Refine
Has Fulltext
- no (10) (remove)
Language
- English (10)
Is part of the Bibliography
- yes (10)
Keywords
- Depression (10) (remove)
Institute
- Department Psychologie (10) (remove)
This longitudinal study investigated patterns of developmental problems across depression, aggression, and academic achievement during adolescence, using two measurement points two years apart (N = 1665; age T1: M = 13.14; female = 49.6%). Latent Profile Analyses and Latent Transition Analyses yielded four main findings: A three-type solution provided the best fit to the data: an asymptomatic type (i.e., low problem scores in all three domains), a depressed type (i.e., high scores in depression), an aggressive type (i.e., high scores in aggression). Profile types were invariant over the two data waves but differed between girls and boys, revealing gender specific patterns of comorbidity. Stabilities over time were high for the asymptomatic type and for types that represented problems in one domain, but moderate for comorbid types. Differences in demographic variables (i.e., age, socio-economic status) and individual characteristics (i.e., self-esteem, dysfunctional cognitions, cognitive capabilities) predicted profile type memberships and longitudinal transitions between types.
Evidence from animal research has revealed that less maternal care results in disturbed emotionality in the offspring. In the present study, the long-term impact of maternal responsiveness and stimulation during early mother child interaction on depressive psychopathology was examined until adulthood. Data are from an epidemiological cohort study of the long-term outcome of early risk factors assessed at birth. At age 3 months, mothers and infants were videotaped during a nursing and playing situation. Maternal responsiveness and stimulation as well as infant responsiveness were evaluated by trained raters. At age 19 years, 314 participants (145 males, 169 females) were characterized on measures of depression through interview and questionnaire. In addition, measures of depression and anxiety were available from assessments in childhood. Results indicated that less maternal stimulation during early interaction was associated with a higher risk of depression in the offspring until the age of 19 years. In addition, children of less stimulating mothers showed more depressive symptoms at age 19 years and displayed more anxiety and depressive symptoms between the ages of 4.5 and 15 years. In contrast, maternal responsiveness was unrelated to children's outcome. In accordance with findings from animal research, the present study provides first longitudinal evidence in humans of a continuous and long-term influence of early maternal interaction behavior on the offspring's psychological adjustment until adulthood. The results suggest that the amount of maternally initiated contact behavior in a very early developmental stage may be crucial for children's mental health, regardless of child and maternal responsiveness.
Child regulative temperament as a mediator of parenting in the development of depressive symptoms
(2017)
Child temperament as well as parenting behaviors have been linked to adolescent depression. Beyond their main effects, the interplay between these factors is of interest. For example, in an interactive model, a differential susceptibility of temperamental variants to parenting has been suggested. However, so far, the differential susceptibility hypothesis has mostly been studied with a focus on externalizing disorders. On the other hand, parenting may shape the child’s temperament and vice versa in a transactional process. In a prospective, longitudinal at-risk sample (163 boys, 176 girls), we assessed emotional (easy–difficult) and regulative (self-control) temperament at ages 4.5, and 8 years, respectively, as well as parenting quality at age 4.5 years using the HOME inventory. Hierarchical linear regression analysis was used to investigate the prediction of depressive symptoms at age 11, measured by the Child Depression Inventory, including interaction terms between the temperament variable and parenting. We additionally tested whether parenting was mediated by child temperament. As previously reported, both self-control and parenting were longitudinally associated with preadolescent depressive symptoms. There were no interactive effects between temperament and parenting. However, the effects of parenting were partly mediated by self-control. Our data do not support a differential susceptibility of temperamental variants in the development of preadolescent depression. However, our results are in line with the assumption that parenting may shape young children’s temperament, with positive parenting in the early childhood fostering the development of regulative temperament.
