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Background Medical students face a variety of stressors associated with their education; if not promptly identified and adequately dealt with, it may bring about several negative consequences in terms of mental health and academic performance. This study examined psychometric properties of the Korean version of the Higher Education Stress Inventory (K-HESI). Methods The reliability and validity of the K-HESI were examined in a large scale multi-site survey involving 7110 medical students. The K-HESI, Beck Depression Inventory (BDI) and questions regarding quality of life (QOL) and self-rated physical health (SPH) were administered. Results Exploratory factor analysis of the K-HESI identified seven factors: Low commitment; financial concerns; teacher-student relationship; worries about future profession; non-supportive climate; workload; and dissatisfaction with education. A subsequent confirmatory factor analysis supported the 7-factor model. Internal consistency of the K-HESI was satisfactory (Cronbach’s α = .78). Convergent validity was demonstrated by its positive association with the BDI. Known group validity was supported by the K-HESI’s ability to detect significant differences on the overall and subscale scores of K-HESI according to different levels of QOL and SPH. Conclusions The K-HESI is a psychometrically valid tool that comprehensively assesses various relevant stressors related to medical education. Evidence-based stress management in medical education empirically guided by the regular assessment of stress using reliable and valid measure is warranted.

Methylenetetrahydrofolate reductase (MTHFR), a critical enzyme in folate metabolism, plays an important role in DNA methylation. It has been suggested that abnormal DNA methylation contributes to the pathogenesis of schizophrenia and congenital anomalies. The previous findings regarding the genetic relationship between MTHFR and schizophrenia are controversial. This study investigated the association of the two functional polymorphisms of MTHFR, C677T and A1298C, with the risk for schizophrenia. Furthermore, we conducted an updated meta-analysis on the two polymorphisms. In addition, we investigated the relationship between the polymorphisms and minor physical anomaly (MPA), which may represent neurodevelopmental aberrations in 201 schizophrenia patients and 350 normal control subjects. There was no significant association between either of the two polymorphisms and the risk of schizophrenia (chi-square = 0.001, df = 1, P = 0.971 for C677T; chi-square = 1.319, df = 1, P = 0.251 for A1298C). However, in meta-analysis, the C677T polymorphism showed a significant association in the combined and Asian populations (OR = 1.13, P = 0.005; OR = 1.21, P = 0.011, respectively) but not in the Korean and Caucasian populations alone. Neither polymorphism was associated with MPAs measured by the Waldrop scale (chi-square = 2.513, df = 2, P = 0.285). In conclusion, the present findings suggest that in the Korean population, the MTHFR polymorphisms are unlikely to be associated with the risk for schizophrenia and neurodevelopmental abnormalities related to schizophrenia.

This nationwide cross-sectional study assessed the prevalence, possible risk factors, and impact of depression among Korean medical students.Of all medical students (14,095) registered in 41 medical schools in 2006 in South Korea, 7,357 (52.2%) completed the survey. Depression was measured using the patient-rated version of the Mini International Neuropsychiatric Interview (MINI-PR). Data on academic functioning, and sociodemographic characteristics were also obtained.Current, one-year, and lifetime prevalence of major depressive disorder (MDD) were 2.9%, 6.5%, and 10.3%, respectively. Possible risk factors for one-year MDD were female gender, lower class years, admission track with exemption from entrance exam, living alone at a lodging house or a rented room, and financial difficulty (P.05). The grade point averages (GPAs) of students with MDD were significantly lower than those of nondepressed students for both semesters (t = 3.8, P.001; t = 4.8, P.001). The odds ratio of students with MDD of receiving a GPA below 2.0 was 1.8 (CI 1.4-2.4) as compared with nondepressed students.This study demonstrated that Korean medical students experience depression frequently. It also highlighted the possible risk factors of MDD among medical students and pervasive association of depression with poor functioning.

Background: Empathy is an essential element of physician professionalism. Thus, proper evaluation and education of empathy in medical students is important for medical education. Purpose: This study was conducted to evaluate the psychometric properties of the Korean Student-Version of the Jefferson Scale of Physician Empathy (JSPE-S). Methods: The scale was completed cross-sectionally by 493 medical students at Seoul National University College of Medicine in Korea. Results: Item-total correlations were all positive and statistically significant. Cronbach’s coefficient alpha was 0.84. A factor structure similar to that from American medical students was observed. The mean score of 5.2 ± 0.6 was obtained. Significant differences in the empathy scores were observed among years in medical school but not between genders. Conclusions: Our findings provide support for the reliability and validity of the Korean JSPE-S and indicate that it can serve as a useful instrument for assessing empathy among Korean medica...

