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There is increasing interest in examining a general psychopathology factor (p factor) in children and adolescents. In previous work, the relationship between the p factor and cognition in youth has largely focused on general intelligence (IQ) and executive functions (EF). Another cognitive construct, processing speed (PS), is dissociable from these cognitive constructs, but has received less research attention despite being related to many different mental health symptoms. This study aimed to examine the association between a latent processing speed factor and the p factor in youth.
Participants and Methods:
The present sample included 795 youth, ages 11-16 from the Colorado Learning Disability Research Center (CLDRC) sample. Confirmatory factor analyses tested multiple p factor models, with the primary model being a novel second-order, multireporter p factor where caregivers reported on externalizing symptoms (oppositional defiant disorder and conduct disorder modules from the Diagnostic Interview for Children and Adolescents [DICA]; aggression, delinquency, and attention problems subscales from the Child Behavior Checklist; and inattentive and hyperactive/impulsive subscales from the Disruptive Behavior Rating Scale) and youth self-reported on internalizing symptoms (Child Depression Inventory, generalized anxiety module from the DICA, and withdrawn, anxious/depression, and somatic subscales from the Youth Self Report). We then tested the correlation between the p factor and a latent PS factor. The latent PS factor was composed of WISC Symbol Search, WISC Coding, Colorado Perceptual Speed Test, and Identical Pictures Test. Three secondary p factor models were examined for comparison to previous literature, including (1) a bifactor, multi-reporter model, (2) a second-order model with just caregiver-report, and (3) a bifactor model with just caregiver-report.
There was a significant, negative correlation between the p factor and PS (r=-0.42, p<.001), indicating that slower processing speed is associated with higher general mental health symptoms. This finding was robust across models that used different raters (youth and caregiver-report vs. caregiver-report only) and modeling approaches (second-order vs. bifactor). This association is stronger than previously reported associations with IQ or EF in the p factor literature. Further, in this sample, we found that the association between PS and the p factor was robust to covariation for general cognition, whereas the correlation between general cognition and the p factor was fully accounted for by PS.
Our findings indicate that PS is related to general psychopathology symptoms, expanding the existing literature relating PS to specific, distinct disorders by showing that PS is related to what is shared across psychopathology. As cognition and psychopathology both undergo significant development across childhood and adolescence, elucidating neurodevelopmental mechanisms that relate to risk for a broad range of symptoms may be critical to informing early intervention and prevention approaches. This research points to processing speed as an important transdiagnostic construct that warrants further attention and exploration across development.
ADHD and anxiety symptoms are highly comorbid in childhood. While worse functional outcomes are typically expected for children with comorbid ADHD and anxiety symptoms, an emerging body of literature has suggested that anxiety symptoms may actually contribute to compensatory effects for executive functioning (EF) skills in children with ADHD symptoms. However, the results of studies investigating this claim have been quite mixed, possibly due to the use of smaller sample sizes and cross-sectional datasets. The current study extends the previous literature by examining the possible compensatory effects of anxiety symptoms in the context of ADHD symptoms on EF abilities (e.g., working memory [WM] and inhibition) both cross-sectionally and longitudinally in a large, well-validated sample.
Participants and Methods:
547 children and adolescents (8-16 years) were included from a population-based sample of twins (CLDRC sample) with enrichment for reading and attention challenges. Participants were retested at a second time point approximately 5 years later. ADHD symptoms (inattention and hyperactivity-impulsivity) were measured by a DSM-based ADHD rating scale, anxiety symptoms were measured by the RCMAS, inhibition was measured by stop-signal reaction time (SSRT), and working memory was measured by Digit Span Backwards (WISC/WAIS-R/III). Covariates included age and sex assigned at birth. Multiple regression models examined cross-sectional and longitudinal associations between ADHD (inattention and H-I) symptoms, anxiety symptoms, and the interaction between ADHD and anxiety symptoms on WM and inhibition abilities.
