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Reports of current ADHD symptoms in adults with a childhood diagnosis of ADHD are often discrepant: While one subgroup reports a particularly high level of current ADHD symptoms, another reports—in contrast—a very low level. The reasons for this difference remain unclear. Although sex might play a moderating role, it has not yet been examined in this regard. In an epidemiological cohort study from birth to young adulthood, childhood ADHD diagnoses were assessed at the ages of 4.5, 8, and 11 years based on parent ratings. Sex-specific development of ADHD symptoms was analyzed from the age of 15 to 25 years via self-reported ADHD symptoms in participants with (n = 47) and without childhood ADHD (n = 289) using a random coefficient regression model. The congruence between parent reports and adolescents’ self-ratings was examined, and the role of childhood ADHD diagnosis, childhood OCC/CD, and childhood internalizing disorder as possible sex-specific predictors of self-reported ADHD symptoms at age 25 years was investigated. With regard to self-reported ADHD symptoms, females with a childhood ADHD diagnosis reported significantly more ADHD symptoms compared to females without childhood ADHD and males with and without ADHD throughout adolescence and young adulthood. In contrast, males with childhood ADHD did not differ from control males either at age 15 or at age 25 years. Only in females did a childhood diagnosis of an externalizing disorder (ADHD and CD/ODD) predict self-reported ADHD symptoms by age 25 years. Our findings suggest that self-reports of young adults with a childhood diagnosis of ADHD are influenced by sex. Specifically, females with childhood ADHD report increased levels of ADHD symptoms upon reaching adulthood. To correctly evaluate symptoms and impairment in this subgroup, other, more objective, sources of information may be advisable, such as neurophysiological measures.
To provide further insight into stress generation patterns in boys and girls around puberty, this study investigated longitudinal reciprocal relations between depressive symptoms, dysfunctional attitudes, and stress generation, the process by which individuals contribute to the occurrence of stress in interpersonal contexts (e.g., problematic social interactions) or in noninterpersonal contexts (e.g., achievement problems). A community sample of N = 924 German children and early adolescents (51.8% male) completed depressive symptoms and dysfunctional attitudes measures at T1 and again 20 months later (T2). Stressful life events were reported at T2. Dysfunctional attitudes were unrelated to stress generation. Interpersonal, but not noninterpersonal, dependent stress partially mediated the relationship between initial and later depressive symptoms, with girls being more likely to generate interpersonal stress in response to depressive symptoms. Findings underscore the role of interpersonal stress generation in the early development of depressive symptomatology, and in the gender difference in depression prevalence emerging around puberty.
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.
Psychische Störungen und Entwicklungsauffälligkeiten früher erkennen mit neuem Kita- Vorsorgebogen
(2007)
Risikofaktoren für Delinquenz bei Jugendlichen und deren Fortsetzung bis in das Erwachsenenalter
(2001)
Background: Evidence from animal studies supports a role for serotonin transporter gene promoter polymorphism (5-HTTLPR) gene-environment interaction (G X E) in the development of excessive alcohol intake. Few studies in humans have been conducted on this topic, yielding inconsistent results. The present study aims to further explore G x E between 5-HTTLPR and exposure to psychosocial adversity on alcohol consumption in a high-risk community sample of young adults. Methods: Data were collected as part of the Mannheim Study of Children at Risk, an ongoing epidemiological cohort study following the outcome of early risk factors from birth into young adulthood. At age 19 years, 309 participants (142 male participants, 167 female participants) were genotyped for the biallelic and triallelic 5-HTTLPR and were administered a 45-day alcohol timeline follow-back interview, providing measures of the total number of drinks and the number of binge drinking days. Psychosocial adversity was assessed at birth (family adversity) and at age 19 (negative life events). Results: In contrast to various previous reports, a significant G x E emerged, indicating that, when exposed to high psychosocial adversity, individuals with the LL genotype of 5-HTTLPR exhibited more hazardous drinking than those carrying the S allele or those without exposure to adversity. This effect, which was confined to male participants, held both for different classifications of 5-HTTLPR and different types of adversity. Conclusions: One explanation for the discrepant results might be heterogeneity in alcohol phenotypes. While the L allele relates more strongly to early-onset alcoholism, the S allele may be linked more closely to alcohol use associated with anxiety and depression.
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.