No previous study has investigated the association between early trauma and suicidal behavior in medical students. We evaluated the types of early trauma which are the most strongly associated with a lifetime history of suicidal behavior in medical students.A total of 6986 medical students completed a self-administered questionnaire (response rates: 49.6% of the entire medical student body in Korea) which included lifetime suicidal behavior, stressors, and the Early Trauma Inventory Self Report-Short Form (ETISR-SF). This was used to evaluate the most serious forms of trauma experienced before the age of 18, including general trauma, physical, emotional and sexual abuse.Among medical students, lifetime prevalence of suicidal behavior was 34.0% for those who experienced early trauma and 18.1% in those without a history of trauma (chi(2)=215.7, p0.0001). Emotional abuse exhibited a higher odds ratio for lifetime suicidal behavior (OR=3.6, 95%CI=2.9-4.4) than other traumas including general trauma (OR=2.1, 95%CI=1.8-2.4), sexual (OR=2.0, 95%CI=1.5-2.8) or physical (OR=1.8, 95%CI=1.5-2.1) abuse, and current stressors including heavy stress (OR=1.5, 95%CI=1.4-1.8), poor physical health (OR=1.3, 95%CI=1.2-1.5), and poor economic status (OR=1.2, 95%CI=1.0-1.3). Emotional abuse also showed a higher odds ratio for lifetime suicidal ideation (OR=3.5, 95%CI=2.8-4.4), plan (OR=3.9, 95%CI=2.4-6.2), and attempt (OR=4.1, 95%CI=2.4-6.8) than other early traumas or stressors. In emotional abuse, a continuously cold or uncaring parental attitude exhibited a stronger association with lifetime suicidal behavior (OR=4.5, 95%CI=2.7-7.7) than other emotional abuse.Emotional abuse, especially continuous parental emotional abuse in childhood, is significantly associated with lifetime suicidal behavior in Korean medical students.

Objectives Depression is more frequently experienced and induces more severe consequences in medical students than in the general population. However, treatment rates for depression in medical students are still low. In this study, the authors investigated factors that affect treatment for depression and dispositions towards treating depression among South Korean medical students. Methods A nationwide, cross-sectional survey was administered to medical students attending all 41 medical schools in South Korea (14 095 students). The questionnaire included the Beck Depression Inventory (BDI) and asked for data on socio-demographic variables, history of diagnosis or treatment for depression, knowledge of mental health problems and disposition to use mental health care. Results A total of 7357 students (52.2%) from 36 schools responded to the survey. Of these, 689 (9.4%) were identified as being depressed via a BDI score higher than 16. Of the depressed respondents, only 61 (8.9%) had been diagnosed with depression and 67 (9.7%) had been treated for depression. Age was significantly associated with treatment behaviour for depression. Correct knowledge about the aetiology of depression and psychiatric medicine was significantly related to students’ disposition to use psychiatric services and to receive psychopharmacotherapy as an option to resolve depression. Conclusions Accurate knowledge of depression and appropriate medication seems to be relevant to students seeking appropriate treatment for depression. The development of education programmes designed to improve medical students’ knowledge of mental health problems and treatments would facilitate treatment seeking in medical students.

To examine regional abnormalities in the brains of patients with obsessive-compulsive disorder (OCD), we assessed the gray matter (GM) density using voxel-based morphometry (VBM). We compared magnetic resonance images (MRIs) acquired from 71 OCD patients and 71 age- and gender-matched normal controls and examined the relationship between GM density and various clinical variables in OCD patients. We also investigated whether GM density differs among the subtypes of OCD compared to healthy controls. We detected significant reduction of GM in the inferior frontal gyrus, the medial frontal gyrus, the insula, the cingulate gyrus, and the superior temporal gyrus of OCD patients. A significant increase in GM density was observed in the postcentral gyrus, the thalamus, and the putamen. Some of these regions, including the insular and postcentral gyrus, were also associated with the severity of obsessive- compulsive symptoms. These findings indicate that the frontal-subcortical circuitry is dysfunctional in OCD, and suggest that the parietal cortex may play a role in the pathophysiology of this disease.

