Objective This study investigated the role of self-regulation of emotion in relation to functional impairment and comorbidity among children with and without AD/HD. Method A total of 358 probands and their siblings participated in the study, with 74% of the sample participants affected by AD/HD. Parent-rated levels of emotional lability served as a marker for self-regulation of emotion. Results Nearly half of the children affected by AD/HD displayed significantly elevated levels of emotional lability versus 15% of those without this disorder. Children with AD/HD also displayed significantly higher rates of functional impairment, comorbidity, and treatment service utilization. Emotional lability partially mediated the association between AD/HD status and these outcomes. Conclusion Findings lent support to the notion that deficits in the self-regulation of emotion are evident in a substantial number of children with AD/HD and that these deficits play an important role in determining functional impairment and comorbidity outcomes.

Objective The purpose of this study was to examine rates and patterns of non-ADHD psychiatric diagnoses among a large group of first-year college students with and without ADHD. Method A total of 443 participants, including 214 males and 229 females ranging in age from 18 to 22-years of age (M= 18.2), were recruited from nine colleges involved in a large scale, multi-site longitudinal investigation. Non-Hispanic Caucasian students represented 67.5% of the total sample. A comprehensive multi-method assessment approach was used in conjunction with expert panel review to determine both ADHD and comorbidity status. Results Significantly higher rates of overall comorbidity were found among college students with well-defined ADHD, with 55.0% exhibiting at least one comorbid diagnosis, and 31.8% displaying two or more, relative to the corresponding rates of non-ADHD diagnoses among Comparison students, which were 11.2% and 4.0%, respectively. These differences in overall comorbidity rates were, in large part, attributable to the increased presence of Depressive and Anxiety Disorders, especially Major Depressive Disorder (active or in partial remission) and Generalized Anxiety Disorder, among the students with ADHD. Within the ADHD group, differential comorbidity rates were observed as a function of ADHD presentation type and gender but not ethnic/racial diversity status. Conclusions The current findings fill a gap in the literature and shed new light on the rates and patterns of comorbidity among emerging adults with ADHD in their first year of college. Implications for providing clinical and support services to college students with ADHD are discussed.

This is a post-peer-review, pre-copyedit version of an article published in Current Attention Disorders Reports.

Objective A family was previously identified that cosegregates a pericentric inversion, inv(3)(p14 : q21), with an early-onset developmental condition, characterized by impulsive behavior and intellectual deficit. The inversion breakpoints lie within DOCK3 and SLC9A9 at the p-arm and q-arm, respectively. Based on this report, these genes were selected to be evaluated in a family-based attention-deficit/hyperactivity disorder (AD/HD) association study. Methods Conners’ Parent (CPRS) and Teacher (CTRS) Rating Scales of AD/HD symptoms and Conners’ Continuous Performance Test (CPT) measures were collected and a minimal number of tagging singlenucleotide polymorphisms (SNPs) in each gene were selected for analysis. Analyses were performed on families who met research criteria for AD/HD. Using the program, QTDT, each tagging SNP was tested for association with T-scores from the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) subscales according to the CTRS and CPRS, and five CPT measures. Results After adjusting for multiple testing, a SNP in the 3′ UTR of SLC9A9, rs1046706, remained significantly associated (false discovery rate, q value < 0.05) with scores on the DSM-IV hyperactive-impulsive and total symptom subscales according to the CTRS and errors of commission on the CPT. In addition, an intronic SLC9A9 SNP, rs2360867, remained significantly associated with errors of commission. Conclusion Our results suggest that SLC9A9 may be related to hyperactive-impulsive symptoms in AD/HD and the disruption of SLC9A9 may be responsible for the behavioral phenotype observed in the inversion family. The association with SLC9A9 is particularly interesting as it was recently implicated in a genome-wide association study for AD/HD. Further investigation of the role of SLC9A9 in AD/HD and other behavioral disorders is warranted.

No abstract