Longitudinal Stability of the CBCL-Juvenile Bipolar Disorder Phenotype: A Study in Dutch Twins

Department of Biological Psychology, Vrije Universiteit, Amsterdam, The Netherlands.
Biological Psychiatry (Impact Factor: 10.26). 12/2006; 60(9):912-20. DOI: 10.1016/j.biopsych.2006.02.028
Source: PubMed


The Child Behavior Checklist-juvenile bipolar disorder phenotype (CBCL-JBD) is a quantitative phenotype that is based on parental ratings of the behavior of the child. The phenotype is predictive of DSM-IV characterizations of BD and has been shown to be sensitive and specific. Its genetic architecture differs from that for inattentive, aggressive, or anxious-depressed syndromes. The purpose of this study is to assess the developmental stability of the CBCL-JBD phenotype across ages 7, 10, and 12 years in a large population-based twin sample and to examine its genetic architecture.
Longitudinal data on Dutch mono- and dizygotic twin pairs (N = 8013 pairs) are analyzed to decompose the stability of the CBCL-JBD phenotype into genetic and environmental contributions.
Heritability of the CBCL-JBD increases with age (from 63% to 75%), whereas the effects of shared environment decrease (from 20% to 8%). The stability of the CBCL-JBD phenotype is high, with correlations between .66 and .77 across ages 7, 10, and 12 years. Genetic factors account for the majority of the stability of this phenotype. There were no sex differences in genetic architecture.
Roughly 80% of the stability in childhood CBCL-JBD is a result of additive genetic effects.

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    • "Twin studies reported relatively high heritability of emotional dysregulation, which ranges from 60% to 80%, depending on the age group of the sample (Althoff et al., 2006; Boomsma et al., 2006; Hudziak et al., 2005; Volk and Todd, 2007). Additive genetic and shared environmental factors represent the major contributions to the variation of this clinical phenotype, with the latter being greater in the youngest children (Boomsma et al., 2006; Hudziak et al., 2005). Although twin studies provide evidence Contents lists available at ScienceDirect journal homepage: www.elsevier.com/locate/jad "
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    ABSTRACT: Background: Two different polymorphisms (TPH2 G-703T and 5-HTTLPR) involved in the serotonergic pathway have been reported to play a role, both alone and in interaction with the environment, in early and adult emotion regulation. As most of these studies are cross-sectional, we know little about the impact of these polymorphisms over time, particularly during adolescence. Methods: Because we were interested in the effects of these polymorphisms and environment (i.e., family structure) at different time-points on the emotional dysregulation profile, we performed a path analysis model in a general adolescent population sample of a five-year follow-up study. Results: We found a high stability of Dysregulation Profile problems independently from the examined allelic variants. We also found that early family structure directly influences the levels of dysregulation problems in early adolescence, both alone and in interaction with TPH2, suggesting the presence of a gene-environment interaction effect. Furthermore, we found that in adolescents homozygous for the TPH2 G allele, the effect of the early family structure remains active during late adolescence, albeit mediated by earlier emotional problems. Limitations: The high attrition rate, the use of only one source on behavioral problems of adolescents, and the focus on a single polymorphism in the investigated genes could limit the generalizability of the present results. Conclusions: These results suggest that early family structure could play a significant role in the development and maintenance of emotional and behavioral problems not only in early adolescence but also in late-adolescence, although this effect was mediated and moderated by behavioral and genetic variables.
    Journal of Affective Disorders 11/2015; 190. DOI:10.1016/j.jad.2015.10.057 · 3.38 Impact Factor
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    • "The childhood dysregulation syndrome has been found to predict negative outcomes in adolescence and adulthood including: anxiety, mood and disruptive behavior disorders, drug abuse (Althoff et al. 2010), suicidality (Holtmann et al. 2011b) and personality disorders (Halperin et al. 2011). Further , research suggests that the childhood dysregulation profile is a stable feature throughout childhood (at 7, 10 and 12 years) (Boomsma et al. 2006). Despite growing interest in the childhood dysregulation syndrome, to our knowledge there are no existing studies exploring whether infant and toddler RPs predict this syndrome . "
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    ABSTRACT: Infant and toddler regulatory problems (RPs) including crying, sleeping and feeding, are a frequent concern for parents and have been associated with negative behavioral outcomes in early and middle childhood. Uncertain is whether infant and toddler RPs predict stable, trait-like dysregulated behavior across childhood. We addressed this gap in the literature using data from the Avon Longitudinal Study of Parents and Children (ALSPAC). RPs at 6, 15-18, & 24-30 months and childhood dysregulated behavior at 4, 7, 8, & 9.5 years were assessed using mother report. Latent Class Growth Analysis (LCGA) indicated that trajectories of childhood dysregulated behavior were stable over time. All single RPs (i.e., crying, sleeping & feeding problems) were significantly associated with childhood dysregulated behavior. For example, crying problems at 6 months after controlling for confounders (Odds Ratios; 95 % Confidence Intervals): Moderate dysregulated behavior: OR = 1.50, 95 % CI [1.09 to 2.06], high dysregulated behavior: OR = 2.13, 95 % CI [1.49 to 3.05] and very high dysregulated behavior: OR = 2.85, 95 % CI [1.64 to 4.94]. Multiple RPs were especially strongly associated with dysregulated behavior. For example, the RP composite at 15-18 months: 1 RP, very high dysregulated behavior: OR = 2.79, 95 % CI [2.17 to 3.57], 2 RPs, very high dysregulated behavior: OR = 3.46, 95 % CI [2.38 to 5.01], 3 RPs, very high dysregulated behavior: OR = 12.57, 95 % CI [6.38 to 24.74]. These findings suggest that RPs in infants and toddlers predict stable dysregulated behavior trajectories across childhood. Interventions for early RPs could help prevent the development of chronic, highly dysregulated behavior.
    Journal of Abnormal Child Psychology 10/2013; 42(5). DOI:10.1007/s10802-013-9813-1 · 3.09 Impact Factor
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    • "is study contributes to the literature on long-term behavioral risk in the adolescent children of teenage mothers. ere are several reasons to expect a higher prevalence of DP in the offspring of teenage mothers than in the general population, including evidence of a strong genetic component [5]. Aside from genetic loading, the children of teenage mothers may experience different rearing environments than children of older mothers, which may also contribute to behavioral dysregulation [55]. "
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    ABSTRACT: Background. Offspring of teenage mothers are at greater risk of early drug use. Research has identified a child behavior checklist (CBCL) profile for children with high levels of comorbid behavior problems, the dysregulation profile (DP), as another risk factor for drug use. Method. Teenage girls (12–18 years old; 71% African-American, 29% White) were recruited during pregnancy. Data were collected during pregnancy and when offspring were 6, 10, and 14 years old ( 𝑛 = 3 1 8 ). Mothers completed the CBCL when children were at ages 6 and 10, and children who scored 60 or higher on all 3 DP subscales (aggression, anxiety/depression, and attention problems) were categorized as dysregulated. At ages 10 and 14, the offspring (50% male, 50% female) reported on their cannabis use and completed the childhood depression inventory (CDI). Results. DP at age 6 and depressive symptoms at age 14 predicted recent cannabis use in the offspring. There was a significant interaction between race and pubertal timing such that White offspring who matured earlier were at greater risk of recent cannabis use. Conclusions. The results of this study suggest that it may be possible to identify a subset of children at risk of dual diagnosis as early as age 6.
    11/2012; 2013(4). DOI:10.1155/2013/659313
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