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Research in Attention-deficit/hyperactivity disorder (ADHD) has had a clear focus on treatment and the dysfunction in specific situation associated with the condition. However, self-report, observational and anecdotal evidence indicates that there are also positive aspects associated with ADHD. Research on the potential positive features in individuals with an ADHD diagnosis is still limited, especially studies with larger representative samples. Here we performed qualitative research to identify positive aspects and strengths associated with ADHD in a large convenience sample from the Dutch organization for people with ADHD, dyslexia and dyscalculia. We sent out open-ended questionnaires to the members of the organization, asking what they consider to be positive aspects of their ADHD. From the responses of individuals with ADHD (n = 206), we extracted 116 codes, which were assigned to thirteen subthemes, which in turn led to five themes. These themes were: Creativity, Being dynamic, Flexibility, Socio-affective skills, and Higher-order cognitive skills. Core symptoms of ADHD such as impulsivity and hyperactivity were also considered positive aspects of ADHD by a minority of participants. After showing our results to a group of additional individuals with ADHD (focus group) they confirmed the identified positive aspects of ADHD. They also helped us with the interpretation of our findings and mentioned certain positive aspects to be a consequence of living with ADHD (being open minded and being honest). In conclusion, experiencing positive aspects seems to be common in ADHD as almost all participants reported positive aspect of ADHD, these aspects cover many different domains. Awareness about ADHD's strengths might help individuals with ADHD and their environment to better cope with, accept or embrace their diagnosis and for example make educational or occupational choices that fit them well. To incorporate these positive aspects in the understanding of ADHD, future research should focus on quantifying strengths in ADHD, and on investigating the link between these aspects and clinical characteristics and how this new knowledge can be implemented in psychoeducation and find its way to education and occupational settings. [ABSTRACT FROM AUTHOR]

Attention-Deficit Hyperactivity Disorder (ADHD) is a complex and heterogeneous neurodevelopmental condition for which curative treatments are lacking. Whilst pharmacological treatments are generally effective and safe, there is considerable interindividual variability among patients regarding treatment response, required dose, and tolerability. Many of the non-pharmacological treatments, which are preferred to drugtreatment by some patients, either lack efficacy for core symptoms or are associated with small effect sizes. No evidence-based decision tools are currently available to allocate pharmacological or psychosocial treatments based on the patient's clinical, environmental, cognitive, genetic, or biological characteristics. We systematically reviewed potential biomarkers thatmay help in diagnosing ADHD and/or stratifying ADHD into more homogeneous subgroups and/or predict clinical course, treatment response, and long-term outcome across the lifespan. Most work involved exploratory studies with cognitive, actigraphic and EEG diagnostic markers to predict ADHD, along with relatively few studies exploring markers to subtype ADHD and predict response to treatment. There is a critical need for multisite prospective carefully designed experimentally controlled or observational studies to identify biomarkers that index inter-individual variability and/or predict treatment response. [ABSTRACT FROM AUTHOR]

Objective: We describe qualitative results on facilitators and barriers to participating in a family mindfulness-based intervention (MBI) for youth with ADHD and their parents and perceived effects on child and parent. Method: Sixty-nine families started the 8-week protocolized group-based MBI called "MYmind." After the MBI, individual semi-structured interviews were conducted with a purposive sample of parents (n = 20), children (n = 17, ages 9–16 years), and mindfulness teachers (n = 3). Interviews were analyzed using Grounded Theory. Results: Facilitators and barriers regarding contextual factors (e.g., time investment), MBI characteristics (e.g., parallel parent–child training), and participant characteristics (e.g., ADHD-symptoms) are described. Perceived effects were heterogeneous: no/adverse effects, awareness/insight, acceptance, emotion regulation/reactivity, cognitive functioning, calmness/relaxation, relational changes, generalization. Conclusion: MYmind can lead to a variety of transferable positively perceived effects beyond child ADHD-symptom decrease. Recommendations on MYmind participant inclusion, program characteristics, mindfulness teachers, and evaluating treatment efficacy are provided. [ABSTRACT FROM AUTHOR]

Objective: The study aimed to identify early childhood risk factors for de novo and subthreshold late-onset ADHD. Method: ADHD symptoms were assessed in 9,875 participants from the Twins Early Development Study (TEDS) using the Conners' Parent Rating Scale at ages 8, 12, 14, and 16 years, along with other childhood characteristics and adolescent outcomes. Multinomial logistic regressions were implemented to identify early childhood predictors of late-onset ADHD and childhood-onset persistent ADHD, with non-ADHD controls as the reference category. Results: Male sex, increased childhood conduct problems, and low socioeconomic status predicted de novo late-onset ADHD. Additional risk factors predicted subthreshold late-onset ADHD and childhood-onset persistent ADHD. Late-onset ADHD symptoms were also accompanied by increased co-occurring behavioral and emotional problems. Conclusion: Findings of different childhood predictors between subthreshold and de novo late-onset ADHD suggest further investigation into time-varying environmental and biological factors driving psychopathological changes is warranted to fully characterize late-onset ADHD. [ABSTRACT FROM AUTHOR]

