Browse
Submit Data
Databases
API
Help

Dataset Information

25 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Attention-deficit/hyperactivity disorder and lifetime cannabis use: genetic overlap and causality.

ABSTRACT: Attention-deficit/hyperactivity disorder (ADHD) is a severely impairing neurodevelopmental disorder with a prevalence of 5% in children and adolescents and of 2.5% in adults. Comorbid conditions in ADHD play a key role in symptom progression, disorder course and outcome. ADHD is associated with a significantly increased risk for substance use, abuse and dependence. ADHD and cannabis use are partly determined by genetic factors; the heritability of ADHD is estimated at 70-80% and of cannabis use initiation at 40-48%. In this study, we used summary statistics from the largest available meta-analyses of genome-wide association studies (GWAS) of ADHD (n = 53,293) and lifetime cannabis use (n = 32,330) to gain insights into the genetic overlap and causal relationship of these two traits. We estimated their genetic correlation to be r² = 0.29 (P = 1.63 × 10^-5) and identified four new genome-wide significant loci in a cross-trait analysis: two in a single variant association analysis (rs145108385, P = 3.30 × 10^-8 and rs4259397, P = 4.52 × 10^-8) and two in a gene-based association analysis (WDPCP, P = 9.67 × 10^-7 and ZNF251, P = 1.62 × 10^-6). Using a two-sample Mendelian randomization approach we found support that ADHD is causal for lifetime cannabis use, with an odds ratio of 7.9 for cannabis use in individuals with ADHD in comparison to individuals without ADHD (95% CI (3.72, 15.51), P = 5.88 × 10^-5). These results substantiate the temporal relationship between ADHD and future cannabis use and reinforce the need to consider substance misuse in the context of ADHD in clinical interventions.

SUBMITTER: Soler Artigas M

PROVIDER: S-EPMC8025199 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

Genetic Investigations of Attention-Deficit/Hyperactivity Disorder

Project description:Genetic Investigations of Attention-Deficit/Hyperactivity Disorder

| PRJNA1114309 | ENA

Genetic Investigations of Attention-Deficit/Hyperactivity Disorder

Project description:Genetic Investigations of Attention-Deficit/Hyperactivity Disorder

| PRJNA1114310 | ENA

Genetic Overlap Between Attention Deficit/Hyperactivity Disorder and Autism Spectrum Disorder in <i>SHANK2</i> Gene.

Project description:Background: Recent findings indicated a high comorbidity between attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD), as well as shared genetic influences on them. The latter might contribute at least partly to the former clinical scenario. This study aimed at investigating whether SHANK genes were potential pleiotropic genes to the two said disorders, underlying their genetic overlap. Methods: This study recruited 298 boys with ADHD (including 256 family trios of 1 ADHD boy and his 2 biological parents), 134 boys with ASD, 109 boys with both ADHD and ASD, and 232 typically developing boys as community controls. They were aged between 6 and 11 years old. Results: There was no significant difference in allele frequency of a number of single nucleotide polymorphisms (SNPs) in SHANK2/SHANK3 between the three clinical groups (ADHD, ASD, and ADHD + ASD) and between the two control groups (community controls and pseudo-controls), respectively. The three clinical groups and the two control groups were thus, respectively, combined. A comparison between the two aggregated samples identified significant evidence of disease association for three SHANK2 SNPs with both ADHD and ASD, even after multiple testing correction: rs11236616 (OR = 0.762, permuted p = 0.0376), rs7106631 (OR = 0.720, permuted p = 0.0034), and rs9888288 (OR = 0.770, permuted p = 0.0407). Comparisons among individual groups pointed to a similar trend of findings. Conclusion: SHANK2 could be considered a potential pleiotropic gene underlying the genetic overlap between ADHD and ASD. This might contribute partly to their high comorbidity in the afflicted children.

| S-EPMC8111170 | biostudies-literature

Thalamocortical functional connectivity and cannabis use in men with childhood attention-deficit/hyperactivity disorder.

