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Why do depression, conduct, and hyperactivity symptoms co-occur across adolescence? The role of stable and dynamic genetic and environmental influences.

ABSTRACT: Depression, conduct, and hyperactivity symptoms are chronic and frequently co-occur in adolescence. Common genetic and environmental vulnerability to these conditions have previously been demonstrated, however, the manner in which common versus disorder-specific etiological influences operate across development and maintain symptom co-occurrence is unclear. Thus, the current study investigated the role of common genetic and environmental influences in the comorbidity of depression, conduct, and hyperactivity across adolescence. Over 10,000 twins and their parents reported adolescents' symptoms at mean ages 11 and 16 years. Biometric independent pathway models were fitted to estimate genetic and environmental contributions to the continuity of symptom co-occurrence over time, as well as time- and symptom-specific influences. Results found that a common stable genetic factor accounted for the concurrent and longitudinal co-occurrence of depression, conduct, and hyperactivity symptoms. New genetic influences common to these three symptom scales emerged at 16 years, and further contributed to symptom co-occurrence. Conversely, environmental influences largely contributed to the time-specific associations. The findings were generally consistent for self- and parent-reported symptoms. Overall, the results suggest that stable, overlapping genetic influences contribute to the co-occurrence of depression, conduct, and hyperactivity symptoms across adolescence. The results are in line with hierarchical causal models of psychopathology, which posit that much of the developmental co-occurrence between different symptoms is due to common liability. Specifically, current findings indicate that only genetic influences constitute common liability over time. Future studies should identify genetically influenced transdiagnostic risk and maintenance factors to inform prevention and treatment of comorbid internalizing and externalizing symptoms in adolescence.

SUBMITTER: Waszczuk MA

PROVIDER: S-EPMC8295149 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:IMPORTANCE:Attention-deficit/hyperactivity disorder (ADHD) is conceptualized as a neurodevelopmental disorder that is strongly heritable. However, to our knowledge, no study to date has examined the genetic and environmental influences explaining interindividual differences in the developmental course of ADHD symptoms from childhood to adolescence (ie, systematic decreases or increases with age). The reason ADHD symptoms persist in some children but decline in others is an important concern, with implications for prognosis and interventions. OBJECTIVE:To assess the proportional impact of genes and the environment on interindividual differences in the developmental course of ADHD symptom domains of hyperactivity/impulsivity and inattention between ages 8 and 16 years. DESIGN, SETTING, AND PARTICIPANTS:A prospective sample of 8395 twin pairs from the Twins Early Development Study, recruited from population records of births in England and Wales between January 1, 1994, and December 31, 1996. Data collection at age 8 years took place between November 2002 and November 2004; data collection at age 16 years took place between February 2011 and January 2013. MAIN OUTCOMES AND MEASURES:Both DSM-IV ADHD symptom subscales were rated 4 times by participants' mothers. RESULTS:Estimates from latent growth curve models indicated that the developmental course of hyperactivity/impulsivity symptoms followed a sharp linear decrease (mean score of 6.0 at age 8 years to 2.9 at age 16 years). Interindividual differences in the linear change in hyperactivity/impulsivity were under strong additive genetic influences (81%; 95% CI, 73%-88%). More than half of the genetic variation was specific to the developmental course and not shared with the baseline level of hyperactivity/impulsivity. The linear decrease in inattention symptoms was less pronounced (mean score of 5.8 at age 8 years to 4.9 at age 16 years). Nonadditive genetic influences accounted for a substantial amount of variation in the developmental course of inattention symptoms (54%; 95% CI, 8%-76%), with more than half being specific to the developmental course. CONCLUSIONS AND RELEVANCE:The large genetic influences on the developmental course of ADHD symptoms are mostly specific and independent of those that account for variation in the baseline level of symptoms. Different sets of genes may be associated with the developmental course vs the baseline level of ADHD symptoms and explain why some children remit from ADHD, whereas others persist. Recent longitudinal imaging data indicate that the maintenance or increase in symptoms is underpinned by atypical trajectories of cortical development. This may reflect a specific genetic liability, distinct from that which contributes to baseline ADHD symptoms, and warrants closer follow-up.

Project description:Decades of research into the etiology of conduct disorder (CD) has yet to yield a consensus on the existence of sex differences in underlying genetic and environmental influences. This may be partly due to the failure of many previous studies to make a distinction between non-aggressive and aggressive CD symptoms or test for potential developmental changes in sex differences in the etiology of conduct problems. To address these gaps, we fit a series of univariate and bivariate biometric sex-difference models to self-reported non-aggressive and aggressive CD symptoms in a community-based sample of twins (N = 1548, ages 9-17 year), grouped into ages 9-13 and 14-17 years. Relative model fit was evaluated using the Bayesian Information Criterion (BIC), which favors parsimony, and by Chi square difference tests. The univariate sex-scalar model provided the best fit to the data for both non-aggressive and aggressive CD symptoms at ages 9-13 and 14-17 years. Thus, the same genetic and environmental factors influenced CD symptoms in both sexes, but the total variability was lower in females than males. At both ages, the heritability of non-aggressive CD symptoms was lower than heritability of aggressive CD symptoms, and shared environmental effects were only observed for non-aggressive CD symptoms. However, estimates for genetic and environmental factors could be not be constrained to be equal across age groups for either CD subtype, suggesting substantive developmental changes in the relative influence of genetic and environmental factors on individual differences in CD symptoms. For both subtypes, the heritability was larger, and shared environmental effect smaller, in the older age group than the younger age group. A bivariate quantitative sex differences model provided the best fit to the data at ages 9-13 years. Covariation between non-aggressive and aggressive CD symptoms was due to overlapping shared and non-shared environmental factors in males and females but the overall covariation was greater in males than females. In contrast, at ages 14-17 years, the sex-scalar bivariate model provided the best fit to the data, and covariation between non-aggressive and aggressive CD symptoms was due to overlapping genetic and non-shared environmental factors. Thus, the etiology of self-reported conduct disorder varied substantially by symptom type and age. However, quantitative sex differences were only apparent when the covariation between the two subtypes was considered.