As expected, higher anxiety, inattention, and H-I symptoms were generally associated with lower inhibition and WM abilities both cross-sectionally and longitudinally. While no significant interactions between ADHD and anxiety symptoms were identified cross-sectionally at Time 1, significant interactions between Time 1 ADHD and anxiety symptoms predicted Time 2 inhibition scores. An inattention x anxiety interaction (p=.002) and a H-I x anxiety (p=.016) interaction significantly predicted Time 2 inhibition. Simple slopes analysis confirmed a compensatory interaction pattern, where ADHD symptoms showed a stronger association with inhibition weaknesses in children without anxiety symptoms compared to those with anxiety symptoms. This suggests that anxiety symptoms may be serving as a compensatory factor for children with ADHD symptoms as compared to their peers without ADHD symptoms.
These findings help clarify a previously mixed literature. Our findings suggest that the compensatory effect of anxiety symptoms on inhibition abilities in children with ADHD symptoms may be a developmental mechanism that takes time to emerge. The fact that the compensatory effect may take time to emerge may explain conflicting results within prior cross-sectional samples. These findings also have implications for research investigating the link between ADHD symptoms and EF abilities, as anxiety symptoms may be an important moderator to consider when attempting to explain why the correlation between ADHD symptoms and EF abilities is often weaker than expected. Finally, clinical implications for this work help to provide empirical evidence to support anecdotal experiences reported by individuals with ADHD and the clinicians who assess them, who often report that anxiety symptoms help them to improve EF performance.
Because of recent concerns about the replication of published results in the behavioral and biomedical sciences (Ioannidis, PLoS Medicine, Vol. 2, 2005, p. e124; Open Science Collaboration, Science, Vol. 349, 2015, p. 943; Pashler & Wagenmakers, Perspectives on Psychological Science, Vol. 7, 2012, pp. 528–530), we have conducted a replication of our recently published analyses of longitudinal reading performance and attention deficit-hyperactivity disorder data from twin pairs selected for reading difficulties (Wadsworth et al., Twin Research and Human Genetics, Vol. 18, 2015, pp. 755–761). Results obtained from univariate and bivariate (DeFries & Fulker, Behavior Genetics, Vol. 15, 1985, pp. 467–473; Acta Geneticae Medicae et Gemellologiae: Twin Research, Vol. 37, 1988, pp. 205–216) analyses of data from a subset of twin pairs tested in the International Longitudinal Twin Study of Early Reading Development at post-4th grade, and its continuation into high school at post-9th grade, were compared to those from our previous report. Similar measures of reading performance, the same measures of inattention and hyperactivity/impulsivity, and similar selection criteria were used in the two studies. In general, the patterns of results obtained from these two independent studies were highly similar. Thus, these results clearly illustrate the principle that findings from studies in quantitative behavioral genetics often replicate (Plomin et al., Perspectives on Psychological Science, Vol. 11, 2016, pp. 3–23).
Approximately 60% of children with reading difficulties (RD) meet criteria for at least one co-occurring disorder. The most common of these, attention deficit-hyperactivity disorder (ADHD), occurs in 20–40% of individuals with RD. Recent studies have suggested that genetic influences are responsible. To assess the genetic etiologies of RD and the comorbidity of RD and two ADHD symptom dimensions –– inattention (IN) and hyperactivity/impulsivity (H/I) –– we are conducting the first longitudinal twin study of RD and ADHD. Data from twin pairs in which at least one member of the pair met criteria for proband status for RD at initial assessment, and were reassessed 5 years later, were subjected to DeFries-Fulker (DF) analysis. Analyses of reading composite data indicated that over 60% of the proband deficit at initial assessment was due to genetic influences, and that reading deficits at follow-up were due substantially to the same genetic influences. When a bivariate DF model was fitted to reading performance and IN data, genetic influences accounted for 60% of contemporaneous comorbidity and over 60% of the longitudinal relationship. In contrast, analysis of the comorbidity between reading performance and H/I indicated that common genetic influences accounted for only about 20% of the contemporaneous and about 10% of the longitudinal relationships. Results indicate that (1) genetic influences on RD are substantial and highly stable; (2) the comorbidity between RD and IN is due largely to genetic influences, both contemporaneously and longitudinally; and (3) genetic influences contribute significantly less to the comorbidity between RD and H/I.
