Showing papers by "Michael Rutter published in 2009"

A genome-wide linkage and association scan reveals novel loci for autism

Abstract: Although autism is a highly heritable neurodevelopmental disorder, attempts to identify specific susceptibility genes have thus far met with limited success. Genome-wide association studies using half a million or more markers, particularly those with very large sample sizes achieved through meta-analysis, have shown great success in mapping genes for other complex genetic traits. Consequently, we initiated a linkage and association mapping study using half a million genome-wide single nucleotide polymorphisms (SNPs) in a common set of 1,031 multiplex autism families (1,553 affected offspring). We identified regions of suggestive and significant linkage on chromosomes 6q27 and 20p13, respectively. Initial analysis did not yield genome-wide significant associations; however, genotyping of top hits in additional families revealed an SNP on chromosome 5p15 (between SEMA5A and TAS2R1) that was significantly associated with autism (P = 2 x 10(-7)). We also demonstrated that expression of SEMA5A is reduced in brains from autistic patients, further implicating SEMA5A as an autism susceptibility gene. The linkage regions reported here provide targets for rare variation screening whereas the discovery of a single novel association demonstrates the action of common variants.

Amygdala, Hippocampal and Corpus Callosum Size Following Severe Early Institutional Deprivation: The English and Romanian Adoptees Study Pilot.

Abstract: The adoption into the UK of children who have been reared in severely deprived conditions provides an opportunity to study possible association between very early negative experiences and subsequent brain development. This cross-sectional study was a pilot for a planned larger study quantifying the effects of early deprivation on later brain structure. We used magnetic resonance imaging (MRI) to measure the sizes of three key brain regions hypothesized to be sensitive to early adverse experiences. Our sample was a group of adoptee adolescents (N = 14) who had experienced severe early institutional deprivation in Romania and a group of non-institutionalised controls (N = 11). The total grey and white matter volumes were significantly smaller in the institutionalised group compared with a group of non-deprived, non-adopted UK controls. After correcting for difference in brain volume, the institutionalised group had greater amygdala volumes, especially on the right, but no differences were observed in hippocampal volume or corpus callosum mid-sagittal area. The left amygdala volume was also related to the time spent in institutions, with those experiencing longer periods of deprivation having a smaller left amygdala volume. These pilot findings highlight the need for future studies to confirm the sensitivity of the amygdala to early deprivation.

Emanuel Miller Lecture: Attachment insecurity, disinhibited attachment, and attachment disorders: where do research findings leave the concepts?

Abstract: Background: Despite the evidence on anomalous attachment patterns, there has been a tendency to interpret most of these as reflecting differences in security/insecurity. Methods: Empirical research findings are reviewed in relation to attachment/insecurity as evident in both infancy and later childhood, disorganised attachment, inhibited attachment disorder, and disinhibited attachment disorder. Findings: Substantial differences are found in the correlates and meaning of these different features, as well as in the patterns associated with conditions such as autism, psychopathy, and Williams syndrome. Conclusions: It is seriously misleading to view all of these patterns through the lens of security/insecurity. This heterogeneity in social relationship features necessarily has implications for the assessment measures for social relationships that need to be used.

Savant skills in autism: psychometric approaches and parental reports

Abstract: Most investigations of savant skills in autism are based on individual case reports. The present study investigated rates and types of savant skills in 137 individuals with autism (mean age 24 years). Intellectual ability ranged from severe intellectual impairment to superior functioning. Savant skills were judged from parental reports and specified as ‘an outstanding skill/knowledge clearly above participant's general level of ability and above the population norm’. A comparable definition of exceptional cognitive skills was applied to Wechsler test scores—requiring a subtest score at least 1 standard deviation above general population norms and 2 standard deviations above the participant's own mean subtest score. Thirty-nine participants (28.5%) met criteria for either a savant skill or an exceptional cognitive skill: 15 for an outstanding cognitive skill (most commonly block design); 16 for a savant skill based on parental report (mostly mathematical/calculating abilities); 8 met criteria for both a cognitive and parental rated savant skill. One-third of males showed some form of outstanding ability compared with 19 per cent of females. No individual with a non-verbal IQ below 50 met criteria for a savant skill and, contrary to some earlier hypotheses, there was no indication that individuals with higher rates of stereotyped behaviours/interests were more likely to demonstrate savant skills.

