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Clinicians are consistently presented with the arduous task of characterizing, identifying, classifying, and evaluating response-to-intervention when treating or examining a broad array of patient populations. The primary aim of this chapter is to outline and define wellness among patients living with chronic medical conditions (PLW-CMC). An operational definition of a chronic medical condition is one requiring ongoing management and treatment over extended periods of time, often comprised of a broad constellation of conditions including heart disease, stroke, cancer, chronic respiratory diseases, infectious diseases, metabolic/endocrine disorders, genetic disorders, and disorders resulting in disability/impairment . The number of persons living with one or more chronic medical conditions continues to increase, both nationally and internationally. Thus, the need for literature pertaining to interventions that optimize a patient's quality of life (QOL) is pertinent, as health status is known to be associated with an individual's perception or appraisal of wellness, life satisfaction, happiness, and overall well-being.
To present a multimodal analysis of psychopathology among African unaccompanied refugee minors (URMs) in Austria. These youths experience well documented war and flight related non-normative stressors on their way from Africa to Europe. We have previously reported 17% of PTSD, a number below expectations. We now report on trauma related personality variables which indicate that these youths are resilient but at high risk for decompensation. We tested the hypothesis that PTSD specific defenses would be high (most notably dissociation, conversion, projection, withdrawal and somatization).
Forty-one URMs participated in the study. The following standardized instruments were used: UCLA PTSD Index for DSM IV, Mini International Neuropsychiatric Diagnostic Interview for Children and Adolescents, Weinberger Adjustment Inventory, Response Evaluation Measure for the measurement of defenses.
Levels of psychopathology were below previously reported levels in URMs. By contrast, all defenses previously reported as elevated in PTSD (conversion, projection, dissociation, withdrawal and somatization) showed significant increases (p < 0.05), putting these defenses in the 80–95TH percentile for the norm population.
While syndromal illness was less than expected, indicators of trauma related habitual function were all elevated. The present findings reveal that URMs manage the extreme stress of their lives by defensive self-regulation. These findings have implications for diagnosis and management.
The present functional magnetic resonance imaging (fMRI) study investigated neural changes in relation to mood biased processing in depression, before and after cognitive behavioral therapy (CBT) using an emotional Stroop task.
Sixteen unmedicated patients (mean age 40 years), fulfilling DSM-IV diagnosis for unipolar major depression underwent fMRI, prior to and after 16 once-weekly sessions of CBT. Sixteen matched healthy volunteers were scanned at similar time intervals. In an emotional Stroop task negative and neutral words were presented in various colors and volunteers had to name the color of words. Latencies were recorded to determine behavioral emotional interference effects. MRI images were acquired using clustered image acquisition. Whole-brain and region of interest analysis examined the neural basis of interference and mood biased processing.
At baseline patients displayed increased latencies during color naming negative words, in comparison to neutral words and in relation to healthy volunteers. After treatment, latencies did not significantly differ between groups. With regard to neural activity, depressed patients showed increased activation at baseline in amygdala, dorsolateral prefrontal cortex (DLPFC), and ventrolateral prefrontal cortex (VLPFC), which normalized after CBT. Additionally, hyperactivation in the rostral anterior cingulate at baseline was positively correlated with symptom reduction after CBT.
Evidence was found for an emotional interference effect during acute states of depression which improved following CBT. The neural basis is associated with increased activity in the amygdala, DLPFC and VLPFC which normalized after treatment. CBT seems to affect behavioral biases and neural circuits involved in processing negative information.
In schizophrenia, sex differences related to age of onset, course of illness and response to antipsychotic treatment may be mirrored by differences in the underlying molecular pathways. We attempted to increase our understanding of these phenomena by carrying out multiplex immunoassay profiling of 95 serum molecules using samples from 4 independent cohorts of male and female first episode antipsychotic naive schizophrenia patients (n=133) and matched controls (n=133). The concentrations of 16 molecules associated with hormonal, inflammation and growth factor pathways showed significant sex differences in schizophrenia patients compared with controls. In line with the numerous sex differences reported in schizophrenia, our findings included alterations in the levels of several hormones, including elevated free and total testosterone in female patients and concomitant sex differences in sex hormone binding globulin and prolactin concentrations. We also found higher levels of thyroxine binding globulin and seven inflammatory markers in male schizophrenia patients only, raising the possibility that some aspects of the widely-reported immunological abnormalities in schizophrenia may be specific for males. Several of these markers showed sexspecific associations with positive and negative syndrome scale (PANSS) scores and changes in concentration after 6 weeks of treatment with antipsychotics. Finally, we also evaluated overlapping and distinct sex-specific biomarkers for schizophrenia, Asperger syndrome, major depressive disorder and bipolar disorder. We propose that future studies should investigate the common and sex-specific aetiologies of schizophrenia, as the current findings suggest that different therapeutic strategies may be required for male and female patients.