It has been suggested that bipolar disorder is associated with altered immune function. Monocyte chemoattractant protien-1 (MCP-1) is a chemokine that influences both neural and immune functions. We thus hypothesized that MCP-1 may be related to the development or pathophysiology of bipolar disorder. In this case–control study, we investigated the association between the A-2518G single nucleotide polymorphism (SNP) of the MCP-1 promoter and bipolar disorder. Patients with bipolar disorder ( n = 183; bipolar I = 145, bipolar II = 38) and healthy controls (350) were recruited for the study. No significant allelic or genotypic association was detected between the A-2518G polymorphism and any sample of bipolar disorder patients. When we pooled the healthy controls and the cases of bipolar I disorder from previous Korean studies and this study, we again found no significant association. No significant difference in either allele frequency or genotype distribution was observed between bipolar I and bipolar II disorders. There was no difference in the age at onset of bipolar disorder among the three genotype groups. Our data suggest that the A-2518G polymorphism of MCP-1 is not a major susceptibility factor for bipolar disorder in the Korean population. However, the physiological role of MCP-1 is highly suggestive of its being associated with bipolar disorder, and further analyses of other SNPs of MCP-1 remain to be performed.

Glycogen synthase kinase-3 (GSK3) is a crucial enzyme contributing to the regulation of neuronal structure, plasticity and survival, is implicated as a contributory factor in prevalent diseases such as Alzheimer's disease and mood disorders and is regulated by a wide range of signaling systems and pharmacological agents. Therefore, factors regulating GSK3 in vivo are currently of much interest. GSK3 is inhibited by phosphorylation of serine-9 or serine-21 in GSK3beta and GSK3alpha, respectively. This study found that accurate measurements of phospho-Ser-GSK3 in brain are confounded by a rapid post-mortem dephosphorylation, with approximately 90% dephosphorylation of both GSK3 isoforms occurring within 2 min post-mortem. Furthermore, three anesthetics, pentobarbital, halothane and chloral hydrate, each caused large in vivo increases in the serine phosphorylation of both GSK3beta and GSK3alpha in several regions of mouse brain. Thus, studies of the phosphorylation state of GSK3 in brain, and perhaps in other tissues, need to take into account post-mortem changes and the effects of anesthetics and there is a direct correlation between anesthesia and high levels of serine-phosphorylated GSK3.

Background Glycogen synthase kinase-3 (GSK3), which is primarily regulated by an inhibitory phosphorylation of an N-terminal serine, has been implicated as contributing to mood disorders by the finding that it is inhibited by the mood stabilizer lithium. Methods This study tested if the antidepressant imipramine or the mood stabilizers lithium and sodium valproate regulated pathophysiological serine-dephosphorylation of GSK3 caused by hypoxia in mouse brain in vivo. Results Hypoxia caused rapid serine-dephosphorylation of both isoforms of GSK3, GSK3β and GSK3α, in mouse cerebral cortex, hippocampus, and striatum. Pretreatment of mice with imipramine, sodium valproate, or lithium attenuated hypoxia-induced serine-dephosphorylation of GSK3β and GSK3α in all three brain regions. Conclusions These results demonstrate that imipramine and mood stabilizers are capable of blocking pathophysiologically induced serine-dephosphorylation of GSK3, supporting the hypothesis that stabilization of serine-phosphorylation of GSK3 contributes to their therapeutic effects.

The goal of this study was to determine if serotonergic activity, which is impaired in depression, regulates the phosphorylation of glycogen synthase kinase-3beta (GSK3beta) in mouse brain in vivo. GSK3beta is inhibited by phosphorylation on serine-9 and is a target of the mood stabilizer lithium. Following administration to mice of d-fenfluramine to stimulate serotonin (5HT) release and reduce its reuptake, and clorgyline to inhibit 5HT catabolism, levels of phospho-Ser9-GSK3beta were 300-400% of control levels in the prefrontal cortex, hippocampus, and striatum. Treatment with monoamine reuptake inhibitors fluoxetine and imipramine also increased the level of phospho-Ser9-GSK3beta. Using receptor selective agonists and antagonists, 5HT1A receptors were found to mediate increases, and 5HT2 receptors decreases, in phospho-Ser9-GSK3beta levels. This indicates that serotonergic regulation of the phosphorylation of GSK3beta is achieved by a balance between the opposing actions of these 5HT receptor subtypes. These findings demonstrate for the first time that serotonergic activity regulates the phosphorylation of GSK3beta and show that this regulation occurs in mammalian brain in vivo. These results raise the possibility that impaired inhibitory control of GSK3beta may occur in conditions where serotonergic activity is dysregulated, such as in mood disorders.