Predictive value of family history on severity of illness: the case for depression, anxiety, alcohol dependence, and drug dependence.

Abstract: Context If family history is associated with clinical features that are thought to index seriousness of disorder, this could inform clinicians predicting patients' prognosis and researchers selecting cases for genetic studies. Although tests of associations between family history and clinical features are numerous for depression, such tests are relatively lacking for other disorders. Objective To test the hypothesis that family history is associated with 4 clinical indexes of disorder (recurrence, impairment, service use, and age at onset) in relation to 4 psychiatric disorders (major depressive episode, anxiety disorder, alcohol dependence, and drug dependence). Design Prospective longitudinal cohort study. Setting New Zealand. Participants A total of 981 members of the 1972 to 1973 Dunedin Study birth cohort (96% retention). Main Outcome Measures For each disorder, family history scores were calculated as the proportion of affected family members from data on 3 generations of the participants' families. Data collected prospectively at the study's repeated assessments (ages 11-32 years) were used to assess recurrence, impairment, and age at onset; data collected by means of a life history calendar at age 32 years were used to assess service use. Results Family history was associated with the presence of all 4 disorder types. In addition, family history was associated with a more recurrent course for all 4 disorders (but not significantly for women with depression), worse impairment, and greater service use. Family history was not associated with younger age at onset for any disorder. Conclusions Associations between family history of a disorder and clinical features of that disorder in probands showed consistent direction of effects across depression, anxiety disorder, alcohol dependence, and drug dependence. For these disorder types, family history is useful for determining patients' clinical prognosis and for selecting cases for genetic studies.

Do prenatal risk factors cause psychiatric disorder? Be wary of causal claims.

Abstract: Many prenatal risk factors are known to have adverse consequences on fetal development and there is increasing interest in effects on the mental health of offspring. However, associations with prenatal risk factors may arise because of postnatal risk or through confounders, including inherited ones. As a result, caution is required in assuming causation.

Gene-environment interactions: biologically valid pathway or artifact?

Abstract: JAMA Interaction Between the Serotonin Transporter Gene (5-HTTLPR), Stressful Life Events, and Risk of Depression: A Meta-analysis Neil Risch, PhD; Richard Herrell, PhD; Thomas Lehner, PhD; Kung-Yee Liang, PhD; Lindon Eaves, PhD; Josephine Hoh, PhD; Andrea Griem, BS; Marika Kovacs, PhD; Jurg Ott, PhD; Kathleen Ries Merikangas, PhD Context: Substantial resources are being devoted to identify candidate genes for complex mental and behavioral disorders through inclusion of environmental exposures following the report of an interaction between the serotonin transporter linked polymorphic region ( 5-HTTLPR ) and stressful life events on an increased risk of major depression. Objective: To conduct a meta-analysis of the interaction between the serotonin transporter gene and stressful life events on depression using both published data and individual-level original data. Data Sources: Search of PubMed, EMBASE, and PsycINFO databases through March 2009 yielded 26 studies of which 14 met criteria for the meta-analysis. Study Selection: Criteria for studies for the meta-analyses included published data on the association between 5-HTTLPR genotype (SS, SL, or LL), number of stressful life events (0, 1, 2, 3) or equivalent, and a categorical measure of depression defined by the Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) or the International Statistical Classification of Diseases, 10th Revision (ICD-10) or use of a cut point to define depression from standardized rating scales. To maximize our ability to use a common framework for variable definition, we also requested original data from all studies published prior to 2008 that met inclusion criteria. Of the 14 studies included in the meta-analysis, 10 were also included in a second sex-specific meta-analysis of original individual-level data. Data Extraction: Logistic regression was used to estimate the effects of the number of short alleles at 5-HTTLPR , the number of stressful life events, and their interaction on depression. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated separately for each study and then weighted averages of the individual estimates were obtained using random-effects meta-analysis. Both sex-combined and sex-specific meta-analyses were conducted. Of a total of 14 250 participants, 1769 were classified as having depression; 12 481 as not having depression. Results: In the meta-analysis of published data, the number of stressful life events was significantly associated with depression (OR, 1.41; 95% CI,1.25-1.57). No association was found between 5-HTTLPR genotype and depression in any of the individual studies nor in the weighted average (OR, 1.05; 95% CI, 0.98-1.13) and no interaction effect between genotype and stressful life events on depression was observed (OR, 1.01; 95% CI, 0.94-1.10). Comparable results were found in the sex-specific meta-analysis of individual-level data. Conclusion: This meta-analysis yielded no evidence that the serotonin transporter genotype alone or in interaction with stressful life events is associated with an elevated risk of depression in men alone, women alone, or in both sexes combined. JAMA. 2009;301(23):2462-2471..

