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Genetics and OUSINS C

DY behaviour A

SK any to complete the following phrase: ‘nature–nurture ______’. A argues that should The answer will no doubt be ‘debate’ or ‘controversy’. But the controversy that prepare to maximise the benefits and minimise the swirled around behavioural genetics in during the 1970s risks that will emerge from DNA research. has largely faded. During the 1980s and, especially, the 1990s, psychology became In my view, this choice represents one as they are to genetic influences. In fact, much more accepting of genetic influence, of the most dramatic shifts in the modern behavioural genetic research provides the as can be seen in the increasing number of . Indeed, the wave strongest available evidence for the behavioural genetic articles in mainstream of acceptance of genetic influence in importance of environmental factors. But psychology journals and in research grants. psychology is growing into a tidal wave in some areas of psychology, especially One symbol of this change was the 1992 that threatens to engulf key messages psychopathology, the pendulum centennial conference of the American coming from behavioural genetic research. representing the accepted view may be Psychological Association. In preparation The first message is that play swinging too far from environmental for the conference, a committee selected a surprisingly important role throughout determinism to genetic determinism. two themes that best represented the past, psychology. But the second message is present, and future of psychology. One of just as important: individual differences Perspectives the two themes chosen was behavioural in psychological traits are due at Behavioural genetics focuses on questions genetics (Plomin & McClearn, 1993). least as much to environmental influences of why individuals within a species differ

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in behaviour (e.g. why children differ in behavioural genetics and evolutionary increase in risk over the general population. rates of language acquisition), whereas psychology are so different that I think it The results of this small study have been much research in psychology investigates causes confusion to conflate the two fields. replicated in other studies (as species-typical behaviour (e.g. the average I should emphasise that perspectives are reviewed by Bailey et al., 1996). age at which children use two-word not right or wrong, just more or less useful sentences). Descriptions and explanations to address particular questions. The twin method Why are identical of species-typical behaviour bear no so much more concordant for autism necessary relationship to descriptions and Autism as an example than non-identical twins? The most explanations of individual differences As recently as the 1970s autism was parsimonious explanation is that identical within a species. For example, the fact that thought to be caused by cold, rejecting twins are much more alike genetically. our species begins to use two-word parents. Certainly, parents whose children Another hypothesis puts the blame on sentences at the average age of 18 months are autistic behave differently towards their prenatal factors. Identical twins often share is an evolutionary adaptation ultimately children compared with parents of non- the same chorion (the outermost membrane due to selection of genes, but this does not autistic children, but the direction-of-effects surrounding the foetus during prenatal mean that genetics is responsible for the question looms large: Are the differences in development), which might make them delayed use of two-word sentences by parenting cause or effect? The accident of more similar than non-identical twins (who some children. nature that results in identical never share the same chorion). So far the The fundamental accomplishment (monozygotic) twins or non-identical scanty evidence relevant to this issue is of genetic research in psychology to date (fraternal or dizygotic) twins provides one mixed (Sokol et al., 1995). Another has been to demonstrate the ubiquitous way to address this question. Identical possibility is that twins may not be importance of genetics throughout twins are like clones, genetically identical representative of the non-twin population psychology. As described later, this to each other because they came from the because of adverse intra-uterine evidence consists of twin studies that same fertilised egg. Non-identical twins, on environments caused by sharing a womb compare the similarity of identical and the other hand, developed from two eggs (Phillips, 1993). However, the statistical non-identical twins; and studies that happened to be fertilised at the same distributions for most psychological that consider the resemblance of adopted- time. Like other siblings, they are only half dimensions and disorders for twins and away children to their biological parents. as similar genetically as identical twins. non-twins are generally similar (e.g. These methods and the theory that At the Institute of Michael Christensen et al., 1995). underlies them are called quantitative Rutter and his colleague Susan Folstein A subtle but important factor is that genetics, in contrast to molecular genetic were the first to use the twin method to identical twins might have more similar research, which attempts to identify investigate the causes of autism (Folstein & experiences than do non-identical twins specific genes. Behavioural genetics Rutter, 1977). They reasoned that if autism after they are born. The use of the twin includes both quantitative genetic research is caused by parental treatment, then non- method is based on the assumption that the and, increasingly, molecular genetic identical twins ought to be as similar environments of non-identical twins reared research. Although this brief target article (concordant) for autism as are identical in the same family are approximately as is limited to human behavioural genetics, twins, because both types of twins are similar as the environments of identical more powerful quantitative genetic and reared by the same parents in the same twins reared in the same family. This molecular genetic methods are available for place and the same time and presumably assumption has been tested in several ways analysing animal behaviour (Plomin et al., get similar treatment. But if autism is and appears reasonable for most traits, 2001). influenced by genes, then non-identical although it has not been tested specifically We can see this focus on species-typical twins ought to be less concordant. Folstein in regard to autism (Bouchard & Propping, behaviour in several key areas of and Rutter located 10 autistic children in 1993). Although the possibility remains psychology. For example, experimental Britain who were non-identical twins. In that identical twins may be treated more psychology implicitly studies species- none of these cases was the other twin also alike by their parents because they are typical behaviour, comparing an autistic. This result was not surprising, more similar in appearance and behaviour, experimental group with a control group because autism is rare (an incidence of the twin method provides a rough but representing typical behaviour, with about one in a thousand) and it was already useful screen to unpack the ‘bottom-line’ individual differences considered as an known that only about 3 per cent of the effects of genes and environment (Martin error term in an analysis of . non-twin siblings of autistic children are et al., 1997). Similarly, much molecular genetic research autistic. The surprise came in the result for consists of experimentally mutating a identical twins. Folstein and Rutter found The adoption method Although there so that it is no longer expressed, and 15 children diagnosed as autistic who were are no adoption studies of autism, the comparing these mutated animals with identical twins. Eight of these children adoption method is another quasi- normal animals; whereas behavioural were in four concordant pairs of twins in experimental design that has a different genetics has focused on naturally occurring which both identical twins were diagnosed of assumptions and potential problems. . Finally, evolutionary as autistic. The incidence of autism in Family members normally share both psychology also focuses on species-typical children who have an autistic sibling, (first-degree relatives correlate behaviour using comparisons between though low in absolute terms, represents .50 genetically) and environment (they species as evidence for evolutionary a risk that is 30 times higher than that for share the same family). Thus, familial adaptations. Although this is a type of children whose siblings are unaffected; the correlations cannot tell us about the relative genetic analysis of behaviour, the incidence in children who have an autistic extent to which genetic and environmental perspectives and empirical foundations for identical twin represents a 500-fold factors contribute to observed resemblance