Based on the neuroinflammatory hypothesis of schizophrenia, we have quantified the numerical density of immunostained CD3+ T-lymphocytes, CD20+ B-lymphocytes, and HLA-DR+ microglial cells in the posterior hippocampus of 17 schizophrenia patients and 11 matched controls. Disease course-related immune alterations were considered by a separate analysis of residual (prevailing negative symptoms, n=7) and paranoid (prominent positive symptoms, n=10) schizophrenia cases. Higher lymphocyte densities were observed in residual schizophrenia. In contrast, HLA-DR+ microglia were increased in paranoid schizophrenia. BBB impairment and infiltration of T cells and B cells may contribute to the pathophysiology of residual schizophrenia, while microglial activation seems to play a role in paranoid schizophrenia. The identification of diverse immune endophenotypes may facilitate the development of distinct anti-inflammatory schizophrenia therapies to normalize BBB function, (auto)antibody production or microglial activity.
There is considerable variation in the prevalence of breastfeeding, which allows for investigation of factors that influence the initiation and duration of breastfeeding and its association with well being of the mother infant dyad.
To better understand factors that influence (1) maternal breastfeeding status and (2) the “effects” of breastfeeding on mothers and infants.
Participants (n = 170) derive from a longitudinal Canadian study “Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN)”, a project designed to understand the pre- and postnatal influences on maternal health and child social-emotional development. Mothers provided data on breastfeeding status, early life adversity, oxytocin gene and oxytocin gene receptor polymorphisms, depression/anxiety, infant temperament and maternal sensitivity.
Early life adversity associated with a shorter breastfeeding duration and higher maternal depression levels. The relation between mothers’ early adversity and the duration of breastfeeding was mediated by mothers’ depression level, but only in women carrying one variant of the oxytocin rs2740210 gene marker (CC genotype). Mothers who breastfeed at 3 months acted more sensitively towards their infants when they were 6 months old and they in turn had infants who at 18 months showed reduced negative affectivity.
Women who have been exposed to early adversity are “living with the past” and they are, to certain extent, protected or more vulnerable to depression, depending on their genotype. Breastfeeding associated with higher maternal sensitivity, which associated with decreased negative emotionality in the infant at 18 months. Our results help to clarify associations between early life experiences, breastfeeding, and the mother-infant relationship.
Disclosure of interest
The authors have not supplied their declaration of competing interest.
Maternal mental well being influences offspring development. Research suggests that an interplay between genetic and environmental factors underlies this familial transmission of mental disorders.
To explore an interaction between genetic and environmental factors to predict trajectories of maternal mental well being, and to examine whether these trajectories are associated with epigenetic modifications in mothers and their offspring.
We assessed maternal childhood trauma and rearing experiences, prenatal and postnatal symptoms of depression and stress experience from 6 to 72 months postpartum, and genetic and epigenetic variation in a longitudinal birth-cohort study (n = 262) (Maternal adversity, vulnerability and neurodevelopment project). We used latent class modeling to describe trajectories in maternal depressive symptoms, parenting stress, marital stress and general stress, taking polygenetic risk for major depressive disorder (MDD), a composite score for maternal early life adversities, and prenatal depressive symptoms into account.
Genetic risk for MDD associated with trajectories of maternal well being in the postpartum, conditional on the experience of early life adversities and prenatal symptoms of depression. We will explore whether these trajectories are also linked to DNA methylation patterns in mothers and their offspring. Preliminary analyses suggest that maternal early life adversities associate with offspring DNA methylation age estimates, which is mediated through maternal mental well being and maternal DNA methylation age estimates.
