Biomedical subjects
J W Gilger
Publications and source records attributed to J W Gilger.
Attention deficit disorder in reading-disabled twins: evidence for a genetic etiology.
In order to assess the genetic etiology of attention deficit hyperactivity disorder (ADHD), the basic regression model for the analysis of selected twin data (DeFries & Fulker, 1985, 1988) was fitted to questionnaire data (DICA: Diagnostic Interview for Children and Adolescents; Herjanic, Campbell, & Reich, 1982) for 37 identical and 37 fraternal twin pairs tested in the Colorado Reading Project. Results of this analysis suggest that ADHD is highly heritable. Moreover, adjusting DICA scores for either IQ or reading performance differences did not substantially change parameter estimates. In future analyses of larger data sets, distinguishing between possible subtypes of attentional problems (e.g., ADD with or without hyperactivity) may facilitate tests of more searching etiological questions.
Reading disability, immune disorders and non-right-handedness: twin and family studies of their relations.
Geschwind and colleagues discussed associations among learning disorders, immune disorders and non-right-handedness. In this study, we examined the associations between reading disability (RD) and both immune disorders (ID) and non-right-handedness (NRH) in family and twin samples (total N = 1731 cases) identified through an RD proband. We also conducted co-segregation analyses to ascertain the degree to which NRH, ID and RD were biologically related. There was little evidence for an overall association between RD and NRH. There was not convergent evidence across all four samples for an association between RD and ID, although we did find an association between RD and ID in two of four samples. Nor was there strong support for a subtype where RD and NRH, or RD and ID, co-segregate in families. These data suggest that the associations postulated by Geschwind and colleagues are not robust in RD samples, although we cannot completely rule out the possibility of an RD plus ID subtype.
Auditory magnetic source localization in twins.
We recorded magnetoencephalographic (MEG) auditory evoked fields (EF) from the L and R hemispheres of 12 paris of twins, 6 monozygotic (MZ), and 6 dizygotic (DZ) and localized the source of the 100 msec latency EF component termed the M100. M100 sources exhibited greater similarity in location in MZ twin pairs, especially in the L hemisphere. These findings support the hypothesis that the functional location of processing of nonmeaningful unattended auditory stimuli may depend more heavily on left hemisphere structures. Furthermore, genetic effects are evident in these left hemisphere structures and their activity, as is a substantial amount of environmental variance.
Gender differences in three-dimensional mental rotation: a replication.
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A twin study of the etiology of comorbidity: attention-deficit hyperactivity disorder and dyslexia.
Monozygotic and dizygotic twin pairs, in which at least one member of each pair is reading disabled (RD), were assessed for attention-deficit hyperactivity disorder (ADHD). Within pair cross-concordances of the RD and ADHD qualitative diagnoses for monozygotic twins were larger than for dizygotic twins, although not significantly so (p less than 0.10). Thus, the data suggest that RD and ADHD may be primarily genetically independent. However, trends in the data and subtype analyses suggest that in some cases RD and ADHD may occur together because of a shared genetic etiology and that a genetically mediated comorbid subtype may exist.
Gender ratios among reading-disabled children and their siblings as a function of parental impairment.
Gender ratios are reported for 374 reading-disabled probands and their 530 siblings included in five independent studies of reading disability. Ratios were tabulated for each study as a function of parental impairment (neither parent affected, mother only affected, father only affected, and both parents affected). Results reveal a small excess of male probands in referred and clinic samples of reading-disabled children, but not in research-identified samples. Gender ratios among siblings of reading-disabled probands are approximately 1:1. In addition, combined results indicate that gender ratios of neither probands nor their siblings vary substantially as a function of parental impairment.
The external validity of age- versus IQ-discrepancy definitions of reading disability: lessons from a twin study.
Recent research has raised the question of whether age- and IQ-discrepancy forms of reading disability (RD) are distinguishable in terms of either their underlying linguistic deficit or their response to treatment, thus threatening the external validity of the traditional distinction between specific reading retardation and reading backwardness. The present study pursued the external validity of this distinction in three domains: (a) genetic etiology, (b) sex ratio and clinical correlates, and (c) neuropsychological profiles. Each of these domains was explored in the RD (n = 640) and control (n = 436) twins participating in the Colorado Reading Project (514 males, 562 females, with an overall mean age of 12.42 years). Little evidence for external validity was found in terms of the clinical correlates of attention deficit-hyperactivity disorder (ADHD), immune disorders, or handedness. Most importantly, there was no evidence of differential genetic etiology of the two phenotypes in this sample, in that deficits in both phenotypes were similarly heritable (h2g = .40 and .46 for age and IQ phenotypes, respectively) and the genetic correlation between them was high (rG = .88 to .96). However, the genetic and neuropsychological profile analyses did suggest that age- and IQ-discrepancy definitions of RD may relate differentially to component reading processes, such as phonological awareness and orthographic coding.
Genetics in disorders of language.