Project description:BackgroundPsychotic experiences (PEs) such as paranoia and hallucinations, and negative symptoms (NS) such as anhedonia and flat affect are common in adolescence. Psychotic experiences and negative symptoms (PENS) increase risk for later psychiatric outcomes, particularly when they persist. The extent to which genetic and environmental influences contribute to the stability of PENS in mid-to-late adolescence is unknown.MethodsUsing the Specific Psychotic Experiences Questionnaire (SPEQ) twice across ~9 months in adolescence, N = 1,448 twin pairs [M = 16.32 (0.68)] reported experiences of paranoia, hallucinations, cognitive disorganization, grandiosity and anhedonia, and their parents reported on a range of NS. Individuals were split into low-scoring, decreasing, increasing and persistent groups for each subscale. Frequencies and mean differences in distress, depression traits and emotional problems were investigated across groups. Longitudinal structural equation modelling was used to estimate the aetiological components underlying the stability of PENS.ResultsPhenotypic stability was moderate for all PENS (r = .59-.69). Persistent PENS across 9 months were associated with greater levels of distress (V = 0.15-0.46, for PEs only), depression traits (d = 0.47-1.67, except grandiosity) and emotional problems (d = 0.47-1.47, except grandiosity and anhedonia) at baseline compared to groups with transitory or low levels of PENS. At both ages PENS were heritable and influenced by shared and nonshared environment. Genetic influences contributed 38%-62% and shared environment contributed 13%-33% to the stability of PENS. Nonshared environment contributed 34%-41% (12% for parent-rated NS). There was strong overlap of genetic and shared environmental influences across time, and lower overlap for nonshared environment. Imperfect stability of PENS was at least partly due to nonshared environmental influences.ConclusionsWhen adolescent PENS persist over time, they are often characterized by more distress, and higher levels of other psychopathology. Both genetic and environmental effects influence stability of PENS.

Project description:ImportanceLess favorable trajectories of depressive mood from adolescence to early adulthood are associated with current and later psychopathology, impaired educational attainment, and social dysfunction, yet the genetic and environmental risk factors associated with these trajectories are not fully established. Examining what risk factors are associated with different trajectories of depressive mood could help identify the nature of depression symptoms and improve preventive interventions for those at most risk.ObjectiveTo examine the differential associations of genetic and environmental risk factors with trajectories of depression symptoms among individuals observed from ages 10 to 24 years.Design, setting, and participantsIn a longitudinal cohort study established in 1990 and currently ongoing (the Avon Longitudinal Study of Parents and Children [ALSPAC]), growth mixture modeling was used to identify trajectories of depression symptoms in 9394 individuals in the United Kingdom. Associations of different risk factors with these trajectories were then examined. Analysis was conducted between August 2018 and January 2019.Main outcomes and measuresTrajectories were composed from depression symptoms measured using the Short Mood and Feelings Questionnaire at 9 occasions from ages 10 to 24 years. Risk factors included sex, a polygenic risk score taken from a recent genome-wide association study of depression symptoms, maternal postnatal depression, partner cruelty to the offspring's mother when the child was aged 2 to 4 years, childhood anxiety at age 8 years, and being bullied at age 10 years.ResultsData on all risk factors, confounders, and the outcome were available for 3525 individuals, including 1771 (50.2%) who were female. Trajectories were assessed between the mean (SD) age of 10.7 (0.3) years and mean (SD) age of 23.8 (0.5) years. Overall, 5 distinct trajectories of depression symptoms were identified: (1) stable low (2506 individuals [71.1%]), (2) adolescent limited (325 individuals [9.2%]), (3) childhood limited (203 individuals [5.8%]), (4) early-adult onset (393 individuals [11.1%]), and (5) childhood persistent (98 individuals [2.8%]). Of all the associations of risk factors with trajectories, sex (odds ratio [OR], 6.45; 95% CI, 2.89-14.38), the polygenic risk score for depression symptoms (OR, 1.47; 95% CI, 1.10-1.96), and childhood anxiety (OR, 1.30; 95% CI, 1.16-1.45) showed the strongest association with the childhood-persistent trajectory of depression symptoms compared with the stable-low trajectory. Maternal postnatal depression (OR, 2.39; 95% CI, 1.41-4.07) had the strongest association with the early-adult-onset trajectory, while partner cruelty to mother (OR, 2.30; 95% CI, 1.36-3.90) had the strongest association with the adolescent-limited trajectory. Bullying (OR, 8.08; 95% CI, 4.92-13.26) showed the strongest association with the childhood-limited trajectory.Conclusions and relevanceThe least favorable trajectories of depression symptoms (childhood persistent and early-adult onset) were associated with both genetic and environmental risk factors, but the 2 trajectories of limited duration that had resolved by early adulthood (childhood limited and adolescent limited) were not associated with the polygenic risk score or maternal postnatal depression. Bullying was strongly associated with both the childhood-persistent and childhood-limited trajectories, suggesting that this risk factor may have a time-specific effect. These findings suggest that examining genetic and multiple time-specific environmental antecedents could help identify trajectories of varying onset and chronicity.

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Why do depression, conduct, and hyperactivity symptoms co-occur across adolescence? The role of stable and dynamic genetic and environmental influences.

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