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between family members. The adoption I found that adoptive families are Another direction for research concerns method separates the effects of nature and reasonably representative of the population the effects of the environment. Because nurture by studying adopted-apart genetic and that selective placement was negligible identical twins are not 100 per cent relatives (to assess the role of genetics) and (Plomin et al., 1997). concordant for autism even though they by studying genetically unrelated Twin and adoption studies can be used are identical genetically, twin studies also individuals brought together by adoption not only to demonstrate the statistical provide strong support for the importance (to assess the role of family environment). significance of genetic influence but also of environmental factors (though no For example, for most psychological to estimate its effect size, called . support for theories that place the blame traits parents and offspring resemble each Heritability is that proportion of the on the parents’ behaviour). Environmental other. Because these are genetic-plus- variance of a particular trait in a population factors must contribute to differences in environmental parents, parent–offspring that can be accounted for by genetic autism for two children – even identical resemblance could be due to nature or factors. twins – growing up in the same family. nurture. ‘Genetic’ parents and their Such environmental influences are called adopted-away offspring do not share Beyond heritability For autism, the twin ‘non-shared’ to distinguish them from postnatal environment and thus their research without the additional weight of shared environmental influences that make resemblance can be attributed to genetics confirming adoption data was responsible children growing up in the same family and (in the case of birth mothers but not for the shift from thinking about autism as similar. What are the specific non-shared fathers) prenatal environment. a disorder caused entirely by environmental environmental factors that make identical ‘Environmental’ parents and their adopted factors to its current status as one of the twins growing up in the same family children do not share heredity and thus most heritable mental disorders. Genetic different and that widen the differences between other sibling pairs? Much remains to be learned about this important issue, for autism and for other psychological characteristics (Harris, 1998). Another example of the use of genetic research to help us understand the environment has been called ‘the nature of nurture’ (Plomin, 1994). Twin and adoption studies have shown that genetic factors can have effects on the environment itself and that such effects can be found on aspects of the environment measured in . Such effects, known as ‘genotype–environment correlations’, could operate in various ways. Genetic factors could affect the reactions we evoke in others and the experiences that we select, construct and re-construct in memory. For OUSINS

