The relationship between executive function, processing speed, and attention-deficit hyperactivity disorder in middle childhood.

Attention-Deficit Hyperactivity Disorder (ADHD) is a heterogeneous disorder that is highly impairing. Early, accurate diagnosis maximizes long-term positive outcomes for youth with ADHD. Tests of executive functioning (EF) are potential tools for screening and differential diagnosis of ADHD subtypes. However, previous research has been inconsistent regarding the specificity and magnitude of EF deficits across ADHD subtypes. Here, we advance knowledge of the EF-ADHD relationship by using: (1) dimensional latent factor models of ADHD that captures the heterogeneity of expression, and (2) a comprehensive, reliable battery of EF tasks and modeling relationships with a general factor of EF ability. We tested 1548 children and adolescents (ages 7-15 years) from the Texas Twin Project, a population-based cohort with a diverse socioeconomic and ethnic composition. We show that EF deficits were specific to the inattention domain of ADHD. Moreover, we found that the association between EF task performance and inattention was stable across sociodemographic groups. Our results demonstrate that failures of executive control are selectively manifested as covert inattentive symptoms, such as trouble with organization, forgetfulness, and distractedness, rather than overt symptoms, such as inappropriate talkativeness and interruption. Future research, utilizing a bifactor characterization of ADHD in clinical samples, is needed to further refine understanding of the nature of cognitive deficits in ADHD across the full range of symptom variation.

Peer Group Similarity in Perceptions of Pubertal Timing.

Self-report measures of perceived pubertal timing correspond only weakly with clinical measures of "objective" physical development. Peer and school contexts shape adolescents' self-perceptions of pubertal timing. The current study examined associations between perceived pubertal timing and the pubertal timing reported by nominated friends and schoolmates. Participants included 2817 adolescents (Mage = 16.6; 49 % female; 16 % Black; 20 % Hispanic) from the National Longitudinal Study of Adolescent Health. Three measures of pubertal timing were included: age-standardized ratings of body changes, comparisons of development relative to peers (relative timing), and, in females, age at menarche. It was hypothesized that relative timing, which explicitly asks adolescents to compare themselves to their peers, would be related to the age-standardized pubertal timing of nominated friends and schoolmates. Surprisingly, there were no associations between relative timing and age-standardized pubertal timing reported by peers, suggesting that pubertal self-perceptions do not fluctuate in response to the average level of development in a friend group. Instead, males were similar to nominated friends and schoolmates in age-standardized ratings of body changes, and females were similar to nominated friends in relative timing, controlling for race, ethnicity, and age. Different self-report measures of pubertal timing index different underlying constructs, and the social processes that influence adolescents' perceptions of pubertal maturation may differ between genders.

Gene×Environment interactions in early externalizing behaviors: parental emotional support and socioeconomic context as moderators of genetic influences?

This study uses longitudinal population-based samples of young siblings to examine the effects of two hypothesized moderators of early externalizing behaviors: parental emotional support and family socioeconomic status. The first sample, a twin sample from the Early Childhood Longitudinal Study-Birth Cohort (ECLS-B), was composed of approximately 600 twin pairs measured on externalizing at ages 4 and 5. Results indicated stronger genetic influences on externalizing at lower levels of parental emotional support but higher levels of socioeconomic status; only the latter interaction remained significant when the two moderators were simultaneously modeled. These moderation effects were not replicated in our analyses of the National Longitudinal Survey of Youth-Child Supplement (CNLSY) data, which contained 1939 pairs of full and half siblings measured on externalizing at ages 4-5 and ages 6-7. Our results highlight the need for replication in quantitative behavior genetics research on externalizing behaviors. Potential causes for non-replication are discussed.

Item-Level Genome-Wide Association Study of the Alcohol Use Disorders Identification Test in Three Population-Based Cohorts.

OBJECTIVE: Genome-wide association studies (GWASs) of the Alcohol Use Disorders Identification Test (AUDIT), a 10-item screen for alcohol use disorder (AUD), have elucidated novel loci for alcohol consumption and misuse. However, these studies also revealed that GWASs can be influenced by numerous biases (e.g., measurement error, selection bias), which may have led to inconsistent genetic correlations between alcohol involvement and AUD, as well as paradoxically negative genetic correlations between alcohol involvement and psychiatric disorders and/or medical conditions. The authors used genomic structural equation modeling to elucidate the genetics of alcohol consumption and problematic consequences of alcohol use as measured by AUDIT. METHODS: To explore these unexpected differences in genetic correlations, the authors conducted the first item-level and the largest GWAS of AUDIT items (N=160,824) and applied a multivariate framework to mitigate previous biases. RESULTS: The authors identified novel patterns of similarity (and dissimilarity) among the AUDIT items and found evidence of a correlated two-factor structure at the genetic level ("consumption" and "problems," rg=0.80). Moreover, by applying empirically derived weights to each of the AUDIT items, the authors constructed an aggregate measure of alcohol consumption that was strongly associated with alcohol dependence (rg=0.67), moderately associated with several other psychiatric disorders, and no longer positively associated with health and positive socioeconomic outcomes. Lastly, by conducting polygenic analyses in three independent cohorts that differed in their ascertainment and prevalence of AUD, the authors identified novel genetic associations between alcohol consumption, alcohol misuse, and health. CONCLUSIONS: This work further emphasizes the value of AUDIT for both clinical and genetic studies of AUD and the importance of using multivariate methods to study genetic associations that are more closely related to AUD.