To get additional insight into the phenotype of attentional problems, we examined to what extent genetic and environmental factors explain covariation between lack of dispositional mindfulness and attention-deficit/hyperactivity disorder (ADHD) traits in youth, and explored the incremental validity of these constructs in predicting life satisfaction. We used data from a UK population-representative sample of adolescent twins (N = 1092 pairs) on lack of dispositional mindfulness [Mindful Attention Awareness Scale (MAAS)], ADHD traits [Conners' Parent Rating Scale-Revised (CPRS-R): inattentive (INATT) and hyperactivity/impulsivity (HYP/IMP) symptom dimensions] and life satisfaction (Students' Life Satisfaction Scale). Twin model fitting analyses were conducted. Phenotypic correlations (rp) between MAAS and CPRS-R (INATT: rp = 0.18, HYP/IMP: rp = 0.13) were small, but significant and largely explained by shared genes for INATT (% rp INATT–MAAS due to genes: 93%, genetic correlation rA = 0.37) and HYP/IMP (% rp HYP/IMP–MAAS due to genes: 81%; genetic correlation rA = 0.21) with no significant contribution of environmental factors. MAAS, INATT and HYP/IMP significantly and independently predicted life satisfaction. Lack of dispositional mindfulness, assessed as self-reported perceived lapses of attention (MAAS), taps into an aspect of attentional functioning that is phenotypically and genetically distinct from parent-rated ADHD traits. The clinically relevant incremental validity of both scales implicates that MAAS could be used to explore the underlying mechanisms of an aspect of attentional functioning that uniquely affects life satisfaction and is not captured by DSM-based ADHD scales. Further future research could identify if lack of dispositional mindfulness and high ADHD traits can be targeted by different therapeutic approaches resulting in different effects on life satisfaction. [ABSTRACT FROM AUTHOR]

Background: Available evidence points towards lower birth weight as a risk factor for the development of attention deficit/hyperactivity disorder (ADHD) symptoms. We probed the causal nature of this putative effect of birth weight on ADHD symptoms using the twin differences design, which accounts for genetic and shared environmental confounds. Method: In a large population‐based twin sample – 3,499 monozygotic (MZ) and 6,698 dizygotic (DZ) pairs – parents, teachers or twins rated the twins’ ADHD symptoms at nine assessment waves (2–16 years). We implemented the twin differences design, which completely accounts for shared environmental and genetic confounding in MZ twins. We tested whether: (a) the lighter‐born twins had elevated ADHD symptoms compared to the heavier‐born twins, by regressing within‐pair differences of ADHD symptoms on within‐pair differences of birth weight among MZ twins; (b) the effect of birth weight on ADHD was moderated by gender, gestational age and low birth weight; (c) this effect changed with age at ADHD assessment using adapted latent growth curve models; and (d) results differed for inattention and hyperactivity/impulsivity. Results: Birth weight significantly predicted ADHD symptoms from early childhood to late adolescence. The lighter‐born twin had more ADHD symptoms than the heavier‐born cotwin among MZ twins across assessment waves and raters. No moderation effect was detected. The magnitude of the effect of birth weight decreased significantly across time for hyperactivity/impulsivity, but the decrease failed to reach significance for inattention. Estimates for inattention were significantly larger than for hyperactivity/impulsivity at each time point, implying stronger effect of birth weight on inattention symptoms. Conclusions: Our findings provide stringent evidence for environmental effect of lower birth weight on the causal pathway to elevated ADHD symptoms. Effect of birth weight persists across a 14‐year period from childhood into late adolescence, in particular for inattention symptoms. [ABSTRACT FROM AUTHOR]

Background: Integration of positive psychology into clinical research and treatment has been slow. This integration can be facilitated by the conceptualisation of mental disorders as the high, symptomatic extreme of continuous normal variation. This assumes that there is also a low, positive extreme, which is, however, unchartered territory. This study aims to examine how well current measures capture the low extreme of mental disorder continua, using attention‐deficit hyperactivity disorder (ADHD) as an example. Methods: The ability of three validated scales to capture ADHD as a continuous trait was examined using Item Response Theory in a sample of 9,882 adolescents from the UK population‐representative Twins Early Development Study. These scales were: the Strengths and Weakness of ADHD Symptoms and Normal behaviour scale (SWAN), Strength and Difficulties Questionnaire (SDQ – hyperactivity subscale), and Conners’ Parent Rating Scale (Conners). Results: Only the SWAN reliably differentiated interindividual differences between participants lying at any level of the continuous ADHD latent trait, including the extreme low, positive end (z‐scores from −3 to +3). The SDQ showed low reliability across the ADHD latent trait. In contrast, the Conners performed best at differentiating individuals scoring at or above the mean to the high symptomatic range (z‐scores from 0 to +3). The SWAN was the only measure to provide indicators of ‘positive mental health’, endorsed in the presence of particularly good attentive abilities. Conclusions: Scales such as the SWAN that reliably capture ADHD as a continuous trait, including the positive end, are important for not missing meaningful variation in population‐based studies. Indicators of positive mental health may be helpful in clinical practice, as positive attributes have been shown to directly influence as well as buffer negative effects of psychiatric symptoms. [ABSTRACT FROM AUTHOR]

