Search PubMed⌕ Search

Biomedical subjects

R Plomin

Publications and source records attributed to R Plomin.

At least 55 records · Page 3Linked to original sources
PubMed2000

Are associations between parental divorce and children's adjustment genetically mediated? An adoption study.

The hypothesis that the association between parental divorce and children's adjustment is mediated by genetic factors was examined in the Colorado Adoption Project, a prospective longitudinal study of 398 adoptive and biological families. In biological families, children who experienced their parents' separation by the age of 12 years exhibited higher rates of behavioral problems and substance use, and lower levels of achievement and social adjustment, compared with children whose parents' marriages remained intact. Similarly, adopted children who experienced their (adoptive) parents' divorces exhibited elevated levels of behavioral problems and substance use compared with adoptees whose parents did not separate, but there were no differences on achievement and social competence. The findings for psychopathology are consistent with an environmentally mediated explanation for the association between parent divorce and children's adjustment; in contrast, the findings for achievement and social adjustment are consistent with a genetically mediated explanation involving passive genotype-environment correlation.

Adaptation, Psychological↗
PubMed1999

Sex-exclusive quantitative trait loci influences in alcohol-related phenotypes.

During the past half century, researchers have identified and examined sex differences in alcohol-related phenotypes, focusing more recently on understanding of the mechanisms underlying these differences. In general, the genetic contributions influencing these differences are not consistent with an interpretation of sex linkage and must, therefore, reflect some form of sex limitation in which allelic differences at particular autosomal loci have different consequences in males and females. Significant sex differences in measures of alcohol consumption in mice have been demonstrated in previous work in our laboratory. To investigate these differences further, we explore the limiting case of sex-exclusive effects using data from (BXD) recombinant inbred (RI) strains of mice and from an intercross derived from the same progenitors, C57BL/6J (B) and DBA/2J (D). By the use of two statistical approaches (examination of residual scores as a sex-exclusive phenotypic value for the RI strains and multivariate regression on sex and genotype in the F(2)) we have identified and confirmed female-exclusive markers for alcohol acceptance on chromosomes 9 and 12 and one marker for alcohol preference on chromosome 2. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:647-652, 1999.

Alcohol-Related Disorders↗
PubMed1999

Genetics and general cognitive ability.

General cognitive ability (g), often referred to as 'general intelligence', predicts social outcomes such as educational and occupational levels far better than any other behavioural trait. g is one of the most heritable behavioural traits, and genes that contribute to the heritability of g will certainly be identified. What are the scientific and social implications of finding genes associated with g?

Genetic Variation↗
PubMed1999

DNA pooling and dense marker maps: a systematic search for genes for cognitive ability.

Pooling DNA from subjects within a group and comparing the pooled DNA across groups for a dense map of DNA markers offers a solution to the conundrum that linkage is systematic but not powerful whereas allelic association is powerful but not systematic. We used DNA pooling to screen 66 markers on chromosome 22 in original and replication samples of children of high general cognitive ability (g) and controls of average g. Although none of these markers survived our three-stage screening design (original pooling, replication pooling, individual genotyping), the results of DNA pooling were largely confirmed by individual genotyping. We can therefore exclude associations of major effect size on chromosome 22 for g, a key variable for cognitive neuroscience research on learning and memory.

Alleles↗
PubMed1999

Relationships between parenting and adolescent adjustment over time: genetic and environmental contributions.

The predictive association between parenting and adolescent adjustment has been assumed to be environmental; however, genetic and environmental contributions have not been examined. This article represents one effort to examine these associations in which a genetically informative design was used. Participants were 395 families with adolescent siblings who participated in the Nonshared Environment in Adolescent Development (D. Reiss et al., 1994) project at 2 times of assessment, 3 years apart. There were 5 sibling types in 2 types of families: 63 identical twins, 75 fraternal twins, and 58 full siblings in nondivorced families and 95 full, 60 half, and 44 genetically unrelated siblings in stepfamilies. Results indicate that the cross-lagged associations between parental conflict-negativity and adolescent antisocial behavior and depressive symptoms can be explained primarily by genetic factors. These findings emphasize the need to recognize and examine the impact that adolescents have on parenting and the contribution of genetic factors to developmental change.

Adolescent↗
PubMed1999

Genetic and environmental origins of verbal and performance components of cognitive delay in 2-year-olds.

