oxidative stress, proteotoxic stress, senescence, genomic instability, and mitochondrial dysfunction. Mechanistically, krill oil increases neuronal resilience through temporal transcriptome rewiring to promote anti-oxidative stress and anti-inflammation via healthspan regulating transcription factors such as SNK-1. Moreover, krill oil promotes dopaminergic neuron survival through regulation of synaptic transmission and neuronal functions via PBO-2 and RIM-1. Collectively, krill oil rewires global gene expression programs and promotes healthy aging via abrogating multiple aging hallmarks, suggesting directions for further pre-clinical and clinical explorations.

Autophagy modulates cell fate decisions during lineage commitment.

Early events during development leading to exit from a pluripotent state and commitment toward a specific germ layer still need in-depth understanding. Autophagy has been shown to play a crucial role in both development and differentiation. This study employs human embryonic and induced pluripotent stem cells to understand the early events of lineage commitment with respect to the role of autophagy in this process. Our data indicate that a dip in autophagy facilitates exit from pluripotency. Upon exit, we demonstrate that the modulation of autophagy affects SOX2 levels and lineage commitment, with induction of autophagy promoting SOX2 degradation and mesendoderm formation, whereas inhibition of autophagy causes SOX2 accumulation and neuroectoderm formation. Thus, our results indicate that autophagy-mediated SOX2 turnover is a determining factor for lineage commitment. These findings will deepen our understanding of development and lead to improved methods to derive different lineages and cell types.Abbreviations: ACTB: Actin, beta; ATG: Autophagy-related; BafA1: Bafilomycin A1; CAS9: CRISPR-associated protein 9; CQ: Chloroquine; DE: Definitive endoderm; hESCs: Human Embryonic Stem Cells; hiPSCs: Human Induced Pluripotent Stem Cells; LAMP1: Lysosomal Associated Membrane Protein 1; MAP1LC3: Microtubule-Associated Protein 1 Light Chain 3; MTOR: Mechanistic Target Of Rapamycin Kinase; NANOG: Nanog Homeobox; PAX6: Paired Box 6; PE: Phosphatidylethanolamine; POU5F1: POU class 5 Homeobox 1; PRKAA2: Protein Kinase AMP-Activated Catalytic Subunit Alpha 2; SOX2: SRY-box Transcription Factor 2; SQSTM1: Sequestosome 1; ULK1: unc-51 like Autophagy Activating Kinase 1; WDFY3: WD Repeat and FYVE Domain Containing 3.

Crosstalk between Different DNA Repair Pathways Contributes to Neurodegenerative Diseases.

Genomic integrity is maintained by DNA repair and the DNA damage response (DDR). Defects in certain DNA repair genes give rise to many rare progressive neurodegenerative diseases (NDDs), such as ocular motor ataxia, Huntington disease (HD), and spinocerebellar ataxias (SCA). Dysregulation or dysfunction of DDR is also proposed to contribute to more common NDDs, such as Parkinson's disease (PD), Alzheimer's disease (AD), and Amyotrophic Lateral Sclerosis (ALS). Here, we present mechanisms that link DDR with neurodegeneration in rare NDDs caused by defects in the DDR and discuss the relevance for more common age-related neurodegenerative diseases. Moreover, we highlight recent insight into the crosstalk between the DDR and other cellular processes known to be disturbed during NDDs. We compare the strengths and limitations of established model systems to model human NDDs, ranging from C. elegans and mouse models towards advanced stem cell-based 3D models.

Barriers to stopping neuroleptic (antipsychotic) treatment in people with schizophrenia, psychosis or bipolar disorder.