Introduction This study aimed to investigate changes in heart rate variability and cardiorespiratory coupling in male college students with problematic Internet use (PIU) excessive gaming type during action video game play to assess the relationship between PIU tendency and central autonomic regulation. Method Electrocardiograms and respiration were simultaneously recorded from 22 male participants with excessive online gaming and 22 controls during action video game play. Sample entropy (SampEn) was computed to assess autonomic regularity, and cross-SampEn was calculated to quantify autonomic coordination. Results During video game play, reduced cardiorespiratory coupling (CRC) was observed in individuals with PIU excessive gaming type compared with controls, implicating central autonomic dysregulation. The PIU tendency was associated with the severity of autonomic dysregulation. Conclusion These findings indicate impaired CRC in PIU excessive gaming type, which may reflect alterations of central inhibitory control over autonomic responses to pleasurable online stimuli.

The purpose of this study was to explore a psychological profile of Internet addiction (IA) considering impulsivity as a key personality trait and as a key component of neuropsychological functioning. Twenty three subjects with IA (Young's Internet Addiction Test scores=70 or more) and 24 sex-, age-, and intelligence-matched healthy controls were enrolled. Participants filled out a questionnaire about trait impulsivity, the Trait Characteristic Inventory, depression, and anxiety. Next, we administered traditional neuropsychological tests including the Stroop et al. and computerized neuropsychological tests using the Cambridge Neuropsychological Test Automated Battery. The IA group exhibited more trait impulsivity than the healthy control group. They also scored higher for novelty seeking and harm avoidance. The IA group performed more poorly than the healthy control group in a computerized stop signal test, a test for inhibitory function and impulsivity; no group differences appeared for other neuropsychological tests. The IA group also scored higher for depression and anxiety, and lower for self-directedness and cooperativeness. In conclusion, individuals with IA exhibited impulsivity as a core personality trait and in their neuropsychological functioning.

Aims: Tolerance to ethanol-induced inhibition of N -methyl-D-aspartate receptors (NMDARs) is thought to underlie the acute adaptive mechanisms against ethanol. To explore these compensatory upregulating mechanisms of NMDARs, we investigated the expression and phosphorylation of NMDAR subunits in vivo following an acute ethanol treatment . Methods: Male Sprague-Dawley rats were given 4 g/kg ethanol, and the phospho-S896-NR1, NR2A and NR2B subunits of NMDAR were immunoblotted from the cerebral cortex and hippocampus. We also examined the mRNAs and ubiquitinated forms of the NR2A and NR2B subunits. Results: Acute ethanol treatment increased phospho-S896-NR1 at 30 min in the cerebral cortex and hippocampus, and the increase was maintained until 2 h in the hippocampus. Ethanol increased total NR2A and NR2B expression at 30 min in the cortex and hippocampus, and the NR2A increase was maintained until 2 h in the hippocampus. The increased expression of the NR2A and NR2B subunits was not associated with statistically significant alterations in mRNA expression or protein ubiquitination. Conclusion: Acute ethanol treatment increased NR1 subunit phosphorylation and NR2A and NR2B subunit expression in the cerebral cortex and hippocampus of rats. These effects of ethanol on the NMDAR subunits may underlie the mechanisms that compensate for ethanol-induced inhibition of NMDARs. However, the regulation of NR2A and NR2B in this paradigm is not dependent on transcriptional changes.

Cyclosporine A (CsA), an immunosuppressant and calcineurin inhibitor, induces hyperlipidemia in humans and animals. AMP-activated protein kinase (AMPK) is involved in metabolic homeostasis and lipid metabolism through modulating downstream molecules acetyl CoA carboxylase (ACC) and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoAR). AMPK activity is regulated by the phosphorylation at the Thr-172 residue by its upstream liver kinase B 1 (LKB1), Ca(2+)/calmodulin-dependent protein kinase kinase β (CaMKKβ) or transforming growth-factor-β-activated kinase 1 (TAK1). AMPK can be deactivated through dephosphorylation by protein phosphatase 2Cα (PP2Cα). In this study, we demonstrated that phosphorylation at Thr-172-AMPK increased with a concurrent increase in the phosphorylation of Ser-431-LKB1 and Thr-184/187-TAK1 in the rat hippocampus at 5 h after an intraperitoneal CsA (50 mg/kg) injection. CsA did not affect the phosphorylation of Thr-196-Ca(2+)/calmodulin-dependent protein kinase 4 (CaMK4) and the amount of PP2Cα. An increased phosphorylation of Ser-79-ACC and Ser-872-HMG-CoAR was also observed. In conclusion, our data indicate that CsA activates the AMPK pathway in the rat hippocampus, which suggests that CsA affects the regulatory signaling pathway of lipid metabolism in the rat brain.

