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The unique phenotypic and genetic aspects of obsessive-compulsive (OCD) and attention-deficit/hyperactivity disorder (ADHD) among individuals with Tourette syndrome (TS) are not well characterized. Here, we examine symptom patterns and heritability of OCD and ADHD in TS families.
OCD and ADHD symptom patterns were examined in TS patients and their family members (N = 3494) using exploratory factor analyses (EFA) for OCD and ADHD symptoms separately, followed by latent class analyses (LCA) of the resulting OCD and ADHD factor sum scores jointly; heritability and clinical relevance of the resulting factors and classes were assessed.
EFA yielded a 2-factor model for ADHD and an 8-factor model for OCD. Both ADHD factors (inattentive and hyperactive/impulsive symptoms) were genetically related to TS, ADHD, and OCD. The doubts, contamination, need for sameness, and superstitions factors were genetically related to OCD, but not ADHD or TS; symmetry/exactness and fear-of-harm were associated with TS and OCD while hoarding was associated with ADHD and OCD. In contrast, aggressive urges were genetically associated with TS, OCD, and ADHD. LCA revealed a three-class solution: few OCD/ADHD symptoms (LC1), OCD & ADHD symptoms (LC2), and symmetry/exactness, hoarding, and ADHD symptoms (LC3). LC2 had the highest psychiatric comorbidity rates (⩾50% for all disorders).
Symmetry/exactness, aggressive urges, fear-of-harm, and hoarding show complex genetic relationships with TS, OCD, and ADHD, and, rather than being specific subtypes of OCD, transcend traditional diagnostic boundaries, perhaps representing an underlying vulnerability (e.g. failure of top-down cognitive control) common to all three disorders.
Genetic–epidemiological studies that estimate the contributions of genetic factors to variation in tic symptoms are scarce. We estimated the extent to which genetic and environmental influences contribute to tics, employing various phenotypic definitions ranging between mild and severe symptomatology, in a large population-based adult twin-family sample.
In an extended twin-family design, we analysed lifetime tic data reported by adult mono- and dizygotic twins (n = 8323) and their family members (n = 7164; parents and siblings) from 7311 families in the Netherlands Twin Register. We measured tics by the abbreviated version of the Schedule for Tourette and Other Behavioral Syndromes. Heritability was estimated by genetic structural equation modeling for four tic disorder definitions: three dichotomous and one trichotomous phenotype, characterized by increasingly strictly defined criteria.
Prevalence rates of the different tic disorders in our sample varied between 0.3 and 4.5% depending on tic disorder definition. Tic frequencies decreased with increasing age. Heritability estimates varied between 0.25 and 0.37, depending on phenotypic definitions. None of the phenotypes showed evidence of assortative mating, effects of shared environment or non-additive genetic effects.
Heritabilities of mild and severe tic phenotypes were estimated to be moderate. Overlapping confidence intervals of the heritability estimates suggest overlapping genetic liabilities between the various tic phenotypes. The most lenient phenotype (defined only by tic characteristics, excluding criteria B, C and D of DSM-IV) rendered sufficiently reliable heritability estimates. These findings have implications in phenotypic definitions for future genetic studies.
Limited evidence has suggested that quitting smoking increases the incidence of major depressive episodes (MDEs), particularly for smokers with a history of depression. Further evidence for this increase would have important implications for guiding smoking cessation.
Spanish- and English-speaking smokers without a current MDE (n=3056) from an international, online smoking cessation trial were assessed for abstinence 1 month after their initial quit date and followed for a total of 12 months. Incidence of screened MDE was examined as a function of abstinence and depression history.
Continued smoking, not abstinence, predicted MDE screened at 1 month [smoking 11.5% v. abstinence 7.8%, odds ratio (OR) 1.36, 95% confidence interval (CI) 1.04–1.78, p=0.02] but not afterwards (smoking 11.1% v. abstinence 9.8%, OR 1.05, 95% CI 0.77–1.45, p=0.74). Depression history predicted MDE screened at 1 month (history 17.1% v. no history 8.6%, OR 1.71, 95% CI 1.29–2.27, p<0.001) and afterwards (history 21.7% v. no history 8.3%, OR 3.87, 95% CI 2.25–6.65, p<0.001), although the interaction between history and abstinence did not.
Quitting smoking was not associated with increased MDE, even for smokers with a history of depression, although a history of depression was. Instead, not quitting was associated with increased MDE shortly following a quit attempt. Results from this online, large, international sample of smokers converge with similar findings from smaller, clinic-based samples, suggesting that in general, quitting smoking does not increase the incidence of MDEs.
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