Most guidelines recommend long-term, indefinite neuroleptic (or antipsychotic) treatment for people with schizophrenia, recurrent psychosis or bipolar disorder, on the basis that these medications reduce the chance of relapse. However, neuroleptics have significant adverse effects, including sexual dysfunction, emotional blunting, metabolic disturbance and brain shrinkage, and patients often request to stop them. Evidence for the benefits of long-term treatment is also not as robust as generally thought. Short-term randomised trials show higher rates of relapse among those whose neuroleptic treatment is discontinued compared with those on maintenance treatment, but they are confounded by adverse effects associated with the withdrawal of established medication. Some longer-term studies show possible advantages of medication reduction and discontinuation in terms of improved social functioning and recovery. Therefore, there is a good rationale for supporting patients who wish to stop their medication, especially given the patient choice agenda favoured by The National Institute for Clinical Excellence (NICE). The major barrier to stopping antipsychotics is an understandable fear of relapse among patients, their families and clinicians. Institutional structures also prioritise short-term stability over possible long-term improvements. The risk of relapse may be mitigated by more gradual reduction of medication, but further research is needed on this. Psychosocial support for patients during the process of reducing medication may also be useful, particularly to enhance coping skills. Guidelines to summarise evidence on ways to reduce medication would be useful. Many patients want to try and stop neuroleptic medication for good reasons, and psychiatrists can help to make this a realistic option by supporting people to do it as safely as possible, with the best chance of a positive outcome.

Collaborative Deprescribing in Borderline Personality Disorder: A Narrative Review.

LEARNING OBJECTIVES: After participating in this activity, learners should be better able to:• Assess medication management in patients with borderline personality disorder (BPD)• Evaluate the role of deprescribing as an active intervention in patients with BPD treated with polypharmacy ABSTRACT: Psychopharmacology in borderline personality disorder (BPD) is complicated by comorbid disorders, substance use, sensitivity to side effects, risk of self-harm through medication misuse, and intense but transient symptoms. Patients' relationships with medications may range from tenuous to highly enmeshed, and may profoundly influence the response to treatment. For these reasons, awareness of current evidence and flexible approaches are particularly relevant to prescribing in BPD. In this narrative review, we illustrate the current status of medication management in BPD by focusing on polypharmacy. We use a single vignette to explore the limitations of prescribing multiple medications and the factors contributing to polypharmacy. With the same vignette, and using the framework of deprescribing, we describe how medication regimens can be reduced to a necessary minimum. Deprescribing, originally developed in geriatric medicine, is an active intervention that involves a risk-benefit analysis for each medication, keeping in mind the patient's medical and psychiatric status and his or her preferences and values. Deprescribing lends itself well to use in psychiatry and especially in BPD because of its emphasis on the patient's preferences and on repeated conversations to revisit and update decisions. In addition to elaborating on the deprescribing framework, we provide recommendations for conducting these critical discussions about medications in BPD, with particular attention to the patient's relationship to the medication. Finally, we summarize our recommendations and strategies for implementing flexible and responsive medication management for patients with BPD. We suggest areas of future research, including testing the efficacy of targeted intermittent medication treatments.

Effects of haloperidol on the delta-9-tetrahydrocannabinol response in humans: a responder analysis.

RATIONALE: Δ-9-Tetrahydrocannabinol (Δ-9-THC) produces psychotomimetic effects in humans. However, the role of dopamine signaling in producing such effects is unclear. We hypothesized that dopaminergic antagonism would reduce the psychotomimetic effect of Δ-9-THC. OBJECTIVE: The objective of this study was to evaluate whether pre-treatment with haloperidol would alter the psychotomimetic and perceptual-altering effects of Δ-9-THC, measured by the Positive and Negative Syndrome Scale for Schizophrenia (PANSS) and the Clinician-Administered Dissociative Symptom Scale (CADSS) in humans. METHODS: In a two-test-day double-blind study, 28 healthy individuals were administered with active (0.057 mg/kg) or placebo oral haloperidol, followed 90 and 215 min later by intravenous administration of active (0.0286 mg/kg) Δ-9-THC and placebo, respectively. This secondary analysis was conducted because of the observation in other studies and in our data that a significant proportion of individuals may not have an adequate response to THC (floor effect), thus limiting the ability to test an interaction. Therefore, this analysis was performed including only responders to THC (n = 10), defined as individuals who had an increase of at least one point on the PANSS positive scale, consistent with prior human laboratory studies. RESULTS: In the 10 responders, Δ-9-THC-induced increases in PANSS positive scores were significantly lower in the haloperidol condition (1.1 + 0.35) compared with the placebo condition (2.9 + 0.92). CONCLUSION: This responder analysis showed that haloperidol did reduce the psychotomimetic effect of Δ-9-THC, supporting the hypothesis that dopaminergic signaling may participate in the psychosis-like effects of cannabinoids.

Radiation induces EIF2AK3/PERK and ERN1/IRE1 mediated pro-survival autophagy.