Project description:Disruptions of the cortico-striato-thalamo-cortical circuit has been implicated in both attention-deficit/hyperactivity disorder and substance use disorder. Given the high prevalence of cannabis use among patients with attention-deficit/hyperactivity disorder, we set out to investigate the relationship between the two in the thalamus. We analyzed resting-state functional magnetic resonance imaging data obtained from the Addiction Connectome Preprocessed Initiative Multimodal Treatment Study of Attention-Deficit/Hyperactivity Disorder database. Functional connectivity maps were extracted to compare thalamic connectivity among adults who had been diagnosed with attention-deficit/hyperactivity disorder during childhood according to whether or not they used cannabis. The study participants included 18 cannabis users and 15 cannabis non-users with childhood attention-deficit/hyperactivity disorder. Our results revealed that adults with attention-deficit/hyperactivity disorder who used cannabis (n = 18) had significantly decreased functional connectivity between the thalamus and parietal regions, which was particularly prominent in the inferior parietal areas, in comparison with those who did not use cannabis (n = 15). Left thalamic functional connectivity with the inferior parietal and middle frontal areas and right thalamic functional connectivity with the inferior parietal and superior frontal areas were increased in non-users of cannabis with attention-deficit/hyperactivity disorder compared with a local normative comparison group (n = 7). In conclusion, adults with a childhood history of attention-deficit/hyperactivity disorder who do not use cannabis often have relatively stronger thalamoparietal and thalamofrontal connectivity, which may help reduce the risk of cannabis use.

| S-EPMC9704667 | biostudies-literature

Adult attention-deficit/hyperactivity disorder: Associations between subtype and lifetime substance use - a clinical study.

Project description:ADHD is the one of the most prevalent childhood disorders and has been associated with impairments persisting into adulthood. Specifically, childhood ADHD is an independent clinical risk factor for the development of later substance use disorders (SUD). Moreover, adults who meet diagnostic criteria for ADHD have shown high rates of comorbid SUDs. Few studies, however, have reported on the relationship between ADHD subtypes and SUD in adult samples. The purpose of this study was to characterize a clinical sample of adults with ADHD and to identify possible associations between ADHD subtypes, lifetime substance use, and if ADHD subtypes may be preferentially associated with specific substances of abuse. We recruited 413 adult ADHD patients, performed an evaluation of their ADHD and conducted an interview on their use of psychotropic substances. Complete data was obtained for 349 patients. Lifetime substance abuse or dependence was 26% and occasional use was 57% in this sample. The inattentive subtype was significantly less likely to abuse or be dependent on cocaine than the combined subtype. Our findings underscore the high rate of comorbidity between substance use and ADHD in adults. The more frequent abuse/dependence of cocaine by adult patients with hyperactive-impulsive symptoms should be kept in mind when treating this patient group.

| S-EPMC5089146 | biostudies-literature

Genetic Overlap Between Attention-Deficit/Hyperactivity Disorder and Bipolar Disorder: Evidence From Genome-wide Association Study Meta-analysis.

Project description:BackgroundAttention-deficit/hyperactivity disorder (ADHD) and bipolar disorder (BPD) are frequently co-occurring and highly heritable mental health conditions. We hypothesized that BPD cases with an early age of onset (≤21 years old) would be particularly likely to show genetic covariation with ADHD.MethodsGenome-wide association study data were available for 4609 individuals with ADHD, 9650 individuals with BPD (5167 thereof with early-onset BPD), and 21,363 typically developing controls. We conducted a cross-disorder genome-wide association study meta-analysis to identify whether the observed comorbidity between ADHD and BPD could be due to shared genetic risks.ResultsWe found a significant single nucleotide polymorphism-based genetic correlation between ADHD and BPD in the full and age-restricted samples (rGfull = .64, p = 3.13 × 10-14; rGrestricted = .71, p = 4.09 × 10-16). The meta-analysis between the full BPD sample identified two genome-wide significant (prs7089973 = 2.47 × 10-8; prs11756438 = 4.36 × 10-8) regions located on chromosomes 6 (CEP85L) and 10 (TAF9BP2). Restricting the analyses to BPD cases with an early onset yielded one genome-wide significant association (prs58502974 = 2.11 × 10-8) on chromosome 5 in the ADCY2 gene. Additional nominally significant regions identified contained known expression quantitative trait loci with putative functional consequences for NT5DC1, NT5DC2, and CACNB3 expression, whereas functional predictions implicated ABLIM1 as an allele-specific expressed gene in neuronal tissue.ConclusionsThe single nucleotide polymorphism-based genetic correlation between ADHD and BPD is substantial, significant, and consistent with the existence of genetic overlap between ADHD and BPD, with potential differential genetic mechanisms involved in early and later BPD onset.

