Hidden scars in depression? Implicit and explicit self-associations following recurrent depressive episodes

To help explain the recurrent nature of major depressive disorder, we tested the hypothesis that depressive episodes and/or the duration of depressive symptoms may give rise to persistent dysfunctional implicit and/or more explicit self-associations, which in turn may place people at risk for the recurrence of symptoms. We therefore examined, in the context of the Netherlands Study of Depression and Anxiety, whether the strength of self-depressed associations at baseline was related to the number of past episodes (retrospective analysis; n = 666), and whether the duration of symptoms between baseline and follow-up predicted self-depressed associations at 2-year follow-up (prospective analysis; n = 726). The lifetime Composite International Diagnostic Interviews and Life Chart Interview were used to index the number of depressive episodes; the Implicit Association Test and its explicit equivalent were used to index self-associations. Consistent with the hypothesis that self-depressed associations strengthen following prolonged activation of negative self-associations during depressive episodes, individuals' implicit and explicit self-depressed associations correlated positively both with the number of prior depressive episodes at baseline and with the duration of depressive symptoms between baseline and 2-year follow-up. There was evidence that these relationships held, particularly in the prospective study, even when controlling for neuroticism and current depressive symptoms, whereas the retrospective relationship between number of episodes and implicit self-associations fell just short of significance

Reduced hypothalamic-pituitary-adrenal axis activity in chronic multi-site musculoskeletal pain : partly masked by depressive and anxiety disorders

Peer reviewedPublisher PD

Evaluating Spectral Models and the X-ray States of Neutron-Star X-ray Transients

We propose a hybrid model to fit the X-ray spectra of atoll-type X-ray transients in the soft and hard states. This model uniquely produces luminosity tracks that are proportional to T^4 for both the accretion disk and boundary layer. The model also indicates low Comptonization levels for the soft state, gaining a similarity to black holes in the relationship between Comptonization level and the strength of integrated rms variability in the power density spectrum. The boundary layer appears small, with a surface area that is roughly constant across soft and hard states. This result may suggestion that the NS radius is smaller than its inner-most stable circular orbit.Comment: 15 pages, 15 figures, accepted for publication in the Ap

Circulating insulin-like growth factor I modulates mood and is a biomarker of vulnerability to stress:from mouse to man

Individual susceptibility to anxiety disorders after maladaptive responses to stress is not well understood. We now report that while exploring stress responses in mice after traumatic brain injury (TBI), a condition associated to stress susceptibility, we observed that the anxiogenic effects of either TBI or exposure to life-threatening experiences (predator) were blocked when both stressors were combined. Because TBI increases the entrance into the brain of serum insulin-like growth factor I (IGF-I), a known modulator of anxiety with a wide range of concentrations in the human population, we then determined whether circulating IGF-I is related to anxiety measures. In mice, anxiety-like responses to predator were inversely related to circulating IGF-I levels. Other indicators of mood regulation such as sensitivity to dexamethasone suppression and expression levels of blood and brain FK506 binding protein 5 (FKBP5), a co-chaperone of the glucocorticoid receptor that regulates its activity, were also associated to circulating IGF-I. Indeed, brain FKBP5 expression in mice was stimulated by IGF-I. In addition, we observed in a large human cohort (n = 2686) a significant relationship between plasma IGF-I and exposure to recent stressful life events, while FKBP5 expression in blood cells was significantly associated to plasma IGF-I levels. Collectively, these data indicate that circulating IGF-I appears to be involved in mood homeostasis across different species. Furthermore, the data in mice allow us to indicate that IGF-I may be acting at least in part by modulating FKBP5 expression

The role of depressive symptoms and symptom dimensions in actigraphy-assessed sleep, circadian rhythm, and physical activity