Cellular effects of ionizing radiation include oxidative damage to macromolecules, unfolded protein response (UPR) and metabolic imbalances. Oxidative stress and UPR have been shown to induce macroautophagy/autophagy in a context-dependent manner and are crucial factors in determining the fate of irradiated cells. However, an in-depth analysis of the relationship between radiation-induced damage and autophagy has not been explored. In the present study, we investigated the relationship between radiation-induced oxidative stress, UPR and autophagy in murine macrophage cells. A close association was observed between radiation-induced oxidative burst, UPR and induction of autophagy, with the possible involvement of EIF2AK3/PERK (eukaryotic translation initiation factor 2 alpha kinase 3) and ERN1/IRE1 (endoplasmic reticulum [ER] to nucleus signaling 1). Inhibitors of either UPR or autophagy reduced the cell survival indicating the importance of these processes after radiation exposure. Moreover, modulation of autophagy affected lethality in the whole body irradiated C57BL/6 mouse. These findings indicate that radiation-induced autophagy is a pro-survival response initiated by oxidative stress and mediated by EIF2AK3 and ERN1. Abbreviations: ACTB: actin, beta; ATF6: activating transcription factor 6; ATG: autophagy-related; BafA1: bafilomycin A1; CQ: chloroquine; DBSA: 3,5-dibromosalicylaldehyde; EIF2AK3: eukaryotic translation initiation factor 2 alpha kinase 3; ERN1: endoplasmic reticulum (ER) to nucleus signaling 1; IR: ionizing radiation; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; 3-MA: 3-methyladenine; MTOR: mechanistic target of rapamycin kinase; NAC: N-acetyl-L-cysteine; PARP1: poly (ADP-ribose) polymerase family, member 1; 4-PBA: 4-phenylbutyrate; Rap: rapamycin; ROS: reactive oxygen species; UPR: unfolded protein response; XBP1: x-box binding protein 1.

Efficacy and safety of a fatty acid amide hydrolase inhibitor (PF-04457845) in the treatment of cannabis withdrawal and dependence in men: a double-blind, placebo-controlled, parallel group, phase 2a single-site randomised controlled trial.

BACKGROUND: Cannabis is one of the most widely used drugs worldwide. Cannabis use disorder is characterised by recurrent use of cannabis that causes significant clinical and functional impairment. There are no approved pharmacological treatments for cannabis use disorder. One approach is to potentiate endocannabinoid signalling by inhibiting fatty acid amide hydrolase (FAAH), the enzyme that degrades the endocannabinoid anandamide. We aimed to test the efficacy and safety of the FAAH-inhibitor PF-04457845 in reduction of cannabis withdrawal and cannabis use in men who were daily cannabis users. METHODS: We did a double-blind, placebo-controlled, parallel group phase 2a trial at one site in men aged 18-55 years with cannabis dependence according to DSM-IV criteria (equivalent to cannabis use disorder in DSM-5). After baseline assessments, participants were randomly assigned (2:1) to receive PF-04457845 (4 mg per day) or placebo using a fixed block size of six participants, stratified by severity of cannabis use and desire to quit. Participants were admitted to hospital for 5 days (maximum 8 days) to achieve abstinence and precipitate cannabis withdrawal, after which they were discharged to continue the remaining 3 weeks of treatment as outpatients. The primary endpoints were treatment-related differences in cannabis withdrawal symptoms during hospital admission, and week 4 (end of treatment) self-reported cannabis use and urine THC-COOH concentrations in the intention-to-treat population. The study is registered at ClinicalTrials.gov, number NCT01618656. FINDINGS: Between Sept 12, 2012, and Jan 18, 2016, 46 men were randomly assigned to PF-04457845 and 24 to placebo. Adherence to study medication was 88%, as confirmed by video-calling and pill count, and corroborated by corresponding drug and anandamide concentrations in blood. Relative to placebo, treatment with PF-04457845 was associated with reduced symptoms of cannabis withdrawal (first day of treatment mean symptom score 11·00 [95% CI 7·78-15·57] vs 6·04 [4·43-8·24]; difference 4·96 [0·71-9·21]; padj=0·048; second day of treatment 11·74 [8·28-16·66] vs 6·02 [4·28-8·47]; difference 5·73 [1·13-10·32]; padj=0·035) and related mood symptoms during the inpatient phase. Additionally, treatment with PF-04457845 was associated with lower self-reported cannabis use at 4 weeks (mean 1·27 joints per day [95% CI 0·82-1·97] vs 0·40 [0·25-0·62]; difference 0·88 [0·29-1·46]; p=0·0003) and lower urinary THC-COOH concentrations (mean 657·92 ng/mL [95% CI 381·60-1134·30] vs 265·55 [175·60-401·57]; difference 392·37 [17·55-767·18)]; p=0·009). Eight (17%) patients in the PF-04457845 group and four (17%) in the placebo group discontinued during the treatment period. During the 4-week treatment phase, 20 (43%) of 46 participants in the PF-04457845 group and 11 (46%) of 24 participants in the placebo group had an adverse event. There were no serious adverse events. INTERPRETATION: PF-04457845, a novel FAAH inhibitor, reduced cannabis withdrawal symptoms and cannabis use in men, and might represent an effective and safe approach for the treatment of cannabis use disorder. FUNDING: United States National Institute of Drug Abuse (NIDA).

