Society and the not-so-new genetics: what are we afraid of? Some future predictions from a social scientist.
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If language is the result of specialized structures in the brain and if these language-specific structures are genetically encoded, one would expect to find evidence of the heritability of language. In this article I review the results of family aggregation, pedigree, sex ratio, commingling, and segregation studies of spoken language disorders. The results of these studies provide evidence that, although spoken language disorders are genetically and behaviorally heterogeneous, genetic factors may play a substantial role in many cases of developmental spoken language disorders.
The most common major comorbid disorders associated with eating disorders include substance use disorders, personality disorders, mood disorders, anxiety disorders, and obesity. To test conceptual models of the relationship between the eating disorders and these comorbid disorders, complex research paradigms are needed, including epidemiological studies, behavior-genetic studies, and longitudinal research designs. Comorbidity may be a significant factor to consider as approaches to the treatment of eating disorders continue to evolve.
The low male/female ratio at birth in African populations has been attributed to a variety of genetic, behavioral, and environmental factors. A low sex ratio at birth has been associated with maternal malnutrition in mammals, but this issue has not been studied in humans. In this study we analyzed the relation between maternal nutritional status and sex ratio at birth in 3282 children born to 684 women from a rural African society. Short maternal stature and obesity were independently related to a low sex ratio at birth. These results are consistent with animal experiments that indicate an adverse effect of maternal malnutrition on male fetuses. The results warrant further research in this area.
Recent behavioral genetic research emphasizes the nonshared family environment as an important contributor to psychological differences between siblings raised in the same family. Most studies of nonshared sibling experiences have examined the effects of differential maternal and paternal treatment separately and have not examined family-level processes. This study attempted to replicate the findings of McHale, Crouter, McGuire, and Updegraff and also of Volling in which relations between family patterns of differential parental treatment, child outcomes, and family functioning were examined. Questionnaire data were collected from 60 maritally intact families with toddler and preschool siblings. Congruence in mothers' and fathers' reports of differential treatment (i.e., similar treatment from both mother and father) was most frequent. Parents' reports of differential enjoyment were related to differential favoritism, whereas their reports of differential discipline were not. Both mothers and fathers were more likely to discipline the older sibling than the younger toddler. Sibling and marital harmony characterized families in which the father disciplined the older sibling more and mothers disciplined the two children equally. Incongruent patterns of differential favoritism (i.e., one parent treats the children equally while the other favors one child) were associated with marital distress. Preschool siblings exhibited greater internalizing and externalizing symptoms when both mothers and fathers disciplined them more than their younger sibling. The findings of this study with very young siblings differ in some respects from those with older children and suggest that future research needs to examine differential parental treatment as a developmental process across childhood.
Direct and indirect behavioral effects of genetic disorders of mental retardation were identified. Three models of direct effects were examined: the no-specific effect model (all genetic disorders lead to identical behavioral outcomes), the totally specific model (each genetic disorder leads to unique outcomes), and the partially specific model (two or more genetic disorders lead to outcomes not shared by others with mental retardation). Although several cases of totally specific outcomes have been identified, partially specific effects most often occur. Persons in the surrounding environment are indirectly affected by behavioral propensities of different genetic disorders. Direct and indirect effects are also related to biological and developmental theory.
A diallel cross involving five noninbred (purebred) lines of Japanese quail indicated that additive and nonadditive genetic effects had important influences on behaviors involved in a detour learning task. Social isolation for 3 hr was used to provide additional motivation which enabled detection of differences among strains. The percentage of quail, within purebred lines, that solved a 4-min detour task three or more consecutive times ranged from 52 to 72. Differences among purebreds were significant for most of the components of the learning task. Further, the data suggested strain differences associated with the successful attainment of the desired goal when there was a similar level of general activity.
In a variety of species, strain differences in aggressive behaviors strongly indicate genetic influences. In people, as suggested, for example, by the work of Kagan, Rothbart, Cloninger, and their collaborators, long-lasting differences in temperament argue for genetic as well as environmental effects. After well-controlled experimentation in mice, we have learned five lessons about gene/behavior causal relations bearing on sociosexual and aggressive behaviors. The effect of a given gene on a given behavior depends upon: (1) exactly when and where that gene is expressed in the brain; (2) the gender of the animal in which it is expressed; (3) the age of the animal; (4) the nature of the opponent; and (5) the form of aggression (e.g., testosterone-facilitated aggression vs. maternal aggression). Moreover, in female mice, better social recognition is correlated with lower levels of aggression. We have gathered evidence for a four-gene micronet involving estrogen receptors alpha and beta, oxytocin, and the oxytocin receptor as expressed in the hypothalamus and amygdala. Normal performance of this micronet is required for social recognition and thus for control over aggression. Underlying certain genetic influences on sociosexual behaviors and aggression may be alterations in generalized brain arousal.
Several studies have been conducted to understand the genetic correlates of Alzheimer disease (AD)-related behavioral and psychological symptoms in dementia (BPSD). However, given that BPSD rarely occur in isolation, it has been suggested that targeting BPSD individually is too narrow of an approach if one wants to accurately define all the associated risk factors. To date, we know of no work on genetic polymorphisms related to behavioral endophenotypes in AD. The present study sought to evaluate the relationship between such behavioral endophenotypes in AD and genetic variations in dopamine- or serotonin-related genes, such as catechol-O-methyltransferase (COMT) or 5-HTT gene-linked promoter region (5-HTTLPR), and apolipoprotein E (APOE). Among 232 AD patients who underwent clinical and neuropsychological examination, a behavioral and psychiatric evaluation, and genotyping at COMT, 5-HTTPLR, and APOE; 66.4% showed more than one behavioral symptom. By Principal Component Analysis of Neuropsychiatric Inventory (NPI) symptoms four endophenotypes were identified, these were termed "psychosis", "moods", "apathy", and "frontal". Modeling NPI symptom-endophenotype-genotype relationships, and taking into account possible confounds (i.e. demographic characteristics, comorbidities, concomitant pharmacological treatments, and disease severity) by latent variable models, COMT and 5-HTTLPR genetic variations correlated with "frontal" and "psychosis" endophenotypes. APOE genotype did not correlate with any endophenotype. These findings suggest that the possibility of identifying distinct phenotypes on a genetic basis among AD patients exists, and suggest that clustering of BPSD into endophenotypes might provide a new strategy for guiding future research on this issue.