We found relevant gene-environment interactions associated with trajectories of maternal well being. Our findings inform research on mechanisms underlying familial transmission of vulnerability for psychopathology and might thus be relevant to prevention and early intervention programs.
Disclosure of interest
The authors have not supplied their declaration of competing interest.
Bipolar disorder (BD) is a psychiatric disorder associated with increased rates of obesity and inflammation. Leptin is an adipokine that is mainly produced by the white adipose tissue in response to insulin. It stimulates the immune system, increasing the production of pro-inflammatory cytokines. There is currently uncertainty regarding possible alterations in peripheral leptin levels across the mood states in BD.
This study comprises a between-group meta-analysis comparing serum and plasma leptin levels in people with BD in mania, depression or euthymia and healthy controls. We conducted a systematic search for all possibly eligible-English and non-English peer-reviewed articles. We calculated the effect size (ES) utilizing Hedges’ adjusted g using random effects.
Eleven studies were included in the meta-analyses, providing data on 1118 participants. Serum and plasma leptin levels were not altered in subjects with BD when compared to healthy controls in mania (g = −0.99, 95% CI −2.43 to 0.43, P = 0.171), in depression (g = 0.17, 95% CI −0.45 to 0.79, P = 0.584), or in euthymia (g = 0.03, 95% CI −0.39 to 0.46, P = 0.882). However, we did observe a stronger association between leptin levels and both age and BMI in patients with BD in euthymia compared to healthy controls, such that the greater the age of the individuals, the greater the difference in leptin levels between BD and controls; and the higher the BMI, the greater the difference in leptin levels between BD and controls.
Our meta-analysis provides evidence that leptin levels are not altered in BD across the mood spectrum compared to healthy controls. The disproportionate increase of leptin levels with increase in BMI in BD speaks in favour of a potential inflammatory role of white adipose tissue in BD and a disproportionate increase of leptin levels with increase in age.
Animal and human studies suggest that individual differences in maternal parenting behaviour are transmitted from one generation to the next.
This study aimed to examine potential psychosocial mechanisms underlying an intergenerational transmission of conceptualization of parenting, including affect, cognition, and parental support.
In a subsample of 201 first-time mothers participating in the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) project, we assessed maternal childhood rearing experiences, using the Parental Bonding Instrument and the Childhood Trauma Questionnaire. At 6 months postpartum, mothers completed questionnaires on parenting stress, symptoms of depression, internalization of maternal care regulation and current relationship with mother and father.
We found significant direct associations of maltreatment and rearing by the grandmother with parenting stress at 6 months. These associations were mediated through distinct psychosocial pathways: the association of maltreatment on higher parenting stress was fully mediated through more maternal symptoms of depression (z = 2.297; P = 022). The association between sub-optimal rearing provided by the mother and higher parenting stress was mediated through lower internalization of maternal care regulation (z = -2.155; P = 031) and to a lesser degree through more symptoms of depression (z = -1.842; P = 065). Finally, higher quality rearing by the grandfather was indirectly related to lower parenting stress through positive current relationship with the father (z = -2.617; P = 009).
There are distinct pathways by which early experiences manifest in parenting stress. By understanding the structure of dysregulated parenting, clinicians will have practical information to specifically target maternal motivation, social supports, and depressed mood to disrupt maladaptive parenting cognitions and practices.
Disclosure of interest
The authors have not supplied their declaration of competing interest.
We examined maternal depression and maternal sensitivity as mediators of the association between maternal childhood adversity and her child's temperament in 239 mother–child dyads from a longitudinal, birth cohort study. We used an integrated measure of maternal childhood adversity that included the Childhood Trauma Questionnaire and the Parental Bonding Index. Maternal depression was assessed with the Edinburgh Postnatal Depression Scale at 6 months postpartum. Maternal sensitivity was assessed with the Ainsworth maternal sensitivity scales at 6 months. A measure of “negative emotionality/behavioral dysregulation” was derived from the Early Childhood Behaviour Questionnaire administered at 36 months. Bootstrapping-based mediation analyses revealed that maternal depression mediated the effect of maternal childhood adversity on offspring negative emotionality/behavioral dysregulation (95% confidence interval [0.026, 0.144]). We also found a serial, indirect effect of maternal childhood adversity on child negative emotionality/behavioral mediated first by maternal depression and then by maternal sensitivity (95% confidence interval [0.031, 0.156]). Results suggest the intergenerational transmission of the effects of maternal childhood adversity to the offspring occurs through a two-step, serial pathway, involving maternal depression and maternal sensitivity.
