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R Plomin

Publications and source records attributed to R Plomin.

At least 73 records · Page 4Linked to original sources
PubMed1998

Genotype-environment correlations in late childhood and early adolescence: antisocial behavioral problems and coercive parenting.

A key question for understanding the interplay between nature and nurture in development is the direction of effects in socialization. A longitudinal adoption design provides a unique opportunity to investigate this issue in terms of genotype-environment correlations for behavioral problems. As part of the Colorado Adoption Project, adopted children were classified as being at genetic risk (N = 38) or not at genetic risk (N = 50) for antisocial behavior based on their biological mothers' self-report history of antisocial behavior collected prior to the birth of the child. From age 7 through age 12, adoptive parents reported on the negative control, positive parenting, and inconsistent parenting they use in managing their child's behavior. Repeated measures analysis of variance indicated that children at genetic risk were consistently more likely to receive negative parenting from their adoptive parents than children not at genetic risk, indicating an evocative genotype-environment correlation. However, the findings also showed that most of the association between negative parenting and children's externalizing behavior was not explicable on the basis of an evocative gene-environment correlation and that an additional environmentally mediated parental effect on children's behavior was plausible.

Adolescent↗
PubMed1998

Longitudinal and cross-sectional twin data on cognitive abilities in adulthood: the Swedish Adoption/Twin Study of Aging.

Cross-sequential methods of analysis, designed to separate age and cohort effects, were applied to data from the Swedish Adoption/Twin Study of Aging. Thirteen cognitive variables were collected at 3 times of measurement separated by 3-year intervals. Data were available from 85 individuals from monozygotic (MZ) pairs reared apart, 132 from MZ pairs reared together, 207 from dizygotic (DZ) pairs reared apart, and 178 from DZ pairs reared together (age range at first assessment: 41-84 years). Time x Cohort interactions were found for mean performance on 8 of the measures, revealing stable mean performance in the younger cohorts and longitudinal decreases in mean performance in the older cohorts. Cohort and time effects for total variance were mixed; little evidence was found for increases in variance with age. Age changes and cohort differences in genetic and environmental components of variance were test-specific; several Cohort x Time interactions attained significance. Heritability of the general cognitive ability factor showed significant longitudinal decreases over time in the older cohorts.

Adolescent↗
PubMed1998

Co-occurrence of depressive symptoms and antisocial behavior in adolescence: a common genetic liability.

Recent reviews of research on child and adolescent psychopathology have highlighted the consistently high rates of co-occurring dimensions of psychopathology, particularly between internalizing and externalizing disorders, and have suggested that further research examining the causes of co-occurring syndromes is needed. The authors examined this question in a national sample of 720 same-sex adolescent siblings between 10 and 18 years of age consisting of monozygotic and dizygotic twins, full siblings, half siblings, and unrelated siblings. Composite measures of adolescent and parent reports and observational measures of depressive symptoms and antisocial behavior were subjected to behavioral genetic models that examine the genetic and environmental influences on individual differences in each dimension as well as in the co-occurrence between dimensions. Results indicated that approximately half of the variability in depressive symptoms and antisocial behavior is attributed to genetic factors; shared and nonshared environmental influences were also significant. The co-occurrence of depressive and antisocial symptoms was explained by genetic and shared and nonshared environmental influences. Specifically, approximately 45% of the observed covariation between depressive and antisocial symptoms could be explained by a common genetic liability. Results are interpreted in light of contribution of genetic studies to debates on child and adolescent psychopathology.

Adolescent↗
PubMed1998

Adoption results for self-reported personality: evidence for nonadditive genetic effects?

Twin studies consistently indicate moderate genetic influence on individual differences in personality as assessed using self-report questionnaires, with heritability estimates typically about 40%. In this first analysis of self-report personality data from the longitudinal Colorado Adoption Project, little evidence is found for additive genetic influence in parent-offspring and sibling adoption analyses based on a foundation sample of 245 adoptive families and 245 nonadoptive families with adopted and nonadopted children assessed yearly from 9 to 16 years. Although several factors might contribute to the discrepancy between twin and adoption results, we suggest that nonadditive genetic influence, which can be detected by twin studies but not by adoption studies, is a likely culprit. These findings have important implications for attempts to identify specific genes responsible for genetic influence on personality.

Adolescent↗
PubMed1998

Genetic influence on language delay in two-year-old children.

Previous work suggests that most clinically significant language difficulties in children do not result from acquired brain lesions or adverse environmental experiences but from genetic factors that presumably influence early brain development. We conducted the first twin study of language delay to evaluate whether genetic and environmental factors at the lower extreme of delayed language are different from those operating in the normal range. Vocabulary at age two was assessed for more than 3000 pairs of twins. Group differences heritability for the lowest 5% of subjects was estimated as 73% in model-fitting analyses, significantly greater than the individual differences heritability for the entire sample (25%). This supports the view of early language delay as a distinct disorder. Shared environment was only a quarter as important for the language-delayed sample (18%) as for the entire sample (69%).

