| 1. |
- Sujan, Ayesha C., et al.
(författare)
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A Genetically Informed Study of the Associations Between Maternal Age at Childbearing and Adverse Perinatal Outcomes
- 2016
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Ingår i: Behavior Genetics. - New York, USA : Springer. - 0001-8244 .- 1573-3297. ; 46:3, s. 431-456
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Tidskriftsartikel (refereegranskat)abstract
- We examined associations of maternal age at childbearing (MAC) with gestational age and fetal growth (i.e., birth weight adjusting for gestational age), using two genetically informed designs (cousin and sibling comparisons) and data from two cohorts, a population-based Swedish sample and a nationally representative United States sample. We also conducted sensitivity analyses to test limitations of the designs. The findings were consistent across samples and suggested that, associations observed in the population between younger MAC and shorter gestational age were confounded by shared familial factors; however, associations of advanced MAC with shorter gestational age remained robust after accounting for shared familial factors. In contrast to the gestational age findings, neither early nor advanced MAC was associated with lower fetal growth after accounting for shared familial factors. Given certain assumptions, these findings provide support for a causal association between advanced MAC and shorter gestational age. The results also suggest that there are not causal associations between early MAC and shorter gestational age, between early MAC and lower fetal growth, and between advanced MAC and lower fetal growth.
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| 2. |
- Wiggs, Kelsey K., et al.
(författare)
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A Family-Based Study of the Association Between Labor Induction and Offspring Attention-Deficit Hyperactivity Disorder and Low Academic Achievement
- 2017
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Ingår i: Behavior Genetics. - Stockholm : Springer. - 0001-8244 .- 1573-3297. ; 47:4, s. 383-393
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Tidskriftsartikel (refereegranskat)abstract
- The current study examined associations between labor induction and both (1) offspring attention-deficit hyperactivity disorder (ADHD) diagnosis in a Swedish birth cohort born 1992-2005 (n = 1,085,008) and (2) indices of offspring low academic achievement in a sub-cohort born 1992-1997 (n = 489,196). Associations were examined in the entire sample (i.e., related and unrelated individuals) with adjustment for measured covariates and, in order to account for unmeasured confounders shared within families, within differentially exposed cousins and siblings. We observed an association between labor induction and offspring ADHD diagnosis and low academic achievement in the population. However, these associations were fully attenuated after adjusting for measured covariates and unmeasured factors that cousins and siblings share. The results suggest that observed associations between labor induction and ADHD and low academic achievement may be due to genetic and/or shared environmental factors that influence both mothers' risk of labor induction and offspring neurodevelopment.
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| 3. |
- Andersson, Anneli, 1992-, et al.
(författare)
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Genetic overlap between ADHD and externalizing, internalizing and neurodevelopmental disorder symptoms : a systematic review and meta-analysis
- 2018
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 48:6, s. 455-456
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Attention-Deficit/Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder (Wilens, Biederman & Spencer 2002) and affects approximately 5% of children (Polanczyk, de Lima, Horta, Biederman & Rohde 2007). About half of those diagnosed in childhood continue to have the diagnosis and symptoms in adulthood (Kessler et al. 2006). The co-occurrence of ADHD with other psychiatric disorder symptoms (Burt et al. 2001; Cole et al. 2009; Polderman et al. 2014) has been suggested to be partly explained by a shared genetic vulnerability (Polderman et al. 2014). However, the strength of the genetic overlap is currently unclear. Also, no study has examined whether the genetic correlations differs between age groups (childhood versus adulthood), by rater (self-report, other informant, combined (parent-teacher, parent-twin, teacher-twin)), or by type of psychiatric disorder symptoms (externalizing, internalizing, neu-rodevelopmental). To address this gap, we conducted