Persistence of literacy problems: spelling in adolescence and at mid-life

Abstract: Background: Developmental reading problems show strong persistence across the school years; less is known about poor readers’ later progress in literacy skills. Method: Poor (n = 42) and normally developing readers (n = 86) tested in adolescence (ages 14/15 years) in the Isle of Wight epidemiological studies were re-contacted at mid-life (ages 44/45 years). Participants completed a spelling test, and reported on educational qualifications, perceived adult spelling competence, and problems in day-to-day literacy tasks. Results: Individual differences in spelling were highly persistent across this 30-year follow-up, with correlations between spelling at ages 14 and 44 years of r = .91 (p < .001) for poor readers and r = .89 (p < .001) for normally developing readers. Poor readers’ spelling remained markedly impaired at mid-life, with some evidence that they had fallen further behind over the follow-up period. Taking account of adolescent spelling levels, continued exposure to reading and literacy demands in adolescence and early adulthood was independently predictive of adult spelling in both samples; family social background added further to prediction among normally developing readers only. Conclusions: By adolescence, individual differences in spelling and its related sub-skills are highly stable. Encouraging young people with reading disabilities to maintain their exposure to reading and writing may be advantageous in the longer term.

Alcohol consumption during pregnancy and its effects on neurodevelopment: what is known and what remains uncertain

Abstract: It has been claimed that mothers' drinking during pregnancy may affect the neurodevelopment of around 1% of all children. If this is true, then prenatal alcohol exposure represents an important risk factor for neurodevelopmental problems, giving rise to a large burden of disability which could be potentially preventable. Evidence to support this idea has come from animal experiments and human observational studies. However, such findings need to be supported by more robust research designs. Because randomized controlled trials in this area are neither feasible nor ethical, suggestions are made for further research making more use of natural experiments.

Dopamine transporter gene polymorphism moderates the effects of severe deprivation on ADHD symptoms: developmental continuities in gene-environment interplay

Abstract: Early institutional deprivation is a risk factor for Attention-Deficit/Hyperactivity Disorder (ADHD) symptoms. However not all individuals are affected. We tested the hypothesis that this heterogeneity is influenced by gene x environment (GxE) interaction and that genetic polymorphisms involved in dopamine neurotransmission moderate the effects of severe early institutional deprivation on symptoms of ADHD (sADHD). Using a prospective-longitudinal design sADHD were measured at ages 6, 11, and 15 years in a sample of individuals who experienced severe institutional deprivation (up to 42 months of age) in Romanian orphanages and a non-institutionalized comparison group. Individuals were genotyped for polymorphisms in the dopamine D4 receptor (DRD4 48-bp VNTR in exon 3) and dopamine transporter gene (DAT1 haplotypes combining a 40-bp VNTR in 3'UTR and a 30-bp VNTR in intron 8). The risk for sADHD associated with early institutional deprivation was moderated by the DAT1 but not the DRD4 genotypes; an effect that was first apparent in early-, and persisted to mid-adolescence. The results (i) provide evidence for developmental continuities in G x E interaction, (ii) explain some of the heterogeneity in ADHD outcomes following institutional deprivation and, (iii) add to our understanding of environmental determinants of sADHD. © 2009 Wiley-Liss, Inc.

The validity of the family history screen for assessing family history of mental disorders.

Abstract: There is a need to collect psychiatric family history information quickly and economically (e.g., for genome-wide studies and primary care practice). We sought to evaluate the validity of family history reports using a brief screening instrument, the Family History Screen (FHS). We assessed the validity of parents' reports of seven psychiatric disorders in their adult children probands from the Dunedin Study (n = 959, 52% male), using the proband's diagnosis as the criterion outcome. We also investigated whether there were informant characteristics that enhanced accuracy of reporting or were associated with reporting biases. Using reports from multiple informants, we obtained sensitivities ranging from 31.7% (alcohol dependence) to 60.0% (conduct disorder) and specificities ranging from 76.0% (major depressive episode) to 97.1% (suicide attempt). There was little evidence that any informant characteristics enhanced accuracy of reporting. However, three reporting biases were found: the probability of reporting disorder in the proband was greater for informants with versus without a disorder, for female versus male informants, and for younger versus older informants. We conclude that the FHS is as valid as other family history instruments (e.g., the FH-RDC, FISC), and its brief administration time makes it a cost-effective method for collecting family history data. To avoid biasing results, researchers who aim to compare groups in terms of their family history should ensure that the informants reporting on these groups do not differ in terms of age, sex or personal history of disorder.