Prenatal adversity shapes child neurodevelopment and risk for later mental health problems. The quality of the early care environment can buffer some of the negative effects of prenatal adversity on child development. Retrospective studies, in adult samples, highlight epigenetic modifications as sentinel markers of the quality of the early care environment; however, comparable data from pediatric cohorts are lacking. Participants were drawn from the Maternal Adversity Vulnerability and Neurodevelopment (MAVAN) study, a longitudinal cohort with measures of infant attachment, infant development, and child mental health. Children provided buccal epithelial samples (mean age = 6.99, SD = 1.33 years, n = 226), which were used for analyses of genome-wide DNA methylation and genetic variation. We used a series of linear models to describe the association between infant attachment and (a) measures of child outcome and (b) DNA methylation across the genome. Paired genetic data was used to determine the genetic contribution to DNA methylation at attachment-associated sites. Infant attachment style was associated with infant cognitive development (Mental Development Index) and behavior (Behavior Rating Scale) assessed with the Bayley Scales of Infant Development at 36 months. Infant attachment style moderated the effects of prenatal adversity on Behavior Rating Scale scores at 36 months. Infant attachment was also significantly associated with a principal component that accounted for 11.9% of the variation in genome-wide DNA methylation. These effects were most apparent when comparing children with a secure versus a disorganized attachment style and most pronounced in females. The availability of paired genetic data revealed that DNA methylation at approximately half of all infant attachment-associated sites was best explained by considering both infant attachment and child genetic variation. This study provides further evidence that infant attachment can buffer some of the negative effects of early adversity on measures of infant behavior. We also highlight the interplay between infant attachment and child genotype in shaping variation in DNA methylation. Such findings provide preliminary evidence for a molecular signature of infant attachment and may help inform attachment-focused early intervention programs.
Prenatal maternal depression and a multilocus genetic profile of two susceptibility genes implicated in the stress response were examined in an interaction model predicting negative emotionality in the first 3 years. In 179 mother–infant dyads from the Maternal Adversity, Vulnerability, and Neurodevelopment cohort, prenatal depression (Center for Epidemiologic Studies Depressions Scale) was assessed at 24 to 36 weeks. The multilocus genetic profile score consisted of the number of susceptibility alleles from the serotonin transporter linked polymorphic region gene (5-HTTLPR): no long-rs25531(A) (LA: short/short, short/long-rs25531(G) [LG], or LG/LG] vs. any LA) and the dopamine receptor D4 gene (six to eight repeats vs. two to five repeats). Negative emotionality was extracted from the Infant Behaviour Questionnaire—Revised at 3 and 6 months and the Early Child Behavior Questionnaire at 18 and 36 months. Mixed and confirmatory regression analyses indicated that prenatal depression and the multilocus genetic profile interacted to predict negative emotionality from 3 to 36 months. The results were characterized by a differential susceptibility model at 3 and 6 months and by a diathesis–stress model at 36 months.