The authors investigated the etiology of several measures of cognitive delay. Verbal (V) and performance (P) abilities were assessed in over 3,000 pairs of 2-year-old twins. Group-differences heritability for general delay (the lowest 5% of the V and P composite) was 35%. However, V and P delays considered independently showed large differences in group heritability (77% for V vs. 40% for P). Specific delays with comorbid cases eliminated showed an even greater difference in group heritability (78% vs. 22%, respectively). The small sample comorbid for both V and P delay also yielded high group heritability for both V (77%) and P (93%) scores. Shared environmental factors also differed in magnitude for V (20%) and P (41%) delays. Because the genetic and environmental origins of V and P delays in infancy differ, they are better considered separately rather than combined into a composite measure of general cognitive delay.

Child, Preschool↗
PubMed1999

DNA pooling identifies QTLs on chromosome 4 for general cognitive ability in children.

General cognitive ability (g), which is related to many aspects of brain functioning, is one of the most heritable traits in neuroscience. Similarly to other heritable quantitatively distributed traits, genetic influence on g is likely to be due to the combined action of many genes of small effect [quantitative trait loci (QTLs)], perhaps several on each chromosome. We used DNA pooling for the first time to search a chromosome systematically with a dense map of DNA markers for allelic associations with g. We screened 147 markers on chromosome 4 such that 85% of the chromosome were estimated to be within 1 cM of a marker. Comparing pooled DNA from 51 children of high g and from 51 controls of average g, 11 significant QTL associations emerged. The association with three of these 11 markers ( D4S2943, MSX1 and D4S1607 ) replicated using DNA pooling in independent samples of 50 children of extremely high g and 50 controls. Furthermore, all three associations were confirmed when each individual was genotyped separately ( D4S2943, P = 0. 00045; MSX1, P = 0.011; D4S1607, P = 0.019). Identifying specific genes responsible for such QTL associations will open new windows in cognitive neuroscience through which to observe pathways between genes and learning and memory.

Adolescent↗
PubMed1999

A genetic study of the family environment in the transition to early adolescence.

The aim of this longitudinal sibling adoption study was to estimate genetic and environmental components of variance in parent- and child-reported measures of the family environment (parental negative affect, negative control, and achievement orientation). Participants included 85 adoptive and 106 nonadoptive sibling pairs from the Colorado Adoption Project. Parents and children completed annual assessments of the family environment when the children were 10, 11, and 12 years old, and genetic and environmental parameter estimates were derived. Genetic influences were found for parent-reported negativity and warmth and child-reported achievement orientation, suggesting child genetic effects on these measures of the family environment. Shared environmental influences were found for parent-reported negativity, inconsistent discipline, warmth, and child-reported positivity. Nonshared environmental variance was substantial for children's ratings, but modest for parents' ratings.

Achievement↗
PubMed1999

Adolescents' relationships to siblings and mothers: a multivariate genetic analysis.

Research has consistently demonstrated that children's behavior toward their siblings tends to resemble interactions occurring in the parent-child relationship. This study examined the relative contributions of genetic and environmental influences to the covariation between sibling relationships and mother-adolescent relationships. Reported and observed family interactions were assessed for 719 same-sex sibling pairs of varying degrees of genetic relatedness. The covariance between mother-adolescent and sibling interactions was decomposed into genetic, shared, and nonshared environmental components. The overlapping effects of shared environment on the two relationship subsystems explained most of the covariance. Smaller but significant genetic and nonshared environmental effects were also found. The consistency of these findings with family processes, such as modeling, is discussed.

Adolescent↗
PubMed1999

The importance of shared environmental influences in explaining the overlap between mother's parenting and sibling relationships: reply to Neale (1999)

This article addresses concerns raised by M. C. Neale (1999) in his commentary on the D. A. Bussell et al. (1999) Nonshared Environment in Adolescent Development (NEAD) study. These concerns fall into two categories: (a) model assumptions and sample design and (b) testing of alternative models. The validity of the assumptions of quantitative genetic models is a concern for all researchers in this area. Discussion of those assumptions in this reply is brief and focuses on those most relevant to the NEAD sample. The two alternative models proposed by Neale were designed to provide alternatives to the large shared environmental effect found in the original report of Bussell et al. Because these alternative models did not provide a better fit, the appropriateness of Bussell et al.'s basic model and the importance of shared environmental influences for explaining the association among family subsystems are supported.

Adolescent↗
PubMed1999

Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.

We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.

Animals↗
PubMed1998

Dopamine markers and general cognitive ability.

Because general cognitive ability (g) is among the most heritable behavioural traits, it is a reasonable target for a search for quantitative trait loci (QTLs). We used a selected-extremes design to test candidate genes for allelic association with g. Polymorphisms in four genes in the dopamine system (DRD2, DRD3, DRD4, DAT1) were genotyped for 51 high g children with IQ scores > 130 and for 51 average g control children. No significant allelic or genotypic differences were found between the high g and average g groups for these markers of the dopamine system, even though the selected-extremes design provides power to detect QTL associations that involve a relative risk of about 1.5.