a systematic literature search to identify relevant twin studies, in PubMed, PsycINFO, and EMBASE. A total of 31 articles were identified and included in the present study. The pooled estimates showed that the comorbidity between ADHD and diverse psychiatric disorder symptoms were explained by shared genetic effectsrg= 0.50 (0.43–0.56). A similar shared genetic overlap between ADHD and psychiatric disorder symptoms was observed in both childhood rg= 0.51(0.42–0.61) and adulthood rg= 0.47 (0.40–0.53). Similar results werealso found for self-reports rg= 0.49 (0.42–0.55), other informants rg= 0.50 (0.40–0.60), and combined raters rg= 0.51 (0.30–0.69). Further, the strength of the genetic correlations of ADHD with the externalizing rg= 0.49 (0.39–0.59), internalizing rg= 0.55 (0.40–0.68) and neurodevelopmental rg= 0.47 (0.40–0.53) spectrums were similar in magnitude. These findings emphasize the presence of a shared genetic liability between ADHD and externalizing, internalizing and neurodevelopmental disorder symptoms, independent of age and rater.ReferencesBurt, S. A., Krueger, R. F., McGue, M., Iacono, W. G. (2001).Sources of covariation among attention-deficit/hyperactivity disorder,oppositional defiant disorder, and conduct disorder: the importance ofshared environment.Journal of Abnormal Psychology, 4, 516–525.Cole, J., Ball, H. A., Martin, N. C., Scourfield, J., McGuffin, P.(2009). Genetic overlap between measures of hyperactivity/inatten-tion and mood in children and adolescents.J Am Acad Child AdolescPsychiatry48, 1094–1101.Kessler, R. C., Adler, L., Barkley, R., Biederman, J., Conners, C.K., Demler, O., Faraone, S. V., Greenhill, L. L., Howes, M. J., Secnik,K., Spencer, T., Ustun, T. B., Walters, E. E., Zaslavsky, A. M. (2006).The prevalence and correlates of adult ADHD in the United States:results from the National Comorbidity Survey Replication.Am JPsychiatry, 163, 716–723.Polanczyk, G., de Lima, M. S., Horta, B. L., Biederman, J., Rohde,L. A. (2007). The worldwide prevalence of ADHD: a systematicreview and metaregression analysis.Am J Psychiatry, 164, 942-8.Polderman, T. J., Hoekstra, R. A., Posthuma, D., Larsson, H.(2014). The co-occurrence of autistic and ADHD dimensions inadults: an etiological study in 17,770 twins.Transl Psychiatry2014;4: e435.Wilens, T. E., Biederman, J., Spencer, T. J. (2002). Attentiondeficit/hyperactivity disorder across the lifespan.Annual Review Med53:113–131.
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| 7. |
- Baker, Laura, et al.
(författare)
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The genetic and environmental etiology of internalizing and externalizing behavior in adolescent twins
- 2011
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Ingår i: Behavior Genetics. - : Springer Science and Business Media LLC. - 0001-8244 .- 1573-3297. ; 41:6, s. 927-927
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Comorbidity between internalizing (anxious, depressive) and externalizing (aggressive, delinquent) behavior is a well-established and common clinical reality throughout the lifespan, but perhaps becomes more significance in adolescence, when individuals are awarded more freedom. However, the genetic and environmental etiology of this comorbidity has rarely been examined in a behavioral genetic setting, especially during the period of adolescence. Additionally, research suggests that while caregivers may be more reliable reporters of externalizing behavior in youth, youth themselves are more reliable reporters of internalizing symptoms, raising the question of how different raters affect data patterns. Using the parent report Child Behavior Checklist (CBCL) as well as the youth report version (Youth Self Report—YSR), this research uses a twin study design to examine the etiology of coexisting internalizing and externalizing symptoms in mid adolescence (age 14–16 years) using a common pathway model that examined all data concurrently. Female comorbidity was accounted for by genetic and shared environmental influences, and male comorbidity by shared environmental influences, exclusively. Genetic influences emerged for all but self-report male externalizing behavior. Every scale showed unique influences as well, some of which were correlated between same-rater scales (e.g. parent report internalizing and externalizing), suggesting that some of the influences on covariation are rater-specific. These results contribute to our understanding of the nature of comorbid psychological disorders during adolescence, and suggest the importance of shared environment to the development of both internalizing and externalizing behavior
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| 8. |
- Baker, Laura, et al.
