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Background: Hyperactivity and inattention, the symptoms of ADHD, are marked by high levels of heritability and intergenerational transmission. Two distinct pathways of genetic intergenerational transmission are distinguished: direct genetic transmission when parental genetic variants are passed to the child's genome and genetic nurture when the parental genetic background contributes to the child's outcomes through rearing environment. This study assessed genetic contributions to hyperactivity and inattention in childhood through these transmission pathways. Methods: The sample included 415 families from the Quebec Newborn Twin Study. Twins' hyperactivity and inattention were assessed in early childhood by parents and in primary school by teachers. The polygenic scores for ADHD (ADHD-PGS) and educational attainment (EA-PGS) were computed from twins' and parents' genotypes. A model of intergenerational transmission was developed to estimate (1) the contributions of parents' and children's PGS to the twins' ADHD symptoms and (2) whether these variances were explained by genetic transmission and/or genetic nurture. Results: ADHD-PGS explained up to 1.6% of the variance of hyperactivity and inattention in early childhood and primary school. EA-PGS predicted ADHD symptoms at both ages, explaining up to 1.6% of the variance in early childhood and up to 5.5% in primary school. Genetic transmission was the only significant transmission pathway of both PGS. The genetic nurture channeled through EA-PGS explained up to 3.2% of the variance of inattention in primary school but this association was non-significant. Conclusions: Genetic propensities to ADHD and education predicted ADHD symptoms in childhood, especially in primary school. Its intergenerational transmission was driven primarily by genetic variants passed to the child, rather than by environmentally mediated parental genetic effects. The model developed in this study can be leveraged in future research to investigate genetic transmission and genetic nurture while accounting for parental assortative mating.
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Study Objective: To investigate whether childhood sleep trajectories are associated with mental health symptoms such as social phobia, generalized anxiety, depression, attention deficit hyperactivity disorder (ADHD), conduct problems, and opposition at age 15. Methods: A total of 2120 children took part in the Quebec Longitudinal Study of Child Development. Childhood sleep trajectories were computed from maternal reports at 2.5, 3.5, 4, 6, 8, 10, and/or 12 years. At age 15, 1446 adolescents filled out mental health and sleep questions. A path analysis model was assessed in the full sample. Results: Four childhood nocturnal sleep duration trajectories were identified: (1) a short pattern (7.5%), (2) a short-increasing pattern (5.8%), (3) a 10 hours pattern (50.7%), and (4) an 11 hours pattern (36.0%). Three childhood sleep latency trajectories were found: (1) a short pattern (31.7%), (2) an intermediate pattern (59.9%), and (3) a long pattern (8.4%). Finally, two childhood wakefulness after sleep-onset trajectories were found: (1) a normative pattern (73.0%) and (2) a long pattern (27.0%). The path analysis model indicated that children following a long childhood sleep latency trajectory were more likely to experience symptoms of depression (ßâ =â 0.06, 95% CI: 0.01 to 0.12), ADHD (ßâ =â 0.07, 95% CI: 0.02 to 0.13), conduct problems (ßâ =â 0.05, 95% CI: 0.00 to 0.10) and opposition (ßâ =â 0.08, 95% CI: 0.02 to 0.13) at age 15. Conclusions: This longitudinal study revealed that children presenting a long sleep latency throughout childhood are at greater risk of symptoms of depression, ADHD, conduct problems, and opposition in adolescence.
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INTRODUCTION: Research shows that parental alcohol use predicts youths' alcohol use, but this intergenerational continuity may vary across countries, and little is known about its moderators. This study examined for the first time the intergenerational continuity in alcohol use in a population sample of families in Canada, and tested whether it varied by youths' sex, family income, or family structure. METHODS: We used prospective longitudinal data on 1632 families from the Quebec Longitudinal Study of Child Development (QLSCD), a representative sample from the province of Quebec, Canada. Youths self-reported alcohol use and binge drinking frequency at seven timepoints from early adolescence to early adulthood. Predictors were mothers' and fathers' self-reported alcohol use from youths' infancy through age 13, and mother-reported socioeconomic variables. RESULTS: We identified three trajectories of alcohol use from ages 13 to 21 years: normative, late-onset and early-onset. Maternal alcohol use increased the youths' risk of following the early-onset trajectory of alcohol use, while both parents' alcohol use decreased the odds of the youths following the late-onset trajectory, compared to the normative trajectory. Insufficient family income increased youths' risk of following either the early-onset or late-onset trajectories. Mothers' and fathers' alcohol use did not interact in predicting youths' trajectory, and we found no moderating effects of the youths' sex, insufficient income, or years as a single-parent family. CONCLUSION: The results suggest modest intergenerational continuity of alcohol use in Quebec families which may be used, with income insufficiency, to help identify at-risk children for targeted interventions.