Cocaine- and amphetamine-regulated transcript (CART) peptide regulates appetite, reward, and mood. CART expression is regulated via the protein kinase A (PKA) pathway, and electroconvulsive shock (ECS), an efficient antipsychotic and antidepressant measure, activates PKA-related signaling. Thus, we hypothesized that ECS may regulate the expression of CART. ECS given daily for five consecutive days increased CART mRNA and protein in the rat nucleus accumbens (NAc), accompanied by an increase in CREB phosphorylation. Our results suggest that ECS-induced CART up-regulation might be associated with PKA-CREB signaling, but the causal direction remains to be elucidated in future studies.

Akt is a serine/threonine protein kinase that plays a vital role in promoting cellular survival. Predominantly cytosolic, upon stimulation with growth-factors or stress, active Akt translocates into mitochondria, but the functions of Akt in mitochondria are not yet fully understood. Mitochondria play a central role in apoptotic pathways and given Akt's functions in the cytoplasm, Akt in mitochondria may help preserve mitochondrial integrity during cellular stress. To test if the translocation of Akt into mitochondria is neuroprotective, adenoviral vectors expressing a constitutively active Akt, Ad-HA-Akt (DD), and a constitutively active Akt with a mitochondrial targeting signal, Ad-Mito-HA-Akt (DD), were generated. Human SH-SY5Y neuroblastoma cells expressing the adenoviral constructs were treated with staurosporine to initiate intrinsic apoptotic cell death and several aspects of the mitochondrial apoptotic pathway were evaluated. Expression of active Akt targeted to mitochondria was found to be sufficient to significantly reduce staurosporine-induced activation of caspase-3 and caspase-9, the release of cytochrome c from mitochondria, and Bax oligomerization at mitochondria. These findings demonstrate that intramitochondrial active Akt results in efficient protection against apoptotic signaling.

Glycogen synthase kinase 3 (GSK3) was recently suggested to be a potential target of psychotropics used in psychiatric illnesses such as schizophrenia and bipolar disorder. Relevant studies have found that antipsychotic drugs regulate GSK3 activity via an increase in either inhibitory serine phosphorylation or amount of GSK3 after acute or subchronic treatment. Recent evidence shows that GSK3 is regulated by dopaminergic or serotonergic systems implicated in the pathophysiology and treatment mechanisms of schizophrenia and bipolar disorder. Therefore, antipsychotics may regulate GSK3 via antagonizing dopaminergic or serotonergic activity. However, the signaling pathway that is involved in GSK3 regulation by dopaminergic or serotonergic systems has not been well established. Haloperidol is a typical antipsychotic with potent dopamine D(2) receptor antagonism. Clozapine is an atypical antipsychotic with potent serotonin 5HT(2) receptor antagonism. We injected rats with haloperidol or clozapine and examined the phosphorylation and amount of GSK3alpha/beta and its well-known upstream regulators Akt and Dvl in the rat frontal cortex by Western blotting. Both haloperidol and clozapine induced Ser21/9 phosphorylation of GSK3GSK3alpha/beta. Haloperidol increased the Ser473 phosphorylation of Akt transiently, whereas clozapine maintained the increase for 1 h. Haloperidol did not affect the phosphorylation and amount of Dvl, whereas clozapine increased both phosphorylation and the amount of Dvl. Our results suggest that GSK3 activity may be regulated by both typical and atypical antipsychotics and that Akt or Dvl, depending on the D(2)- or 5HT(2)- receptor antagonism properties of typical and atypical antipsychotics, mediate the regulation differently.

