The physical and psychological health benefits of positive emotional writing:Investigating the moderating role of Type D (distressed) personality

Objectives Type D personality is associated with psychological and physical ill‐health. However, there has been limited investigation of the role of Type D personality in interventions designed to enhance well‐being. This study investigated associations between Type D personality and the efficacy of positive emotional writing for reducing stress, anxiety, and physical symptoms. Design A between‐subjects longitudinal design was employed. Method Participants (N = 71, Mage = 28.2, SDage = 12.4) completed self‐report measures of Type D personality, physical symptoms, perceived stress, and trait anxiety, before completing either (1) positive emotional writing or (2) a non‐emotive control writing task, for 20 min per day over three consecutive days. State anxiety was measured immediately before and after each writing session, and self‐report questionnaires were again administered 4 weeks post‐writing. Results Participants in the positive emotional writing condition showed significantly greater reductions in (1) state anxiety and (2) both trait anxiety and perceived stress over the 4‐week follow‐up period, compared to the control group. While these effects were not moderated by Type D personality, a decrease in trait anxiety was particularly evident in participants who reported both high levels of social inhibition and low negative affectivity. Linguistic analysis of the writing diaries showed that Type D personality was positively associated with swear word use, but not any other linguistic categories. Conclusion These findings support the efficacy of positive emotional writing for alleviating stress and anxiety, but not perceived physical symptoms. Swearing may be a coping strategy employed by high Type D individuals

A shortened protocol for assessing cognitive bias in rats

Reliable measurement of affective state in animals is a significant goal of animal welfare. Such measurements would also improve the validity of pre-clinical mental health research which relies on animal models. However, at present, affective states in animals are inaccessible to direct measurement. In humans, changes in cognitive processing can give reliable indications of emotional state. Therefore, similar techniques are increasingly being used to gain proxy measures of affective states in animals. In particular, the ‘cognitive bias’ assay has gained popularity in recent years. Major disadvantages of this technique include length of time taken for animals to acquire the task (typically several weeks), negative experiences associated with task training, and issues of motivation. New method Here we present a shortened cognitive bias protocol using only positive reinforcers which must actively be responded to. Results The protocol took an average of 4 days to complete, and produced similar results to previous, longer methods (minimum 30 days). Specifically, rats housed in standard laboratory conditions demonstrated negative cognitive biases when presented with ambiguous stimuli, and took longer to make a decision when faced with an ambiguous stimulus. Comparison with existing methods Compared to previous methods, this protocol is significantly shorter (average 4 days vs. minimum 30 days), utilises only positive reinforcers to avoid inducing negative affective states, and requires active responses to all cues, avoiding potential confounds of motivational state. Conclusions We have successfully developed a shortened cognitive bias protocol, suitable for use with laboratory rats. Keywords Cognitive bias; Emotion; Affect; Rat; Protoco

Cis-effects on gene expression in the human prenatal brain associated with genetic risk for neuropsychiatric disorders

The majority of common risk alleles identified for neuropsychiatric disorders reside in non-coding regions of the genome and are therefore likely to impact gene regulation. However, the genes that are primarily affected and the nature and developmental timing of these effects remain unclear. Given the hypothesised role for early neurodevelopmental processes in these conditions, we here define genetic predictors of gene expression in the human fetal brain with which we perform transcriptome-wide association studies (TWASs) of attention deficit hyperactivity disorder (ADHD), autism spectrum disorder, bipolar disorder, major depressive disorder and schizophrenia. We identify prenatal cis-regulatory effects on 63 genes and 166 individual transcripts associated with genetic risk for these conditions. We observe pleiotropic effects of expression predictors for a number of genes and transcripts, including those of decreased DDHD2 expression in association with risk for schizophrenia and bipolar disorder, increased expression of a ST3GAL3 transcript with risk for schizophrenia and ADHD, and increased expression of an XPNPEP3 transcript with risk for schizophrenia, bipolar disorder and major depression. For the protocadherin alpha cluster genes PCDHA7 and PCDHA8, we find that predictors of low expression are associated with risk for major depressive disorder while those of higher expression are associated with risk for schizophrenia. Our findings support a role for altered gene regulation in the prenatal brain in susceptibility to various neuropsychiatric disorders and prioritize potential risk genes for further neurobiological investigation

Polygenic risk for schizophrenia and subcortical brain anatomy in the UK Biobank cohort

Research has shown differences in subcortical brain volumes between participants with schizophrenia and healthy controls. However, none of these differences have been found to associate with schizophrenia polygenic risk. Here, in a large sample (n = 14,701) of unaffected participants from the UK Biobank, we test whether schizophrenia polygenic risk scores (PRS) limited to specific gene-sets predict subcortical brain volumes. We compare associations with schizophrenia PRS at the whole genome level (‘genomic’, including all SNPs associated with the disorder at a p-value threshold < 0.05) with ‘genic’ PRS (based on SNPs in the vicinity of known genes), ‘intergenic’ PRS (based on the remaining SNPs), and genic PRS limited to SNPs within 7 gene-sets previously found to be enriched for genetic association with schizophrenia (‘abnormal behaviour,’ ‘abnormal long-term potentiation,’ ‘abnormal nervous system electrophysiology,’ ‘FMRP targets,’ ‘5HT2C channels,’ ‘CaV2 channels’ and ‘loss-of-function intolerant genes’). We observe a negative association between the ‘abnormal behaviour’ gene-set PRS and volume of the right thalamus that survived correction for multiple testing (ß = −0.031, pFDR = 0.005) and was robust to different schizophrenia PRS p-value thresholds. In contrast, the only association with genomic PRS surviving correction for multiple testing was for right pallidum, which was observed using a schizophrenia PRS p-value threshold < 0.01 (ß = −0.032, p = 0.0003, pFDR = 0.02), but not when using other PRS P-value thresholds. We conclude that schizophrenia PRS limited to functional gene sets may provide a better means of capturing differences in subcortical brain volume than whole genome PRS approaches