| S-EPMC7027938 | biostudies-literature

Attention-deficit hyperactivity disorder.

Project description:Attention-deficit hyperactivity disorder (ADHD), like other psychiatric disorders, represents an evolving construct that has been refined and developed over the past several decades in response to research into its clinical nature and structure. The clinical presentation and course of the disorder have been extensively characterised. Efficacious medication-based treatments are available and widely used, often alongside complementary psychosocial approaches. However, their effectiveness has been questioned because they might not address the broader clinical needs of many individuals with ADHD, especially over the longer term. Non-pharmacological approaches to treatment have proven less effective than previously thought, whereas scientific and clinical studies are starting to fundamentally challenge current conceptions of the causes of ADHD in ways that might have the potential to alter clinical approaches in the future. In view of this, we first provide an account of the diagnosis, epidemiology, and treatment of ADHD from the perspective of both the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders and the eleventh edition of the International Classification of Diseases. Second, we review the progress in our understanding of the causes and pathophysiology of ADHD on the basis of science over the past decade or so. Finally, using these discoveries, we explore some of the key challenges to both the current models and the treatment of ADHD, and the ways in which these findings can promote new perspectives.

| S-EPMC7880081 | biostudies-literature

Inattentiveness in attention-deficit/hyperactivity disorder.

Project description:Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder with a long-term impact on functioning, productivity and quality of life of patients. This impact is largely due to the symptoms of inattentiveness. However, despite its impairing role in the lives of ADHD patients, inattentiveness has been studied relatively less frequently than have symptoms of impulsivity/hyperactivity and problems with executive function. This review therefore seeks to integrate the neuropsychological theories and current findings in the research fields of neuropsychology, neurophysiology, and neuroimaging, in an attempt to gain a more complete understanding of the role that inattentiveness plays in ADHD, as well as to suggest directions for future studies. The need for a more comprehensive understanding of inattentiveness and ADHD, which integrates findings from each of the three disciplines mentioned above, is emphasized.

| S-EPMC4440572 | biostudies-other

Use of stimulants for attention deficit hyperactivity disorder: FOR.

Project description: Not available

| S-EPMC523123 | biostudies-literature

ADHDgene: a genetic database for attention deficit hyperactivity disorder.

Project description:With a worldwide prevalence of ~5%, attention deficit hyperactivity disorder (ADHD) has become one of the most common psychiatric disorders. The polygenetic nature of ADHD indicates that multiple genes jointly contribute to the development of this complex disease. Studies aiming to explore genetic susceptibility of ADHD have been increasing in recent years. There is a growing need to integrate the genetic data from various genetic studies to provide a comprehensive data set and uniform access for convenience of in-depth data mining. So far, there has been no such effort for ADHD. To address the genetic complexity of ADHD, we developed the ADHDgene database by integrating ADHD-related genetic factors by profound literature reading. Based on the data from the literature, extended functional analysis, including linkage disequilibrium analysis, pathway-based analysis and gene mapping were performed to provide new insights into genetic causes of ADHD. Moreover, powerful search tools and a graphical browser were developed to facilitate the navigation of the data and data connections. As the first genetic database for ADHD, ADHDgene aims to provide researchers with a central genetic resource and analysis platform for ADHD and is freely available at http://adhd.psych.ac.cn/.

| S-EPMC3245028 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data