Background: The appetite-stimulating hormone ghrelin is a fundamental regulator of human energy metabolism. A series of studies support the notion that long-term appetite and weight regulation may be already programmed in early life and it could be demonstrated that the intrauterine environment affects the ghrelin system of the offspring. Animal studies have also shown that intrauterine programming of orexigenic systems persists even until adolescence/adulthood. Methods: We hypothesized that plasma ghrelin concentrations in adulthood may be associated with the intrauterine exposure to cigarette smoke. We examined this hypothesis in a sample of 19-year-olds followed up since birth in the framework of the Mannheim Study of Children at Risk, an ongoing epidemiological cohort study of the long-term outcome of early risk factors. Results: As a main finding, we found that ghrelin plasma concentrations in young adults who had been exposed to cigarette smoke in utero were significantly higher than in those without prenatal smoke exposure. Moreover, individuals with intrauterine nicotine exposure showed a significantly higher prevalence of own smoking habits and lower educational status compared to those in the group without exposure. Conclusion: Smoking during pregnancy may be considered as an adverse intrauterine influence that may alter the endocrine-metabolic status of the offspring even until early adulthood.
In order to clarify further the role of Beck’s vulnerability-stress model in the early development of depression, this longitudinal study tested a threshold model of dysfunctional attitudes in children and adolescents. An initially asymptomatic sample of 889 youths aged 9–18 years completed measures of dysfunctional attitudes and depressive symptoms. Twenty months later, participants reported stressful life events and current depressive symptoms. Results support a threshold view of cognitive vulnerability as only dysfunctional attitudes above a certain threshold significantly interacted with life events to predict depressive symptoms. Thus, findings suggest that dysfunctional attitudes must exceed a certain threshold to confer vulnerability to depressive symptomatology in youth. The term “dysfunctional” might therefore only apply to higher levels of the “dysfunctional attitudes” proposed by A. T. Beck. Results also indicate that studies using non-clinical samples may systematically underestimate the effect of dysfunctional attitudes when relying on conventional linear methods.
Accumulating research suggests a moderating role for the corticotropin-releasing hormone receptor 1 gene (CRHR1) in the association between childhood adversity and adult depression. The present study aims to replicate recent findings using different genetic variants and measures of early adversity assessed both prospectively and retrospectively. Data were collected in the context of an ongoing epidemiological cohort study following the outcome of early risk factors from birth into adulthood. 300 participants (137 males, 163 females) were genotyped for four CRHR1 SNPs (rs7209436, rs110402, rs242924, and rs17689882) and completed the Beck Depression Inventory at ages 19, 22 and 23 years. Childhood adversity was assessed using the Childhood Trauma Questionnaire and by a standardized parent interview yielding an index of family adversity. Our results indicate that CRHR1 and childhood adversity interacted to predict depressive symptoms in young adults. Specifically, we found that the impact of childhood maltreatment on adult depressive symptoms was significantly higher in individuals (i) with two copies of the CRHR1 TAT haplotype, and (ii) homozygous for the G allele of rs17689882. The interaction was demonstrated for exposure to childhood maltreatment as assessed by retrospective self-report, but not to prospectively ascertain objective family adversity. The present study partially replicates recent findings of a CRHR1 by childhood adversity interaction with regard to adult depression highlighting the subjective characteristics of the environmental pathogen that is operative in this interaction.
Objective: The purpose of this systematic review and meta-analysis was to examine the effects of exercise on depression and anxiety in people living with HIV (PLWH), and to evaluate, through subgroup analysis, the effects of exercise type, frequency, supervision by exercise professionals, study quality, and control group conditions on these outcomes. Method: A literature search was conducted through four electronic databases from inception to February 2019. Considered for inclusion were randomized controlled trials (RCTs) investigating exercise interventions and depression or anxiety as outcomes in people living with HIV (>= 18 years of age). Ten studies were included (n = 479 participants, 49.67% females at baseline), and the standardized mean difference (SMD) and heterogeneity were calculated using random-effect models. An additional pre-post meta-analysis was also conducted. Results: A large effect in favor of exercise when compared to controls was found for depression (SMD = -0.84, 95%CI = [-1.57, -0.11], p = 0.02) and anxiety (SMD = -1.23, 95%CI = [-2.42, 0.04], p = -0.04). Subgroup analyses for depression revealed large effects on depression for aerobic exercise only (SMD = -0.96, 95%CI = [-1.63, -0.30], p = 0.004), a frequency of >= 3 exercise sessions per week (SMD = -1.39, 95%CI = [-2.24, -0.54], p < 0.001), professionally supervised exercise (SMD = -1.40, 95%CI = [-2.46, -0.17], p = 0.03]), and high-quality studies (SMD = -1.31, 95%CI = [-2.46, -0.17], p = 0.02). Conclusion: Exercise seems to decrease depressive symptoms and anxiety in PLWH, but other larger and high-quality studies are needed to verify these effects.
