Michael Rutter

Bio: Michael Rutter is an academic researcher from King's College London. The author has contributed to research in topics: Autism & Conduct disorder. The author has an hindex of 188, co-authored 676 publications receiving 151592 citations. Previous affiliations of Michael Rutter include VCU Medical Center & Center for Advanced Study in the Behavioral Sciences.

Addressing the issue of fractionation in autism spectrum disorder: A commentary on Brunsdon and Happé, Frazier et al., Hobson and Mandy et al.:

Abstract: It seems decidedly odd that after more than half a century of both research and clinical experience with autism spectrum disorders (ASDs), there continue to be arguments on the nature of autism. Diagnostic and Statistical Manual of Mental Disorders–Fifth Edition (DSM-5; American Psychiatric Association (APA), 2013) has not helped in this connection. It abolished the subcategories of ASDs because it had become obvious that, as specified in both Diagnostic and Statistical Manual of Mental Disorders–Fourth Edition (DSM-IV) and International Statistical Classification of Diseases, Tenth Revision (ICD-10), they had not worked. One alternative would have been to seek to devise better specifications, but this was not done – perhaps because there was limited evidence on what would work better and because it was doubted that a new scheme would achieve general acceptance. On the other hand, it is generally assumed that ASDs will prove to be heterogeneous. We know already that they differ in the genes involved (Rutter and Thapar, in press), and it is highly likely that they will also differ in other aspects of biology. So what is all the disagreement about? Let me turn to the four articles. It is appropriate to begin by considering the article by Brunsdon and Happé because it is the only one to provide a thoughtful, empirically based discussion of the evidence both against and for the fractionation of autism at the cognitive level. Table 1 in their article provides a most useful summary of the relevant research findings. As they point out, the evidence indicates that ASDs cannot be accounted for by a single underlying cognitive deficit, at least with respect to those they considered, but nevertheless, there are significant associations between some cognitive skills and not others. The greatest area of ignorance concerns the connections between cognitive test performance and real-life behaviour. Most crucially, too, it is necessary to ask about developmental changes. Both increased and decreased modularisations are possible. Thus, as Pellicano (2013) suggested, even initially separate traits may become more inter-correlated as a result of contextual effects. Conversely, as Karmiloff-Smith et al. (2012) have argued, modularisation cannot be assumed to be innate. Sometimes, features change during the course of development. Autism and Williams syndrome appear to have a very different pattern of cognitive performance when the children are young, but they come closer together with increasing age. Training studies may also be helpful in delineating causal pathways by showing the direction of different effects. What Brunsdon and Happé do not do, however, is consider the evidence that, at some level, there is a coherence to the concept of ASDs. Hobson, by contrast, argues forcefully that there is a coherence to autism, although it is not at all clear how such a proposition might be tested. He rightfully claims that coherence cannot possibly require all individuals with ASD to have all the symptoms. That would not apply to most medical conditions. The example he cites – borderline personality disorder – is unfortunate in view of the major disputes as to whether it exists as a meaningful diagnosis. Nevertheless, diabetes does show both heterogeneity in manifestation and coherence. Hobson then goes on to consider the case of autism arising in congenitally blind children. His own evidence indicated that the course was atypical as compared with autism in non-blind children, but he infers coherence on the basis that the autism fitted in with intersubjectivity theory. Hobson is undoubtedly correct in arguing that autism is a multifactorial disorder in which the particular mix of causal influences will vary from child to child. He is also right to point out that it may well be misleading to suppose some ‘true’ type of autism. But that is where there is a problem in defining autism on the basis of particular features without considering a broader pattern (see below). Frazier et al. put all their reliance on the factor structure of autism symptomatology as measured by Constantino’s social responsiveness scale. They argue that their evidence suggests five highly inter-related factors and that the factor structure may yield important insights into the biology of ASDs. Maybe, but why should it do so? It makes no sense to reduce ASDs to just behavioural dimensions. What about the associations with both savant skills (Howlin et al., 2009) and intellectual impairment (Dykens and Lense, 2011)? What about the strong association with a phase of temporary loss of social and language skills (Pickles et al., 2009), which is much less common in other developmental disorders? What about the development of epileptic Addressing the issue of fractionation in autism spectrum disorder: A commentary on Brunsdon and Happé, Frazier et al., Hobson and Mandy et al. 513522 AUT18110.1177/1362361313513522AutismCommentary 2013