Autism spectrum disorder (ASD) symptoms frequently occur in individuals with attention-deficit/hyperactivity disorder (ADHD). While there is evidence that both ADHD and ASD have differential structural brain correlates, knowledge of the structural brain profile of individuals with ADHD with raised ASD symptoms is limited. The presence of ASD-like symptoms was measured by the Children's Social Behavior Questionnaire (CSBQ) in a sample of typically developing controls (n = 154), participants with ADHD (n = 239), and their unaffected siblings (n = 144) between the ages of 8 and 29. Structural magnetic resonance imaging (MRI) correlates of ASD ratings were analysed by studying the relationship between ASD ratings and grey matter volumes using mixed effects models which controlled for ADHD symptom count and total brain volume. ASD ratings were significantly elevated in participants with ADHD relative to controls and unaffected siblings. For the entire group (participants with ADHD, unaffected siblings and TD controls), mixed effect models revealed that the left caudate nucleus volume was negatively correlated with ASD ratings (t = 2.83; P = 0.005). The current findings are consistent with the role of the caudate nucleus in executive function, including the selection of goals based on the evaluation of action outcomes and the use of social reward to update reward representations. There is a specific volumetric profile associated with subclinical ASD-like symptoms in participants with ADHD, unaffected siblings and controls with the caudate nucleus and globus pallidus being of critical importance in predicting the level of ASD-like symptoms in all three groups. [ABSTRACT FROM AUTHOR]

Background: Data on structural brain alterations in patients with attention-deficit/hyperactivity disorder (ADHD) have been inconsistent. Both ADHD and brain volumes have a strong genetic loading, but whether brain alterations in patients with ADHD are familial has been underexplored. We aimed to detect structural brain alterations in adolescents and young adults with ADHD compared with healthy controls. We examined whether these alterations were also found in their unaffected siblings, using a uniquely large sample. Methods: We performed voxel-based morphometry analyses on MRI scans of patients with ADHD, their unaffected siblings and typically developing controls. We identified brain areas that differed between participants with ADHD and controls and investigated whether these areas were different in unaffected siblings. Influences of medication use, age, sex and IQ were considered. Results: Our sample included 307 patients with ADHD, 169 unaffected siblings and 196 typically developing controls (mean age 17.2 [range 8-30] yr). Compared with controls, participants with ADHD had significantly smaller grey matter volume in 5 clusters located in the precentral gyrus, medial and orbitofrontal cortex, and (para)cingulate cortices. Unaffected siblings showed intermediate volumes significantly different from controls in 4 of these clusters (all except the precentral gyrus). Medication use, age, sex and IQ did not have an undue influence on the results. Limitations: Our sample was heterogeneous, most participants with ADHD were taking medication, and the comparison was cross-sectional. Conclusion: Brain areas involved in decision making, motivation, cognitive control and motor functioning were smaller in participants with ADHD than in controls. Investigation of unaffected siblings indicated familiality of 4 of the structural brain differences, supporting their potential in molecular genetic analyses in ADHD research. [ABSTRACT FROM AUTHOR]

Background Although attention deficit hyperactivity disorder ( ADHD) is thought to reflect a continuously distributed quantitative trait, it is assessed through binary diagnosis or skewed measures biased towards its high, symptomatic extreme. A growing trend is to study the positive tail of normally distributed traits, a promising avenue, for example, to study high intelligence to increase power for gene-hunting for intelligence. However, the emergence of such a 'positive genetics' model has been tempered for ADHD due to poor phenotypic resolution at the low extreme. Overcoming this methodological limitation, we conduct the first study to assess the aetiologies of low extreme ADHD traits. Methods In a population-representative sample of 2,143 twins, the Strength and Weaknesses of ADHD Symptoms and Normal behaviour ( SWAN) questionnaire was used to assess ADHD traits on a continuum from low to high. Aetiological influences on extreme ADHD traits were estimated using DeFries-Fulker extremes analysis. ADHD traits were related to behavioural, cognitive and home environmental outcomes using regression. Results Low extreme ADHD traits were significantly influenced by shared environmental factors (23-35%) but were not significantly heritable. In contrast, high-extreme ADHD traits showed significant heritability (39-51%) but no shared environmental influences. Compared to individuals with high extreme or with average levels of ADHD traits, individuals with low extreme ADHD traits showed fewer internalizing and externalizing behaviour problems, better cognitive performance and more positive behaviours and positive home environmental outcomes. Conclusions Shared environmental influences on low extreme ADHD traits may reflect passive gene-environment correlation, which arises because parents provide environments as well as passing on genes. Studying the low extreme opens new avenues to study mechanisms underlying previously neglected positive behaviours. This is different from the current deficit-based model of intervention, but congruent with a population-level approach to improving youth wellbeing. [ABSTRACT FROM AUTHOR]