BACKGROUND: Considering the heterogeneity of depression, distinct depressive symptom dimensions may be differentially associated with more objective actigraphy-based estimates of physical activity (PA), sleep and circadian rhythm (CR). We examined the association between PA, sleep, and CR assessed with actigraphy and symptom dimensions (i.e. mood/cognition, somatic/vegetative, sleep).METHODS: Fourteen-day actigraphy data of 359 participants were obtained from the Netherlands Study of Depression and Anxiety. PA, sleep, and CR estimates included gross motor activity (GMA), sleep duration (SD), sleep efficiency (SE), relative amplitude between daytime and night-time activity (RA) and sleep midpoint. The 30-item Inventory of Depressive Symptomatology was used to assess depressive symptoms, which were categorised in three depression dimensions: mood/cognition, somatic/vegetative, and sleep.RESULTS: GMA and RA were negatively associated with higher score on all three symptom dimensions: mood/cognition (GMA: β = -0.155, p &lt; 0.001; RA: β = -0.116, p = 0.002), somatic/vegetative (GMA: β = -0.165, p &lt; 0.001; RA: β = -0.133, p &lt; 0.001), sleep (GMA: β = -0.169, p &lt; 0.001; RA: β = -0.190, p &lt; 0.001). The association with sleep was more pronounced for two depression dimensions: longer SD was linked to somatic/vegetative (β = 0.115, p = 0.015) dimension and lower SE was linked to sleep (β = -0.101, p = 0.011) dimension.CONCLUSION: As three symptom dimensions were associated with actigraphy-based low PA and dampened CR, these seem to be general indicators of depression. Sleep disturbances appeared more linked to the somatic/vegetative and sleep dimensions; the effectiveness of sleep interventions in patients reporting somatic/vegetative symptoms may be explored, as well as the potential of actigraphy to monitor treatment response to such interventions.</p

Discovery of kilohertz quasi-periodic oscillations in the Z source GX 340+0

We have discovered two simultaneous kHz quasi-periodic oscillations (QPOs) in the Z source GX 340+0 with the Rossi X-ray Timing Explorer. The X-ray hardness-intensity and color-color diagram each show a full Z-track, with an extra limb branching off the flaring branch of the Z. Both peaks moved to higher frequencies when the mass accretion rate increased. The two peaks moved from 247 +/- 6 and 567 +/- 39 Hz at the left end of the horizontal branch to 625 +/- 18 and 820 +/- 19 Hz at its right end. The higher frequency peak's rms amplitude (5-60 keV) and FWHM decreased from ~5% and 383 +/- 135 Hz to ~2%, and 145 +/- 62 Hz, respectively. The rms amplitude and FWHM of the lower peak were consistent with being constant near 2.5 % and 100 Hz. The kHz QPO separation was consistent with being constant at 325 +/- 10 Hz. Simultaneous with the kHz QPOs we detected the horizontal branch oscillations (HBO) and its second harmonic, at frequencies between 20 and 50 Hz, and 38 and 69 Hz, respectively. The normal branch oscillations were only detected on the upper and middle normal branch, and became undetectable on the lower normal branch. The HBO frequencies do not fall within the range predicted for Lense-Thirring (LT) precession, unless either the ratio of the neutron star moment of inertia to neutron star mass is at least 4, 10^45 gcm^2/M_sun, the frequencies of the HBO are in fact the sub-harmonic oscillations, or the observed kHz peak difference is half the spin frequency and not the spin frequency. During a 1.2 day gap between two observations, the Z-track in the hardness-intensity diagram moved to higher count rates by about 3.5%. Comparing data before and after this shift, we find that the HBO properties are determined by position on the Z-track and not directly by count rate or X-ray colors.Comment: 12 pages including 4 figures. Accepted for publication in ApJ Letter

The role of depressive symptoms and symptom dimensions in actigraphy-assessed sleep, circadian rhythm, and physical activity