C example, autistic children evoke distancing DY

A responses in others and select non-social experiences that reinforce their genetic their resemblance can be attributed to research has now moved on to other tendency towards social and family environment. The adoption method issues. One direction is to examine, using communication abnormalities. also includes siblings or twins reared apart. , the genetic links Environmental influences need to be Because the twin and adoption methods are between autism and other problems. The examined in genetically sensitive designs, so different, greater confidence is genetic vulnerability to autism has been and genetic influences need to be examined warranted when results from these two shown to extend well beyond classic in environmentally sensitive designs that methods converge on the same conclusion diagnostic symptoms: it includes milder incorporate specific measures of the – as they usually do. social and communication difficulties that environment (Rutter et al., 1997). One issue for adoption studies is that are found to be more common in the A new direction for research is to adoptees and their adoptive families might biological relatives of autistic people attempt to identify some of the specific not be representative of the population as (Rutter et al., 1999). genes responsible for the genetic a whole, either because they have distinctive characteristics or because they span a narrower range. There is also the possibility that adopted children might be HYPERACTIVITY selectively placed with adoptive parents Several twin studies of attention deficit hyperactivity disorder (ADHD) have been matched to the birth parents. These issues carried out in recent years.These studies have consistently pointed to high heritability can be examined empirically. For example, for hyperactive symptoms and for the ADHD diagnosis itself.Again, genetic links between in a longitudinal prospective adoption the normal and abnormal have been found. Several molecular genetic studies have study of normal behavioural development indicated a role for dopamine genes in the aetiology of hyperactivity (Thapar et al., 1999). that began in 1975, my colleagues and

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of for genetic influence is general READING DISABILITY cognitive ability (g), although it remains Reading disability shows moderate heritability – concordances for non-identical and controversial in psychology (Plomin et al., identical twins are about 40 per cent and 70 per cent respectively. As with autism and 2001). Dozens of studies including more many other disorders, the genetic liability for reading disability extends beyond the than 8000 parent–offspring pairs, 25,000 dichotomy imposed by a yes-or-no diagnostic procedure. On average, the non-identical pairs of siblings, 10,000 twin pairs, and twins of reading-disabled probands (index cases) are much better readers than the hundreds of adoptive families all converge probands themselves, but they are significantly worse readers than the rest of the on the conclusion that genetic factors population. In contrast, the identical twins of reading-disabled probands read almost as contribute substantially to g. Estimates of poorly as the probands.As with autism, these results suggest a genetically influenced the effect size, called heritability, vary from continuum between normal and abnormal.That is, genetic factors that affect diagnosed 40 to 80 per cent; but estimates based on reading disability may be the same genetic factors that contribute to the quantitative the entire body of data are about 50 per dimension of reading ability (DeFries & Alarcón, 1996). cent, indicating that genes account for Results that demonstrate a continuum between the normal and abnormal have major about half of the variance in g. Sorting implications for molecular genetic research, because they imply that many different genes the results by age indicates that heritability contribute to the heritability of common disorders (Plomin et al., 1994). Unlike the increases from about .20 in infancy to relatively rare disorders in which a single gene is necessary and sufficient for the about .40 in childhood to .60 or higher development of the disorder, common disorders like reading disability are complex traits later in life (McGue et al., 1993), even for influenced by environmental factors and by many genes of varying but relatively small individuals 80+ years old (McClearn et al., effect size (called quantitative trait loci or QTLs). Multiple-gene systems require more 1997). powerful genetic designs that can