IMPORTANCE: Attention-deficit/hyperactivity disorder (ADHD) is a heritable neurodevelopmental disorder. It has been linked to reductions in total brain volume and subcortical abnormalities. However, owing to heterogeneity within and between studies and limited sample sizes, findings on the neuroanatomical substrates of ADHD have shown considerable variability. Moreover, it remains unclear whether neuroanatomical alterations linked to ADHD are also present in the unaffected siblings of those with ADHD. OBJECTIVE: To examine whether ADHD is linked to alterations in whole-brain and subcortical volumes and to study familial underpinnings of brain volumetric alterations in ADHD. DESIGN, SETTING, AND PARTICIPAN: ts In this cross-sectional study, we included participants from the large and carefully phenotyped Dutch NeurolMAGE sample (collected from September 2009-December 2012) consisting of 307 participants with ADHD, 169 of their unaffected siblings, and 196 typically developing control individuals (mean age, 17.21 years,- age range, 8-30 years). MAIN OUTCOMES AND MEASURES: Whole-brain volumes (total brain and gray and white matter volumes) and volumes of subcortical regions (nucleus accumbens, amygdala, caudate nucleus, globus pallidus, hippocampus, putamen, thalamus, and brainstem) were derived from structural magnetic resonance imaging scans using automated tissue segmentation. RESULTS: Regression analyses revealed that relative to control individuals, participants with ADHD had a 2.5% smaller total brain ((3 = -31.92; 95% Cl, -52.69 to -11.16; P = .0027) and a 3% smaller total gray matter volume (P = -22.51; 95% Cl, -35.07 to -9.96; P = .0005), while total white matter volume was unaltered (P = -10.10; 95% Cl, -20.73 to 0.53; P = .06). Unaffected siblings had total brain and total gray matter volumes intermediate to participants with ADHD and control individuals. Significant age-by-diagnosis interactions showed that older age was linked to smaller caudate (P < .001) and putamen (P = .01) volumes (both corrected for total brain volume) in control individuals, whereas age was unrelated to these volumes in participants with ADHD and their unaffected siblings. Attention-deficit/ hyperactivity disorder was not significantly related to the other subcortical volumes. CONCLUSIONS AND RELEVANCE: Global differences in gray matter volume may be due to alterations in the general mechanisms underlying normal brain development in ADHD. The age-by-diagnosis interaction in the caudate and putamen supports the relevance of different brain developmental trajectories in participants with ADHD vs control individuals and supports the role of subcortical basal ganglia alterations in the pathophysiology of ADHD. Alterations in total gray matter and caudate and putamen volumes in unaffected siblings suggest that these volumes are linked tofamilial risk for ADHD. [ABSTRACT FROM AUTHOR]

Background Attention-Deficit/Hyperactivity Disorder ( ADHD) is a risk factor for substance use disorders ( SUDs) and nicotine dependence ( ND). Neurocognitive deficits may predict the increased risk of developing SUDs and nicotine dependence. Methods This study comprised three groups derived from the Dutch part of the International Multicenter ADHD Genetics ( IMAGE) study: ADHD probands ( n = 294), unaffected siblings ( n = 161), and controls ( n = 214). At baseline (age = 12.2), a range of neurocognitive functions was assessed including executive functions (inhibition, working memory, timing), measures of motor functioning (motor timing and tracking) and IQ. After a mean follow-up of 4.2 years, SUDs and ND were assessed. Results None of the neurocognitive functions predicted later SUDs or ND in ADHD probands, even after controlling for medication use and conduct disorder. Slower response inhibition predicted later nicotine dependence in unaffected siblings ( OR = 2.06, 95% CI = 1.22-3.48), and lower IQ predicted increased risk for SUDs in controls ( OR = 1.96, 95% CI = 1.12-3.44). Conclusions Cold executive functions, motor functioning, and IQ did not predict the elevated risk of SUDs and ND in ADHD. Future studies should target 'hot' executive functions such as reward processing as risk factors for SUDs or ND. [ABSTRACT FROM AUTHOR]

While the negative association between ADHD symptoms and IQ is well documented, our knowledge about the direction and aetiology of this association is limited. Here, we examine the association of ADHD symptoms with verbal and performance IQ longitudinally in a population-based sample of twins. In a population-based sample of 4,771 twin pairs, DSM-IV ADHD symptoms were obtained from the Conners’ Parent Rating Scale-Revised. Verbal (vocabulary) and performance (Raven’s Progressive Matrices) IQ were assessed online. ADHD symptom ratings and IQ scores were obtained at ages 12, 14 and 16 years. Making use of the genetic sensitivity and time-ordered nature of our data, we use a cross-lagged model to examine the direction of effects, while modelling the aetiologies of the association between ADHD symptoms with vocabulary and Raven’s scores over time. Although time-specific aetiological influences emerged for each trait at ages 14 and 16 years, the aetiological factors involved in the association between ADHD symptoms and IQ were stable over time. ADHD symptoms and IQ scores significantly predicted each other over time. ADHD symptoms at age 12 years were a significantly stronger predictor of vocabulary and Raven’s scores at age 14 years than vice versa, whereas no differential predictive effects emerged from age 14 to 16 years. The results suggest that ADHD symptoms may put adolescents at risk for decreased IQ scores. Persistent genetic influences seem to underlie the association of ADHD symptoms and IQ over time. Early intervention is likely to be key to reducing ADHD symptoms and the associated risk for lower IQ. [ABSTRACT FROM AUTHOR]