BACKGROUND: Considering the heterogeneity of depression, distinct depressive symptom dimensions may be differentially associated with more objective actigraphy-based estimates of physical activity (PA), sleep and circadian rhythm (CR). We examined the association between PA, sleep, and CR assessed with actigraphy and symptom dimensions (i.e. mood/cognition, somatic/vegetative, sleep).METHODS: Fourteen-day actigraphy data of 359 participants were obtained from the Netherlands Study of Depression and Anxiety. PA, sleep, and CR estimates included gross motor activity (GMA), sleep duration (SD), sleep efficiency (SE), relative amplitude between daytime and night-time activity (RA) and sleep midpoint. The 30-item Inventory of Depressive Symptomatology was used to assess depressive symptoms, which were categorised in three depression dimensions: mood/cognition, somatic/vegetative, and sleep.RESULTS: GMA and RA were negatively associated with higher score on all three symptom dimensions: mood/cognition (GMA: β = -0.155, p &lt; 0.001; RA: β = -0.116, p = 0.002), somatic/vegetative (GMA: β = -0.165, p &lt; 0.001; RA: β = -0.133, p &lt; 0.001), sleep (GMA: β = -0.169, p &lt; 0.001; RA: β = -0.190, p &lt; 0.001). The association with sleep was more pronounced for two depression dimensions: longer SD was linked to somatic/vegetative (β = 0.115, p = 0.015) dimension and lower SE was linked to sleep (β = -0.101, p = 0.011) dimension.CONCLUSION: As three symptom dimensions were associated with actigraphy-based low PA and dampened CR, these seem to be general indicators of depression. Sleep disturbances appeared more linked to the somatic/vegetative and sleep dimensions; the effectiveness of sleep interventions in patients reporting somatic/vegetative symptoms may be explored, as well as the potential of actigraphy to monitor treatment response to such interventions.</p

Recovery of the X-Ray Transient QX Nor (=X1608-52) in Outburst and Quiescence

We present optical and near-IR observations of QX Nor, the counterpart to the recurrent soft X-ray transient X1608-52, after its reappearance following the X-ray outburst in February 1996. The object has been seen only once before, during an X-ray outburst in 1977. Data from 3-5 months after the outburst show the counterpart at a mean magnitude of R=20.2 and variable on timescales of days. A comparison with identical observations in 1995 implies that the object has brightened by at least 1.8 mag in R following the X-ray outburst. We also detected QX Nor in the IR in both quiescence and outburst. A faint source is visible in the J but not the R band in May 1995. These first observations in the quiescent state yield magnitudes and colors consistent with optical emission from a low mass companion in the binary system, as is true in other soft X-ray transients.Comment: 10 pages including 4 figures and 2 tables; Uses AASTeX 4.0; Accepted for publication in The Astrophysical Journal, Volume 485, August 20, 199

The association of childhood maltreatment with depression and anxiety is not moderated by the oxytocin receptor gene

Background: The oxytocin receptor (OXTR) gene may be involved in resilience or vulnerability towards stress, and hence in the development of stress-related disorders. There are indications that OXTR single nucleotide polymorphisms (SNPs) interact with early life stressors in predicting levels of depression and anxiety. To replicate and extend these findings, we examined whether three literature-based OXTR SNPs (rs2254298, rs53576, rs2268498) interact with childhood maltreatment in the development of clinically diagnosed depression and anxiety disorders. Methods: We included 2567 individuals from the Netherlands Study of Depression and Anxiety. This sample consisted of 387 healthy controls, 428 people with a current or past depressive disorder, 243 people with a current or past anxiety disorder, and 1509 people with both lifetime depression and anxiety diagnoses. Childhood maltreatment was measured with both an interview and via self-report. Additional questionnaires measured depression and anxiety sensitivity. Results: Childhood maltreatment was strongly associated with both lifetime depression and anxiety diagnoses, as well as with depression and anxiety sensitivity. However, the OXTR SNPs did not moderate these associations nor had main effects on outcomes. Conclusions: The three OXTR gene SNPs did not interact with childhood maltreatment in predicting lifetime depression and anxiety diagnoses or sensitivity. This stresses the importance of replication studies with regard to OXTR gene variants in general populations as well as in clearly established clinical samples