Child, Preschool↗
PubMed1998

A simple method for analyzing microsatellite allele image patterns generated from DNA pools and its application to allelic association studies.

Allelic association studies provide the most powerful method for locating genes of small effect contributing to complex diseases and traits. However, in outbred populations, allelic association is usually maintained only over distances of <=1 cM. Therefore, systematic searches over large regions are costly. Here we present a method involving DNA pooling that can be used as a rapid preliminary screen for allelic association with the most common class of polymorphic markers, single-sequence repeats. Patient and control samples are pooled separately, and markers are typed in the two pools. By use of primers with fluorescent 5' ends, PCR products can be analyzed on an automated sequencing apparatus. Allele image patterns (AIPs) produced for the two groups are overlaid and differences in pattern area between pools computed. From this, a DeltaAIP statistic is calculated from the difference in areas between the two AIPs expressed as a fraction of the total shared and nonshared area. AIPs of a range of different-sized pools were generated by computer simulation for markers with a range of allele sizes and frequencies. DeltaAIPs from pools and chi2 values for individual genotypings were compared, with both simulated and real data from microsatellite markers. The results demonstrated a high correlation between DeltaAIP and chi2 values. DeltaAIP analysis of real microsatellite data indicated the feasibility of using this method in systematic searches for allelic association and generated a small number of false positives but few false negatives. We conclude that DeltaAIP analysis of DNA pools can be used effectively and efficiently as a rapid screen for allelic association in case-control studies.

Alleles↗
PubMed1998

Exploring the genetic and environmental etiology of high general cognitive ability in fourteen- to thirty-six-month-old twins.

Although numerous theories have attempted to explain the origins of high general cognitive ability (g), the genetic and environmental etiology of high g during infancy and early childhood has not previously been investigated. We report results of a twin study of high cognitive ability at 14, 20, 24, and 36 months using twins from the more than 600 children participating in the MacArthur Longitudinal Twin Study. High g groups were formed from the ninetieth percentile and above at each age, with IQ equivalent means at or above 126 across the ages. Results suggest increasing genetic influence and increasing genetic stability from 14 to 36 months using DeFries-Fulker multiple regression analyses. However, genetic influences are substantial when examining individuals who possess high g scores averaged across all 4 ages. These results suggest that, although high cognitive ability may be genetically influenced in early childhood, these influences differ in magnitude from 14 to 36 months.

Child Development↗
PubMed1998

Molecular genetic studies of cognitive ability.

Given that the evidence of a substantial genetic contribution to cognitive ability is now convincing, the next challenge is to locate and identify the genes involved. It is likely that there are several genes, each of only small effect. Detection of such so-called quantitative trait loci contributing to polygenic traits in plants and animals is facilitated by the ability to carry out experimental crosses. However, in humans detection of quantitative trait loci depends on studies of siblings or other relative pairs or on allelic association studies aimed at detecting linkage disequilibrium in populations. The allelic association approach is currently being applied to investigate cognitive ability by using both candidate genes and DNA pooling methods that potentially allow rapid screening of the whole genome for quantitative trait loci.

Animals↗
PubMed1998

Genetic contributions to continuity, change, and co-occurrence of antisocial and depressive symptoms in adolescence.

In adolescence, antisocial and depressive symptoms are moderately stable and modestly correlated with each other. We examined the genetic and environmental origins of the stability and change of antisocial and depressive symptoms and their co-occurrence cross-sectionally and longitudinally in a national sample of 405 adolescents. Monozygotic (MZ) and dizygotic (DZ) twins and full, half, and unrelated siblings 10-18 years of age from non-divorced and step-families were studied over a 3-year period. Composite measures of adolescent self-reports, parent reports, and observational measures of antisocial and depressive symptoms were analysed in multivariate behavioural genetic models. Results indicated that the majority of the stability in and co-occurrence between dimensions could be accounted for by genetic factors. Non-shared environmental risks and, for antisocial symptoms, shared environmental risks also contributed to the stability. Genetic influences on change were observed, but only for antisocial behaviour. In addition, the longitudinal association between antisocial behavioural and later depressive symptoms was also found to be genetically mediated, but this effect was nonsignificant after controlling for stability. Results were discussed in light of the potential contributions of development behavioural genetic research in understanding individual differences in the stability and change of maladjustment.

Adolescent↗
PubMed1998

An adoption study of depressive symptoms in middle childhood.

Several twin studies of children and adolescents have found significant heritability of depressive symptoms. In contrast, the sole adoption study of biologically related and biologically unrelated adopted siblings found no evidence for genetic influence. The present study attempts to confirm these results in middle childhood using two adoption designs. The sample, from the Colorado Adoption Project, included 180 adopted children (77 with adoptive siblings) and their biological and adoptive mothers, and 227 nonadopted children (93 with biological siblings) and their mothers. Mothers reported their own neuroticism, and children's depressive symptoms were reported by the parents and by the children themselves. For both the sibling adoption and the parent-offspring designs heritability was negligible, shared environment modest, and non-shared environment substantial, irrespective of child gender. Although the power of the sibling data is low, the combined findings from the two designs suggest that genetic effects on depressive symptoms in childhood may be somewhat smaller than previously estimated in twin studies.