detect genes of small effect. Reading disability is the This increase in the heritability of g first common behavioural disorder to which a QTL approach was applied.A linkage throughout the lifespan is interesting between reading disability and DNA markers on the short arm of 6 because it is counterintuitive in relation to (Cardon et al., 1994) has been consistently replicated (e.g. Gayán et al., 1999).This QTL the accumulation of life’s experiences. It appears to be broad in its effect, involving both phonological (auditory) and orthographic may be that heritability increases because (visual) aspects of reading disability. individuals seek and create environments correlated with their genetic propensities. That is, genetic propensities might be best contribution to various disorders, even genetic influence than common medical considered as appetites rather than though it seems likely that the target is disorders such as breast cancer or heart aptitudes, making some children hungrier many genes of small effect size rather than disease (Plomin et al., 1994). The reason for knowledge and more able to digest it. one or two genes of major effect. An for the greater genetic influence for Molecular genetic studies are also international team initially led by Rutter behavioural disorders may be that many beginning to identify genes associated and Monaco has identified a region on different biological pathways can affect with g (Fisher et al., 1999). chromosome 7 that may be linked with behaviour. Behaviour can be seen as the vulnerability to autism (International downstream outcome of many different New avenues Genetic research to date Molecular Genetic Study of Autism biological systems; thus, genetic influences has only scratched the surface of possible Consortium, 1998). Finding specific genes can operate on behaviour via all of the applications in psychology, even within the that contribute to vulnerability to autism upstream systems. best-studied domains of psychopathology, and other behavioural disorders and Genetic influences are not limited to , and cognitive disabilities and dimensions will provide the strongest disorders, they also contribute to normal abilities. For psychopathology, genetic evidence for genetic influence and will variation in personality (Loehlin, 1992) and research has just begun to consider make it easier to explore the developmental in cognitive abilities (Plomin & DeFries, disorders other than and interplay between nature and nurture 1998), as well as to psychopathology. For the major mood disorders. Developmental (Plomin & Rutter, 1998). self-report questionnaires, most personality psychopathology has recently become an traits show moderate genetic influence, active area of genetic research (Rutter et Other examples with twin correlations of about 0.50 for al., 1999). Personality is so complex that For milder psychological disorders too, identical twins and 0.20 for non-identical it can keep researchers busy for decades, a more balanced view that accepts the role twins. In the case of self-report personality especially as they go beyond self-report of nature as well as nurture is beginning to questionnaires, the far fewer adoption questionnaires to use other measures such prevail, and researchers are making studies appear to suggest only about half as and ratings by others progress in identifying specific genes. Two as much genetic influence as twin studies, (Riemann et al., 1997). A rich territory further examples are reading disability and perhaps because twin studies capture for future exploration is the links between hyperactivity (see boxes). different types of genetic variance than psychopathology and personality (Nigg & adoption studies (Plomin & Caspi, 1998). Goldsmith, 1994). New directions for Other behavioural disorders and Genetic factors even appear to be involved genetic research on cognitive abilities and dimensions Moderate genetic influence in social and political attitudes and disabilities includes the systematic analysis has been found for most behavioural occupational interests (Plomin et al., 2001). of psychological theories of cognition disorders that have been studied to date, Genes responsible for the heritability of (Mackintosh, 1998), the use of information- including schizophrenia, mood disorders personality are beginning to be identified processing measures of reaction times (e.g. and anxiety (Plomin et al., 2001). Indeed, (Hamer & Copeland, 1998). Neubauer et al., 2000), and brain-imaging behavioural disorders tend to show greater One of the best documented cases in all measures (Kosslyn & Plomin, 2001).

