Nature, Nurture, and the Transition to Early Adolescence

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As with the results found in the univariate case, biologically related siblings were more similar across measurement occasions than were adoptive siblings, suggesting genetic influences on the age-to-age stability of general cognitive ability. A significant adoptive cross-sibling correlation between Year 1 and Year 2 suggests moderate shared environmental influences on the stability of cognitive ability, most consistently in the first 2 years of life.

Numbers of double-entered sibling pairs appear in parentheses. The standardized estimates from the full model are presented in Table 5. These estimates suggest a high degree of genetic stability. Age-specific genetic influences were negligible after Year 1, and genetic stability was divided between the general factor and simplex transmission. That is, whenever simplex transmission was high e. Shared environmental influences suggest a similar pattern: In contrast, age-specific effects were most consistent in the nonshared environmental estimates.

Age-specific parameters are expressed as variances; general-factor and simplex parameters are expressed in standard deviation units. These standardized parameter estimates, by themselves, do not provide a clear picture of the overall magnitude of genetic, shared environmental, and nonshared environmental influences. Heritability and nonshared environment were consistently moderate to high in effect from ages 1 through 16 see Table 6. Shared environmental influences, in contrast, were small in effect, ranging from. Six submodels were fit to the data to test the significance of age-to-age stability as well as the significance of the genetic, shared environmental, and nonshared environmental components of this stability see Table 7.

The first two submodels tested whether the stability of cognitive ability was influenced by a general factor or simplex transmission, irrespective of etiology. The first submodel No simplex transmission dropped all 21 simplex pathways 7 from genetics, 7 from the shared environment, 7 from the nonshared environment. The second No common factor dropped all pathways from the genetic, shared environmental, and nonshared environmental common factors.

Both submodels fit significantly worse than the full model, suggesting that the general factor and simplex transmission were important to stability. The remaining four submodels tested the magnitude of genetic, shared environmental, and nonshared environmental influences on stability as well as instability. First, all shared environmental pathways were dropped from the model No shared environment.

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This model did not result in a significant decrease in model fit, suggesting that the shared environment was not significant to either the stability or instability of general cognitive ability. Submodels of the genetic pathways suggested that it was possible to drop all simplex and age-specific pathways No specific genetic or genetic simplex transmission without significantly reducing model fit. However, it was not possible to drop the general factor No genetic common factor. Thus, only the genetic variance relating to the general factor was significant in the current study.

Finally, it was also possible to drop all stability pathways No nonshared environmental common factor or nonshared environmental transmission from the nonshared environment without significantly reducing model fit.

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Given that the unique environmental innovation term incorporates experimental error, these parameters cannot be dropped. Collectively, these results support the significance of genetic overlap across years and suggest that age-specific nonshared environmental experiences and error are responsible for age-to-age instability.

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These correlations estimate the overlap between the genetic variance found at two measurement occasions. The results are consistent with a large degree of genetic overlap from age 1 to age Between Years 2 and 3 the genetic correlation is. Moreover, aside from Year 1, the genetic correlations among the remaining years are consistently high and stable, irrespective of the number of years between measurement occasions.

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  • The results of the current analysis suggest that the nonshared environment is primarily responsible for instability and genetics are primarily responsible for stability in cognitive performance from age 1 to age The model-fitting results suggested that cognitive abilities in adolescence are significantly correlated with abilities at earlier measurement occasions in childhood and that genes are primarily responsible for this overlap. The nonshared environment including error was primarily responsible for instability. Shared environmental influences were nonsignificant in the current study.

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    An examination of the estimates from the full model see Table 5 , the model-fitting results see Table 7 , as well as the genetic correlations see Table 8 suggests that simplex transmission may be significant but that it was not possible to distinguish genetic from nonshared environmental contributions to simplex transmission.

    Moreover, the magnitude of genetic simplex transmission from age 2 to age 3 and from age 3 to age 4 is so high.

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    It is difficult to distinguish simplex from general- factor transmission when simplex transmission approaches 1. Despite the lack of clarity concerning the precise mechanism, the current study suggests that genetic influences are primarily responsible for covariance among cognitive skills from age 1 to age 16 and that this covariance is significant and substantial from early childhood through adolescence. These results build on previous studies though they differ slightly in the characterization of the pattern of genetic and environmental influences throughout this period.

    Significant genetic simplex transmission in early childhood was not found in our analyses. Because results for each study were estimated through a simultaneous analysis of the data, the point estimates for genetic and environmental effects are similar, but they are not the same across both studies.

