Single Nucleotide Polymorphism Heritability of a General Psychopathology Factor in Children

Neumann, Alexander; Pappa, Irene; Lahey, Benjamin B.; Verhulst, Frank C.; Medina‐Gomez, Carolina; Jaddoe, Vincent W. V.; Bakermans‐Kranenburg, Marian J.; Moffitt, Terrie E.; IJzendoorn, Marinus H. van; Tiemeier, Henning

doi:10.1016/j.jaac.2016.09.498

Cited by 123 publications

(153 citation statements)

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“…This structure has replicated in multiple youth samples (e.g., Castellanos-Ryan et al, 2016; Martel et al, 2017; Neumann et al, 2016; Snyder, Young, & Hankin, 2017; Tackett et al, 2013; Waldman, Poore, van Hulle, Rathouz, & Lahey, 2016). Converging evidence demonstrates the p factor is moderately heritable (Neumann et al, 2016; Waldman et al, 2016), has strong distress-related psychopathology loadings (Waldman et al, 2016) and is associated with negative emotionality (Castellanos-Ryan et al, 2016; Tackett et al, 2013) and poor executive function (Castellanos-Ryan et al, 2016; Huang-Pollock, Shapiro, Galloway-Long, & Weigard, 2016; Martel et al, 2017). Thus, one way to conceptualize the p factor is as shared (partially genetic) liability for psychopathology, characterized by transdiagnostic distress, potentially through the endophenotype of poorly-regulated emotion and cognition (e.g., Beauchaine & Zisner, 2017).…”

mentioning

confidence: 78%

Chronic Stress Exposure and Generation Are Related to the P-Factor and Externalizing Specific Psychopathology in Youth

Snyder

Young

Hankin

2017

Journal of Clinical Child & Adolescent Psychology

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Objective Psychopathology is posited to be transdiagnostically linked to chronic stress. Yet efforts to understand the specificity and directionality of these links have been sparse, and the ubiquitous comorbidity of psychopathology has made the seemingly non-specific links between psychological disorders and chronic stress difficult to interpret. The current study used a latent dimensional bifactor model of psychopathology to account for comorbidity and a multi-wave prospective design to disentangle temporal associations between psychopathology and chronic stress longitudinally during the critical adolescent period for psychopathology risk and stress reactivity. Method A community sample of 567 youth (55.5% female, age M=11.8 at baseline, M=15.1 at end of study) were followed prospectively for three years, with chronic stress assessed with the Youth Life Stress Interview and psychopathology symptoms assessed via both self and parent report. Results Exposure to chronic stress predicted what is common across forms of psychopathology (the p factor), which in turn predicted generation of chronic stress over time. After accounting for comorbidity via the p factor, externalizing behaviors also had specific transactional links to chronic stress, whereas links between internalizing psychopathology and chronic stress were completely accounted for by common psychopathology. Conclusions The results provide the first direct evidence that chronic stress is transdiagnostically and reciprocally linked to psychopathology, during a critical youth period for psychopathology onset and stress reactivity.

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mentioning

confidence: 78%

Chronic Stress Exposure and Generation Are Related to the P-Factor and Externalizing Specific Psychopathology in Youth

Snyder

Young

Hankin

2017

Journal of Clinical Child & Adolescent Psychology

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“…Genetic influences on the general factor were moderate (h 2 = .43), with moderate shared environmental influences (c 2 = .25) and nonshared environmental influences as well (e 2 = .32). Consistent with these estimates, the heritability of a general factor of psychopathology was estimated from single nucleotide polymorphisms to be .37 in a large representative sample of children (Neumann et al, in press). …”

Section: Genetic and Environmental Structure Of Psychopathologymentioning

confidence: 91%

A hierarchical causal taxonomy of psychopathology across the life span.