Adoption↗
PubMed1998

Confirmation of quantitative trait loci for alcohol preference in mice.

An F2 intercross derived from C57BL/6 and DBA/2 progenitor inbred strains was used to test for replication of quantitative trait loci (QTLs) for alcohol preference nominated by a previous study using BXD recombinant inbred (RI) strains (Rodriguez et al., Alcohol. Clin. Exp. Res. 19:367-379, 1995). Fourteen provisional QTLs were nominated in the original RI study with a p < 0.05 criterion. In the present study, a genome scan (101 microsatellite markers) was conducted on an F2 population (n = 218). Three significant QTLs were detected on chromosomes 1, 4, and 9, and three suggestive QTLs were detected on chromosomes 2, 3, and 10. Of these six QTLs, four were consistent with the previous RI nominations. The replication rate of 28.6% (4 of 14) is in agreement with the results of simulation studies performed by Belknap et al. (Behav. Genet. 26:149-160, 1996) and supports the methodological argument for a multistage research design for nominating and replicating QTLs.

Alcohol Drinking↗
PubMed1998

Child development, molecular genetics, and what to do with genes once they are found.

Genes associated with behavioral dimensions and disorders are beginning to be identified. Although it is difficult and expensive to find genes associated with behavior, it is relatively easy and inexpensive to use genes that have already been identified. We describe how genes are found, but the main goal of this article is to outline what developmentalists can do with genes once they are found and, hence, to encourage the use of DNA markers in developmental research. We suggest that genes can be used to answer questions about developmental continuities, about psychopathological patterns, and about environmental risk mechanisms. Developmental questions include the causal mechanisms involved in heterotypic continuity. Questions on psychopathological patterns address heterogeneity (Do gene-behavior associations apply to disorders or to separate components representing risk or protective factors?), comorbidity (Are gene-behavior associations diagnosis-specific?), and the links between normality and disorder (Does a gene-behavior association for a disorder extend to related dimensions of normal variation and vice versa?). Questions about environmental risk mechanisms are informed by study of gene-environment interaction (Are individuals who are at genetic risk more sensitive to specific psychosocial risks?) and gene-environment correlation (Are individuals who are at genetic risk more likely to be exposed to psychosocial risk?).

Bioethics↗
PubMed1997

Substantial genetic influence on cognitive abilities in twins 80 or more years old.

General and specific cognitive abilities were studied in intact Swedish same-sex twin pairs 80 or more years old for whom neither twin had major cognitive, sensory, or motor impairment. Resemblance for 110 identical twin pairs significantly exceeded resemblance for 130 fraternal same-sex twin pairs for all abilities. Maximum-likelihood model-fitting estimates of heritability were 62 percent for general cognitive ability, 55 percent for verbal ability, 32 percent for spatial ability, 62 percent for speed of processing, and 52 percent for memory. There was also evidence for the significant influence of idiosyncratic experience as the environmental component that most determines individual differences in cognitive abilities late in life.

Aged↗
PubMed1997

The serotonin transporter gene and peer-rated neuroticism.

Polymorphisms in the serotonin transporter gene (5HTT) have been reported to be associated with neuroticism (emotionality) and with depression. A recent report of an association between 5HTT and neuroticism involved unselected samples and self-report questionnaires. We attempted to extend these findings using a selected extremes design and peer ratings. From a sample of 2085 individuals, each assessed on neuroticism by two independent peers, we selected 52 individuals from the top 5% and 54 individuals from the bottom 5%. No association was found for either a functional 44 bp insertion/deletion polymorphism in 5HTT regulatory sequence (5HTTLPR) or for a non-functional variable number tandem repeat 5HTT polymorphism.

Adolescent↗
PubMed1997

Human behavioural genetics of cognitive abilities and disabilities.

Although neither the genome nor the environment can be manipulated in research on human behaviour, some of the new tools of molecular genetics can be brought to bear on human behavioural disorders (e.g. cognitive disabilities) and quantitative traits (e.g. cognitive abilities). The inability to manipulate the human genome experimentally has had the positive effect of focusing attention on naturally occurring genetic variation responsible for behavioural differences among individuals in all their complex multifactorial splendour. Genes in such complex multiple-gene systems are called quantitative trait loci (QTLs), which merge the two worlds of genetic research, quantitative genetics and molecular genetics. Although most genetic research on complex human behaviour has focused on severe mental disorders, cognitive abilities and disabilities may be even more immediately relevant to neuroscience. For example, verbal ability and spatial ability are two of the most heritable cognitive abilities, and reading disability is the first behavioural disability for which replicated QTL linkage has been found. The purpose of this essay is to provide an overview of the genetics of cognitive abilities and disabilities as an example of the impending merger of quantitative genetics and molecular genetics in QTL analysis of complex traits.

Achievement↗