The effects of cannabidiol (CBD) on cognition and symptoms in outpatients with chronic schizophrenia a randomized placebo controlled trial.

RATIONALE: Preliminary evidence suggests that cannabidiol (CBD) may be effective in the treatment of neurodegenerative disorders; however, CBD has never been evaluated for the treatment of cognitive impairments associated with schizophrenia (CIAS). OBJECTIVE: This study compared the cognitive, symptomatic, and side effects of CBD versus placebo in a clinical trial. METHODS: This study was a 6-week, randomized, placebo-controlled, parallel group, fixed-dose study of oral CBD (600 mg/day) or placebo augmentation in 36 stable antipsychotic-treated patients diagnosed with chronic schizophrenia. All subjects completed the MATRICS Consensus Cognitive Battery (MCCB) at baseline and at end of 6 weeks of treatment. Psychotic symptoms were assessed using the Positive and Negative Syndrome Scale (PANSS) at baseline and biweekly. RESULTS: There was no main effect of time or drug on MCCB Composite score, but a significant drug × time effect was observed (p = 0.02). Post hoc analyses revealed that only placebo-treated subjects improved over time (p = 0.03). There was a significant decrease in PANSS Total scores over time (p < 0. 0001) but there was no significant drug × time interaction (p = 0.18). Side effects were similar between CBD and placebo, with the one exception being sedation, which was more prevalent in the CBD group. CONCLUSIONS: At the dose studied, CBD augmentation was not associated with an improvement in MCCB or PANSS scores in stable antipsychotic-treated outpatients with schizophrenia. Overall, CBD was well tolerated with no worsening of mood, suicidality, or movement side effects. TRIAL REGISTRATION: https://clinicaltrials.gov/ct2/show/NCT00588731.

Online Sales of Unscheduled Pharmaceutical Agents: A Case Report of Tianeptine Use in the United States.

: Tianeptine is a tricyclic antidepressant that stimulates mu-opioid receptors at high doses. It is marketed and used across Europe and Latin America as an antidepressant, but is not approved by the Food and Drug Administration for use in the United States. In the United States, tianeptine is sold through online health stores as a cognition enhancer, dietary supplement, or as research chemical. We report the case of a 36-year-old man with a history of major depressive disorder, responsive to sertraline, who turned to the unmonitored use of tianeptine purchased online to treat residual feelings of apathy and boredom. His use of tianeptine was marked by rapidly escalating doses and a significant withdrawal syndrome that made discontinuation of this substance difficult. This case serves as a reminder that unscheduled pharmaceutical agents are available for misuse by the general population and have the potential to cause significant harm. Therefore, medical providers must be aware of and screen for the use of such products amongst their patients.

The Nucleus Accumbens and Ketamine Treatment in Major Depressive Disorder.