Lahey¹,

Krueger²,

Rathouz³

et al. 2017

Psychological Bulletin

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We propose a taxonomy of psychopathology based on patterns of shared causal influences identified in a review of multivariate behavior genetic studies that distinguish genetic and environmental influences that are either common to multiple dimensions of psychopathology or unique to each dimension. At the phenotypic level, first-order dimensions are defined by correlations among symptoms; correlations among first-order dimensions similarly define higher-order domains (e.g., internalizing or externalizing psychopathology). We hypothesize that the robust phenotypic correlations among first-order dimensions reflect a hierarchy of increasingly specific etiologic influences. Some nonspecific etiologic factors increase risk for all first-order dimensions of psychopathology to varying degrees through a general factor of psychopathology. Other nonspecific etiologic factors increase risk only for all first-order dimensions within a more specific higher-order domain. Furthermore, each first-order dimension has its own unique causal influences. Genetic and environmental influences common to family members tend to be nonspecific, whereas environmental influences unique to each individual are more dimension-specific. We posit that these causal influences on psychopathology are moderated by sex and developmental processes. This causal taxonomy also provides a novel framework for understanding the heterogeneity of each first-order dimension: Different persons exhibiting similar symptoms may be influenced by different combinations of etiologic influences from each of the three levels of the etiologic hierarchy. Furthermore, we relate the proposed causal taxonomy to transdimensional psychobiological processes, which also impact the heterogeneity of each psychopathology dimension. This causal taxonomy implies the need for changes in strategies for studying the etiology, psychobiology, prevention, and treatment of psychopathology.

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“…One study estimated the SNPheritability as 18% for maternal ratings of total problems on the Child Behavior Checklist, which measures internalizing, externalizing, and attention problems [35]. Similarly, another study estimated the SNP heritability as 38% for a general psychopathology factor derived from childhood psychopathology symptoms assessed by multiple raters [36]. These studies also support spectrum-specific genetic factors, such as genetic factors that load specifically on externalizing disorders [31].…”

Section: Psychiatric Comorbiditymentioning

confidence: 97%

Genetics of attention deficit hyperactivity disorder

2018

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Decades of research show that genes play an vital role in the etiology of attention deficit hyperactivity disorder (ADHD) and its comorbidity with other disorders. Family, twin, and adoption studies show that ADHD runs in families. ADHD's high heritability of 74% motivated the search for ADHD susceptibility genes. Genetic linkage studies show that the effects of DNA risk variants on ADHD must, individually, be very small. Genome-wide association studies (GWAS) have implicated several genetic loci at the genome-wide level of statistical significance. These studies also show that about a third of ADHD's heritability is due to a polygenic component comprising many common variants each having small effects. From studies of copy number variants we have also learned that the rare insertions or deletions account for part of ADHD's heritability. These findings have implicated new biological pathways that may eventually have implications for treatment development.Attention deficit hyperactivity disorder (ADHD) is a childhood-onset condition with impairing symptoms of inattention, impulsivity, and hyperactivity. Decades of research have documented and replicated key facts about the disorder (for a review, see ref.[1]). It occurs in about 5% of children with little geographic or cross-cultural variation in prevalence and often co-occurs with other conditions, including mood, anxiety, conduct, learning, and substance use disorders. Longitudinal studies show that two-thirds of ADHD youth will continue to have impairing symptoms of ADHD in adulthood. People with ADHD are at risk for a wide range of functional impairments: school failure, peer rejection, injuries due to accidents, criminal behavior, occupational failure, divorce, suicide, and premature death. Although many details of ADHD's pathophysiology are unknown, neuropsychological and neuroimaging studies implicate brain circuits regulating executive functioning, reward processing, timing, and temporal information processing.This article reviews data about the role that genes play in the etiology of ADHD from two perspectives. Family, twin, and adoption studies provide a firm foundation for asserting that genes are involved in the etiology of ADHD. The view from molecular genetics provides a basis for understanding mechanisms whereby genes affect biological pathways that lead to ADHD. Family, twin and adoption studies of ADHDEvidence for heritability from family, adoption, and twin studies A study of 894 ADHD probands and 1135 of their siblings aged 5-17 years old found a ninefold increased risk of ADHD in siblings of ADHD probands compared with siblings of controls [2]. Adoption studies suggest that the familial factors of ADHD are attributable to genetic factors rather than shared environmental factors [3,4] with the most recent one reporting rates of ADHD to be greater among biological relatives of non-adopted ADHD children than adoptive relatives of adopted ADHD children. The adoptive relatives had a risk for ADHD like the risk in relatives of control childr...

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Single Nucleotide Polymorphism Heritability of a General Psychopathology Factor in Children

Cited by 123 publications

References 37 publications

Chronic Stress Exposure and Generation Are Related to the P-Factor and Externalizing Specific Psychopathology in Youth

Chronic Stress Exposure and Generation Are Related to the P-Factor and Externalizing Specific Psychopathology in Youth

A hierarchical causal taxonomy of psychopathology across the life span.

Genetics of attention deficit hyperactivity disorder

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