The Greek-Orthodox version of the Brief Religious Coping (B-RCOPE) instrument: psychometric properties in three samples and associations with mental disorders, suicidality, illness perceptions, and quality of life

Background: The B-RCOPE is a brief measure assessing religious coping. We aimed to assess the psychometric properties of its Greek version in people with and without long-term conditions (LTCs). Associations between religious coping and mental illness, suicidality, illness perceptions, and quality of life were also investigated. Methods: The B-RCOPE was administered to 351 patients with diabetes, chronic pulmonary obstructive disease (COPD), and rheumatic diseases attending either the emergency department (N = 74) or specialty clinics (N = 302) and 127 people without LTCs. Diagnosis of mental disorders was established by the MINI. Associations with depressive symptom severity (PHQ-9), suicidal risk (RASS), illness perceptions (B-IPQ), and health-related quality of life (WHOQOL-BREF) were also investigated. Results: The Greek version of B-RCOPE showed a coherent two-dimensional factor structure with remarkable stability across the three samples corresponding to the positive (PRC) and negative (NRC) religious coping dimensions. Cronbach’s alphas were 0.91–0.96 and 0.77–0.92 for the PRC and NRC dimensions, respectively. Furthermore, NRC was associated with poorer mental health, greater depressive symptom severity and suicidality, and impaired HRQoL. In patients with LTCs, PRC correlated with lower perceived illness timeline, while NRC was associated with greater perceived illness consequences, lower perceived treatment control, greater illness concern, and lower illness comprehensibility. Conclusions: These findings indicate that the Greek-Orthodox B-RCOPE version may reliably assess religious coping. In addition, negative religious coping (i.e., religious struggle) is associated with adverse illness perceptions, and thus may detrimentally impact adaptation to medical illness. These findings deserve replication in prospective studies

Stress exposure alters brain mRNA expression of the genes involved in insulin signalling, an effect modified by a high fat/high fructose diet and cinnamon supplement

In occidental societies, high fat and high sugar diets often coincide with episodes of stress. The association is likely to modify brain energy control. Brain insulin signalling is rarely studied in stressed individuals consuming high fat diets. Furthermore the effects of cinnamon supplement are not known in these conditions. Therefore, we exposed rats, over a 12-week period, to a control (C) or a high fat/high fructose (HF/HFr) diet that induces peripheral insulin resistance. A cinnamon supplement (C+CN and HF/HFr +CN) was added or not. After diet exposure, one group of rats was exposed to a 30-min restraint followed by a 10-min open-field test, their combination featuring a moderate stressor, the other rats staying unstressed in their home cages. The insulin signalling in hippocampus and frontal cortex was studied through the mRNA expression of the following genes: insulin receptor (Ir), insulin receptor substrate (Irs1), glucose transporters (Glut1 and Glut3), glycogen synthase (Gys1) and their modulators, Akt1 and Pten. In C rats, stress enhanced the expression of Ir, Irs1, Glut1, Gys1 and Akt1 mRNA. In C+CN rats, stress induced an increase in Pten but a decrease in Gys1 mRNA expression. In HF/HFr rats, stress was associated with an increase in Pten mRNA expression. In HF/HFr+CN rats, stress increased Pten mRNA expression but also decreased Gys1 mRNA expression. This suggests that a single moderate stress favours energy refilling mechanisms, an effect blunted by a previous HF/HFr diet and cinnamon supplement

No differences between drug naive and drug experienced unipolar depressed patients in terms of neurobiological testing: A cross sectional study

Successful antidepressant treatment has been associated with concomitant changes in brain function, consolidated as long as treatment is continued and remission is preserved. The present study aimed at assessing the impact of prior antidepressant treatment on brain function in currently depressed but unmedicated individuals by investigating for any differences between antidepressant-naive vs. antidepressant-experienced subjects. Fifty right-handed patients (22 medication-naive vs. 28 medication-experienced), suffering from major depression participated in the study. They all underwent a standardised clinical interview and psychometric assessment combined with neurobiological tests (brain SPECT, Dexamethasone Suppression Test, Dexfenfluramine Challenge Test, electro-oculogram, flash-electroretinogram and flash-visual evoked potentials and pattern-reversal visual evoked potentials). No significant differences between medication-naive and medication-experienced depressed subjects were found in terms of the neurobiological markers assessed, after controlling for age, sex, age at onset, number of depressive episodes, depression subtype (melancholic, atypical or undifferentiated) and severity of current episode. Unmedicated currently depressed patients, no matter their previous exposure to antidepressants, show similar changes in brain function. This does not necessarily mean that antidepressants do not have a long term effect on brain physiology, since not all patients relapse. However, it seems that those patients who relapse after stopping medication, seem to 'regress' to an 'as if never medicated' state, with regard to brain function. These findings might suggest that continuous maintenance treatment with antidepressants is essential for patients at high risk to relapse. Alternatively, they might suggest that our methodology assesses only a shallow and mainly state part of the pathophysiology of depression