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PubMed1987

Research strategies in human behaviour genetics.

Genetic variation influencing normal and abnormal human behaviour has been studied since Francis Galton's work in the second half of the 19th century. However, most of these studies have consisted of biometric analysis of complex phenotypes; the genotype has been treated as a 'black box'. The concepts and analytical tools of modern genetics have rarely been used. In this lecture, some examples are given of approaches combining tools from genetics, cytogenetics, and various fields of neurobiology which might help in the analysis of genetic mechanisms leading, in interaction with the environment, to individual differences in behaviour, mental performance, and susceptibility to mental diseases.

Genetics, Behavioral↗
PubMed2006

Towards unbiased parentage assignment: combining genetic, behavioural and spatial data in a Bayesian framework.

Inferring the parentage of a sample of individuals is often a prerequisite for many types of analysis in molecular ecology, evolutionary biology and quantitative genetics. In all but a few cases, the method of parentage assignment is divorced from the methods used to estimate the parameters of primary interest, such as mate choice or heritability. Here we present a Bayesian approach that simultaneously estimates the parentage of a sample of individuals and a wide range of population-level parameters in which we are interested. We show that joint estimation of parentage and population-level parameters increases the power of parentage assignment, reduces bias in parameter estimation, and accurately evaluates uncertainty in both. We illustrate the method by analysing a number of simulated test data sets, and through a re-analysis of parentage in the Seychelles warbler, Acrocephalus sechellensis. A combination of behavioural, spatial and genetic data are used in the analyses and, importantly, the method does not require strong prior information about the relationship between nongenetic data and parentage.

Animals↗
PubMed2000

Personality disorder traits, family environment, and alcohol misuse: a multivariate behavioural genetic analysis.

AIMS: This study seeks to estimate the extent to which a common genetic and environmental basis is shared between (i) traits delineating specific aspects of antisocial personality and alcohol misuse, and (ii) childhood family environments, traits delineating broad domains of personality pathology and alcohol misuse. DESIGN: Postal survey data were collected from monozygotic and dizygotic twin pairs. SETTING: Twin pairs were recruited from Vancouver, British Columbia and London, Ontario, Canada using newspaper advertisements, media stories and twin clubs. PARTICIPANTS: Data obtained from 324 monozygotic and 335 dizygotic twin pairs were used to estimate the extent to which traits delineating specific antisocial personality traits and alcohol misuse shared a common genetic and environmental aetiology. Data from 81 monozygotic and 74 dizygotic twin pairs were used to estimate the degree to which traits delineating personality pathology, childhood family environment and alcohol misuse shared a common aetiology. MEASUREMENTS: Current alcohol misuse and personality pathology were measured using scales contained in the self-report Dimensional Assessment of Personality Pathology. Perceptions of childhood family environment were measured using the self-report Family Environment Scale. FINDINGS: Multivariate genetic analyses showed that a subset of traits delineating components of antisocial personality (i.e. grandiosity, attention-seeking, failure to adopt social norms, interpersonal violence and juvenile antisocial behaviours) are influenced by genetic factors in common to alcohol misuse. Genetically based perceptions of childhood family environment had little relationship with alcohol misuse. CONCLUSIONS: Heritable personality factors that influence the perception of childhood family environment play only a small role in the liability to alcohol misuse. Instead, liability to alcohol misuse is related to genetic factors common a specific subset of antisocial personality traits describing conduct problems, narcissistic and stimulus-seeking behaviour.

Adolescent↗
PubMed1995

Alcohol and drug problems: a multivariate behavioural genetic analysis of co-morbidity.