Glycogen synthase kinase-3 (GSK3) has recently been linked to mood disorders and schizophrenia, and the neurotransmitter systems and therapeutic treatments associated with these diseases. GSK3 is a widely influential enzyme that is capable of phosphorylating, and thereby regulating, over forty known substrates. Four mechanisms regulating GSK3 (phosphorylation, protein complexes, localization, and substrate phosphorylation) combine to provide substrate-specific regulation of the actions of GSK3. Several intracellular signaling cascades converge on GSK3 to modulate its activity, and several neurotransmitter systems also regulate GSK3, including serotonergic, dopaminergic, cholinergic, and glutamatergic systems. Because of changes in these neurotransmitter systems and the actions of therapeutic drugs, GSK3 has been linked to the mood disorders, bipolar disorder and depression, and to schizophrenia. Inhibition of GSK3 may be an important therapeutic target of mood stabilizers, and regulation of GSK3 may be involved in the therapeutic effects of other drugs used in psychiatry. Dysregulated GSK3 in bipolar disorder, depression, and schizophrenia could have multiple effects that could impair neural plasticity, such as modulation of neuronal architecture, neurogenesis, gene expression, and the ability of neurons to respond to stressful, potentially lethal, conditions. In part because of these key actions of GSK3 and its associations with mood disorders and schizophrenia, much research is currently being devoted to identifying new selective inhibitors of GSK3.

Repeated administrations of NMDA receptor antagonists induce behavioural changes which resemble the symptoms of schizophrenia in animals. ERK and GSK-3beta associated signalling pathways have been implicated in the pathogenesis of psychosis and in the action mechanisms of various psychotropic agents. Here, we observed the phosphorylations of ERK and GSK-3beta and related molecules in the rat frontal cortex after repeated intraperitoneal injections of MK-801, over periods of 1, 5, and 10 d. Repeated treatment with 0.5, 1, and 2 mg/kg MK-801 increased the phosphorylation levels of the MEK-ERK-p90RSK and Akt-GSK-3beta pathways and concomitantly and significantly increased CREB phosphorylation in the rat frontal cortex. However, single MK-801 treatment did not induce these significant changes. In addition, the immunoreactivities of HSP72, Bax, and PARP were not altered, which suggests that neuronal damage may not occur in the rat frontal cortex in response to chronic MK-801 treatment. These findings suggest that chronic exposure to MK-801 may induce pro-survival and anti-apoptotic activity without significant neuronal damage in the rat frontal cortex. Moreover, this adaptive change might be associated with the psychotomimetic action of MK-801.

Akt (protein kinase B, PKB) is one of the major downstream pathways of neurotrophin signaling and plays important roles in the cell survival and synaptic plasticity of the central nervous system. Electroconvulsive shock (ECS) has neurotrophic effect and it affects the synaptic plasticity. It can activate another major pathway of neurotrophin signaling, i.e., Ras–Raf–MEK–Erk cascade. In this paper, the authors investigated whether ECS can activate Akt signaling in the rat hippocampus. After a single ECS, the phosphorylation of Akt was increased, as were the signals detected by phospho-PDK1 substrate antibody, which suggests the activation of PDK1, an upstream molecule of Akt. The phosphorylation of downstream molecules of Akt, forkhead transcription factors (FKHR), endothelial nitric oxide synthase (eNOS), and glycogen synthase kinase-3β (GSK-3β) was also increased. The increased phosphorylation of Akt appeared within 5 min of ECS and its time frame paralleled that of the phosphorylation of Erks. Taken together, these results suggest that ECS activates Akt signaling over a similar time scale to that of Erks in the rat hippocampus.

group there were high rates of positive family history for endocrine disease and 40% were ethnically vulnerable to endocrine disease. The mean waist circumference, weight, BMI and fasting cholesterol were elevated for both groups. There were no cases of type 2 diabetes in the FEPP group vs. 10 cases in the ROMHC group. Conclusions: Although the FEPP group was younger and psychiatrically ill for a shorter duration, their anthropometric, and metabolic parameters were similar to the chronic group. This may be explained due to the higher proportion of individuals with ethnic vulnerability to type 2diabetes in the FEPP group. However, despite the elevated risk factors in the FEPP group, there were no cases o f type 2 diabetes. This indicates a window of opportunity to intervene with prevention strategies. References [1] Brown, S., Inskip, H., & Barraclough, B. (2000). Causes of the excess mortality of schizophrenia. Br.J.Psychiatry, 177, 212-217. [2] Horrobin, D.F. & Bennett, C.N. (1999). Depression and bipolar disorder: relationships to impaired fatty acid and phospholipid metabolism and to diabetes, cardiovascular disease, immunological abnormalities, cancer, ageing and osteoporosis. Possible candidate genes. Prostaglandins Leukot.Essent.Fatty Acids, 60, 217-234. [3] Dixon, L.B., Kreyenbuhl, J.A., Dickerson, F.B., Donner, T.W., Brown, C.H., Wolheiter, K. et al. (2004). A comparison of type 2 diabetes outcomes among persons with and without severe mental illnesses. Psychiatr. Serv., 55, 892-900.