Autism spectrum disorder (ASD) symptoms frequently occur in subjects with attention deficit/hyperactivity disorder (ADHD). While there is evidence that both ADHD and ASD have differential structural correlates, no study to date has investigated these structural correlates within a framework that robustly accounts for the phenotypic overlap between the two disorders. The presence of ASD symptoms was measured by the parent-reported Children’s Social and Behavioural Questionnaire (CSBQ) in ADHD subjects (n = 180), their unaffected siblings (n = 118) and healthy controls (n = 146). ADHD symptoms were assessed by a structured interview (K-SADS-PL) and the Conners’ ADHD questionnaires. Whole brain T1-weighted MPRAGE images were acquired and the structural MRI correlates of ASD symptom scores were analysed by modelling ASD symptom scores against white matter (WM) and grey matter (GM) volumes using mixed effects models which controlled for ADHD symptom levels. ASD symptoms were significantly elevated in ADHD subjects relative to both controls and unaffected siblings. ASD scores were predicted by the interaction between WM and GM volumes. Increasing ASD score was associated with greater GM volume. Equivocal results from previous structural studies in ADHD and ASD may be due to the fact that comorbidity has not been taken into account in studies to date. The current findings stress the need to account for issues of ASD comorbidity in ADHD. [ABSTRACT FROM AUTHOR]

Background Attention-deficit/hyperactivity disorder ( ADHD) symptoms and mathematics ability are associated, but little is known about the genetic and environmental influences underlying this association. Methods Data came from more than 6,000 twelve-year-old twin pairs from the UK population-representative Twins Early Development Study. Parents rated each twin's behaviour using a DSM- IV-based 18-item questionnaire of inattentive and hyperactive-impulsive ADHD symptoms. Mathematics tests based on the UK National Curriculum were completed by each twin. The twins also completed standardised tests of reading and general cognitive ability. Multivariate twin model fitting was applied. Results Inattentive and hyperactive-impulsive ADHD symptoms were highly heritable (67% and 73% respectively). Mathematics ability was moderately heritable (46%). Mathematics ability and inattentiveness showed a significantly greater phenotypic correlation ( rp = −.26) and genetic correlation ( rA = −.41) than mathematics ability and hyperactivity-impulsivity ( rp = −.18; rA = −.22). The genetic correlation between inattentiveness and mathematics ability was largely independent from hyperactivity-impulsivity, and was only partially accounted for by genetic influences related to reading and general cognitive ability. Conclusions Results revealed the novel finding that mathematics ability shows significantly stronger phenotypic and genetic associations with inattentiveness than with hyperactivity-impulsivity. Genetic associations between inattentiveness and mathematics ability could only partially be accounted for by hyperactivity-impulsivity, reading and general cognitive ability. Results suggest that mathematics ability is associated with ADHD symptoms largely because it shares genetic risk factors with inattentiveness, and provide further evidence for considering inattentiveness and hyperactivity-impulsivity separately. DNA markers for ADHD symptoms (especially inattentiveness) may also be candidate risk factors for mathematics ability and vice versa. [ABSTRACT FROM AUTHOR]

Background: Attention deficit hyperactivity disorder (ADHD) is a common and highly heritable neurodevelopmental disorder with a complex aetiology. The identification of candidate intermediate phenotypes that are both heritable and genetically linked to ADHD may facilitate the detection of susceptibility genes and elucidate aetiological pathways. Very low-frequency (VLF; <0.5 Hz) electroencephalographic (EEG) activity represents a promising indicator of risk for ADHD, but it currently remains unclear as to whether it is heritable or genetically linked to the disorder. Methods: Direct-current (DC)-EEG was recorded during a cognitive activation condition in 30 monozygotic and dizygotic adolescent twin pairs concordant or discordant for high ADHD symptom scores, and 37 monozygotic and dizygotic matched-control twin pairs with low ADHD symptom scores. Structural equation modelling was used to quantify the genetic and environmental contributions to the phenotypic covariance between ADHD and VLF activity. Results: Attention deficit hyperactivity disorder was significantly associated with reduced VLF power during cognitive activation, which suggests reduced synchronization of widespread neuronal activity. Very low-frequency power demonstrated modest heritability (0.31), and the genetic correlation (−0.80) indicated a substantial degree of overlap in genetic influences on ADHD and VLF activity. Conclusions: Altered VLF activity is a potential candidate intermediate phenotype of ADHD, which warrants further investigation of underlying neurobiological and genetic mechanisms. [ABSTRACT FROM AUTHOR]