Childhood adversity plays an important role for development of major depressive disorder (MDD). There are differences in subcortical brain structures between patients with MDD and healthy controls, but the specific impact of childhood adversity on such structures in MDD remains unclear. Thus, aim of the present study was to investigate whether childhood adversity is associated with subcortical volumes and how it interacts with a diagnosis of MDD and sex. Within the ENIGMA-MDD network, nine university partner sites, which assessed childhood adversity and magnetic resonance imaging in patients with MDD and controls, took part in the current joint mega-analysis. In this largest effort world-wide to identify subcortical brain structure differences related to childhood adversity, 3036 participants were analyzed for subcortical brain volumes using FreeSurfer. A significant interaction was evident between childhood adversity, MDD diagnosis, sex, and region. Increased exposure to childhood adversity was associated with smaller caudate volumes in females independent of MDD. All subcategories of childhood adversity were negatively associated with caudate volumes in females - in particular emotional neglect and physical neglect (independently from age, ICV, imaging site and MDD diagnosis). There was no interaction effect between childhood adversity and MDD diagnosis on subcortical brain volumes. Childhood adversity is one of the contributors to brain structural abnormalities. It is associated with subcortical brain abnormalities that are relevant to psychiatric disorders such as depression. (C) 2016 Published by Elsevier Ltd.
The goal of this study was to determine the prevalence of depression and its risk factors in patients with late-onset rheumatoid arthritis (RA) treated in German primary care practices. Longitudinal data from general practices (n=1072) throughout Germany were analyzed. Individuals initially diagnosed with RA (2009-2013) were identified, and 7301 patients were included and matched (1:1) to 7301 controls. The primary outcome measure was the initial diagnosis of depression within 5 years after the index date in patients with and without RA. Cox proportional hazards models were used to adjust for confounders. The mean age was 72.2 years (SD: 7.6 years). A total of 34.9 % of patients were men. Depression diagnoses were present in 22.0 % of the RA group and 14.3 % of the control group after a 5-year follow-up period (p < 0.001). In the multivariate regression model, RA was a strong risk factor for the development of depression (HR: 1.55, p < 0.001). There was significant interaction of RA and diagnosed inflammatory polyarthropathies (IP) (RA*IP interaction: p < 0.001). Furthermore, dementia, cancer, osteoporosis, hypertension, and diabetes were associated with a higher risk of developing depression (p values < 0.001). The risk of depression is significantly higher in patients with late-onset RA than in patients without RA for subjects treated in primary care practices in Germany. RA patients should be screened routinely for depression in order to ensure improved treatment and management.
Recent studies have emphasized an important role for neurotrophins, such as brain-derived neurotrophic factor (BDNF), in regulating the plasticity of neural circuits involved in the pathophysiology of stress-related diseases. The aim of the present study was to examine the interplay of the BDNF Val(66)Met and the serotonin transporter promoter (5-HTTLPR) polymorphisms in moderating the impact of early-life adversity on BDNF plasma concentration and depressive symptoms. Participants were taken from an epidemiological cohort study following the long-term outcome of early risk factors from birth into young adulthood. In 259 individuals (119 males, 140 females), genotyped for the BDNF Val(66)Met and the 5-HTTLPR polymorphisms, plasma BDNF was assessed at the age of 19 years. In addition, participants completed the Beck Depression Inventory (BDI). Early adversity was determined according to a family adversity index assessed at 3 months of age. Results indicated that individuals homozygous for both the BDNF Val and the 5-HTTLPR L allele showed significantly reduced BDNF levels following exposure to high adversity. In contrast, BDNF levels appeared to be unaffected by early psychosocial adversity in carriers of the BDNF Met or the 5-HTTLPR S allele. While the former group appeared to be most susceptible to depressive symptoms, the impact of early adversity was less pronounced in the latter group. This is the first preliminary evidence indicating that early-life adverse experiences may have lasting sequelae for plasma BDNF levels in humans, highlighting that the susceptibility to this effect is moderated by BDNF Val(66)Met and 5-HTTLPR genotype.