Where are the strongest associations between autistic traits and traits of ADHD? evidence from a community-based twin study

Taylor, Mark J.; Charman, Tony; Ronald, Angelica

doi:10.1007/s00787-014-0666-0

Cited by 55 publications

(57 citation statements)

References 45 publications

(57 reference statements)

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“…Low genetic correlations (0.27) between ASD and ADHD traits have been reported in 2-year-olds [27], whereas stronger genetic correlations (~0.40-0.60) have been reported in childhood age twin samples [5,16,20,23,28]. This contrast with the high genetic correlation (0.87) between ASD and ADHD in a sample of young adolescents (12 years old) [15], albeit findings in a similar age group suggest genetic correlations may be symptom domain specific [moderately strong between communication difficulties and traits of ADHD (~0.50), but low to moderate for other ASD domains (~0.05-0.30)] [31,32]. A sample of late adolescent/young adults (18-33 years) showed a moderately strong genetic correlation (~0.70) between ASD and ADHD traits [24], albeit studies including a similar age range found lower genetic correlations (~0.20-0.60), strongest between repetitive behaviors and ADHD symptoms ( [21]; see also [16]).…”

Section: Shared Heritability Of Asd and Adhd Across The Lifespanmentioning

confidence: 84%

Review: changing (shared) heritability of ASD and ADHD across the lifespan

Rommelse

Hartman

2016

Eur Child Adolesc Psychiatry

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been strongly focused on childhood. The age of onset for ASD and ADHD is nearly always in childhood ([18]; but see [17]), which is the likely reason for this bias. However, given that it is already well known that developmental changes take place in both ADHD and ASD symptom domains separately, a focus beyond childhood is needed to further understand the potentially changing etiology of ADHD-ASD co-occurrence. Heritability of ADHD across the lifespanSeveral longitudinal twin studies on ADHD symptoms report that new, age-specific genetic effects influence ADHD symptoms in adolescence and adulthood, suggesting that ADHD symptoms are a developmentally complex phenotype characterized by both continuity and change across the life span [3,9,12,13,19]. In addition, only a modest overlap between longitudinal genetic effects underlying both symptom domains (inattention versus hyperactivity/impulsivity) appears present, suggesting it is necessary to study both separately. Moreover, several longitudinal studies report that subgroups may be formed based on various combinations of symptoms in both domains across the longitudinal course that likely has partly distinct genetic underpinnings ([7, 14, 25]). These findings strongly suggest that genetic effects implicated in childhood ADHD may not at all be directly comparable to those that influence ADHD in adulthood. This concurs with a review on molecular genetics in adult ADHD, where it was concluded that only some genes potentially related to childhood ADHD have been replicated in adults with the disorder [8]. In addition, in some cases the same genes were implicated, but different alleles increased the risk for ADHD in children versus adults (for instance, the 10-repeat in the dopamine transporter gene [DAT1] increased the risk for ADHD in children, but decreased the risk in adults) [8]. Note though that currently

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Section: Shared Heritability Of Asd and Adhd Across The Lifespanmentioning

confidence: 84%

Review: changing (shared) heritability of ASD and ADHD across the lifespan

Rommelse

Hartman

2016

Eur Child Adolesc Psychiatry

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“…For this, we investigate a phenotypically rich longitudinal population-based cohort from the UK, the Avon Longitudinal Study of Parents and Children (ALSPAC), as well as summary statistics from the largest publicly available clinical ADHD and ASD samples collected by the Psychiatric Genomics Consortium (PGC) [22, 33]. Given the strong genetic overlap between communication difficulties and ADHD traits in community twin samples [34], we selected social-communication difficulties as well as combined hyperactive-impulsive and inattentive ADHD symptoms for the study on the population level. Here, we (a) report and characterise genetic links between longitudinally assessed social-communication difficulties and combined hyperactive-impulsive and inattentive ADHD symptoms within the general population across ages 7 to 17 years, (b) confirm that these traits genetically overlap with clinical disorder assuming a uni-dimensional behavioural continuum (unless already reported) and (c) study the cross-dimensional trait-disorder overlap between these longitudinally assessed population-based traits with respect to both clinical ADHD and ASD.…”