(författare)
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The Relationship between IQ and PM2.5 : Findings from the University of Southern California Twin Study
- 2016
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 46:6, s. 772-773
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Tidskriftsartikel (refereegranskat)abstract
- We examined the longitudinal relationship between IQ and fine particulate matter (\2.5lm aerodynamic diameters; PM2.5) exposure in urban-dwelling children, using prospective longitudinal data from the USC Twin Study of Risk Factors for Antisocial Behavior (RFAB; Baker et al. 2013). Residential addresses were collected via selfreports. Verbal and Performance IQ during childhood (age 9–10) and young adulthood (age 19–20) were evaluated by the Wechsler Abbreviated Intelligence Scale (Wechsler, 1999) using four subtests: VIQ=Vocabulary Similarities; PIQ=Block Design Matrices. Based on residential addresses and spatiotemporal generalized additive model of local monitoring data for PM2.5, we estimated 1-year average exposure before each assessment. A three-level mixed effects model regressing IQ scores at each assessment on time-varying air pollution exposures, accounting for both within-family (random intercepts) and within-individual (random slopes) was used. PM2.5 exposure had significant adverse effects on PIQ (95 % CI of b:-7.29 to-1.01, p\.05) but not VIQ (95 % CI of b:-4.50 to-1.96). Adverse effects of PM2.5 exposure remained significant after adjusting for age, family SES, sex, race/ethnicity, parental cognitive abilities, neighborhood SES, neighborhood quality and neighborhood greenness; the association was still significant after further adjusting for traffic distance (300 m), temperature, humidity and annual NOx. PM2.5 exposure confers stronger adverse effects on PIQ in low SES families, males, and during pre-adolescence. Our findings reveal social disparities and sexual dimorphism in the adverse PM2.5 exposure effects on PIQ. Baker, L., Tuvblad, C., Wang, P., Gomez, K., Bezdjian, S., Niv, S., & Raine, A. (2013). The Southern California Twin Register at the University of Southern California: III. Twin Research and Human Genetics, 16(1), 336–343; Wechsler, D. (1999). Wechsler Abbreviated Scale of Intelligence (WASI). San Antonio, Texas: Harcourt Assessment.
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| 9. |
- Baldwin, Jessie R., et al.
(författare)
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Adverse Childhood Experiences and Mental Health : A Genetically Informed Study
- 2021
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 51:6, s. 691-692
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Children exposed to adverse childhood experiences (ACEs) have an elevated risk of mental health problems, but it is unclear whether these associations reflect genetic confounding. We tested (1) whether children with genetic liability to psychopathology are more likely to experience ACEs, and (2) the extent to which the associations between ACEs and mental health are genetically confounded. Par-ticipants were 6411 children from the Avon Longitudinal Study of Parents and Children (ALSPAC). ACEs (including maltreatment, domestic violence, and parental psychopathology, substance abuse, criminality, and separation) were prospectively measured through parent reports at multiple assessments between birth and age 9. Internalizing and externalizing problems at age 9 were assessed through parent reports on the Development and Wellbeing Assessment. We derived polygenic scores for a range of psychiatric disorders. Children with greater genetic liability to psychopathology had a small elevation in risk of ACEs (pooled odds ratio = 1.05, 95% CI 1.01–1.09). Measured polygenic scores accounted for a very small proportion of the associations between ACEs with internalizing problems (pooled average across ACEs = 3.6%) and externalizing problems (pooled average = 4.8%). However, latent polygenic scores capturing SNP heritability in mental health outcomes explained a larger proportion of the associations between ACEs with internalizing problems (pooled average = 63%) and externalizing problems (pooled average = 17%). Risk of mental health problems in children exposed to ACEs is partly, but not completely driven by pre-existing genetic liability to psychopathology. Assuming the absence of nongenetic confounding, these findings are consistent with a partly causal effect of ACEs on mental health.
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| 11. |
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| 12. |
- Beam, Christopher R., et al.