Understanding and testing risk mechanisms for mental disorders.

Abstract: Over the past 50 years there has been a virtual revolution in thinking about risk mechanisms. The key areas of challenge and opportunity include: identification of environmental causes; use of natural experiments; gene-environment interaction; testing for mediation; developmental moderation; biological programming; and developmental perturbations.

Epidemiological methods to tackle causal questions

Abstract: It is a dull day when there is not at least one media report of a claim that research has identified some new environmental cause of disease. Such claimed causes concern a wide range of supposed hazards including medical interventions such as the measlesmumps-rubella (MMR) vaccine, the thimerasol (mercury) preservative in other vaccines, dietary factors of many different kinds (coffee, alcohol, food additives, etc.), prenatal stresses or the intra-uterine exposure to the effects of maternal smoking or ingestion of alcohol, use of mobile phones, and living near radiation sources—to mention just a few examples. It is problematic, however, that many of these claims are not confirmed by other research and some are even reversed. Unsurprisingly both professionals and the lay public have developed a scepticism about claims on environmental causes of disease. Because much of the evidence derives from epidemiological studies of one kind or another, epidemiological science itself has come under scrutiny both within and outside the profession. Some have argued that only laboratory experiments and randomized controlled trials (RCT) can provide acceptable evidence on causation. That cannot be a solution, however, because so many of the putative environmental causes are ones that cannot be manipulated in humans—for a mixture of both ethical and practical reasons. Because the identification of environmental causes is of such importance, and because the solution of the causal inference problem has no obvious single, simple solution, the Academy of Medical Sciences set up a working party (made up of clinical scientists, epidemiologists, statisticians, policy leaders and scientific media specialists) to answer the key questions of ‘how should we decide what to believe and when to take action?’ The report emphasized the need to focus on individual components in the causal process and not on some misleading abstract notion of a single basic cause. It also notes the many reasons why an observed association or correlation might not reflect an environmentally mediated causal effect. Such reasons include genetic mediation of the causal risk effect, social selection (allocation bias), and reverse causation to mention but three out of a much longer list of possibilities. It was also noted that the main problem in moving from an observed association to a causal inference did not lie in the effect of known, measured confounders, but rather in the effect of unknown, unmeasured confounders.

Pathways from science findings to health benefits

Abstract: There have been numerous exhortations for more 'translational research'. A selective review of historical examples of research leading to health benefits is used to consider the various forms of successful interplay between basic science and clinical applications. This is followed by a consideration of key neuroscience findings that might be relevant for translation, and then by a discussion of the challenges and opportunities in relation to mental disorders. The time-frame for the pathway from science findings to health benefits is usually long, and generally requires an interactive interplay among different scientific strategies. There is a false dichotomy between so-called basic and applied research and translation needs to proceed from the bedside to the laboratory as well as in the opposite direction. There is a key need for bridging research of the hypothesis-testing experimental medicine variety. Health benefits may involve either public health considerations or the treatment of individual patients, or both. There are now some opportunities for direct translational research but there is a much greater need for hypothesis-based bridging studies that occupy a crucial mid-phase in the pathway from science findings to health benefits.

