Showing papers by "Michael Rutter published in 2012"
TL;DR: Evidence on turning point effects associated with experiences that increase opportunities and enhance coping and Gene–environment interaction findings are considered, and it is noted that there is some evidence that the genetic influences concerns responsivity to all environments and not just bad ones.
Abstract: The concept of resilience has as its starting point the recognition that there is huge heterogeneity in people's responses to all manner of environmental adversities. Resilience is an inference based on evidence that some individuals have a better outcome than others who have experienced a comparable level of adversity; moreover, the negative experience may have either a sensitizing effect or a strengthening "steeling" effect in relation to the response to later stress or adversity. After noting the crucial importance of first testing for the environmental mediation of risk through "natural experiments," findings are reviewed on "steeling effects" in animal models and humans. Gene-environment interaction findings are considered, and it is noted that there is some evidence that the genetic influences concerns responsivity to all environments and not just bad ones. Life course effects are reviewed in relation to evidence on turning point effects associated with experiences that increase opportunities and enhance coping. Attention is drawn to both research implications and substantive findings as features that foster resilience.
1,152 citations
Trinity College, Dublin1, University of Pittsburgh2, University of Toronto3, Icahn School of Medicine at Mount Sinai4, University of Bologna5, Guy's and St Thomas' NHS Foundation Trust6, Goethe University Frankfurt7, King's College London8, Pasteur Institute9, University of Paris10, University College Dublin11, University of Lisbon12, Instituto Gulbenkian de Ciência13, University of Michigan14, Vanderbilt University15, Utrecht University16, University of Washington17, University of Oxford18, Memorial University of Newfoundland19, University of Miami20, McGill University21, University of Gothenburg22, University of Pennsylvania23, University of Manchester24, University of Illinois at Chicago25, Newcastle University26, New York University27, Nathan Kline Institute for Psychiatric Research28, University of Manitoba29, Cornell University30, Stanford University31, University of Toulouse32, Indiana University33, Harvard University34, National and Kapodistrian University of Athens35, Carnegie Mellon University36, Medical Research Council37, University of Iowa38, McMaster University39, Yale University40, University of Alberta41, University of British Columbia42, University of California, Los Angeles43, University of Utah44, Autism Speaks45, University of North Carolina at Chapel Hill46, Veterans Health Administration47, German Cancer Research Center48, Tufts University49, French Institute of Health and Medical Research50, Centre national de la recherche scientifique51, Pierre-and-Marie-Curie University52, Ohio State University53
TL;DR: Stage 2 of the Autism Genome Project genome-wide association study is reported, adding 1301 ASD families and bringing the total to 2705 families analysed, and it is reasonable to conclude that common variants affect the risk for ASD but their individual effects are modest.
Abstract: While it is apparent that rare variation can play an important role in the genetic architecture of autism spectrum disorders (ASDs), the contribution of common variation to the risk of developing ASD is less clear. To produce a more comprehensive picture, we report Stage 2 of the Autism Genome Project genome-wide association study, adding 1301 ASD families and bringing the total to 2705 families analysed (Stages 1 and 2). In addition to evaluating the association of individual single nucleotide polymorphisms (SNPs), we also sought evidence that common variants, en masse, might affect the risk. Despite genotyping over a million SNPs covering the genome, no single SNP shows significant association with ASD or selected phenotypes at a genome-wide level. The SNP that achieves the smallest P-value from secondary analyses is rs1718101. It falls in CNTNAP2, a gene previously implicated in susceptibility for ASD. This SNP also shows modest association with age of word/phrase acquisition in ASD subjects, of interest because features of language development are also associated with other variation in CNTNAP2. In contrast, allele scores derived from the transmission of common alleles to Stage 1 cases significantly predict case status in the independent Stage 2 sample. Despite being significant, the variance explained by these allele scores was small (Vm< 1%). Based on results from individual SNPs and their en masse effect on risk, as inferred from the allele score results, it is reasonable to conclude that common variants affect the risk for ASD but their individual effects are modest.