(författare)
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Midlife study of the Louisville Twins : Connecting cognitive development to biological and cognitive aging
- 2020
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 50:2, s. 73-83
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Tidskriftsartikel (refereegranskat)abstract
- The Louisville Twin Study (LTS) began in 1958 and became a premier longitudinal twin study of cognitive development. The LTS continuously collected data from twins through 2000 after which the study closed indefinitely due to lack of funding. Now that the majority of the sample is age 40 or older (61.36%, N = 1770), the LTS childhood data can be linked to midlife cognitive functioning, among other physical, biological, social, and psychiatric outcomes. We report results from two pilot studies in anticipation of beginning the midlife phase of the LTS. The first pilot study was a participant tracking study, in which we showed that approximately 90% of the Louisville families randomly sampled (N = 203) for the study could be found. The second pilot study consisted of 40 in-person interviews in which twins completed cognitive, memory, biometric, and functional ability measures. The main purpose of the second study was to correlate midlife measures of cognitive functioning to a measure of biological age, which is an alternative index to chronological age that quantifies age as a function of the breakdown of structural and functional physiological systems, and then to relate both of these measures to twins’ cognitive developmental trajectories. Midlife IQ was uncorrelated with biological age (−.01) while better scores on episodic memory more strongly correlated with lower biological age (−.19 to −.31). As expected, midlife IQ positively correlated with IQ measures collected throughout childhood and adolescence. Additionally, positive linear rates of change in FSIQ scores in childhood significantly correlated with biological age (−.68), physical functioning (.71), and functional ability (−.55), suggesting that cognitive development predicts lower biological age, better physical functioning, and better functional ability. In sum, the Louisville twins can be relocated to investigate whether and how early and midlife cognitive and physical health factors contribute to cognitive aging.
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| 15. |
- Brikell, Isabell, et al.
(författare)
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The contribution of ADHD genetic risk to somatic health in late life
- 2019
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 49:6, s. 514-514
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Genetic risk variants associated with ADHD have been linked to comorbid psychiatric health problems, however less is known about how these genetic factors contribute to somatic health across the life-span. The aim of this study is to assess whether polygenic risk scores (PRS) for ADHD are associated with late-life somatic health problems in a general population sample never diagnosed with ADHD.We derived ADHD PRS for 15,701 Swedish twins born 1911–1958 using results from an independent ADHD genome-wide association study meta-analysis (Demontis et al, 2018). Somatic health outcomes in cardiovascular, metabolic, autoimmune, and neurological domains were defined via self-report in the Screening Across the Lifespan Twin study (Lichtenstein et al. 2006) and from clinical diagnoses in the National Swedish Patient Register. Associations between ADHD PRS and somatic health problems were estimated using generalized estimating equations.Higher ADHD PRS were associated with a small increased risk of coronary heart disease based on self-report (OR = 1.11, 95% CI = 1.02–1.20) and clinical diagnoses (OR = 1.09, 95% CI = 1.02–1.16), after false discovery rate correction. We also found statistically significant associations between ADHD PRS and obesity, type 1 diabetes, arthritis, psoriasis, and migraine, although results varied by information source. Our results suggest that polygenic risk for ADHD is associated with small increases to risk of somatic health problems in cardiovascular and autoimmune domains. These findings warrant further research into mechanisms influencing long-term health outcomes in ADHD. Next, we will test for mediation via socioeconomic variables, evaluate genetic causality using twin-comparison methods, and test for replication in a younger, clinical ADHD sample.
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| 16. |
- Burt, S. Alexandra, et al.
(författare)
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Additional evidence against shared environmental contributions to attention-deficit/hyperactivity problems
- 2012
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Ingår i: Behavior Genetics. - New York, USA : Springer. - 0001-8244 .- 1573-3297. ; 42:5, s. 711-721
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Tidskriftsartikel (refereegranskat)abstract
- A recent meta-analysis "Burt (Psychol Bull 135:608-637, 2009)" indicated that shared environmental influences (C) do not contribute to Attention-Deficit/Hyperactivity Disorder (ADHD). Unfortunately, the meta-analysis relied almost exclusively on classical twin studies. Although useful in many ways, some of the assumptions of the classical twin model (e.g., dominant genetic and shared environmental influences do not simultaneously influence the phenotype) can artifactually decrease estimates of C. There is thus a need to confirm that dominant genetic influences are not suppressing estimates of C on ADHD. The current study sought to do just this via the use of a nuclear twin family model, which allows researchers to simultaneously model and estimate dominant genetic and shared environmental influences. We examined two independent samples of child twins: 312 pairs from the Michigan State University Twin Registry and 854 pairs from the PrE School Twin Study in Sweden. Shared environmental influences were found to be statistically indistinguishable from zero and to account for less than 5 % of the variance. We conclude that the presence of dominant genetic influences does not account for the absence of C on ADHD.
