525 research outputs found
The important gain is that we are lumpers and splitters now; it is the splitting that needs our hard work
Examining inflammation, health, stress and lifestyle variables linking low socioeconomic status with poorer cognitive functioning during adolescence
Higher C-reactive protein (CRP) is associated with cognitive difficulties. The nature of this association remains unclear given that multiple other variables are linked with both CRP and cognitive difficulties, which may confound the association. The goal of the current study is to determine whether low socioeconomic status (SES) is associated with worse cognitive functioning via higher CRP and whether this association is independent of known associations with other health, stress and lifestyle factors (e.g., depression, physical activity, body mass). Assessments in a longitudinal study of 1,029 Dutch adolescents were based on a combination of self-report and parent-report questionnaires, diagnostic assessment, behavioral testing, and blood assay. We estimated latent variables for cognitive functioning (executive functioning, verbal fluency, episodic memory) and used structural equation analysis to test whether SES (wave 1: 11.08 years (SD=0.55); 55% female] was associated with worse cognitive outcomes (wave 4: aged 18.97 years; SD=0.55) via increased CRP, depression, stress, body mass, substance use or physical inactivity (wave 3: aged 16.17 years; SD=0.61). Low SES was associated with worse cognitive functioning via increased CRP. Additionally, low SES was associated with (i) worse executive func-tioning via higher body mass, higher levels of sedentary behavior, and higher stress, (ii) worse verbal fluency via higher levels of sedentary behavior and (iii) worse episodic memory via sedentary behaviors, body mass, and substance use. These results confirm the link between SES, CRP and cognitive functioning and additionally identify four modifiable lifestyle factors that may be implicated in the link between low SES and worse per-formance on tests of cognitive functioning
Stress-related exposures amplify the effects of genetic susceptibility on depression and anxiety
It is unclear whether and to what extent stress-related exposures moderate the effects of polygenic risk scores (PRSs) on depression and anxiety. We aimed to examine such moderation effects for a variety of stress-related exposures on depression and anxiety. We included 41,810 participants with both genome-wide genetic data and measurements of depression and anxiety in the Lifelines Cohort Study. Current depression and anxiety were measured by the MINI International Neuropsychiatric Interview. Stress-related exposures included long-term difficulties, stressful life events, reduced social support, childhood trauma, and loneliness, which were measured by self-report questionnaires. PRSs were calculated based on recent large genome-wide association studies for depression and anxiety. We used linear mixed models adjusting for family relationships to estimate the interactions between PRSs and stress-related exposures. Nine of the ten investigated interactions between the five stress-related exposures and the two PRSs for depression and anxiety were significant (Ps < 0.001). Reduced social support, and higher exposure to long-term difficulties, stressful life events, and loneliness amplified the genetic effects on both depression and anxiety. As for childhood trauma exposure, its interaction with the PRS was significant for depression (P = 1.78 × 10 -05) but not for anxiety (P = 0.32). Higher levels of stress-related exposures significantly amplify the effects of genetic susceptibility on depression and anxiety. With a large sample size and a comprehensive set of stress-related exposures, our study provides powerful evidence on the presence of polygenic risk-by-environment interactions in relation to depression and anxiety. </p
Correction to: Familial co-aggregation and shared heritability between depression, anxiety, obesity and substance use
Structural brain imaging correlates of ASD and ADHD across the lifespan:a hypothesis-generating review on developmental ASD-ADHD subtypes
Contains fulltext :
169832.pdf (publisher's version ) (Open Access)We hypothesize that it is plausible that biologically distinct developmental ASD-ADHD subtypes are present, each characterized by a distinct time of onset of symptoms, progression and combination of symptoms. The aim of the present narrative review was to explore if structural brain imaging studies may shed light on key brain areas that are linked to both ASD and ADHD symptoms and undergo significant changes during development. These findings may possibly pinpoint to brain mechanisms underlying differential developmental ASD-ADHD subtypes. To this end we brought together the literature on ASD and ADHD structural brain imaging symptoms and particularly highlight the adolescent years and beyond. Findings indicate that the vast majority of existing MRI studies has been cross-sectional and conducted in children, and sometimes did include adolescents as well, but without explicitly documenting on this age group. MRI studies documenting on age effects in adults with ASD and/or ADHD are rare, and if age is taken into account, only linear effects are examined. Data from various studies suggest that a crucial distinctive feature underlying different developmental ASD-ADHD subtypes may be the differential developmental thinning patterns of the anterior cingulate cortex and related connections towards other prefrontal regions. These regions are crucial for the development of cognitive/effortful control and socio-emotional functioning, with impairments in these features as key to both ASD and ADHD