353 citations
University College Dublin1, Instituto Nacional de Saúde Dr. Ricardo Jorge2, Instituto Gulbenkian de Ciência3, Trinity College, Dublin4, Center for Autism and Related Disorders5, University of Bologna6, University of British Columbia7, Guy's Hospital8, Newcastle University9, King's College London10, University of Paris11, University of Illinois at Chicago12, University of Michigan13, University of Oxford14, Autism Speaks15, University of North Carolina at Chapel Hill16, Utrecht University17, Goethe University Frankfurt18, University of Washington19, Memorial University of Newfoundland20, University of Miami21, McGill University22, University of Gothenburg23, University of Pennsylvania24, Boston Children's Hospital25, German Cancer Research Center26, Icahn School of Medicine at Mount Sinai27, University of Manchester28, French Institute of Health and Medical Research29, Nathan Kline Institute for Psychiatric Research30, New York University31, Vanderbilt University32, University of Toulouse33, University of Toronto34, Indiana University35, University of Utah36, University of California, Los Angeles37, National and Kapodistrian University of Athens38, McMaster University39, Yale University40, University of Iowa41, University of Birmingham42, University of Alberta43, Stanford University44, Ohio State University45
TL;DR: A large scale analysis to identify candidate genes which may contain low-frequency recessive variation contributing to ASD while taking into account the potential contribution of population differences to the genetic heterogeneity of ASD highlights the applicability of HH mapping in complex disorders such as ASD and offers an alternative approach to the analysis of genome-wide association data.
Abstract: Autism spectrum disorder (ASD) is a highly heritable disorder of complex and heterogeneous aetiology. It is primarily characterized by altered cognitive ability including impaired language and communication skills and fundamental deficits in social reciprocity. Despite some notable successes in neuropsychiatric genetics, overall, the high heritability of ASD (~90%) remains poorly explained by common genetic risk variants. However, recent studies suggest that rare genomic variation, in particular copy number variation, may account for a significant proportion of the genetic basis of ASD. We present a large scale analysis to identify candidate genes which may contain low-frequency recessive variation contributing to ASD while taking into account the potential contribution of population differences to the genetic heterogeneity of ASD. Our strategy, homozygous haplotype (HH) mapping, aims to detect homozygous segments of identical haplotype structure that are shared at a higher frequency amongst ASD patients compared to parental controls. The analysis was performed on 1,402 Autism Genome Project trios genotyped for 1 million single nucleotide polymorphisms (SNPs). We identified 25 known and 1,218 novel ASD candidate genes in the discovery analysis including CADM2, ABHD14A, CHRFAM7A, GRIK2, GRM3, EPHA3, FGF10, KCND2, PDZK1, IMMP2L and FOXP2. Furthermore, 10 of the previously reported ASD genes and 300 of the novel candidates identified in the discovery analysis were replicated in an independent sample of 1,182 trios. Our results demonstrate that regions of HH are significantly enriched for previously reported ASD candidate genes and the observed association is independent of gene size (odds ratio 2.10). Our findings highlight the applicability of HH mapping in complex disorders such as ASD and offer an alternative approach to the analysis of genome-wide association data.
182 citations
01 Jan 2012
TL;DR: In this paper, the author distinguishes resilience from concepts of positive psychology and competence by showing that there is heterogeneity in how humans respond to environmental hazards, whether those are physical or psychological.
Abstract: The author distinguishes resilience from concepts of positive psychology and competence by showing that there is heterogeneity in how humans respond to environmental hazards, whether those are physical or psychological. His goal is to explore these different responses in order to discover the causal processes that relate to resilience. His chapter shows the wisdom that comes with more than four decades of research in this area.
129 citations
TL;DR: Feeding and eating disorders should be merged into a single grouping with categories applicable across age groups and the category of anorexia nervosa should be broadened through dropping the requirement for amenorrhoea, extending the weight criterion to any significant underweight, and extending the cognitive criterion to include developmentally and culturally relevant presentations.
127 citations
TL;DR: The majority of individuals with high callous-unemotional traits did not show conduct disorder in this special sample of children, supporting the view that, while common, an overlap between these aspects of psychopathology is not inevitable and so provides evidence for the dissociation of these two concepts.
Abstract: Background
There is a debate over whether disruptive behaviour should be regarded as a central component of, or rather as an epiphenomenon with little diagnostic value for, psychopathy.
Aims
To test whether callous–unemotional traits and conduct disorder can be dissociated in the English and Romanian Adoptee Study, a prospective longitudinal study of adopted individuals with a history of severe early institutional deprivation.