Epidemiology of melanoma in rural southern Queensland

Objective: The objective of this study is to define the epidemiology of melanoma in rural communities in southern Queensland. Design: The design used was a 6‐year clinical record audit of melanoma cases identified by billing records and electronic clinical records, confirmed and typed with histology. Setting and Participants: This study was based on seven agricultural communities on the Darling Downs with patients presenting to local primary care clinics. Main outcome measures: Outcomes measured were confirmed type, depth and anatomic distribution of melanoma identified at these practices during the study period. Results: The results from 317 cases of melanoma found anatomic distribution was significantly different (χ2 = 9.6, P < 0.05) to that reported previously from the Queensland Cancer Registry. A high proportion (87%) of melanoma diagnosed by these general practitioners were 1 mm or less when treated. Conclusions: Conclusions drawn from these findings are that melanoma risk is not so much lesser in rural, inland communities compared with coastal and metropolitan regions, but different. Differences may relate to comprehensive data capture available in rural community studies and to different sun exposure and protection behaviours. The higher proportion of melanoma identified at early stages suggests rural primary care is an effective method of secondary prevention

Road to Nowhere? A Critical Consideration of the Use of the Metaphor ‘Care Pathway’ in Health Services Planning, Organisation and Delivery

AbstractMetaphors are inescapable in human discourse. Policy researchers have suggested that the use of particular metaphors by those implementing policy changes both influences perceptions of underlying reality and determines what solutions seem possible, and that exploring ‘practice languages’ is important in understanding how policy is enacted. This paper contributes to the literature exploring the generative nature of metaphors in policy implementation, demonstrating their role in not just describing the world, but also framing it, determining what is seen/unseen, and what solutions seem possible. The metaphor ‘care pathway’ is ubiquitous and institutionalised in healthcare. We build upon existing work critiquing its use in care delivery, and explore its use in health care commissioning, using evidence from the recent reorganisation of the English NHS. We show that the pathways metaphor is ubiquitous, but not necessarily straightforward. Conceptualising health care planning as ‘designing a pathway’ may make the task more difficult, suggesting a limited range of approaches and solutions. We offer an alternative metaphor: the service map. We discuss how approaches to care design might be altered by using this different metaphor, and explore what it might offer. We argue not for a barren language devoid of metaphors, but for their more conscious use.</jats:p

Summaries of plenary, symposia, and oral sessions at the XXII World Congress of Psychiatric Genetics, Copenhagen, Denmark, 12-16 October 2014

The XXII World Congress of Psychiatric Genetics, sponsored by the International Society of Psychiatric Genetics, took place in Copenhagen, Denmark, on 12-16 October 2014. A total of 883 participants gathered to discuss the latest findings in the field. The following report was written by student and postdoctoral attendees. Each was assigned one or more sessions as a rapporteur. This manuscript represents topics covered in most, but not all of the oral presentations during the conference, and contains some of the major notable new findings reported

Amino acid residues in five separate HLA genes can explain most of the known associations between the MHC and primary biliary cholangitis.

Primary Biliary Cholangitis (PBC) is a chronic autoimmune liver disease characterised by progressive destruction of intrahepatic bile ducts. The strongest genetic association is with HLA-DQA1*04:01, but at least three additional independent HLA haplotypes contribute to susceptibility. We used dense single nucleotide polymorphism (SNP) data in 2861 PBC cases and 8514 controls to impute classical HLA alleles and amino acid polymorphisms using state-of-the-art methodologies. We then demonstrated through stepwise regression that association in the HLA region can be largely explained by variation at five separate amino acid positions. Three-dimensional modelling of protein structures and calculation of electrostatic potentials for the implicated HLA alleles/amino acid substitutions demonstrated a correlation between the electrostatic potential of pocket P6 in HLA-DP molecules and the HLA-DPB1 alleles/amino acid substitutions conferring PBC susceptibility/protection, highlighting potential new avenues for future functional investigation

A transcriptome-wide association study implicates specific pre- and post-synaptic abnormalities in schizophrenia

chizophrenia is a complex highly heritable disorder. Genome-wide association studies (GWAS) have identified multiple loci that influence the risk of developing schizophrenia, although the causal variants driving these associations and their impacts on specific genes are largely unknown. We identify a significant correlation between schizophrenia risk and expression at 89 genes in dorsolateral prefrontal cortex (P ≤ 9.43x10−6), including 20 novel genes. Genes whose expression correlate with schizophrenia were enriched for those involved in abnormal CNS synaptic transmission (PFDR = 0.02) and antigen processing and presentation of peptide antigen via MHC class I (PFDR = 0.02). Within the CNS synaptic transmission set, we identify individual significant candidate genes to which we assign direction of expression changes in schizophrenia. The findings provide strong candidates for experimentally probing the molecular basis of synaptic pathology in schizophrenia