Background: Attention deficit hyperactivity disorder (ADHD) and reading disability commonly co-occur because of shared genetic risk factors. However, the stability and change of these genetic influences and the predictive relationships underlying this association longitudinally remain unclear. Methods: ADHD symptoms and reading were assessed as continuous dimensions in a UK general population sample of approximately 7,000 twin pairs. Parent ratings of ADHD symptoms and teacher ratings of reading were obtained at two ages: middle childhood (ages 7-8 years) and early adolescence (ages 11-12 years). Cross-lagged quantitative genetic analyses were applied. Results: ADHD symptoms and reading significantly predicted each other over time. However, ADHD symptoms were a significantly stronger predictor of reading than vice versa. Inattentive and hyperactive-impulsive symptoms of ADHD both contributed to the prediction of reading, but inattentiveness was a significantly stronger predictor. Furthermore, ADHD symptoms and reading were highly heritable, and their association was primarily attributable to shared genetic influences. Despite notable genetic innovation for each trait, genetic factors involved in the association of ADHD symptoms and reading over time were highly stable. Conclusions: ADHD symptoms may put children at increased risk for reading problems and vice versa. Moreover, enduring genetic mechanisms appear to be important in the association of ADHD symptoms and reading over time. [ABSTRACT FROM AUTHOR]

DSM-IV distinguishes two symptom domains of attention deficit hyperactivity disorder (ADHD): inattentiveness and hyperactivity-impulsivity. The present study examines the aetiologies and developmental relations underlying the associations between inattentiveness and hyperactivity-impulsivity over time, based on a representative population sample from the United Kingdom of approximately 7,000 twin pairs. ADHD symptoms were assessed as continuous dimensions using the DSM-IV items from the Conners' Parent Rating Scale at two ages: middle childhood (age 1) and early adolescence (age 2). Quantitative genetic cross-lagged analyses showed that the association of the ADHD dimensions over time is influenced by stable as well as newly developing genetic factors. Moreover the longitudinal relationship between the ADHD dimensions appears to be unidirectional, with hyperactivity-impulsivity in middle childhood predicting the presence of inattentiveness in early adolescence, but not vice versa. Thus, hyperactivity-impulsivity may serve to exacerbate inattentiveness over time. Findings are discussed in the context of developmental changes in ADHD symptoms. [ABSTRACT FROM AUTHOR]

Objective: To assess the genetic and environmental etiology of the co-occurence of ADHD symptoms and reading difficulties using the largest sample to date, distinguishing two dimensions of ADHD and two of reading. Method: Data were obtained from 6428 12-year old twin pairs drawn from the population-based Twins Early Development Study. ADHD symptoms (combined ADHD, inattentiveness and hyperactivity-impulsivity) were assessed using parent ratings. Reading was assessed using a battery of reading comprehension and word decoding tests. Results: Heritabilities were high, around 70% for ADHD symptoms and 45-65% for the reading measures. Some of the same genes affected combined ADHD and reading with a genetic correlation of -.31. The most notable finding was that the genetic correlation with reading was significantly greater for inattentiveness (-.31) than for hyperactivity-impulsivity (-.16), suggesting that genetic overlap between combined ADHD and reading is largely driven by inattentiveness. Moreover results showed that it is word decoding rather than reading comprehension that is differentially related to the ADHD dimensions (lower genetic correlation to hyperactivity-impulsivity than to inattentiveness). Conclusions: Genetic overlap between ADHD and reading is largely driven by inattentiveness rather than hyperactivity-impulsivity. [ABSTRACT FROM AUTHOR]

A previous paper in this journal revealed substantial genetic overlap between the ADHD dimensions of hyperactivity-impulsivity and inattentiveness in a sample of 8-year old twins drawn from a UK-representative population sample. Four years later, when the twins were 12 years old, more than 5,500 pairs drawn from the same sample were rated again on the DSM-IV based Revised Conners' Parent Rating Scale to assess symptoms on both ADHD dimensions. Heritabilities were high (around 70%) for both hyperactivity-impulsivity and inattentiveness and evidence for etiological sex differences was absent. The critical finding was a genetic correlation of 0.55, indicating that hyperactivity-impulsivity and inattentiveness are substantially influenced by the same genes but that the two dimensions also show large and significant unique genetic effects. These results in early adolescence confirm our findings in middle childhood, providing evidence for substantial genetic overlap as well as genetic heterogeneity of the ADHD dimensions. Future genetic studies should investigate the ADHD dimensions separately. [ABSTRACT FROM AUTHOR]

We investigated gene-environment interaction in ADHD traits, focusing on environmental variables related to personality traits, school environment, satisfaction with life, and callousness. Using data from 2170 16-year-old twins and state-of-the-art methodology to prevent spurious findings due to measurement scale artifacts, gene-environment interaction models were estimated separately for the two core ADHD dimensions, hyperactivity-impulsivity, and inattentiveness. Based on scores on the SWAN questionnaire, where high scores are reflective of low ADHD traits, results showed that additive genetic influences were more important in explaining individual differences in the degree of hyperactivity-impulsivity in twins with a high score on the trait conscientiousness than in twins with a moderate or low score (e.g., a positive gene-environment interaction). Similarly, additive genetic influences were relatively more important in explaining individual differences in the degree of inattentiveness in twins with a high score on conscientiousness or satisfaction with oneself. Lastly, a negative gene-environment interaction was found: For twins with a high score on the trait callousness, additive genetic influences were less important in explaining differences in the degree of inattentiveness than in twins with an average or low score on the trait. The finding of these specific gene-environment interactions is important for a deeper understanding of the etiology of ADHD traits and may assist in developing targeted interventions for genetically vulnerable individuals. [ABSTRACT FROM AUTHOR]