Animal models of depression repeatedly showed stress-induced nucleus accumbens (NAc) hypertrophy. Recently, ketamine was found to normalize this stress-induced NAc structural growth. Here, we investigated NAc structural abnormalities in major depressive disorder (MDD) in two cohorts. Cohort A included a cross-sectional sample of 34 MDD and 26 healthy control (HC) subjects, with high-resolution magnetic resonance imaging (MRI) to estimate NAc volumes. Proton MR spectroscopy (1H MRS) was used to divide MDD subjects into two subgroups: glutamate-based depression (GBD) and non-GBD. A separate longitudinal sample (cohort B) included 16 MDD patients who underwent MRI at baseline then 24 h following intravenous infusion of ketamine (0.5 mg/kg). In cohort A, we found larger left NAc volume in MDD compared to controls (Cohen's d=1.05), but no significant enlargement in the right NAc (d=0.44). Follow-up analyses revealed significant subgrouping effects on the left (d⩾1.48) and right NAc (d⩾0.95) with larger bilateral NAc in non-GBD compared to GBD and HC. NAc volumes were not different between GBD and HC. In cohort B, ketamine treatment reduced left NAc, but increased left hippocampal, volumes in patients achieving remission. The cross-sectional data provided the first evidence of enlarged NAc in patients with MDD. These NAc abnormalities were limited to patients with non-GBD. The pilot longitudinal data revealed a pattern of normalization of left NAc and hippocampal volumes particularly in patients who achieved remission following ketamine treatment, an intriguing preliminary finding that awaits replication.

Evidence for the role of lipid peroxides on glycation of hemoglobin and plasma proteins in non-diabetic asthma patients.

BACKGROUND: Collective evidences reveal that malondialdehyde (MDA), reduced glutathione (GSH) and ascorbic acid can modulate protein glycation. We investigated the concentrations of MDA, GSH, ascorbic acid and protein glycation in asthma patients to delineate the possible association among these parameters. METHODS: Blood was collected from 18 asthma patients and 16 age and sex matched control subjects. Glycated hemoglobin (HbA1C), GSH, MDA, vitamin C, fructosamine and glucose were assessed in both groups. The effect of H2O2 on glycation of hemoglobin was studied by incubating normal healthy erythrocytes with either 5 or 50 mmol/l glucose concentration. RESULTS: Plasma of asthma patients revealed significantly higher concentrations of lipid peroxides and fructosamine concentrations than the matched controls. Glycated hemoglobin concentrations were also found to be significantly increased. Ascorbic acid and GSH concentrations were decreased significantly in the test group when compared with the healthy control group. When the effects of fasting glucose, GSH and ascorbic acid on the concentrations of HbA1C and fructosamine were refuted by partial correlation analysis, MDA was found to be a significant determinant of HbA1c and fructosamine in patients with asthma. The in vitro model with human erythrocytes showed an enhancement of protein glycation by H2O2. CONCLUSION: An increased glycation of proteins was found in asthma patients. These data also support the premise that lipid peroxides per se do have a role to play in glycation of hemoglobin and plasma proteins.

A Prescription for "Deprescribing" in Psychiatry.

The term "deprescribing," initially coined in geriatric medicine, describes a process of pharmacologic regimen optimization through reduction or cessation of medications for which benefits no longer outweigh risks. Burgeoning rates of polypharmacy, growing appreciation of long-term adverse effects, and a focus on patient-centered practice present specific indications for deprescribing in psychiatry. A strong therapeutic alliance, appropriate timing, and consideration of the meaning of medication for the patient must accompany the following established elements: review of all medications, identification of medications that could be ceased or reduced, collaborative planning of the deprescribing regimen, and provision of review and support to the patient and caregivers. The authors discuss how deprescribing might be adapted for and implemented in psychiatry, identify potential barriers, and make recommendations for future directions.

The early identification of psychosis: can lessons be learnt from cardiac stress testing?

Psychotic disorders including schizophrenia are amongst the most debilitating psychiatric disorders. There is an urgent need to develop methods to identify individuals at risk with greater precision and as early as possible. At present, a prerequisite for a diagnosis of schizophrenia is the occurrence of a psychotic episode. Therefore, attempting to detect schizophrenia on the basis of psychosis is analogous to diagnosing coronary artery disease (CAD) after the occurrence of a myocardial infarction (MI). The introduction of cardiac stress testing (CST) has revolutionized the detection of CAD and the prevention and management of angina and MI. In this paper, we attempt to apply lessons learnt from CST to the early detection of psychosis by proposing the development of an analogous psychosis stress test. We discuss in detail the various parameters of a proposed psychosis stress test including the choice of a suitable psychological or psychopharmacological "stressor," target population, outcome measures, safety of the approach, and the necessary evolution of test to become clinically informative. The history of evolution of CST may guide the development of a similar approach for the detection and management of psychotic disorders. The initial development of a test to unmask latent risk for schizophrenia will require the selection of a suitable and safe stimulus and the development of outcome measures as a prelude to testing in populations with a range of risk to determine predictive value. The use of CST in CAD offers the intriguing possibility that a similar approach may be applied to the detection and management of schizophrenia.