Children's Pronoun Interpretation Problems Are Related to Theory of Mind and Inhibition, But Not Working Memory
In several languages, including English and Dutch, children’s acquisition of the interpretation of object pronouns (e.g., him) is delayed compared to that of reflexives (e.g., himself). Various syntactic and pragmatic explanations have been proposed to account for this delay in children’s acquisition of pronoun interpretation. This study aims to provide more insight into this delay by investigating potential cognitive mechanisms underlying this delay. Dutch-speaking children between 6 and 12 years old with autism spectrum disorder (ASD; n = 47), attention-deficit/hyperactivity disorder (ADHD; n = 36) or typical development (TD; n = 38) were tested on their interpretation and production of object pronouns and reflexives and on theory of mind, working memory, and response inhibition. It was found that all three groups of children had difficulty with pronoun interpretation and that their performance on pronoun interpretation was associated with theory of mind and inhibition. These findings support an explanation of object pronoun interpretation in terms of perspective taking, according to which listeners need to consider the speaker’s perspective in order to block coreference between the object pronoun and the subject of the same sentence. Unlike what is predicted by alternative theoretical accounts, performance on pronoun interpretation was not associated with working memory, and the children made virtually no errors in their production of object pronouns. As the difficulties with pronoun interpretation were similar for children with ASD, children with ADHD and typically developing children, this suggests that certain types of perspective taking are unaffected in children with ASD and ADHD
Reward Sensitivity at Age 13 Predicts the Future Course of Psychopathology Symptoms
BACKGROUND: There are numerous observations of reward sensitivity being associated with different psychiatric disorders. Nonetheless, most studies investigating this relationship have been cross-sectional. Additionally, current knowledge is fragmentary as studies often investigate only one disorder at a time. The present study addresses these gaps by investigating whether reward sensitivity at age 13 predicts the course of nine psychopathology domains (attention and hyperactivity, autism spectrum, reactive aggression, proactive aggression, mood, anxiety, smoking, alcohol use, and cannabis use) over a 14-year follow-up period. METHODS: We used dimensional outcomes on 2,523 individuals over five measurement waves between ages 13 and 26 of the Dutch Tracking Adolescents' Individual Lives Survey (TRAILS). Reward sensitivity was measured with the Behavioral Activation System (BAS) scale. The longitudinal associations between reward sensitivity and psychopathology were examined using growth curve analysis within a multilevel framework. RESULTS: Reward sensitivity at age 13 was associated with changes in psychopathology over time. Reward sensitivity had a stable main effect on the future course of reactive and proactive aggression problems and anxiety problems. The effect of reward sensitivity increased over time for alcohol and cannabis use. Post-hoc analyses showed that reward sensitivity also had a stable effect on attention problems and hyperactivity and smoking when based on the fun-seeking subscale for both domains and when changing the informant who reported on attention problems and hyperactivity. No evidence was found for a longitudinal association between reward sensitivity and autism spectrum problems and mood problems. CONCLUSION: The current study provides evidence for the long-lasting effects of reward sensitivity on the course of different domains of psychopathology
Chronic Stressors and Adolescents' Externalizing Problems:Genetic Moderation by Dopamine Receptor D4. The TRAILS Study
The existing literature does not provide consistent evidence that carriers of the Dopamine D4 Receptor 7-repeat allele are more sensitive to adverse environmental influences, resulting in enhanced externalizing problems, compared to noncarriers. One explanation is that the adverse influences examined in prior studies were not severe, chronic, or distressing enough to reveal individual differences in sensitivity reflected by DRD4-7R. This study examined whether the 7-repeat allele moderated the association between chronic stressors capturing multiple stressful aspects of individuals' lives and externalizing problems in adolescence. We expected that chronic stressor levels would be associated with externalizing levels only in 7-repeat carriers. Using Linear Mixed Models, we analyzed data from 1621 Dutch adolescents (52.2% boys), obtained in three measurement waves (mean age approximately 11, 13.5, and 16 years) from the TRacking Adolescents' Individual Lives Survey (TRAILS) population-based birth cohort and the parallel clinic-referred cohort. Across informants, we found that higher levels of chronic stressors were related to higher externalizing levels in 7-repeat carriers but not in noncarriers, as hypothesized. Although previous studies on the 7-repeat allele as a moderator of environmental influences on adolescents' externalizing problems have not convincingly demonstrated individual differences in sensitivity to adverse environmental influences, our findings suggest that adolescent carriers of the Dopamine D4 Receptor 7-repeat allele are more sensitive to chronic, multi-context stressors than noncarriers
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