Sleep duration and depressive symptoms: a gene-environment interaction.

OBJECTIVE: We used quantitative genetic models to assess whether sleep duration modifies genetic and environmental influences on depressive symptoms. METHOD: Participants were 1,788 adult twins from 894 same-sex twin pairs (192 male and 412 female monozygotic [MZ] pairs, and 81 male and 209 female dizygotic [DZ] pairs] from the University of Washington Twin Registry. Participants self-reported habitual sleep duration and depressive symptoms. Data were analyzed using quantitative genetic interaction models, which allowed the magnitude of additive genetic, shared environmental, and non-shared environmental influences on depressive symptoms to vary with sleep duration. RESULTS: Within MZ twin pairs, the twin who reported longer sleep duration reported fewer depressive symptoms (ec = -0.17, SE = 0.06, P < 0.05). There was a significant gene × sleep duration interaction effect on depressive symptoms (a'c = 0.23, SE = 0.08, P < 0.05), with the interaction occurring on genetic influences that are common to both sleep duration and depressive symptoms. Among individuals with sleep duration within the normal range (7-8.9 h/night), the total heritability (h2) of depressive symptoms was approximately 27%. However, among individuals with sleep duration within the low (< 7 h/night) or high (≥ 9 h/night) range, increased genetic influence on depressive symptoms was observed, particularly at sleep duration extremes (5 h/night: h2 = 53%; 10 h/night: h2 = 49%). CONCLUSION: Genetic contributions to depressive symptoms increase at both short and long sleep durations.

A twin study of genetic influences on diurnal preference and risk for alcohol use outcomes.

OBJECTIVE: The population-based University of Washington Twin Registry (UWTR) was used to examine (1) genetic influences on chronobiology and (2) whether these genetic factors influence alcohol-use phenotypes. METHODS: We used a reduced Horne-Östberg Morningness-Eveningness Questionnaire (rMEQ) to survey UWTR participants for diurnal preference. Frequency and quantity of alcohol use, as well as binge drinking (6+ drinks per occasion), were assessed on a 5-point Likert scale. Both diurnal preference and alcohol use were self-reported. Twin data were analyzed by using structural equation models. RESULTS: The sample consisted of 2,945 participants (mean age = 36.4 years), including 1,127 same-sex and opposite-sex twin pairs and 691 individual twins. The rMEQ range was 4-25, with a mean score of 15.3 (SD 4.0). Diurnal "morning types" comprised 30.7% (N = 903) of participants, while 17.4% (N = 513) were "evening types." Regarding alcohol use, 21.2% (N = 624) reported never drinking. Among drinkers, 35.7% (N = 829) reported ≥ 3 drinks per occasion and 48.1% (N = 1,116) reported at least one instance of binge drinking. Genetic influences accounted for 37% of the variance in diurnal preference, with the remaining 63% due to non-shared environmental influences. Genetic propensities toward diurnal eveningness were significantly associated with increased alcohol quantity (ß = -0.17; SE = 0.05, p < 0.001) and increased binge drinking (ß = -0.19; SE = 0.04, p < 0.001), but not with frequency of alcohol use. Environmental paths between diurnal preference and alcohol use phenotypes were not significant. CONCLUSIONS: Genetic influences on diurnal preference confer elevated risk for problematic alcohol use, including increased quantity and binge drinking. Differences in circadian rhythm may be an important and understudied pathway of risk for genetic influences on alcohol use.

Sleep duration and body mass index in twins: a gene-environment interaction.

STUDY OBJECTIVES: To examine whether sleep duration modifies genetic and environmental influences on body mass index (BMI). DESIGN: Genotype-environment interaction twin study. SETTING: University of Washington Twin Registry. PATIENTS OR PARTICIPANTS: A population-based sample of US twins (1,088 pairs, 604 monozygotic, 484 dizygotic; 66% female; mean age = 36.6 yr, standard deviation (SD) = 15.9 yr). INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Participants self-reported information on height, weight, and sleep. Mean BMI was calculated as 25.3 kg/m² (SD = 5.4) and mean habitual sleep duration was 7.2 hr/night (SD = 1.2). Data were analyzed using biometric genetic interaction models. Overall the heritability of sleep duration was 34%. Longer sleep duration was associated with decreased BMI (P < 0.05). The heritability of BMI when sleep duration was < 7 hr (h² = 70%) was more than twice as large as the heritability of BMI when sleep duration was ≥ 9 hr (h² = 32%); this interaction was significant (P < 0.05). CONCLUSIONS: Shorter sleep duration is associated with increased BMI and increased genetic influences on BMI, suggesting that shorter sleep duration increases expression of genetic risks for high body weight. At the same time, longer sleep duration may suppress genetic influences on body weight. Future research aiming to identify specific genotypes for BMI may benefit by considering the moderating role of sleep duration.