Linkages between neuropsychological functioning (i.e., response inhibition, processing speed, reaction time variability) and word reading have been documented among children with attention-deficit/hyperactivity disorder (ADHD) and children with Reading Disorders. However, associations between neuropsychological functioning and other aspects of reading (i.e., fluency, comprehension) have not been well-documented among children with comorbid ADHD and Reading Disorder. Children with ADHD and poor word reading (i.e., ≤25th percentile) completed a stop signal task (SST) and tests of word reading, reading fluency, and reading comprehension. Multivariate multiple regression was conducted predicting the reading skills from SST variables [i.e., mean reaction time (MRT), reaction time standard deviation (SDRT), and stop signal reaction time (SSRT)]. SDRT predicted word reading, reading fluency, and reading comprehension. MRT and SSRT were not associated with any reading skill. After including word reading in models predicting reading fluency and reading comprehension, the effects of SDRT were minimized. Reaction time variability (i.e., SDRT) reflects impairments in information processing and failure to maintain executive control. The pattern of results from this study suggest SDRT exerts its effects on reading fluency and reading comprehension through its effect on word reading (i.e., decoding) and that this relation may be related to observed deficits in higher-level elements of reading. (JINS, 2014, 20, 1–10)
The augmented multiple regression model for the analysis of data from selected
twin pairs was extended to facilitate analyses of data from twin pairs and
nontwin siblings. Fitting this extended model to data from both selected twin
pairs and siblings yields direct estimates of heritability (h2) and
the difference between environmental influences shared by members of twin pairs
and those of sib or twin–sib pairs (i.e., c2(t)
– c2 (s)). When this model was fitted to reading
performance data from 293 monozygotic and 436 dizygotic pairs selected for
reading difficulties, and 291 of their nontwin siblings, h2 = .48
± .22, p = .03, and c2 (t) –
c2 (s) = .22 ± .12, p = .06. Although the test
for differential shared environmental influences is only marginally significant,
the results of this analysis suggest that environmental influences on reading
performance that are shared by members of twin pairs (.36) may be substantially
greater than those for less contemporaneous twin–sibling pairs
Few studies have investigated the role of gene × environment interactions (G × E) in speech, language, and literacy disorders. Currently, there are two theoretical models, the diathesis–stress model and the bioecological model, that make opposite predictions about the expected direction of G × E, because environmental risk factors may either strengthen or weaken the effect of genes on phenotypes. The purpose of the current study was to test for G × E at two speech sound disorder and reading disability linkage peaks using a sib-pair linkage design and continuous measures of socioeconomic status, home language/literacy environment, and number of ear infections. The interactions were tested using composite speech, language, and preliteracy phenotypes and previously identified linkage peaks on 6p22 and 15q21. Results showed five G × E at both the 6p22 and 15q21 locations across several phenotypes and environmental measures. Four of the five interactions were consistent with the bioecological model of G × E. Each of these four interactions involved environmental measures of the home language/literacy environment. The only interaction that was consistent with the diathesis–stress model was one involving the number of ear infections as the environmental risk variable. The direction of these interactions and possible interpretations are explored in the discussion.
This study investigated the association between reading disability (RD) and internalizing
and externalizing psychopathology in a large community sample of twins with (N = 209) and
without RD (N = 192). The primary goals were to clarify the relation between RD and
comorbid psychopathology, to test for gender differences in the behavioral correlates of RD,
and to test if common familial influences contributed to the association between RD and
other disorders. Results indicated that individuals with RD exhibited significantly higher
rates of all internalizing and externalizing disorders than individuals without RD. However,
logistic regression analyses indicated that RD was not significantly associated with symptoms
of aggression, delinquency, oppositional defiant disorder, or conduct disorder after
controlling for the significant relation between RD and ADHD. In contrast, relations
between RD and symptoms of anxiety and depression remained significant even after
controlling for comorbid ADHD, suggesting that internalizing difficulties may be specifically
associated with RD. Analyses of gender differences indicated that the significant relation
between RD and internalizing symptoms was largely restricted to girls, whereas the
association between RD and externalizing psychopathology was stronger for boys. Finally,
preliminary etiological analyses suggested that common familial factors predispose both
probands with RD and their non-RD siblings to exhibit externalizing behaviors, whereas
elevations of internalizing symptomatology are restricted to individuals with RD.
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