The role of conduct disorder in the association between ADHD and alcohol use (disorder). Results from the Netherlands Mental Health Survey and Incidence Study-2.
ABSTRACT Much is unclear about the association between attention-deficit/hyperactivity disorder (ADHD) and alcohol use (disorder). Research on this subject is hindered by the role of conduct disorder (CD). We investigate whether (1) childhood ADHD is associated with higher prevalence and earlier onset of alcohol initiation, regular alcohol use and alcohol use disorder (AUD) (2) CD mediates or modifies this association.
Data were derived from the baseline assessment of the Netherlands Mental Health Survey and Incidence Study-2, a general population study. ADHD and CD were assessed among respondents aged 18-44 (n=3309). ADHD, CD, and alcohol use (disorder) were assessed using the Composite International Diagnostic Interview 3.0.
Lifetime prevalence was 2.9% for ADHD, 5.6% for CD, 94.3% for alcohol initiation, 85.7% for regular alcohol use and 19.0% for AUD; mean ages of onset were 6.7, 11.5, 14.8, 16.7 and 19.2 years, respectively. After correction for gender and age, ADHD was associated with a higher prevalence of all three stages of alcohol use, but not with earlier onset of these stages. The association between ADHD and prevalence of AUD was fully explained by a mediating role of CD. CD did not modify the associations between ADHD and prevalence and onset of alcohol use (disorder).
The mediating role of CD in the association between ADHD and AUD suggests a developmental pathway from ADHD to CD and subsequent AUD. Early interventions in children with ADHD may prevent CD and subsequent onset of AUD.
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ABSTRACT: Background Alcohol consumption levels and alcohol use disorder (AUD) symptoms may serve as easily quantifiable markers for AUD relapse after remission and might help prevention workers identify at-risk individuals. We investigated the predictive value of alcohol consumption and AUD symptoms on relapse. Methods Data are from the Netherlands Mental Health Survey and Incidence Study-2 (NEMESIS-2). We selected 506 people in ≥12-month DSM-5 AUD remission at baseline and assessed their status at 3-year follow-up. AUD symptoms and drinking patterns were assessed using the Composite International Diagnostic Interview 3.0. Time since remission was assessed retrospectively at baseline and ranged from 1 to 48 years. Predictors for relapse were examined using Cox regression analysis. Results Cumulative AUD relapse rate was 5.6% at 5 years, 9.1% at 10 years and 12.0% at 20 years. Relapse was predicted by both medium [15-28/22-42 drinks weekly for women/men] and high [≥29/43] past alcohol intake, 6+ lifetime AUD symptoms, ‘impaired control over use’, and at-risk [≥8/15] current intake. The risk of relapse was especially high when medium or high past intake or 6+ lifetime symptoms coincided with current at-risk drinking. Conclusions Only a minority of people in DSM-5 AUD remission relapsed, but the risk of relapse increased substantially with the presence of at least one of the risk factors. Moreover, at-risk current drinking coupled with other risk factors substantially increased the likelihood of relapse. Therefore, current drinking may provide an adequate reference point for relapse prevention.Drug and alcohol dependence 01/2014; · 3.60 Impact Factor
- American Journal of Medical Genetics Part B Neuropsychiatric Genetics 07/2013; · 3.23 Impact Factor
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ABSTRACT: Single nucleotide polymorphisms (SNPs) in the tachykinin receptor 1 gene (TACR1) are nominally associated with bipolar affective disorder (BPAD) in a genome-wide association study and in several case-control samples of BPAD, alcohol dependence syndrome (ADS) and attention-deficit hyperactivity disorder (ADHD). Eighteen TACR1 SNPs were associated with BPAD in a sample (506 subjects) from University College London (UCL1), the most significant being rs3771829, previously associated with ADHD. To further elucidate the role of TACR1 in affective disorders, rs3771829 was genotyped in a second BPAD sample of 593 subjects (UCL2), in 997 subjects with ADS, and a subsample of 143 individuals diagnosed with BPAD and comorbid alcohol dependence (BPALC). rs3771829 was associated with BPAD (UCL1 and UCL2 combined: P = 2.0 × 10−3), ADS (P = 2.0 × 10−3) and BPALC (P = 6.0 × 10−4) compared with controls screened for the absence of mental illness and alcohol dependence. DNA sequencing in selected cases of BPAD and ADHD who had inherited TACR1-susceptibility haplotypes identified 19 SNPs in the promoter region, 5′ UTR, exons, intron/exon junctions and 3′ UTR of TACR1 that could increase vulnerability to BPAD, ADS, ADHD, and BPALC. Alternative splicing of TACR1 excludes intron 4 and exon 5, giving rise to two variants of the neurokinin 1 receptor (NK1R) that differ in binding affinity of substance P by 10-fold. A mutation in intron four, rs1106854, was associated with BPAD, although a regulatory role for rs1106854 is unclear. The association with TACR1 and BPAD, ADS, and ADHD suggests a shared molecular pathophysiology between these affective disorders. © 2014 The Authors. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics Published by Wiley Periodicals.American Journal of Medical Genetics Part B Neuropsychiatric Genetics 05/2014; · 3.23 Impact Factor