Developments in Child and Adolescent Psychiatry Over the Last 50 Years

Abstract: The development of child and adolescent psychiatry in the first half of the 20th century was well described by Achenbach (1974), Cameron (1956), Kanner (1959), Parry-Jones (1989) and Warren (1974) with respect to both its strengths and limitations. The establishment of community child guidance clinics, much influenced by the Mental Hygiene movement, had the value of viewing psychopathology in the context of young people’s real-life circumstances. The cost, however, was that there was both geographical and professional isolation from general psychiatry, pediatrics and academic research. Most treatment tended to be very open-ended and prolonged, usually without a well-defined focus (Rutter, 1982a). There tended, also, to be a rigid separation in the functioning of the unholy trinity of the psychiatrist, the psychologist and the psychiatric social worker. In addition, there was a tendency to blame parents for the disorders of their children – as indexed by concepts of the schizophrenogenic mother (Jackson, 1960) and “refrigerator” parents (Bettelheim, 1967), in relation to schizophrenia and autism, respectively. The dominant theories were the several varieties of psychoanalysis (Eisenberg, 2001), clinical practice was mostly not evidence-based, and there was a paucity of specific treatments (Chess, 1988). Furthermore, very little attention was paid to diagnosis. The prevailing terminology concerned “maladjustment” and official classifications referred only to “behavior disorders of childhood.” However, very important changes were afoot (Rutter, 1998). Although systematic diagnosis was not yet in fashion, Kanner (who wrote the first definitive English-language textbook in 1935) had already done much to foster critical thinking about different patterns of psychopathology and to encourage a questioning approach (as exemplified by his 1969 paper on differential diagnosis). Also, his first description of autism (Kanner, 1943) not only provided a model of top-level clinical observation, but established the reality of a disorder that was distinctively different from others. Similarly, approaching diagnosis psychometrically rather than clinically, Hewitt and Jenkins (1946) wrote a pioneering monograph identifying different patterns of psychopathology. The tide was beginning to turn with respect to both diagnosis and classification in both child and adult psychopathology (Meehl, 1954). Although biological causes had only a very limited role in clinical thinking at that time, Pasamanick and Knobloch (1966), in relation to their concept of a continuum of reproductive casualty, postulated the importance of prenatal and perinatal risk factors. Studies of children with epilepsy as, for example, by Pond (1961) and by Ounsted (1955) were also influential in pointing to the interplay between biological and psychosocial risk factors. The concept of so-called “minimal brain dysfunction” was beginning to be established. It did not stand the test of empirical investigation (Rutter, 1982b) but, nevertheless, it did force people to pay attention to biological risk factors. In the realm of treatment, the value of stimulants in the treatment of children with hyperkinetic disorders was beginning to be appreciated and, in adult psychiatry, neuroleptics were starting to be developed for the treatment of schizophrenia. At about the same time, there was the birth of behavioral therapies (Wolpe, 1958). At first, these were largely considered in relation to adults, rather than children, but the application to children soon followed (Rachman, 1962; Yule & Berger, 1972). Academic child and adolescent psychiatry scarcely existed in the 1950s although there were some chairs in the subject in North America and mainland Europe and there were the beginnings of systematic clinical research (Hersov, 1986; Remschmidt & van Engeland, 1999; Schowalter, 2000). However, the report that probably did most to change the field in a radical fashion was Bowlby’s (1951) review of “maternal deprivation” for the World Health Organization. Spitz and Goldfarb had previously drawn attention to the damaging effects of institutional care but Bowlby drew on a much wider range of evidence and did most to pull together the ideas. For quite a while, his views were treated with extreme hostility by both academic psychologists and by psychoanalysts. The former pointed to the weakness of much of the research and the latter to the heresy that the causal factors lay in real-life experiences rather than internal conflict. Despite the controversies, Bowlby’s observations on young children’s responses to separation from their parents led to enduring changes in hospital practice. Professionals, almost for the first time, were forced to become aware of young