Cannabinoids and Psychosis.

There is growing interest in the relationship between cannabis and psychosis. The link between cannabis use and psychosis comprises three distinct relationships: acute psychosis associated with cannabis intoxication, acute psychosis that lasts beyond the period of acute intoxication, and persistent psychosis not time-locked to exposure. Experimental studies reveal that cannabis, tetrahydrocannabinol (THC) and synthetic cannabinoids reliably produce transient positive, negative, and cognitive symptoms in healthy volunteers. Case-studies indicate that cannabinoids can induce acute psychosis which lasts beyond the period of acute intoxication and persisting as long as a month. Exposure to cannabis in adolescence is associated with an increased risk for later psychotic disorder in adulthood; this association is consistent, somewhat specific, shows a dose-response, and is biologically plausible. The link between cannabinoids and psychosis is greater with earlier age of exposure to cannabinoids, childhood abuse and genetic vulnerability. However, cannabinoids are neither necessary nor sufficient to cause a persistent psychotic disorder. More likely cannabinoids are a 'component cause' interacting with other known (family history) and unknown factors to result in psychosis outcomes. While more research is needed to better understand the relationship between cannabinoid use and psychosis, and the neural underpinnings of this link, clinicians should be mindful of the potential risk of psychosis especially in vulnerable populations, including adolescents and those with a psychosis diathesis.

The Denial of Death: A Three-decade Long Case of Absent Grief.

Bereavement reactions are associated with numerous physical and mental complications. Atypical bereavement reactions have been described but their place in the classificatory system has not been established. We present the case of an eighty-year-old woman who came with the belief that her deceased son was alive. We discuss the diagnostic dilemma she posed and conclude that it may be difficult to differentiate atypical bereavement from other psychiatric illnesses.

Personality disorders: prevalence and demography at a psychiatric outpatient in North India.

BACKGROUND: Even though personality disorders are common among psychiatric populations, the data from India on their prevalence and demography are sparse. AIM: To profile the prevalence and demography of personality disorders in North India. METHODS: The retrospective study was based on patients attending the outpatient of a general hospital psychiatric centre in North India between June 1996 and June 2006. The specified data were collected from the case records of those receiving a primary or comorbid ICD-10 diagnosis of a personality disorder. RESULTS: Personality disorders had a prevalence of 1.07%, with a preponderance of those aged 21-40 years (69.4%), men (64.9%), employed and students (37.3% and 32.8% respectively), unmarried (56%), graduates and undergraduates (27.6% each), and referred by the family (68.7%). The most common personality disorders were anxious-avoidant and borderline. Compared with the anxious-avoidant group, the borderline group was younger (mean age 24.44 vs 29.66 years) and had a preponderance of females (60% vs 27.1%). CONCLUSION: The prevalence of personality disorders among the psychiatric outpatients was low compared to most of the research literature reporting clinically diagnosed personality disorders. The differences between the borderline and anxious-avoidant personality disorder subjects were largely explained by interrelated demographic variables.

Relationship between religiosity and psychopathology in patients with depression.

OBJECTIVE: To compare the psychopathology between depressed patients with low religiosity and those with high religiosity and to correlate the level of religiosity with the psychopathology in the psychiatric clinic of a general hospital in Chandigarh, North India. MATERIALS AND METHODS: Thirty depressed patients with low religiosity and 30 patients with high religiosity were assessed on the Religiosity Scale, Beck Depression Inventory, Hamilton Depression Rating Scale, Beck Hopelessness Scale and Suicidal Intent Questionnaire. RESULTS: In the patients with depression, hopelessness and suicidal intent correlated negatively with the level of religiosity. CONCLUSION: In depressed patients, hopelessness and suicidal intent are inversely related to the level of religiosity.