Illness severity and biomarkers in depression: Using a unidimensional rating scale to examine BDNF.

BACKGROUND: Numerous studies have reported reduced peripheral brain-derived neurotrophic factor (BDNF) in major depression (MD). However, most of these studies used multidimensional depression rating scales, and failed to identify a relationship between BDNF levels and depression severity. Unidimensional scales are a more valid measure of syndrome severity. In these scales, items are ordered in increasing severity, so that as scores increase, syndrome severity increases; thus, each item adds unique information, and items can be totaled to a meaningful sum. The current study used the HAM-D6, a unidimensional measure of depression, to examine if it could identify a correlation between serum BDNF and depression severity. METHODS: Serum BDNF levels and symptom severity were assessed in 163 depressed patients, including those with both unipolar (84.0%) and bipolar (16.0%) depression. The evaluation of depression severity included the total HAM-D17 and 3 subscales, including the HAM-D6. RESULTS: On average, patients presented moderate to severe depression (HAM-D17=21.2±5.5). Overall BDNF levels were 60.4±22.6ng/mL. The correlation between serum BDNF and depression severity was modest and not different when assessed by the HAM-D6 subscale or the HAM-D17 as a whole (z=0.951; p=0.341), despite being statistically significant for the HAM-D6 (r=-0.185; p=0.019; 95% CI: -0.335 to -0.033), but not for the entire HAM-D17 (r=-0.127; p=0.108; 95% CI: -0.272 to 0.027). CONCLUSION: We could not identify a strong relationship between serum BDNF levels and depression severity using the HAM-D6. This is in concordance with results of previous studies that reported no correlation between these variables, and indicates that the properties of the clinical measures used cannot explain the results these studies.

Childhood trauma and dimensions of depression: a specific association with the cognitive domain

Objective: To investigate associations between a history of childhood trauma and dimensions of depression in a sample of clinically depressed patients. Methods: A sample of 217 patients from a mood-disorder outpatient unit was investigated with the Beck Depression Inventory, the Hamilton Depression Rating Scale, the CORE Assessment of Psychomotor Change, and the Childhood Trauma Questionnaire. A previous latent model identifying six depressive dimensions was used for analysis. Path analysis and Multiple Indicators Multiple Causes (MIMIC) models were used to investigate associations between general childhood trauma and childhood maltreatment modalities (emotional, sexual, and physical abuse; emotional and physical neglect) with dimensions of depression (sexual, cognition, insomnia, appetite, non-interactiveness/retardation, and agitation). Results: The overall childhood trauma index was uniquely associated with cognitive aspects of depression, but not with any other depressive dimension. An investigation of childhood maltreatment modalities revealed that emotional abuse was consistently associated with depression severity in the cognitive dimension. Conclusion: Childhood trauma, and specifically emotional abuse, could be significant risk factors for the subsequent development of cognitive symptoms of major depression. These influences might be specific to this depressive dimension and not found in any other dimension, which might have conceptual and therapeutic implications for clinicians and researchers alike.

Childhood trauma and dimensions of depression: a specific association with the cognitive domain.

OBJECTIVE: To investigate associations between a history of childhood trauma and dimensions of depression in a sample of clinically depressed patients. METHODS: A sample of 217 patients from a mood-disorder outpatient unit was investigated with the Beck Depression Inventory, the Hamilton Depression Rating Scale, the CORE Assessment of Psychomotor Change, and the Childhood Trauma Questionnaire. A previous latent model identifying six depressive dimensions was used for analysis. Path analysis and Multiple Indicators Multiple Causes (MIMIC) models were used to investigate associations between general childhood trauma and childhood maltreatment modalities (emotional, sexual, and physical abuse; emotional and physical neglect) with dimensions of depression (sexual, cognition, insomnia, appetite, non-interactiveness/retardation, and agitation). RESULTS: The overall childhood trauma index was uniquely associated with cognitive aspects of depression, but not with any other depressive dimension. An investigation of childhood maltreatment modalities revealed that emotional abuse was consistently associated with depression severity in the cognitive dimension. CONCLUSION: Childhood trauma, and specifically emotional abuse, could be significant risk factors for the subsequent development of cognitive symptoms of major depression. These influences might be specific to this depressive dimension and not found in any other dimension, which might have conceptual and therapeutic implications for clinicians and researchers alike.

Angiotensin-converting enzyme gene polymorphism in preeclampsia and normal pregnancy.

OBJECTIVE: The purpose of this study was to evaluate the angiotensin-converting enzyme gene polymorphism in pregnant women with and without preeclampsia. STUDY DESIGN: Preeclampsia was defined as hypertension and pathologic proteinuria in pregnant women after gestational week 20. Genomic DNA was isolated from leukocytes. The insertion-deletion polymorphism in intron 16 of the angiotensin-converting enzyme gene was detected in DNA samples with the use of the polymerase chain reaction. Chi-squared and Student t tests were used for statistical analysis. RESULTS: In preeclampsia (n=51 women) angiotensin-converting enzyme genotypes were deletion-D (DD) in 16 women (31%), insertion-I (II) in 12 women (24%), and insertion-deletion in 23 women (45%); in the control group (n=71), the angiotensin-converting enzyme genotypes were DD in 21 women (30%), II in 17 women (24%), and insertion-deletion in 33 women (46%). Angiotensin-converting enzyme genotype distribution and allelic frequencies were not different between groups. CONCLUSION: No difference in the angiotensin-converting enzyme genotype distribution was found between preeclampsia and normal pregnancy. The results showed no association between angiotensin-converting enzyme polymorphism and the development of preeclampsia.