Method
The Child and Adolescent Psychiatric Assessment was used to establish DSM-IV diagnoses for conduct disorder (and also oppositional defiant disorder) at the 15-year follow-up stage. The Inventory of Callous–Unemotional Traits questionnaire was administered to assess psychopathy traits.
Results
There was no significant association between callous–unemotional traits and conduct disorder, both according to parent and youth self-report assessed categorically and dimensionally after controlling for confounds.
Conclusions
The majority of individuals with high callous–unemotional traits did not show conduct disorder in this special sample of children. This supports the view that, while common, an overlap between these aspects of psychopathology is not inevitable and so provides evidence for the dissociation of these two concepts. In terms of classification, we argue for a diagnostic scheme where psychopathy can be diagnosed independently of conduct disorder.
80 citations
TL;DR: The findings in the literature are discussed in relation to the biological effects of supposedly positive or normal experiences, the use of natural experiments to determine the causal effects of early experience, the heterogeneity of social adversity, the possible mediators of the biological embedding, gene–environment interdependence, and remaining challenges.
Abstract: The starting point for the study of adverse experiences is that some have enduring consequences that continue after the period of exposure to the adversity. That raises four basic issues: whether social adversities can be considered homogeneous, whether the crucial effect lies in the “objective” or subjectively perceived “effective” environment, whether the effects are environmentally mediated, and whether the form of biological embedding involves psychological or health consequences. The findings in the literature are discussed in relation to the biological effects of supposedly positive or normal experiences, the use of natural experiments to determine the causal effects of early experience, the heterogeneity of social adversity, the possible mediators of the biological embedding, gene–environment interdependence, and remaining challenges.
75 citations
TL;DR: "Pure" psychosocial deprivation (in the absence of subnutrition) had a profound effect on psychological functioning in the form of DSPs.
Abstract: Objective To summarize the advantages and limitations of general population, high-risk and "natural experiment" longitudinal studies for studying psychological change. The English and Romanian Adoptees study is used as an example of a "natural experiment," and detailed findings are provided. Method What is new is a focus on the young people who spent the whole of their life in institutional care up to the time of adoption and who did not show subnutrition. The results were compared with a composite comparison group who had not experienced institutional care or who were adopted before the age of 6 months. The outcomes were assessed in terms of previously established deprivation-specific patterns (DSPs). Results "Pure" psychosocial deprivation was associated with a substantial increase in the rate of DSPs. It was not associated with significantly impaired head growth if institutional care lasted less than 6 months, whereas thereafter there was a 2.5 standard deviation reduction. Subnutrition differed in being accompanied by impaired head and body growth even with institutional care lasting less than 6 months. In the pure psychosocial deprivation group, 45.5% showed a DSP at 15 years compared with 1.3% in the comparison group. Conclusion "Pure" psychosocial deprivation (in the absence of subnutrition) had a profound effect on psychological functioning in the form of DSPs. Subnutrition had a surprisingly small effect on DSPs.
64 citations
TL;DR: Evidence from multiple lines of research converges to indicate that current classifications contain excessively large numbers of categories of limited validity and psychiatric research should discard the assumption that current classification is valid.
Abstract: To examine whether and how the classification of mental disorders can be based on research, we evaluate the relevance of psychiatric science to the major questions in classification. We conclude that most studies cannot inform the validity of diagnostic categories because they are constrained by the classification through a top-down diagnostic approach. Analyses of relationships between diagnostic categories suggest that most interdiagnostic boundaries in current classifications lack validity. Likewise, genetic studies show that the susceptibility to mental illness is at most partly disorder-specific. Neuroimaging research is uninformative due to unsystematic single-diagnosis studies, use of super-healthy controls, and publication bias. Treatment research suggests moderate specificity in several areas of psychopathology (e.g. lithium for bipolar disorder), but lack of specificity is the rule (e.g. the broad indications of serotonin-reuptake inhibitors). In summary, evidence from multiple lines of research converges to indicate that current classifications contain excessively large numbers of categories of limited validity. Dimensional classification will not solve the problem because the number of dimensions is as uncertain as the number of categories. Psychiatric research should discard the assumption that current classification is valid. Instead of diagnosis-specific investigations, studies of unselected groups assessed with bottom-up approaches are needed to advance psychiatry.
61 citations
TL;DR: In this article, the practical utility of finding susceptibility genes with a very small effect is questioned and the empirical findings and implications of developmental perturbations, epigenetics, gene-environment correlations and interactions are discussed.