Adolescent↗
PubMed1998

High genetic susceptibility to ethanol withdrawal predicts low ethanol consumption.

C57BL/6J (B6) inbred mice are well known to drink large amounts of alcohol (ethanol) voluntarily and to have only modest ethanol-induced withdrawal under fixed dose conditions. In contrast, DBA/2J (D2) mice are "teetotallers" and exhibit severe ethanol withdrawal. Speculation that an inverse genetic relationship existed between these two traits was substantiated by meta-analysis of existing data collected in multiple genetic models, including large panels of standard and recombinant inbred strains, their crosses, and selectively bred mouse lines. Despite methodological differences among laboratories in measurement of both preference drinking and withdrawal, a nearly universal finding was that genotypes consuming large amounts of 10% ethanol (calculated as g/kg/day) during two-bottle choice preference drinking were genetically predisposed to low withdrawal scores in independent studies after either acute or chronic ethanol treatment. Conversely, low-drinking genotypes had higher withdrawal severity scores. The genetic relationship appears to be strongest in populations derived from B6 and D2, where data from more genotypes (BXD RIs, B6D2F2s, BXD RI F1s, and B6D2F2-derived selectively bred lines) were available for analysis. Gene mapping studies in these populations identified four chromosome regions [on Chromosomes (Chrs) 1, 2, 4, and 15] where genes might potentially influence both traits. Among genotypes with greater genetic diversity (for example, a panel of standard inbred strains or selectively bred lines), the relationship was less pronounced. Thus, reduced susceptibility to the development of high alcohol use may be supported by increased genetic susceptibility to ethanol withdrawal symptoms.

Alcohol Drinking↗
PubMed1998

Developmental loss of effect of a Chromosome 15 QTL on alcohol acceptance.

Human alcohol abuse and alcoholism have clear developmental features, suggesting the possibility of changes over time in heritability and in quantitative genetic architecture, and raising prospects of identifying individual genes or quantitative trait loci (QTLs) that display different influence on alcohol-related phenotypes at different ages. The identification of specific loci showing such age-related changes will open up opportunities of focused association studies and of genotype manipulation by various mating procedures. Most animal model research in alcohol assesses the phenotypes of the animals at an early age; developmental studies are rare. Here we report on a QTL on Chromosome (Chr) 15 of the mouse that has been shown in several populations, including BXD recombinant inbred strains, an F2, and genotypically selected lines, to affect a measure of alcohol consumption. In the present study, we measured alcohol acceptance in the genotypically selected animals and in an F4 sample at about 100 days and again at about 300 days of age. In both groups, and in both sexes, significant differences were observed at 100 days between animals that were homozygous for the "increasing" haplotype defining the QTL region and those homozygous for the "decreasing" haplotype. At 300 days of age, the effect is absent in females and has diminished or disappeared in males. The results provide a further confirmation of the Chr 15 QTL in young mice, offer a new perspective on the development of alcohol-related phenotypes, and have strong implications for research design.

Alcohol Drinking↗
PubMed1998

Multivariate path analysis of specific cognitive abilities data at 12 years of age in the Colorado Adoption Project.

A parent-offspring multivariate conditional path model was fitted to specific cognitive abilities data from the Colorado Adoption Project (CAP) when the offspring were 12 years of age. The sample included 175 adoptees, 175 sets of adoptive parents, 175 biological mothers, 34 biological fathers, and 209 nonadopted children and their parents. Consistent with results obtained from multivariate genetic analyses of CAP data obtained at earlier ages, the effects of familial environmental transmission on individual differences in specific cognitive abilities were not significant. Assuming complete isomorphism (i.e., that the genetic and environmental etiologies of individual differences are the same) between the child and the adult measures, the heritability estimates for verbal, spatial, perceptual speed, and visual memory were .26, .35, .38, and .53, respectively. Although the heritability estimate for visual memory is somewhat higher than those for verbal, spatial, and perceptual speed abilities, these estimates are not significantly different. These estimates are higher than those obtained when the adoptees and controls were 4 years old (Rice et al., 1986, 1989); thus, heritabilities of specific cognitive abilities may increase as a function of cognitive development. Alternatively, genetic stability from childhood to adulthood may be greater from 12 years than from 4 years, which would be interpreted as greater heritability by the CAP parent-offspring design. The genetic correlations among the four measures were substantial, ranging from .27 between verbal and spatial abilities to .78 between spatial ability and perceptual speed. However, differences among these correlations are not significant, suggesting that their covariation may be due to general cognitive ability. Finally, estimates of bivariate-heritability indicate that on average about half of the phenotypic correlations among the four specific cognitive ability measures are due to genetic effects.

Adoption↗