Disorganized attachment is an important early risk factor for socioemotional problems throughout childhood and into adulthood. Prevailing models of the etiology of disorganized attachment emphasize the role of highly dysfunctional parenting, to the exclusion of complex models examining the interplay of child and parental factors. Decades of research have established that extreme child birth weight may have long-term effects on developmental processes. These effects are typically negative, but this is not always the case. Recent studies have also identified the dopamine D4 receptor (DRD4) as a moderator of childrearing effects on the development of disorganized attachment. However, there are inconsistent findings concerning which variant of the polymorphism (seven-repeat long-form allele or non–seven-repeat short-form allele) is most likely to interact with caregiving in predicting disorganized versus organized attachment. In this study, we examined possible two- and three-way interactions and child DRD4 polymorphisms and birth weight and maternal caregiving at age 6 months in longitudinally predicting attachment disorganization at 36 months. Our sample is from the Maternal Adversity, Vulnerability and Neurodevelopment project, a sample of 650 mother–child dyads. Birth weight was cross-referenced with normative data to calculate birth weight percentile. Infant DRD4 was obtained with buccal swabs and categorized according to the presence of the putative allele seven repeat. Macroanalytic and microanalytic measures of maternal behavior were extracted from a videotaped session of 20 min of nonfeeding interaction followed by a 10-min divided attention maternal task at 6 months. Attachment was assessed at 36 months using the Strange Situation procedure, and categorized into disorganized attachment and others. The results indicated that a main effect for DRD4 and a two-way interaction of birth weight and 6-month maternal attention (frequency of maternal looking away behavior) and sensitivity predicted disorganized attachment in robust logistic regression models adjusted for social demographic covariates. Specifically, children in the midrange of birth weight were more likely to develop a disorganized attachment when exposed to less attentive maternal care. However, the association reversed with extreme birth weight (low and high). The DRD4 seven-repeat allele was associated with less disorganized attachment (protective), while non–seven-repeat children were more likely to be classified as disorganized attachment. The implications for understanding inconsistencies in the literature about which DRD4 genotype is the risk direction are also considered. Suggestions for intervention with families with infants at different levels of biological risk and caregiving risk are also discussed.
Dysfunctional attitudes are a feature of depression that has been correlated with receptor binding abnormalities in limbic and cortical regions. We sought to investigate the functional neuroanatomy of dysfunctional attitudes in major depressive disorder (MDD) and the effects of treatment with cognitive–behavioural therapy (CBT).
Participants were 16 patients with unipolar depression in an acute depressive episode (mean age 40.0 years) and 16 matched healthy controls (mean age 39.9 years). Patients were medication free and received a course of treatment with CBT. All participants underwent functional magnetic resonance imaging (fMRI) scans at baseline and at week 16, prior to the initiation of therapy and following the course of CBT for patients. During each fMRI scan, participants indicated their attributions to statements from a modified Dysfunctional Attitudes Scale (mDAS-48).
MDD patients in an acute depressive episode endorsed a greater number of extreme responses to DAS statements, which normalized following CBT treatment. Extreme attributions were associated with greater activation in the left hippocampal region, inferior parietal lobe and precuneus in MDD patients as compared with healthy controls as a main effect of group. An interaction effect was found in the left parahippocampal region, which showed less attenuation in MDD patients at the follow-up scan relative to healthy controls.
Attenuation of activity in the parahippocampal region may be indicative of an improvement in dysfunctional thinking following CBT treatment in depression, while persistent engagement of regions involved in attentional processing and memory retrieval with extreme attributions reflects a trait feature of depression.
Context: we present a study of the central 200 pc of NGC 6951, in the optical and NIR, taken with the Gemini North Telescope integral field spectrographs, with resolution of ~ 0”.1 Methods: we used a set of image processing techniques, as the filtering of high spatial and spectral frequencies, Richardson-Lucy deconvolution and PCA Tomography (Steiner et al.2009) to map the distribution and kinematics of the emission lines. Results: we found a thick molecular disk, with the ionization cone highly misaligned.
High post-release survival, low dispersal and the recruitment of captive-reared individuals into the wild population are critical to the success of any reintroduction programme. Reintroducing a migratory species poses an additional challenge as success also depends on the return of captive-reared individuals to breeding grounds in subsequent years. We investigated the effects of seven husbandry and management factors on the return rate of captive-reared eastern loggerhead shrikes Lanius ludovicianus migrans and documented the recruitment of returning individuals. During 2004–2010, 564 juveniles were released in Ontario, Canada, as part of a field propagation and release programme and there were 27 confirmed sightings of returning birds during 2005–2011. Returning birds were significantly more likely to have been released in large groups of juveniles (9–10 birds) at 5.5 weeks post-fledging from the Carden field propagation site. Comparisons of the number of young fledged and survival to 2 weeks post-fledging revealed similar results for pairs comprising one captive-reared and one wild-reared individual and pairs comprising two wild individuals. These results highlight the contribution of captive-reared shrikes to the recovery of the wild population and the importance of monitoring outcomes and evaluating techniques.