Section: Introductionmentioning

confidence: 99%

Shared genetic influences between dimensional ASD and ADHD symptoms during child and adolescent development

et al. 2017

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BackgroundShared genetic influences between attention-deficit/hyperactivity disorder (ADHD) symptoms and autism spectrum disorder (ASD) symptoms have been reported. Cross-trait genetic relationships are, however, subject to dynamic changes during development. We investigated the continuity of genetic overlap between ASD and ADHD symptoms in a general population sample during childhood and adolescence. We also studied uni- and cross-dimensional trait-disorder links with respect to genetic ADHD and ASD risk.MethodsSocial-communication difficulties (N ≤ 5551, Social and Communication Disorders Checklist, SCDC) and combined hyperactive-impulsive/inattentive ADHD symptoms (N ≤ 5678, Strengths and Difficulties Questionnaire, SDQ-ADHD) were repeatedly measured in a UK birth cohort (ALSPAC, age 7 to 17 years). Genome-wide summary statistics on clinical ASD (5305 cases; 5305 pseudo-controls) and ADHD (4163 cases; 12,040 controls/pseudo-controls) were available from the Psychiatric Genomics Consortium. Genetic trait variances and genetic overlap between phenotypes were estimated using genome-wide data.ResultsIn the general population, genetic influences for SCDC and SDQ-ADHD scores were shared throughout development. Genetic correlations across traits reached a similar strength and magnitude (cross-trait r g ≤ 1, p min = 3 × 10−4) as those between repeated measures of the same trait (within-trait r g ≤ 0.94, p min = 7 × 10−4). Shared genetic influences between traits, especially during later adolescence, may implicate variants in K-RAS signalling upregulated genes (p-meta = 6.4 × 10−4).Uni-dimensionally, each population-based trait mapped to the expected behavioural continuum: risk-increasing alleles for clinical ADHD were persistently associated with SDQ-ADHD scores throughout development (marginal regression R 2 = 0.084%). An age-specific genetic overlap between clinical ASD and social-communication difficulties during childhood was also shown, as per previous reports. Cross-dimensionally, however, neither SCDC nor SDQ-ADHD scores were linked to genetic risk for disorder.ConclusionsIn the general population, genetic aetiologies between social-communication difficulties and ADHD symptoms are shared throughout child and adolescent development and may implicate similar biological pathways that co-vary during development. Within both the ASD and the ADHD dimension, population-based traits are also linked to clinical disorder, although much larger clinical discovery samples are required to reliably detect cross-dimensional trait-disorder relationships.Electronic supplementary materialThe online version of this article (doi:10.1186/s13229-017-0131-2) contains supplementary material, which is available to authorized users.

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“…Similarly, having a diagnosis of ASD may in some cases further exacerbate other problems, making it harder to cope. This is particularly important to examine in more detail in light of the vast literature exploring the common co-morbidities which frequently present in individuals with ASD, most notably, mood disorders such as depression and anxiety (e.g., Ghaziuddin, Ghaziuddin, & Greden, 2002;Hammond & Hoffman, 2014;Matson & Williams, 2014;Moss, Howlin, Savage, Bolton, & Rutter, 2015;Bruggink, Huisman, Vuijk, Kraaij, & Garnefski, 2016), and behavioral disorders such as attention-deficit/hyperactivity disorder (ADHD) (e.g., Chen et al, 2015;Taylor, Charman, & Ronald, 2015;Antshel, Zhang-James, Wagner, Ledesma, & Faraone, 2016). Such comorbidities may further intensify an individual with ASD's impaired ability to cope with problems in his or her life.…”

Section: Discussionmentioning

confidence: 99%