    Despite these differences, both analyses are in agreement that the stability of cognitive skills from infancy, through childhood, and into adolescence is due primarily to genetic influences. In a separate study, Bartels et al.

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    Though this latter pattern is a considerable departure from the current and previous adoption studies, U. Another possible explanation is that there was a greater proportion of same-sex siblings among biological siblings in the CAP than among adoptive siblings. This dissonance may have resulted in an underestimation of adoptive sibling correlations, thus depressing the shared environment. Although we do not have power to examine the potential effects of this difference in the current study, results from the parent-offspring CAP data suggest that adoptive children are unrelated to their adoptive parents except very early in early childhood.

    Instead, adoptive children are most closely related to their biological parents, yielding heritability estimates similar to those found in the current study using sibling data Plomin et al. Given the sample size and the number of variables estimated in the current analyses, it was not possible to address these issues with sufficient power. Another limitation of the current study is that it used a single measure of cognitive ability at each age.

    In the current study, we assumed that these measures index general cognitive ability. However, what is emerging from the behavioral genetic literature is that the overlap among different cognitive abilities is largely due to genetic overlap see Petrill, Thus, it is likely that the genetic variance we are measuring in the current study is highly correlated with the genetic variance found in other measures of cognitive ability.

    Despite these limitations, the CAP is the only study in existence that can examine the genetic and environmental influences on cognitive skills in an adoptive sample assessed longitudinally from 1 to 16 years. It is also important to consider that the siblings, although possessing test scores at the same chronological age, were tested several years apart. The results of the current study suggest that to the extent that there is genetic variance, it is associated with stability, not instability. Furthermore, to the extent that the environment is important, it contributes primarily to instability and is associated with the nonshared environment.

    Given the amount of growth from early childhood through adolescence, it is surprising that there is any stability in cognitive ability. A child just learning to speak cannot be assessed with the same measurements as a teenager. Despite the difference in performance measurement, previous studies have validated the use of these measures across early childhood through adolescence Sattler, Taken together, genetic influences not only are significant and substantial but are increasingly correlated from birth through adolescence. Although these data suggest significant covariance in cognitive ability from age 1 to age 16, there is also a great deal of instability, particularly in early childhood.

    Thus, it is important to point out that although genetic factors are important to understanding why there is stability, these genetic factors do not explain all of the variability in general cognitive ability at a given age.

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    As the present results suggest, genetic mechanisms play a highly consistent and considerable role in the stability of cognitive ability during the first 16 years of life. This genetic stability is likely to be associated with brain-based, neuroanatomical, and neurophysiological mechanisms. In the context of the stability of general cognitive ability throughout development, a discussion of these neurobiological substrates might prove valuable. The present results also suggest that likely candidates for influencing changes in cognitive performance are age-specific unique environmental experiences.

    Cooperation between these genetic, or neurobiological, mechanisms and environmental influences suggests that these neurobiological substrates of cognition are flexible and responsive to external stimuli. This flexibility undoubtedly is a feature of the molecular genetic mechanisms that construct this responsive neurobiological system. The system responsible for cognitive performance is the local and global neural architecture of the brain.

    A potential mechanism of change and stability within this system is the neuronal mechanism of plasticity Garlick, During this early part of life, long-term changes that may occur include the rewiring of existing networks and the establishment of new sets of connections, the results of which include increased capacity and improved efficiency.

    Changes that occur throughout life, that are the predominant mode of plasticity later in life Huttenlocher, ; Rakic, , involve changes in local circuitry such as modifications in receptors, neurotransmitter release, or the formation of new dendritic or axonal synaptic connections in response to external stimulation Crutcher, This dendritic or axonal plasticity strengthens preexisting circuits and improves the efficiency of local neuronal transmission Tang et al.

    Changes in myelination are another neurobiological mechanism that may influence cognitive ability by affecting information transfer along axons. These neural mechanisms ultimately allow subsequent experiences to elicit more meaningful responses and thus may serve to directly impact cognitive ability. This research capitalizes on the resources of the Colorado Adoption Project CAP , the only ongoing, long-term longitudinal adoption study of behavioral development. Its foundation sample includes adopted children whose biological parents and adoptive parents were tested on a three-hour battery of social and behavioral measures.

    These adoptive families were matched to nonadoptive families; that is, to parents rearing their own biological children. This full adoption design assesses genetic and environmental effects of parents on their children by comparing children to genetic parents i. Leia mais Leia menos. Detalhes do produto Formato: Compartilhe seus pensamentos com outros clientes.

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