Multivariate biometrical genetic analyses of self-report questionnaire items assessing problem alcohol and drug use were performed on data obtained from a sample of 438 volunteer twin pairs (236 monozygotic twin pairs, 247 dizygotic twin pairs). Additive genetic influences were moderate for all alcohol abuse items (21-46%), frequency of drug use (32%) and illicit drug use (32%). Prescribed drug use and debilitating drug use were largely environmentally determined (86% and 94%, respectively). The influence of environmental factors that influence all members of a family to the same degree (shared family environment) on each item was generally small (0-20%), whereas the influence of environmental factors unique to each family member (non-shared environment) comprised over half of the total variance on all items. Genetic factor analyses identified three uncorrelated common genetic factors. The first genetic factor appears to represent problems associated with alcohol and drug use, such as the inability to fulfil obligations at home, work or school. The second genetic factor is more specific to drug use and represents a general liability towards drug use, illicit or otherwise. The third genetic factor is specific to the alcohol use items only. The observed co-morbidity of alcohol and drug misuse can be attributed largely to a non-shared environmental factor common to both domains. Genetic co-morbidity appears to be limited to alcohol and substance misuse behaviours that interfere with normal daily functioning.

Adolescent↗
PubMed2003

Genetics, behaviour and psychiatry: historical burdens and perspective.

Familiar, twin, adoption and linkage studies represent the usual tools for assessing the possible role of genetics in mental disease. These genetic approaches have been refined in the last years and a number of methodological problems are absent in recent approaches. While there is no doubt that schizophrenia, mood disorders and autism are characterized by a genetic component no linkage study has been successful up to date, apart, probably, the case of autism. The existence of a genetic component does not minimize the role of the environment and of critical life events. It is also evident that no major genes are responsible for these psychiatric diseases: thus, quantitative trait loci analyses might prove fruitful in future research to track the role of different genes contributing to the outcome of different psychopathologies. The main problem, however, is the difficulty of carrying out quantitative analyses since the today's diagnostic tools do not allow a quantitative approach to these phenotypes.

Behavior↗
PubMed1984

Behavioural genetics of early childhood: fears, restlessness, motion sickness and enuresis.

Seventy-nine pairs of same-sex twins were examined at the age of three years at a municipal clinic and their mothers were interviewed to assess the twins' current and past behaviours. The zygosity was determined after the interview by fingerprints and/or bloodtyping in the majority of cases. The following significant differences in concordance between monozygotic and dizygotic twins were found: fear of strangers during observation at the clinic; marked fear of strangers in the first year of life; whether or not the child was startled by sudden noises during infancy; whether or not the child was able to sleep alone at three years without a parent sitting nearby; susceptibility to motion sickness; nocturnal enuresis; short attention span or restlessness during the test.

Child Behavior Disorders↗
PubMed1990

Genetic behaviour of tumorigenicity in human cancer.

The technique of somatic cell hybridization and the concept of tumour suppressor genes share a common history. Somatic cell hybrids between mammalian tumour cells and their normal cellular counterparts invariably are non-tumorigenic, establishing the recessive genetic nature of tumorigenicity. The development of cytogenetics and microcell hybridization has provided methods for localization of the tumour suppressor genes to specific chromosomal regions. Continuing studies of this type will facilitate the isolation of these genes by molecular methods including differential cDNA screening and 'reverse genetics'.

Chromosome Mapping↗
PubMed2006

Examining the state-trait anxiety relationship: a behavioural genetic approach.

State and trait anxiety define different aspects of anxiety, and may represent environmentally and genetically mediated components of this phenotype. Furthermore their relationship, where trait anxiety is expressed through levels of state anxiety under threatening circumstances, may represent a process of interplay between a genetic vulnerability factor and an environmental stressor. To test these hypotheses, we explored genetic and environmental influences on measures of state and trait anxiety in a sample of 1058 twins (521 males and 537 females) aged 8-16. The results were consistent with these hypotheses. State anxiety is largely influenced by environmental factors in males and females whereas trait anxiety shows moderate genetic effects and substantial non-shared environment effects. Their association was accounted for by non-shared environmental effects, with modest genetic and shared environmental inputs. The implications of these results for vulnerability mechanisms involving stress reactivity on anxiety are discussed.

Adolescent↗
PubMed1998

Behavioural genetics: molecular genetics meets feeding ecology.

Fruit fly larvae occur as either 'rovers', which move a long way to find food, or 'sitters', which stay within a more restricted area. This polymorphism is determined by alleles of a cyclic GMP-dependent protein kinase gene; rovers are at an advantage in crowded populations, while sitters have the edge at low population density.

Alleles↗