Tremendous progress in the field of human genetics has made a major impact over the last two decades into our understanding of many Mendelian disorders affecting humans. It is much more difficult to approach the genetics of complex disorders and is particularly challenging in the case of dissecting genetics of the wide range of behavioral variation in the general population. Knowledge of the biology and genetics of Mendelian traits is beginning to inform studies in complex genetics. Furthermore, the convergence of this growing knowledge with increasingly powerful new tools now put complex genetics of behavior within reach. The bottleneck in such studies and the greatest challenge to investigators is the rigorous phenotyping of human research subjects.
OBJECTIVES: To assess the longitudinal covariance between emotionality, activity, and sociability (EAS) temperamental traits and anxious/depressed behavior, attention problems, delinquent behavior, and aggressive behavior and to assess the significance of genetic and common environmental influences on the temperament and behavior relations. METHOD: Parental responses to the Child Behavior Checklist and the EAS Temperament Survey were collected from five national cohorts of Norwegian same-sex twins. The final sample consisted of 759 twin pairs aged 7 through 17 at 2-year follow-up. RESULTS: High emotionality predicted anxious/depressed behavior, attention problems, delinquent behavior, and aggressive behavior. The influence on delinquent and aggressive behavior was stronger in boys. Aggressive behavior was further predicted by high activity scores, especially in younger children. Significant genetic influence was found for the covariance between emotionality and attention problems and emotionality and aggressive behavior. CONCLUSION: Emotionality was the strongest temperamental predictor of behavior problems. The mechanisms involved in the associations between temperament and behavior problems appeared to differ with kind of behavior problems.
The effects of intracerebral infection with herpes simplex virus on the subsequent behavior of two strains of mice were examined. Infected Nya:NYLAR mice were hyperactive and did not show any deficits in the acquisition or reversal of a spatial learning task. In contrast, infected Nya:(SW) mice were hypoactive and made more errors than controls during both phases of the learning tasks. These differences in the nature of the sequelae to infection were related to an overall higher virus titer in the brains of Nya:(SW) mice, an effect particularly marked in the cerebral hemispheres. The results suggest that herpes encephalitis may produce a variety of behavioral syndromes, depending in part on the genetic background of the host. The relevance of these findings to clinical disorders produced by viral infection is discussed.
A genetic screen using mice was performed to identify dominant loci affecting behavior. Mice were mutagenized with ENU, then bred to examine their G1 offspring for behavioral abnormalities. Potentially mutant G1 pups were screened through a variety of behavioral assays, including tests of learning and memory, sensorimotor gating, fear and anxiety, nociception (pain perception) and locomotor activity. Mice falling outside the normal performance distribution in these tests were considered potential behavioral mutants and were bred for further analysis. Outliers included both animals with very discrete defects and animals with abnormal performance across a range of tests. To date, we have identified two confirmed mutants affecting sensorimotor gating. These results provide further impetus for the use of random mutagenesis screens as a tool for dissecting the genetic basis of brain and behavior.
Mating of Drosophila melanogaster is a sterotypically patterned behavior consisting of a fixed sequence of actions that are primarily under genetic control. Mutations that disrupt specific aspects of mating activities offer a starting point for exploring the molecular machineries underlying sexual behavior. Several genes, identified as causing aberrant sexual behavior when mutated, have been isolated and cloned, providing molecular probes for expression and mosaic analyses that can be used in specifying the cells responsible for the behavior. This review presents current understandings of mating behavior obtained by such molecular and cellular approaches and provides an overview of future directions of research in behavioral genetics.
The genetic basis of insertion behavior of laboratory strains of Drosophila melanogaster was examined. Reciprocal crosses among five strains revealed a significant effect of interaction between cytoplasmic/maternal factors and the chromosomal genotype in determining the insertion tendency, thus complicating the characterization of the dominant/recessive nature of the insertion genes. The majority of heterozygous combinations demonstrated dominance or partial dominance for the higher insertion tendency over low insertion, while a few combinations produced results to the contrary. These could be due to a more complex genetic basis of insertion behavior than a simple dominant/recessive relationship or else to the cytoplasmic/maternal-chromosome interactions. Examination of the effects of each chromosome revealed the greatest contributions to insertion tendency from the second and third chromosomes, with a significant effect of interaction or nonadditivity of the insertion genes in these two chromosomes in the genotypes tested. The X and fourth chromosomes appear to contribute a small effect in some strains.
It can be hypothesized that children inherit their parents' driving habits both through genetic disposition and model learning. A few studies have shown indeed that parents' and their children's traffic convictions and accidents correlate which, however, may be due to life style and other exposure factors. This study aimed at investigating the relationships between parents' and their children's self-reported driving behavior. The subjects were 174 parent-child pairs who independently completed a questionnaire. Driving behavior-driving style-was evaluated by means of Manchester driver behavior questionnaire (DBQ), while data about driving exposure, life style, accidents, and traffic tickets were also collected. A series of regression models indicated that parents' self-reported driving behavior explains their children's respective self-reported behavior, even when exposure and demographic and life-style factors are controlled.