As is typical in science, early work in an area is bound to have weaknesses. Therefore, it is not unexpected that the extent to which conclusions can be drawn from the current research on the genetics of DLD is limited. These limitations stem from the use of heterogeneous samples, the use of overly broad phenotypes, survey rather than objective test data, and only a few studies looking beyond simple familiarity. Future research is in progress that attempts to correct for these weaknesses. Still, some practically useful information can be gleaned from the work done thus far. First, we can now hypothesize something about the pathway from gene to DLD phenotype. Much of DLD, like RD, may be a manifestation of early genetic effects on the structural development of the brain (e.g., Plante, Swisher, and Vance, 1991; Plante, 1991; Molfese and Betz, 1988). However, consequences of these genetic effects for language development can still be modified by environmental events (e.g., treatment). Furthermore, genetic effects do not act in isolation and they are not necessarily static. A number of genetic and non-genetic events in the course of development may positively or negatively modify the disorder (e.g., Tomblin, 1989, Tallal et al., 1991; Molfese and Holcomb, 1989). A related point is that there is evidence for genetic heterogeneity in DLD. That different modes of transmission have been put forth by different authors, suggests that a variety of genetic forms of DLD may exist. This idea is further supported by noting that DLD is a common outcome of a number of clinical syndromes having very different genetic bases (e.g., Williams syndrome, Down syndrome, fragile X, etc.; Siegel-Sadewitz and Shprintzen, 1982; Bellugi et al., 1991). This does not rule out the possibility that a majority of nonsyndromic DLD is due to one or a few major genes, however. Finally, there is also evidence for behavioral heterogeneity in DLD. The data suggest that the genes for DLD are variably expressed. For example, in families selected through a DLD proband, a number of different language-related problems have been noted. Furthermore, when a globally defined DLD individual is examined closely, it is common to find a collection of symptoms, sometimes spanning all the major domains of language (Weiss and Lillywhite, 1981). Overall, the data and concepts presented in this article suggest that the clinician should take careful family histories of clients and, when doing so, attempt to ascertain the specific symptoms that family members other than the client exhibit.(ABSTRACT TRUNCATED AT 400 WORDS)
Evidence for major gene transmission of developmental dyslexia.
OBJECTIVE: --There is strong evidence that developmental dyslexia is both familial and heritable, but the mode of genetic transmission has remained unclear. In this article, we examine specific genetic hypotheses about the mode of transmission of developmental dyslexia by performing complex segregation analyses. DESIGN: --A family study method was applied, whereby the relatives of dyslexic probands were examined for dyslexia. The families studied represent four independently ascertained samples. SETTING: --The four samples of families were primarily from rural and suburban communities of Colorado, Washington State, and Iowa. PARTICIPANTS: --A total of 204 families and 1698 individuals in the four samples combined. MAIN OUTCOME MEASURES: --The complex segregation program, POINTER, was used to test competing genetic hypotheses of how a categorical trait (dyslexia) is transmitted in families. RESULTS: --The results were consistent with major locus transmission in three of four samples and with polygenic transmission in the fourth. In these three samples, the estimates of penetrance for the AA, Aa, and aa genotypes (where A is the abnormal allele) were, respectively, 1.000, 1.000, and 0.001 to 0.039 in males, and 0.560 to 1.000, 0.550 to 0.897, and 0.000 in females. The estimated gene frequency of the major locus was between 3% and 5%. CONCLUSIONS: --Sex-influenced, additive, or dominant transmission occurs in a significant proportion of dyslexic families. Other evidence indicates, however, that dyslexia is etiologically heterogeneous and that there is genetic heterogeneity even among families selected for apparent dominant transmission. Thus, while no single major locus may account for all of dyslexia, it is important to pursue potential major loci for dyslexia using linkage techniques.
Differential assortative mating found for academic and demographic variables as a function of time of assessment.
The purpose of this study was to examine changes in spousal similarity that occur as a function of time of assessment and to assess the extent to which assortment is a function of initial versus "realized" similarity. Similarity for academic achievement test scores obtained when adults were in elementary and high-school grades was examined in approximately 170 couples. Similarity for occupational and educational traits achieved in adulthood and during marriage was also assessed. The data suggest small but significant assortative mating for test data obtained while husbands and wives were in elementary school. This is in contrast to the larger and significant spousal correlations observed for high-school test scores. Further adjustment procedures indicated that most of the significant high-school test score correlations remained, even after elementary school academic abilities were controlled for. Moreover, spousal correlations for academic-related variables assessed after marriage, such as occupation and college education, were only slightly higher than high-school test score correlations and showed some shrinkage after controlling for school-aged academic performance. Some minor convergence was found for one of the variables assessed after marriage using a multiple regression procedure advocated by Price and Vandenburg (1980). The discontinuity in assortment found for elementary, high-school, and adult variables is related to the mate selection procedure and how it appears to be based on the phenotype best approximating that of an adult.
Comment on analysis of psychiatric comorbidity in twins.
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Reliability and validity of retrospective self-reports of the age of pubertal onset using twin, sibling, and college student data.
This study presents a methodology, derived from behavioral genetic research, designed to evaluate the validity of retrospective self-report inventories. The application of this technique to college student, twin, and sibling data demonstrated the reliability and validity of a retrospective self-report questionnaire on the timing of pubertal onset. Support was provided by four main findings: (1) substantial test-retest reliability coefficients for individual items (r ranged from .73 to .97) were obtained for a sample of college students; (2) nearly all of the monozygotic twin (MZ) intraclass correlations exceeded those for dizygotic twins (DZ); (3) the magnitude of the test-retest and intraclass correlations for recall of the timing of pubertal onset followed theoretical expectations for a trait demonstrating significant genetic influence (i.e., r for the same individual tested twice greater than r for MZs greater than r for DZs greater than r for siblings); (4) the expected secular trend of a cross-generational decrease in the age of sexual maturation was demonstrated for retrospective self-reports of family members representing three different generations. Moreover, the size of the mean differences across generations mirrored those reported for nonretrospective assessments of the actual age of pubertal onset. Finally, the value of retrospective self-report surveys in psychological research is discussed, and the relative merits of these instruments as indices of individual differences in pubertal development, as opposed to indices of the actual age of sexual maturation, are emphasized.