Background: Self-control in childhood has been linked to long-term and cascading effects on health, academic, criminality, wealth and parenting outcomes. Hence it is important to target self-control deficits early in life. Self-control deficits are a hallmark of Attention Deficit/Hyperactivity Disorder (ADHD). Even after receiving care-as-usual (CAU) for ADHD, impaired self-control often remains. Pharmacotherapy can be hampered by side-effects, low adherence and short-term effectiveness. Other limitations of CAU are decreased effectiveness when parents have ADHD and little effect on parental well-being. Mindfulness-Based Interventions (MBIs) are an emerging non-pharmacological approach with potential to improve self-control and well-being in both children and parents. However, there is a lack of sufficiently powered randomised controlled trials (RCTs) to establish their effects in families with ADHD. This study protocol describes an RCT to investigate the effectiveness of a family MBI as an add-on to CAU in treatment of youth with ADHD, and is described in accordance with Standard Protocol Items: Recommendations for Interventional Trials (SPIRIT). Methods/design: An RCT will be conducted in N = 100 children (aged 8–16 years) with ADHD and their parents. The experimental condition will consist of a family MBI (MYmind): 8-week group-based MBI for youth combined with parallel group-based Mindful Parenting for their parents, as an add-on to CAU. The control condition will consist of CAU-only. Assessments will take place at baseline, end of treatment (3 months later), 2 and 6 months' follow-up. Primary outcome measure will be an ecologically valid assessment of child self-control with the parent-rated Behaviour Rating Inventory of Executive Function (BRIEF). Secondary child outcome measures will be teacher-rated BRIEF, computerised self-control tasks and questionnaires on psychological symptoms (e.g. ADHD, symptoms of autism), well-being and mindfulness. For parental outcomes, secondary measures will be self-rated BRIEF, computerised self-control tasks and questionnaires on psychological symptoms, well-being and mindful parenting. Discussion: The proposed RCT will take account of methodological limitations of previous studies on MBIs in child ADHD populations. The current study will provide valuable information on family MBI as a potential effective intervention in targeting self-control deficits for youth with ADHD and their parents. Trial registration: ClinicalTrials.govNCT03220308. Retrospectively registered 18 July 2017. [ABSTRACT FROM AUTHOR]

Cognitive control has been strongly linked to midfrontal theta (4–8 Hz) brain activity. Such control processes are known to be impaired in individuals with psychiatric conditions and neurodevelopmental diagnoses, including attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). Temporal variability in theta, in particular, has been associated with ADHD, with shared genetic variance underlying the relationship. Here, we investigated the phenotypic and genetic relationships between theta phase variability, theta-related signals (the N2, error-related negativity, and error positivity), reaction time, and ADHD and ASD longitudinally in a large twin study of young adults to investigate the stability of the genetic relationships between these measures over time. Genetic multivariate liability threshold models were run on a longitudinal sample of 566 participants (283 twin pairs). Characteristics of ADHD and ASD were measured in childhood and young adulthood, while an electroencephalogram was recorded in young adulthood during an arrow flanker task. Cross-trial theta phase variability in adulthood showed large positive phenotypic and genetic relationships with reaction time variability and both childhood and adult ADHD characteristics. Error positivity amplitude was negatively related phenotypically and genetically to ADHD and ASD at both time points. We showed significant genetic associations between variability in theta signaling and ADHD. A novel finding from the current study is that these relationships were stable across time, indicating a core dysregulation of the temporal coordination of control processes in ADHD that persists in individuals with childhood symptoms. Error processing, indexed by the error positivity, was altered in both ADHD and ASD, with a strong genetic contribution. [ABSTRACT FROM AUTHOR]

Background Attention-deficit/hyperactivity disorder (ADHD) is associated with structural abnormalities in total gray matter, basal ganglia, and cerebellum. Findings of structural abnormalities in frontal and temporal lobes, amygdala, and insula are less consistent. Remarkably, the impact of comorbid oppositional defiant disorder (ODD) (comorbidity rates up to 60%) on these neuroanatomical differences is scarcely studied, while ODD (in combination with conduct disorder) has been associated with structural abnormalities of the frontal lobe, amygdala, and insula. The aim of this study was to investigate the effect of comorbid ODD on cerebral volume and cortical thickness in ADHD. Methods Three groups, 16 ± 3.5 years of age (mean ± SD; range 7–29 years), were studied on volumetric and cortical thickness characteristics using structural magnetic resonance imaging (surface-based morphometry): ADHD+ODD ( n = 67), ADHD-only ( n = 243), and control subjects ( n = 233). Analyses included the moderators age, gender, IQ, and scan site. Results ADHD+ODD and ADHD-only showed volumetric reductions in total gray matter and (mainly) frontal brain areas. Stepwise volumetric reductions (ADHD+ODD < ADHD-only < control subjects) were found for mainly frontal regions, and ADHD+ODD was uniquely associated with reductions in several structures (e.g., the precuneus). In general, findings remained significant after accounting for ADHD symptom severity. There were no group differences in cortical thickness. Exploratory voxelwise analyses showed no group differences. Conclusions ADHD+ODD and ADHD-only were associated with volumetric reductions in brain areas crucial for attention, (working) memory, and decision-making. Volumetric reductions of frontal lobes were largest in the ADHD+ODD group, possibly underlying observed larger impairments in neurocognitive functions. Previously reported striatal abnormalities in ADHD may be caused by comorbid conduct disorder rather than ODD. [ABSTRACT FROM AUTHOR]