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The vast majority of human genetic research in psychology has centred on psychopathology, personality, and cognitive disabilities and abilities because these areas have long been the focus of research on individual differences. Three new areas of psychology that are beginning to be explored genetically are psychology and aging, , and (Plomin et al., 2001). Some of the oldest areas of psychology – and , for example – have not emphasised individual differences and as a result have yet to be explored systematically from a genetic perspective.

Entire disciplines within the social and OUSINS behavioural , such as economics, C DY education, and sociology, are still A essentially untouched by genetic research. becoming available that can genotype several million DNA bases that differ Genetic research in psychology is thousands of genes in a few minutes at among us. The future of genetic research moving beyond heritability, as illustrated costs that will eventually be very low per lies in moving from finding genes by the examples of autism, reading individual. () to finding out how genes work disability and hyperactivity. Asking Although some psychology departments (functional genomics). Functional whether and how much genetic factors already have DNA laboratories, it is likely genomics is usually considered in terms of affect psychological dimensions and that most psychological research with DNA bottom-up at the cellular disorders are important first steps in will be accomplished through level of analysis. However, a top-down understanding the origins of individual collaborations with molecular or psychological level of analysis may be differences, but these questions are only through commercial arrangements. It is even more valuable in understanding how a beginning. The next step involves the critical for the future of psychology as a genes work at the level of the intact question ‘how’ – that is, the study of the science that we be prepared to use DNA in organism, in understanding interactions mechanisms by which genes have their our research and eventually in our clinics. and correlations between genes and effects. Avenues for genetic research in What has happened in the area of dementia environment, and in leading to new psychology include developmental change in the elderly will be played out in many treatments and interventions. For example, and continuity, links between the normal areas of psychology. The only known risk top-down approaches for genes associated and abnormal, multivariate genetic analysis factor for late-onset Alzheimer’s disease with learning and memory could trace the of heterogeneity and comorbidity, and the (LOAD) is a gene, effects of genes through cognitive interplay between genes and environment. (ApoE), involved in cholesterol transport. processes as outlined by theories of An especially exciting direction for A form of the gene called 4 (e.g. Mackintosh, research is identification of some of quadruples the risk for LOAD but is 1998), in contrast to a bottom-up approach the specific genes responsible for the neither necessary nor sufficient to produce that begins with the cellular functioning of heritability of psychological disorders the disorder; hence it is a QTL. The neuroreceptors. The phrase ‘behavioural and dimensions. association between allele 4 and LOAD genomics’ has been suggested to emphasise was first reported only in 1993, but it has the importance of top-down levels of DNA already become de rigueur in research on analysis in understanding how genes work Although attention is now focused on dementia to genotype subjects for ApoE to (Plomin & Crabbe, in press). Bottom-up finding specific genes associated with ascertain whether the results differ for and top-down levels of analysis of complex traits, the greatest impact on individuals with and without this genetic gene–behaviour pathways will eventually psychology will come after genes have risk factor. Genotyping ApoE will become meet in the brain. The grandest been identified. clinically routine if this genetic risk factor implication for science is that DNA will is found to predict differential response to serve as an integrating force across diverse Using DNA Few psychologists are likely interventions or treatments. disciplines. to join the hunt for genes because it is difficult and expensive, but once genes are Scientific implications Among Clinical implications Geneticists need found, it is relatively easy and inexpensive geneticists it is generally believed that to define , to use them (Plomin & Rutter, 1998). DNA we will be awash in genes associated with to design treatment, intervention and can be obtained from cheek swabs, rather complex traits including behaviour in the prevention programmes, and to evaluate than blood, at a cost of less than £10 per next few years. This is especially likely these programmes. For clinical psychology, individual. One cheek swab yields enough as the Human Project completes DNA may eventually lead to gene-based DNA to genotype thousands of genes, and sequencing all 3.5 billion DNA bases (the diagnoses and treatment programmes. The several genes can be genotyped for less four-letter alphabet of the genome that most exciting potential is secondary than £5 per individual. Microarrays the size forms the steps in the spiral staircase of prevention. Because DNA analysis can of a postage stamp, called DNA chips, are DNA) and identifies all genes and the be used to predict genetic risk for an

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individual, it offers the hope for genetics implies therapeutic nihilism, even genetics justifies the status quo (Rutter & intervention before disorders create for a single-gene disorder. This point is Plomin, 1997). cascades of complications. even more important in relation to complex Interventions for complex psychological disorders that are influenced by many ‘DNA’ For these reasons, it is crucial that traits, and even for single-gene disorders, genes and by many environmental factors psychologists be prepared to maximise the are likely to involve environmental rather as well. benefits and minimise the risks that will than . For example, emerge from DNA research. Students in phenylketonuria (PKU), a metabolic Social implications Psychologists psychology must be taught about genetics disorder that can cause severe mental should participate constructively in the to prepare them for this future. Otherwise retardation, is caused by a single gene on discussion of scientific, clinical and social this opportunity for psychology will slip chromosome 12. A particular form of the implications of the advances brought about away by default to geneticists, and genetics gene, found in 1 in 10,000 babies, damages by DNA research. The search for genes is much too important a topic to be left to the developing brain postnatally. This form involved in behaviour has led to a number geneticists! Clinical psychologists use the of mental retardation has been largely of ethical concerns: there is fear that the acronym ‘DNA’ to note that their clients prevented, not by high-tech solutions such results will be used to justify social ‘did not attend.’ It is critical to the future as correcting the mutant DNA or by inequality, to select individuals for of psychology as a science that, for all eugenic programmes or by , but education or employment, or to enable psychologists, DNA denotes deoxyribonucleic rather by a change in diet that prevents the parents to pick and choose among their acid rather than ‘did not attend’. mutant DNA from having its damaging foetuses. These concerns are largely based effects. For this reason newborns have been on misunderstandings about how genes Professor Robert Plomin is at the screened for decades for PKU to identify affect complex traits such as the mistaken Social, Genetic and Developmental those with the disorder so their diet can be implication of therapeutic nihilism Psychiatry Research Centre, Institute of changed. The example of PKU serves as an mentioned earlier, the assumption that Psychiatry, London. Tel: 020 7848 0894; antidote to the mistaken notion that genetic factors imply determinism, or that e-mail: [email protected].

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