Causal Factors of Increased Smoking in ADHD: A Systematic Review

Amsterdam, Jan van; Velde, Bauke van der; Schulte, Mieke H J; Brink, Wim van den

doi:10.1080/10826084.2017.1334066

Cited by 49 publications

(66 citation statements)

References 125 publications

(144 reference statements)

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“…While previous observational studies may have been biased by (unmeasured) confounding, our approach of using genetic variants as instrumental variables is more robust to confounding and reverse causality. We were not able to identify the exact mechanism of causation, but it seems plausible that higher levels of impulsivity may lead individuals with ADHD liability to try out cigarettes or cannabis without considering their possible negative consequences 5,49 . Another potential mechanism is 'selfmedication', whereby a substance is used because of its (real or perceived) positive effects on ADHD symptomatology -even though such effects might not actually exist 50 .…”

Section: Discussionmentioning

confidence: 96%

“…There is extensive research showing that genetic influences on smoking initiation are mediated via impulsivity-related traits 5 . This was confirmed by our findings that the genetic instrument for smoking initiation also showed strong evidence for a causal effect on ADHD symptoms in children <13 years (who would not yet have started smoking).…”

Section: Discussionmentioning

confidence: 99%

“…Around 5.9-7.1% of children and adolescents and 5.0% of adults are thought to meet the diagnostic criteria for ADHD 2 , and genetic studies support the notion that a clinical diagnosis represents the extreme end of a continuum of impulsivity and/or attention problems in the general population 3,4 . Both ADHD diagnosis and higher levels of impulsivity and attention problems are associated with higher levels of cigarette smoking 5,6 , cannabis use 7,8 , alcohol use 7,9 and caffeine consumption 10,11 . The exact nature of these associations is not fully understood, which hampers the development of evidence-based interventions and public health messages.…”

Section: Introductionmentioning

confidence: 99%

“…If variable X causes variable Y, it follows that any environmental or genetic risk factor causing variable X will also be associated (indirectly) with variable Y. The current literature has mostly focused on causal pathways from ADHD to substance use, with longitudinal cohort studies showing that externalizing symptoms in early adolescence predict onset of smoking and faster progression to daily smoking, and that ADHD medication reduces early onset smoking and alleviates smoking withdrawal 5 .…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Investigating causal pathways between liability to ADHD and substance use, and liability to substance use and ADHD risk, using Mendelian randomization

Treur

Demontis

Sallis

et al. 2019

Preprint

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BackgroundAttention-deficit hyperactivity disorder (ADHD) has consistently been associated with substance (ab)use, but the nature of this association is not fully understood. In view of preventive efforts, a vital question is whether there are causal effects, from ADHD to substance use and/or from substance use to ADHD.MethodsWe applied bidirectional Mendelian randomization using summary-level data from the largest available genome-wide association studies (GWASs) on ADHD, smoking (initiation, cigarettes/day, cessation, and a compound measure of lifetime smoking), alcohol use (drinks/week and alcohol use disorder), cannabis use (initiation and cannabis use disorder (CUD)) and coffee consumption (cups/day). Genetic variants robustly associated with the ‘exposure’ were selected as instruments and then identified in the ‘outcome’ GWAS. Effect estimates from individual genetic variants were combined with inverse-variance weighted regression and five sensitivity analyses were applied (weighted median, weighted mode, MR-Egger, generalized summary-data-based MR, and Steiger filtering).ResultsWe found strong evidence that liability to ADHD increases likelihood of smoking initiation and also cigarettes per day among smokers, decreases likelihood of smoking cessation, and increases likelihood of cannabis initiation and CUD. In the other direction, there was evidence that liability to smoking initiation and CUD increase ADHD risk. There was no clear evidence of causal effects between liability to ADHD and alcohol or caffeine consumption.ConclusionsWe find evidence for causal effects of liability to ADHD on smoking and cannabis use, and of liability to smoking and cannabis use on ADHD risk, indicating bidirectional pathways. Further work is needed to explore causal mechanisms.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Investigating causal pathways between liability to ADHD and substance use, and liability to substance use and ADHD risk, using Mendelian randomization