The cognitive development and school achievement of adopted adolescents: The Greek “Metera” study

Abstract: The cognitive development and school performance of 52 adopted adolescents, who spent their first two years of life in “Metera” Babies Center in Athens, Greece, were compared with those of 36 who were brought up in their biological families. Adopted adolescents had significantly lower cognitive development and school performance scores than their comparisons, although within the average range according to general population norms. The higher maternal education in the adoptive mothers was associated with higher cognitive scores in adolescence.

Risks for conduct disorder symptoms associated with parental alcoholism in stepfather families versus intact families from a community sample.

Abstract: BACKGROUND: It is not known if the prevalence of parental psychiatric disorders is higher in stepfather than intact families, or if parental alcoholism is differentially associated with risk for conduct disorder (CD) symptoms in stepfather families versus intact families. METHOD: The sample comprised 839 girls and 741 boys from 792 intact families and 99 girls and 67 boys from 83 stepfather families from a population-based registry of twins aged between 8 and 17 years. Children's current psychiatric symptoms were assessed at personal interview with the child, mother and father. Parental histories of psychiatric disorder were assessed at personal interview with each residential parent. Associations between CD symptoms and parental alcoholism were characterized using both linear and Poisson regression, and results are presented with and without adjustment for maternal drug use during pregnancy, parental conflict, and estimated socioeconomic status (SES) based on census tract data. RESULTS: Mothers from stepfather families had a higher lifetime prevalence of alcoholism, antisocial personality disorder, depression and social phobia than mothers from intact families. Stepfathers had a higher lifetime prevalence of alcoholism and depression than biological fathers from intact families. Children from stepfather families had more externalizing (CD/ODD) symptoms than children from intact families. Girls who lived with an alcoholic stepfather had significantly more CD symptoms than girls who lived with an alcoholic biological father. Boys who lived with an alcoholic stepfather had significantly fewer CD symptoms than boys who lived with an alcoholic biological father. This sex difference was statistically significant. Adjustment for maternal drug use during pregnancy, parental conflict, and estimated SES based on census tract data did not change these findings. CONCLUSIONS: Children living in stepfather families are exposed to more parental psychiatric risk factors than children from intact families. The increased risk for CD symptoms in girls (but not boys) from stepfather families is partly mediated by or associated with the stepfather's history of alcoholism.

Implications of Genetic Research for Child Psychiatry

Abstract: Objective:To review implications of genetic research in child psychiatry.Method:Key advances in quantitative and molecular genetics are noted and findings are summarized with respect to autism, att...

The need to belong: Desire for interpersonal attachments as a fundamental human motivation.

Abstract: A hypothesized need to form and maintain strong, stable interpersonal relationships is evaluated in light of the empirical literature. The need is for frequent, nonaversive interactions within an ongoing relational bond. Consistent with the belongingness hypothesis, people form social attachments readily under most conditions and resist the dissolution of existing bonds. Belongingness appears to have multiple and strong effects on emotional patterns and on cognitive processes. Lack of attachments is linked to a variety of ill effects on health, adjustment, and well-being. Other evidence, such as that concerning satiation, substitution, and behavioral consequences, is likewise consistent with the hypothesized motivation. Several seeming counterexamples turned out not to disconfirm the hypothesis. Existing evidence supports the hypothesis that the need to belong is a powerful, fundamental, and extremely pervasive motivation.