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| 17. |
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| 18. |
- Chen, Cen, et al.
(författare)
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Chronic Pain Conditions and Risk of Suicidal Behavior : A 10-Year Longitudinal Co-twin Control Study
- 2022
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 52:6, s. 351-351
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Understanding the relationship between chronic pain conditions and suicidal behavior is imperative for suicide prevention efforts. Although chronic pain conditions are associated with suicidal behaviors, these associations might be attributed to unmeasured confounding, or mediated via pain comorbidity. We linked a population-based Swedish twin study (N = 17 148 twins) with 10 years of longitudinal, nationwide records of suicidal behavior from health and mortality registers through 2016. To investigate whether pain comorbidity versus specific pain conditions were more important for later suicidal behavior, we modeled a general factor of pain and two independent specific pain factors (measuring pain-related somatic symptoms and neck-shoulder pain, respectively) based on 9 self-reported chronic pain conditions. To examine whether the pain-suicidal behavior associations were attributable to familial confounding, we applied a co-twin control model. Individuals scoring one standard deviation above the mean on the general pain factor had 51% higher risk of experiencing suicidal behavior (Odds Ratio (OR), 1.51; 95% Confidence Interval (CI), 1.34–1.72). The specific factor of somatic pain was also associated with increased risk for suicidal behavior (OR, 1.80; 95% CI, 1.45–2.22]). However, after adjustment for familial confounding, the associations were greatly attenuated and not statistically significant within monozygotic twin pairs (general pain factor OR, 0.89; 95% CI, 0.59–1.33; somatic pain factor OR, 1.02; 95% CI, 0.49–2.11) Clinicians might benefit from measuring not only specific types of pain, but also pain comorbidity; however, treating pain might not necessarily reduce future suicidal behavior, as the associations appeared attributable to familial confounding.
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| 19. |
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| 20. |
- Codita, Alina, et al.
(författare)
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Effects of spatial and cognitive enrichment on activity pattern and learning performance in three strains of mice in the IntelliMaze.
- 2012
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Ingår i: Behavior Genetics. - : Springer Science and Business Media LLC. - 0001-8244 .- 1573-3297. ; 42:3, s. 449-460
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Tidskriftsartikel (refereegranskat)abstract
- The IntelliMaze allows automated behavioral analysis of group housed laboratory mice while individually assigned protocols can be applied concomitantly for different operant conditioning components. Here we evaluate the effect of additional component availability (enrichment) on behavioral and cognitive performance of mice in the IntelliCage, by focusing on aspects that had previously been found to consistently differ between three strains, in four European laboratories. Enrichment decreased the activity level in the IntelliCages and enhanced spatial learning performance. However, it did not alter strain differences, except for activity during the initial experimental phase. Our results from non-enriched IntelliCages proved consistent between laboratories, but overall laboratory-consistency for data collected using different IntelliCage set-ups, did not hold for activity levels during the initial adaptation phase. Our results suggest that the multiple conditioning in spatially and cognitively enriched environments are feasible without affecting external validity for a specific task, provided animals have adapted to such an IntelliMaze.
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| 21. |
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| 22. |
- de Frias, Cindy M, et al.
(författare)
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COMT gene polymorphism is associated with declarative memory in adulthood and old age.