Treur

Demontis

Sallis

et al. 2019

Preprint

View full text Add to dashboard Cite

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“…Recent studies have established the clinical relevance of ADHD symptoms (impulsivity, disinhibition, executive function deficits, and slowed mental processing) for the prediction of SUD development and persistence [19, 20]. These studies suggested that treatment outcomes for SUD may be improved by early and accurate identification and targeting ADHD symptoms in this population.…”

Section: Introductionmentioning

confidence: 99%

The Utility of the CPT in the Diagnosis of ADHD in Individuals with Substance Abuse: A Systematic Review

Slobodin

2020

Eur Addict Res

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Background: Early identification of attention-deficit/hyperactivity disorder (ADHD) in individuals with substance use disorders (SUD) is important because ADHD has an adverse effect on the development and course of SUD. Given the limited validity of self-report measures of ADHD in individuals with SUD, it is important to investigate the utility of the continuous performance test (CPT) in classifying ADHD in adults with SUD. Objective: This review aims to examine the quantitative similarities and differences in CPT performance of adults with ADHD, SUD, and their comorbidity to determine if a distinct neurocognitive profile exists for each. Method: A systematic review of CPT studies that included patients with the comorbidity of ADHD and SUD and a comparison group of one of the disorders alone was conducted. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were used. Results: Eight studies were identified with sample sizes ranging from n = 17 to n = 386. The comorbidity of ADHD and SUD was, mostly, not associated with higher rates of commission and omission errors than either disorder alone. However, the comorbidity of ADHD and SUD was more likely to be associated with increased deficits in response time variability compared with individuals with ADHD alone. Conclusions: This review highlights the shortage of large-scale CPT research involving patients with ADHD and SUD. The CPT might be sensitive to attentional deficits, but it lacks specificity for the classification of adult ADHD, SUD, or their comorbidity, and the CPT is thus not useful in discriminating comorbid ADHD and SUD from either disorder alone. Future CPT research should explore whether specific attentional deficits account for the development and persistence of SUD. Such research should also reach beyond traditional CPT measures and include other cognitive and behavioral deficits that were associated with ADHD, such as distractibility and hyperactivity.

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Investigating genetic correlation and causality between nicotine dependence and ADHD in a broader psychiatric context

Vink

Treur

Pasman

et al. 2020

American J of Med Genetics Pt B

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People with attention-deficit/hyperactivity disorder (ADHD) or other psychiatric disorders show high rates of nicotine dependence (ND). This comorbidity might be (partly) explained by shared genetic factors. Genetic correlations between ND and ADHD (or other psychiatric disorders) have not yet been estimated. A significant genetic correlation might indicate genetic overlap, but could also reflect a causal relationship. In the present study we investigated the genetic correlation (with LD score regression analyses) between ND and ADHD, as well as between ND and other major psychiatric conditions (major depressive disorder, schizophrenia, anxiety, bipolar disorder, autism spectrum, anorexia nervosa, and antisocial behavior) based on the summary statistics of large Genome Wide Association studies. We explored the causal nature of the relationship between ND and ADHD using two-sample Mendelian randomization. We found a high genetic correlation between ND and ADHD (r g = .53, p = 1.85 × 10 −13 ), and to a lesser extent also between ND-major depressive disorder (r g = .42, p = 3.6 × 10 −11 ) and ND-schizophrenia (r g = .18, p = 1.1 × 10 −3 ).We did not find evidence for a causal relationship from liability for ADHD to ND (which could be due to a lack of power). The strong genetic correlations might reflect different phenotypic manifestations of (partly) shared underlying genetic vulnerabilities. Combined with the lack of evidence for a causal relationship from liability for ADHD to ND, these findings stress the importance to further investigate the underlying genetic vulnerability explaining co-morbidity in psychiatric disorders.

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Causal Factors of Increased Smoking in ADHD: A Systematic Review

Cited by 49 publications

References 125 publications

Investigating causal pathways between liability to ADHD and substance use, and liability to substance use and ADHD risk, using Mendelian randomization

Investigating causal pathways between liability to ADHD and substance use, and liability to substance use and ADHD risk, using Mendelian randomization

The Utility of the CPT in the Diagnosis of ADHD in Individuals with Substance Abuse: A Systematic Review

Investigating genetic correlation and causality between nicotine dependence and ADHD in a broader psychiatric context

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