The Strengths and Difficulties Questionnaire: A Research Note

Abstract: A novel behavioural screening questionnaire, the Strengths and Difficulties Questionnaire (SDQ), was administered along with Rutter questionnaires to parents and teachers of 403 children drawn from dental and psychiatric clinics. Scores derived from the SDQ and Rutter questionnaires were highly correlated; parent-teacher correlations for the two sets of measures were comparable or favoured the SDQ. The two sets of measures did not differ in their ability to discriminate between psychiatric and dental clinic attenders. These preliminary findings suggest that the SDQ functions as well as the Rutter questionnaires while offering the following additional advantages: a focus on strengths as well as difficulties; better coverage of inattention, peer relationships, and prosocial behaviour; a shorter format; and a single form suitable for both parents and teachers, perhaps thereby increasing parent-teacher correlations.

Prevalence, Severity, and Comorbidity of 12-Month DSM-IV Disorders in the National Comorbidity Survey Replication

Abstract: Background Little is known about the general population prevalence or severity of DSM-IV mental disorders. Objective To estimate 12-month prevalence, severity, and comorbidity of DSM-IV anxiety, mood, impulse control, and substance disorders in the recently completed US National Comorbidity Survey Replication. Design and Setting Nationally representative face-to-face household survey conducted between February 2001 and April 2003 using a fully structured diagnostic interview, the World Health Organization World Mental Health Survey Initiative version of the Composite International Diagnostic Interview. Participants Nine thousand two hundred eighty-two English-speaking respondents 18 years and older. Main Outcome Measures Twelve-month DSM-IV disorders. Results Twelve-month prevalence estimates were anxiety, 18.1%; mood, 9.5%; impulse control, 8.9%; substance, 3.8%; and any disorder, 26.2%. Of 12-month cases, 22.3% were classified as serious; 37.3%, moderate; and 40.4%, mild. Fifty-five percent carried only a single diagnosis; 22%, 2 diagnoses; and 23%, 3 or more diagnoses. Latent class analysis detected 7 multivariate disorder classes, including 3 highly comorbid classes representing 7% of the population. Conclusion Although mental disorders are widespread, serious cases are concentrated among a relatively small proportion of cases with high comorbidity.

Human biochemical genetics

Abstract: So far in this course we have dealt entirely with the evolution of characters that are controlled by simple Mendelian inheritance at a single locus. There are notes on the course website about gametic disequilibrium and how allele frequencies change at two loci simultaneously, but we didn’t discuss them. In every example we’ve considered we’ve imagined that we could understand something about evolution by examining the evolution of a single gene. That’s the domain of classical population genetics. For the next few weeks we’re going to be exploring a field that’s actually older than classical population genetics, although the approach we’ll be taking to it involves the use of population genetic machinery. If you know a little about the history of evolutionary biology, you may know that after the rediscovery of Mendel’s work in 1900 there was a heated debate between the “biometricians” (e.g., Galton and Pearson) and the “Mendelians” (e.g., de Vries, Correns, Bateson, and Morgan). Biometricians asserted that the really important variation in evolution didn’t follow Mendelian rules. Height, weight, skin color, and similar traits seemed to

Adolescence-limited and life-course-persistent antisocial behavior: A developmental taxonomy.

Abstract: This chapter suggests that delinquency conceals two distinct categories of individuals, each with a unique natural history and etiology: A small group engages in antisocial behavior of one sort or another at every life stage, whereas a larger group is antisocial only during adolescence. According to the theory of life-course-persistent antisocial behavior, children's neuropsychological problems interact cumulatively with their criminogenic environments across development, culminating m a pathological personality. According to the theory of adolescence-limited antisocial behavior, a contemporary maturity gap encourages teens to mimic antisocial behavior in ways that are normative and adjustive. There are marked individual differences in the stability of antisocial behavior. The chapter reviews the mysterious relationship between age and antisocial behavior. Some youths who refrain from antisocial behavior may, for some reason, not sense the maturity gap and therefore lack the hypothesized motivation for experimenting with crime.