Objective: The objectives of this study were to model more homogeneous subgroups within autism spectrum disorder (ASD) based on early trajectories of core symptoms; and to further characterize these subgroups in terms of trajectories of language, cognition, co-occurring (attention-deficit/hyperactivity disorder [ADHD]-related) traits and clinical outcome diagnosis.Method: Children (N = 203) referred for possible ASD at ages 1 to 4 years were assessed at three time points at intervals ranging from 9 months to 3 years. Assessments included standardized measures for ASD (Autism Diagnostic Observation Schedule [ADOS]), language (ADOS-language item), nonverbal IQ (NV-IQ; different tests adequate to chronological/mental age), and parent-reported behavioral problems (Infant-Toddler Social and Emotional Assessment, Child Behavior Checklist).Results: Latent-class growth curve analysis with ADOS total scores led to the identification of three main stable and two small improving groups: a severe-stable group (19.5% of sample)-the only group without considerable language improvement-showed persistent low NV-IQ and marked increase in attention problems over time; a moderate-stable group (21.7%) with below-average increasing NV-IQ; and a mild-stable group (48%) with stable-average NV-IQ and the highest scores on ADHD-related traits, whose ASD outcome diagnoses increased despite stable-low ASD scores. Two groups (each 5.4%) improved: one moved from severe to moderate ASD scores, and the other moved from moderate to mild/nonspectrum scores. Both of these groups improved on language, NV-IQ, and ADHD-related traits.Conclusion: Results support the high stability of ASD symptoms into various severity levels, but also highlight the significant contribution of non-ASD domains in defining and explaining the different ASD trajectories. [ABSTRACT FROM AUTHOR]

Objective: The aims of this study were to elucidate the influence of common genetic variants on childhood attention-deficit/hyperactivity disorder (ADHD) symptoms, to identify genetic variants that explain its high heritability, and to investigate the genetic overlap of ADHD symptom scores with ADHD diagnosis.Method: Within the EArly Genetics and Lifecourse Epidemiology (EAGLE) consortium, genome-wide single nucleotide polymorphisms (SNPs) and ADHD symptom scores were available for 17,666 children (<13 years of age) from nine population-based cohorts. SNP-based heritability was estimated in data from the three largest cohorts. Meta-analysis based on genome-wide association (GWA) analyses with SNPs was followed by gene-based association tests, and the overlap in results with a meta-analysis in the Psychiatric Genomics Consortium (PGC) case-control ADHD study was investigated.Results: SNP-based heritability ranged from 5% to 34%, indicating that variation in common genetic variants influences ADHD symptom scores. The meta-analysis did not detect genome-wide significant SNPs, but three genes, lying close to each other with SNPs in high linkage disequilibrium (LD), showed a gene-wide significant association (p values between 1.46 × 10(-6) and 2.66 × 10(-6)). One gene, WASL, is involved in neuronal development. Both SNP- and gene-based analyses indicated overlap with the PGC meta-analysis results with the genetic correlation estimated at 0.96.Conclusion: The SNP-based heritability for ADHD symptom scores indicates a polygenic architecture, and genes involved in neurite outgrowth are possibly involved. Continuous and dichotomous measures of ADHD appear to assess a genetically common phenotype. A next step is to combine data from population-based and case-control cohorts in genetic association studies to increase sample size and to improve statistical power for identifying genetic variants. [ABSTRACT FROM AUTHOR]

Objective: Attention-deficit/hyperactivity disorder (ADHD) is more frequent in males than in females. The "female protective effect" posits that females undergo greater exposure to etiological factors than males in order to develop ADHD, leading to the prediction that relatives of females with ADHD will display more ADHD behaviors. We thus tested whether cotwins of females displaying extreme ADHD traits would display more ADHD traits than cotwins of males displaying extreme ADHD traits.Method: Parents of approximately 7,000 pairs of nonidentical twins in Sweden, and approximately 4,000 pairs of twins in England and Wales, completed dimensional assessments of ADHD traits. Probands were selected on the basis of scoring within the highest 10% of the distribution in each sample. Dimensional scores of cotwins of probands, as well as the categorical recurrence rate, were investigated by proband sex.Results: Cotwins of female probands displayed higher mean ADHD trait scores (mean = 0.62-0.79) than cotwins of male probands (mean = 0.38-0.55) in both samples. This trend was significant in the Swedish sample (p < .01) and when the 2 samples were merged into a single, larger sample (p < .001). When the samples were merged, there was also a significant association between proband sex and cotwin's categorical status, with more cotwins of female probands also being probands than cotwins of male probands.Conclusion: These findings support a female protective effect against ADHD behaviors, suggesting that females require greater exposure to genetic and environmental factors associated with ADHD in order to develop the condition. [ABSTRACT FROM AUTHOR]