ABSTRACT
Previous studies suggest that individual preferences for medication- or psychotherapy-based treatments for depression may affect outcomes in clinical trials that compare these two forms of treatment. We assessed patients' beliefs about the causes of their depression, their preferred treatment, and strength of that preference in 80 patients participating in a 12-week clinical trial evaluating neuroimaging predictors of response to cognitive behavior therapy (CBT) or escitalopram. Forty-five patients expressed a preference for one of the 2 treatments, but being matched to preference did not influence remission or completion rates. Medication-preferring patients were more likely to terminate the trial early, regardless of treatment received. CBT-preferring patients rarely endorsed unknown causes for their depression, and medication-preferring patients were highly unlikely to identify pessimistic attitudes as a source of their depression. Among patients willing to be randomized to treatment, preference does not appear to strongly influence outcome. Specific preferences for CBT or medication may reflect differing conceptualizations about depressive illness, knowledge of which may enhance treatment retention and efficacy.
Subject(s)
Antidepressive Agents/therapeutic use , Cognitive Behavioral Therapy/methods , Depressive Disorder, Major , Patient Preference/psychology , Remission Induction/methods , Adult , Culture , Depressive Disorder, Major/diagnosis , Depressive Disorder, Major/psychology , Depressive Disorder, Major/therapy , Diagnostic and Statistical Manual of Mental Disorders , Double-Blind Method , Female , Health Knowledge, Attitudes, Practice , Humans , Interview, Psychological , Male , Middle Aged , Neuroimaging/methods , Outcome and Process Assessment, Health Care , Patient Dropouts/psychology , Treatment OutcomeABSTRACT
Variations of the corticotropin-releasing hormone receptor 1 (CRHR1) gene appear to moderate the development of depression after childhood trauma. Depression more frequently affects women than men. We examined sex differences in the effects of the CRHR1 gene on the relationship between childhood trauma and adult depression. We recruited 1,063 subjects from the waiting rooms of a public urban hospital. Childhood trauma exposure and symptoms of depression were assessed using dimensional rating scales. Subjects were genotyped for rs110402 within the CRHR1 gene. An independent sample of 78 subjects underwent clinical assessment, genotyping, and a dexamethasone/CRH test. The age range at recruitment was 18-77 years and 18-45, for the two studies respectively. In the hospital sample, the protective effect of the rs110402 A-allele against developing depression after childhood trauma was observed in men (N = 424), but not in women (N = 635). In the second sample, the rs110402 A-allele was associated with decreased cortisol response in the dexamethasone/CRH test only in men. In A-allele carriers with childhood trauma exposure women exhibited increased cortisol response compared men; there were no sex differences in A-allele carriers without trauma exposure. This effect may, however, not be related to gender differences per se, but to differences in the type of experienced abuse between men and women. CRHR x environment interactions in the hospital sample were observed with exposure to physical, but not sexual or emotional abuse. Physical abuse was the most common type of abuse in men in this cohort, while sexual abuse was most commonly suffered by women. Our results suggest that the CRHR1 gene may only moderate the effects of specific types of childhood trauma on depression. Gender differences in environmental exposures could thus be reflected in sex-specific CRHR1 x child abuse interactions.
ABSTRACT
OBJECTIVE: The authors sought to determine innate immune system activation following psychosocial stress in patients with major depression and increased early life stress. METHOD: Plasma interleukin (IL)-6, lymphocyte subsets, and DNA binding of nuclear factor (NF)-kB in peripheral blood mononuclear cells were compared in medically healthy male subjects with current major depression and increased early life stress (N=14) versus nondepressed male comparison subjects (N=14) before and after completion of the Trier Social Stress Test. RESULTS: Trier Social Stress Test-induced increases in IL-6 and NF-kappaB DNA-binding were greater in major depression patients with increased early life stress and independently correlated with depression severity, but not early life stress. Natural killer (NK) cell percentages also increased following stress. However, there were no differences between groups and no correlation between NK cell percentage and stress-induced NF-kappaB DNA-binding or IL-6. CONCLUSIONS: Male major depression patients with increased early life stress exhibit enhanced inflammatory responsiveness to psychosocial stress, providing preliminary indication of a link between major depression, early life stress and adverse health outcomes in diseases associated with inflammation.