Abstract: The modern understanding of genetic influences, of environmental effects, of mental disorder, and of heritabilities is noted. The practical utility of finding susceptibility genes with a very small effect is questioned. The empirical findings and implications of developmental perturbations, epigenetics, gene–environment correlations and interactions are then discussed. It is noted that the genes involved in gene–environment interactions may be concerned with susceptibility to all environments and not just adverse ones.
46 citations
TL;DR: Research has now extended the concept of psychopathy to childhood and has produced evidence that it is meaningfully distinct from antisocial behaviour, and it is proposed that psychopathy should be accepted as a meaningful diagnosis in childhood.
Abstract: Psychopathy is not included in either of the main classification systems (ICD-10 or DSM-IV). Research has now extended the concept of psychopathy to childhood and has produced evidence that it is meaningfully distinct from antisocial behaviour. It is proposed that psychopathy should be accepted as a meaningful diagnosis in childhood.
15 Mar 2012
TL;DR: Hagell and Witherspoon as discussed by the authors investigated the relationship between adolescents' emotional and behavioural problems and time trends in time adolescent time use in the United Kingdom, and their implications for understanding trends in mental health.
Abstract: Foreword by Professor Sir Michael Rutter Introduction~ Ann Hagell Time trends in young people's emotional and behavioural problems, 1975-2005 Stephan Collishaw Stress and mental health in adolescence: interrelationship and time trends ~ Ann Hagell, Seija Sandberg and Robert MacDonald Trends in time adolescent time use in the United Kingdom ~ Ann Hagell, Stephen Peck, Nicole Zarrett, J. Ignacio Gimenez-Nadal and Jennifer Symonds Trends in parenting: can they help explain time trends in problem behaviour? ~ Frances Gardner, Stephan Collishaw, Barbara Maughan, Jacqueline Scott, Karen Schepman and Ann Hagell Educational changes and possible links with adolescent well-being: 1970s to 2000s Ann Hagell, John Gray, Maurice Galton and Colleen McLaughlin Trends in adolescent substance use, and their implications for understanding trends in mental health ~ Ann Hagell, Judith Aldridge, Petra Meier, Tim Millar, Jennifer Symonds and Michael Donmall Some thoughts on the broader context: neighbourhoods and peers ~ Ann Hagell, Sarah Curtis, Shari Daya, Yasmin Khatib, Rachel Pain, Catherine Rothon, Stephen Stansfeld and Sara Fuller Reflections and implications ~ Ann Hagell and Sharon Witherspoon
TL;DR: The major advances that have taken place over the last half century are reviewed with a focus on those that are particularly important with respect to classification issues in the field of child and adolescent psychopathology.
Abstract: The major advances that have taken place over the last half century are reviewed with a focus on those that are particularly important with respect to classification issues in the field of child and adolescent psychopathology. Attention is paid to the conceptual issues in DSM and ICD development and differences between the two classifications. Specific recommendations for changes in ICD-11 are presented and an online supplement provides specific details with respect to diagnostic categories that are in need of further testing.
TL;DR: In this article, a high measure of agreement on the key issues concerning gene-environment interdependence is found, and it is suggested that robust replication using the same constructs is needed.
Abstract: There is a high measure of agreement on the key issues concerning gene–environment interdependence. Contrary to arguments on the need for direct exact replication of findings, it is suggested that “robust” replication using the same constructs is needed. RCTs have an important role for testing for environmental mediation but cannot be used for environmental risks in childhood that show G×E in relation to adult outcomes. Instead, greater use needs to be made of natural experiments. Experimental methods are needed to study biological mediating mechanisms and these should include both animal models and human brain imaging studies. In addition to further research on G×E, further studies of gene–environment correlations are required. Many challenges remain but the future for gene–environment interdependence is bright.
01 Jan 2012
TL;DR: The modern understanding of genetic influences, of environmental effects, of mental disorder, and of heritabilities is noted and the practical utility of finding susceptibility genes with a very small effect is questioned.
Abstract: The modern understanding of genetic influences, of environmental effects, of mental disorder, and of heritabilities is noted. The practical utility of finding susceptibility genes with a very small effect is questioned. The empirical findings and implications of developmental perturbations, epigenetics, gene– environment correlations and interactions are then discussed. It is noted that the genes involved in gene–environment interactions may be concerned with susceptibility to all environments and not just adverse ones.