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Cognitive Distortions in Relation to Plasma Cortisol and Oxytocin Levels in Major Depressive Disorder.

ABSTRACT: Negative thinking is prominent in major depressive disorder (MDD). Cognitive models propose that negative thinking influences the hypothalamus-pituitary-adrenal axis and cortisol release. Oxytocin is also linked to MDD, social and affective processing, and stress buffering. Little research has examined direct relationships between negative cognitions, cortisol, and oxytocin. Methods:Sixty-one unmedicated participants meeting DSM-5 criteria for MDD and 60 healthy controls completed measures of psychopathology, stress, and cognitions. Plasma samples were analyzed for cortisol and oxytocin. Between-group analyses of variance were conducted along with correlational, regression and mediation analyses. Results:Depressed participants reported greater frequency and believability of negative thoughts than controls. Cortisol levels were positively, and oxytocin inversely, correlated with negative thinking. Cortisol and negative thinking accounted for unique variance in depression, and the relationship between stress and cortisol depended on the extent of negative cognitions. Conclusions:The results support long-standing cognitive models which propose that negative thoughts are important in the relationship between stress and cortisol levels.

SUBMITTER: Thomas SJ

PROVIDER: S-EPMC6987429 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Cognitive Distortions in Relation to Plasma Cortisol and Oxytocin Levels in Major Depressive Disorder.

Thomas Susan Jennifer SJ Larkin Theresa T

Frontiers in psychiatry 20200122

Negative thinking is prominent in major depressive disorder (MDD). Cognitive models propose that negative thinking influences the hypothalamus-pituitary-adrenal axis and cortisol release. Oxytocin is also linked to MDD, social and affective processing, and stress buffering. Little research has examined direct relationships between negative cognitions, cortisol, and oxytocin.<h4>Methods</h4>Sixty-one unmedicated participants meeting DSM-5 criteria for MDD and 60 healthy controls completed measure ...[more]

PMID: 32038321

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Project description:AimsMajor Depressive Disorder (MDD) is associated with an increased risk of chronic disease related to weight gain, problematic eating behaviours and neuroendocrine changes. MDD is frequently associated with altered hypothalamic-pituitary-adrenal axis activity and cortisol secretion, where cortisol has been implicated in regulating energy balance, food intake and depressogenic weight changes. However, little research has examined the relationships between cortisol, adiposity and depressogenic problematic eating behaviours.MethodPlasma cortisol concentrations were compared between 37 participants with MDD reporting appetite/weight loss, 43 participants with MDD reporting appetite/weight gain, and 60 healthy controls, by sex. Associations between cortisol, indices of adiposity and problematic eating behaviours were then assessed after accounting for demographic variables and depressive symptoms. Depressive symptoms were assessed using the Depression subscale of the Depression, Anxiety and Stress Scale, and eating behaviours with the Dutch Eating Behaviours Questionnaire and Yale Food Addiction Scale.ResultsParticipants with MDD reporting appetite/weight loss had higher cortisol compared to controls, and marginally higher cortisol than those with MDD reporting appetite/weight gain. Cortisol negatively and significantly accounted for unique variance in body mass index and waist circumference after accounting for variance associated with age, sex and depressive symptoms, however it was not a significant predictor of problematic eating behaviours, such as emotional eating or food addiction. Cortisol concentrations did not differ between sexes.ConclusionThe results indicate that cortisol is related to lower indices of adiposity and depressogenic symptoms of appetite/weight loss but is not related to problematic eating behaviours and appetite increases in MDD. These findings provide further evidence that the melancholic and atypical subtypes of MDD are associated with differential neuroendocrine and anthropometric indices, as well as behavioural and symptom profiles. Further research investigating the temporal nature of the identified relationships may assist in facilitating the development of improved interventions for individuals affected by weight changes in MDD.

Project description:Background: Major Depressive Disorder (MDD) is a moderately heritable disorder with a high lifetime prevalence. At present, laboratory blood tests to support MDD diagnosis are not available. Methods: We used a classifier approach on blood gene expression profiles of a unique set of non-medicated subjects (MDD patients and controls) to select genes of which expression is predictive for disease status. To reveal blood gene expression changes related to MDD disease, we applied a powerful ex vivo stimulus to the blood, i.e. incubation with lipopolysaccharide (LPS; 10 ng/ml blood). Results: Based on LPS-stimulated blood gene expression using whole-genome microarrays in 42 subjects (primary cohort; 21 MDD patients (mean age 42.3 years), 21 healthy controls (mean age 41.9 years)), we identified a set of genes (CAPRIN1, CLEC4A, KRT23, MLC1, PLSCR1, PROK2, ZBTB16) that serves as a molecular signature of MDD. These findings were validated for the primary cohort using an independent quantitative PCR method (P = 0.007). The difference between depressive patients and controls was confirmed (P = 0.019) in a replication cohort of 13 patients with MDD (mean age 42.8 years) and 14 controls (mean age 45.6 years). The MDD-signature score comprised of expression levels of 7 genes could discriminate depressive patients from controls with sensitivity of 76.9% and specificity of 71.8%. Conclusions: We show for the first time that molecular analysis of stimulated blood cells can be used as an endophenotype for MDD diagnosis, which is a milestone in establishing biomarkers for neuropsychiatric disorders with moderate heritability in general. Our results may provide a new entry point for following and predicting treatment outcome, as well as prediction of severity and recurrence of MDD. In total, 33 MDD patients and 34 healthy controls were analyzed using basal gene expression in whole blood, and gene expression from whole blood that was stimulated with LPS for 5-6 h, using microarrays. Patients were arbitrarily selected from all patients to serve as primary cohort (nMDD = 21 (MDD01-MDD21); nControls = 21 (Con01-Con21)), or replication cohort (nMDD = 12 (MDD22-MDD35); nControls = 13 (Con22-Con37)) using microarrays. This submission does not include Samples CON21_LPS or CON30_LPS.

Dataset Information

Cognitive Distortions in Relation to Plasma Cortisol and Oxytocin Levels in Major Depressive Disorder.

Publications

Cognitive Distortions in Relation to Plasma Cortisol and Oxytocin Levels in Major Depressive Disorder.

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