- 2004
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Ingår i: Behavior genetics. - New York : Kluwer Academic Publishers. - 0001-8244 .- 1573-3297. ; 34:5, s. 533-9
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Tidskriftsartikel (refereegranskat)abstract
- Variation in memory performance is to a large extent explained by genes. In the prefrontal cortex, the catechol O-methyltransferase (COMT) gene is essential in the metabolic degradation of dopamine, a neurotransmitter implicated in cognitive functions. The present study examined the effect of a polymorphism in the COMT gene on individual differences and changes in memory in adulthood and old age. Tests assessing episodic and semantic memory were administered to 286 men (initially aged 35-85 years) from a random sample of the population (i.e., the Betula prospective cohort study) at two occasions followed over a 5-year period. Carriers of the Met/Met genotype (with low enzyme activity) performed better on episodic and semantic memory, as compared to carriers of the Val allele (with higher enzyme activity). Division of episodic memory into its recall and recognition components showed that the difference was specific to episodic recall, not recognition tasks; an effect that was observed across three age groups (middle-age, young-old, and old-old adults) and over a 5-year period. The COMT gene is a plausible candidate gene for memory functioning in adulthood and old age.
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| 24. |
- Dinkler, Lisa, et al.
(författare)
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Heritability of the Avoidant/Restrictive Food Intake Disorder (ARFID) Phenotype in 6-to-12-Year-Old Swedish Twins
- 2022
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 52:6, s. 357-357
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Little is known about the etiology of avoidant/restrictive food intake disorder (ARFID) and no twin studies of ARFID exist yet. Validated screening instruments for ARFID are only starting to emerge and accordingly, few large-scale epidemiological studies specifically aimed at measuring ARFID are available. We leveraged the rich existing datasets of the Swedish Twin Registry to develop a proxy for the ARFID phenotype and determine its twin-based heritability. We extracted all data relevant to ARFID from the Child and Adolescent Twin Study in Sweden and national health registers, and identified children with avoidant/restrictive eating with clinically significant impact, but without body image concerns such as fear of weight gain and excluding major medical illnesses that could account for the eating behavior. Among 34,382 twins born 1992–2010, 678 children (2.0%, 39% female) were identified with the ARFID phenotype between age 6 and 12 years. In the best fitting model, variation in the liability to ARFID was largely explained by additive genetic factors (0.80, 95% confidence interval [CI] 0.71–0.86), with significant contributions from non-shared environmental factors (0.20, 95% CI 0.14–0.29) and sibling contrast effects (-0.11, 95% CI -0.16—-0.04). Prevalence and sex distribution of the ARFID phenotype were similar to previous studies, supporting the use of epidemiological data to identify ARFID. This first heritability estimate of ARFID suggests that ARFID is highly heritable, encouraging future twin and molecular genetic studies. In a next step we will use multivariate twinmodels to test whether, etiologically, ARFID is related to neurod-velopmental disorders.
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| 25. |
- Dominicus, Annica, et al.
(författare)
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Likelihood ratio tests in behavioral genetics: Problems and solutions
- 2006
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 36:2, s. 331-340
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Tidskriftsartikel (refereegranskat)abstract
- The likelihood ratio test of nested models for family data plays an important role in the assessment of genetic and environmental influences on the variation in traits. The test is routinely based on the assumption that the test statistic follows a chi-square distribution under the null, with the number of restricted parameters as degrees of freedom. However, tests of variance components constrained to be non-negative correspond to tests of parameters on the boundary of the parameter space. In this situation the standard test procedure provides too large p-values and the use of the Akaike Information Criterion (AIC) or the Bayesian Information Criterion (BIC) for model selection is problematic. Focusing on the classical ACE twin model for univariate traits, we adapt existing theory to show that the asymptotic distribution for the likelihood ratio statistic is a mixture of chi-square distributions, and we derive the mixing probabilities. We conclude that when testing the AE or the CE model against the ACE model, the p-values obtained from using the v2 (1 df) as the reference distribution should be halved. When the E model is tested against the ACE model, a mixture of v2(0 df), v2(1 df) and v2 (2 df) should be used as the reference distribution, and we provide a simple formula to compute the mixing probabilities. Similar results for tests of the AE, DE and E models against the ADE model are also derived. Failing to use the appropriate reference distribution can lead to invalid conclusions.
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