Commentary: Fact and artefact in the secular increase in the rate of autism

Abstract: King and Bearman sought to determine whether the increased prevalence of an autism diagnosis in California was due to diagnostic substitution of autism in place of mental retardation (MR). They make good use of systematic administrative data from the California Department of Developmental Services between 1992 and 2005 for this purpose, with the conclusion that changes in diagnostic practices accounted for a quarter of the observed increase in diagnosed autism over this time period. They discuss this finding as reflecting diagnostic substitution or accretion, but it is clear that there was almost no substitution. Thus, in 95% of the cases the change was from ‘pure’ MR to MR plus autism. Figure 3 in King & Bearman indicates a substantial increase in MR between 1992 and 2005, although the proportional increase for autism was greater. Most of the rise applied to ‘pure’ autism, about a quarter to ‘pure’ MR being changed to MR and autism, and very little to MR being replaced by autism. In other words, the main change in diagnostic practice concerned an increased willingness to note co-morbidity. Given that the increase in ‘pure’ autism between 1992 and 2005 was huge (from 4446 to 28 046 cases)—a much greater rise than for co-morbidity (3210–10 410), it is dubious whether the latter increase does much to help in resolving the key basic issue of whether there has been a true increase over time in the incidence of autism. That is particularly so when the available evidence suggests that the main rise has not predominantly involved autism associated with intellectual disability; rather, it seems to have particularly involved autism in individuals with non-verbal IQ in the normal range. King and Bearman quite properly pointed out that they could not examine that suggestion in their dataset. Nevertheless, the consequence is that their main focus was off-target with respect to the observed rise. Almost all reviews have concluded that a substantial part of the rise in the rate of diagnosed autism has been due to a combination of better ascertainment and a broadening of the diagnostic concept, but has there been, in addition, a true rise in incidence? In my view, we simply do not know. The rise has been seen in Europe, the USA and Japan, but there is a geographic variability in whether the main rise began in the 1970s and 80s, or rather in the 1990s. The claims that the so-called ‘epidemic’ of autism was due to either the measles–mumps–rubella (MMR) vaccine or mercury-containing preservative thimerosal that used to be present in many vaccines are not supported by the evidence. Most crucially, in Japan, where MMR was discontinued at a time when it remained in wide use in other countries, the removal of MMR was not followed by any fall in the rate of autism, or even by a reduction in the rate of rise. Similarly, the discontinuation of use of thimerosal in Scandanavia was not followed by any change in the rising rate of autism. Nevertheless, these findings do not rule out a risk effect from other prenatal or postnatal toxins or other hazards. Large-scale prospective epidemiological/longitudinal studies with good biological measures and good diagnostic procedures are needed to test that possibility. The ongoing MoBa study of mothers and babies in Norway constitutes one good example of what is needed in that connection. It should be added that the factor responsible for a real rise in autism (if that truly has occurred) need not necessarily be a specific environmental hazard. The trigger could be a rising age of parenthood, given the evidence that high paternal age is associated with an increased rate of autism in the offspring. How might that operate? One possibility is that it increases the rate of developmental perturbations such as copy number variation (i.e. submicroscopic substitutions or deletion) or minor congenital anomalies or chromosomal anomalies, all of which have been found to be more common in autism. Whilst there is value in considering the role of changing concepts and better ascertainment in the observed rise in the rate of diagnosed autism, and there is still uncertainty on whether or not there has been a true rise in incidence, the greater the need is for hypothesis-testing focused research on possible causal mechanisms that could lead to changes in incidence. MRC SGDP Centre, PO 80, Institute of Psychiatry, King’s College London, De Crespigny Park, Denmark Hill, London SE5 8AF, UK. E-mail: camilla.azis@kcl.ac.uk Published by Oxford University Press on behalf of the International Epidemiological Association

Parents' Evaluation of Adoption Success: A Follow‐Up Study of Intercountry and Domestic Adoptions

Abstract: Parents of 165 children adopted from Romania and 52 children adopted from within the United Kingdom rated the success of the adoptions when the children were 11 years old. As was the case at two earlier study waves, satisfaction was found to be extremely high. Both positive and negative assessments were generally stable between ages 6 and 11, although for the children who had more problems there was an increase in negative evaluation, albeit within an overall positive picture. Parents' evaluations were somewhat more negative for this group of children; however, parents reported that having the child as part of their family was very rewarding. Negative evaluation was not directly related to age at placement, but appeared to be a reflection of the later-placed children's higher rates of problem behavior. As found at earlier assessment waves, child factors, in particular conduct problems and inattention or overactivity, were key in predicting parental evaluations at age 11, as were four domains closely associated with institutional deprivation, namely cognitive impairment, quasi-autistic patterns, inattention or overactivity, and disinhibited attachment. The findings emphasize the need for early intervention for children in severely deprived conditions, and for access to postadoption services that target the particular problem behaviors the children may exhibit.

Effects of profound early institutional deprivation: An overview of findings from a UK longitudinal study of Romanian adoptees.

Abstract: A randomly selected sample of 165 children from Romania (of whom 144 had been reared in institutions) who were adopted by UK families, with placement before the age of 42 months, was studied at 4, 6, and 11 years of age. Comparisons were made with a sample of 52 non-institutionalized UK children adopted before the age of 6 months, who were studied in the same way. The paper briefly summarizes circumstances at the time of adoption and then reports findings at age 11, focusing on changes between 6 and 11. Marked catch-up in psychological functioning was evident following adoption, but significant problems continued in a substantial minority of the children placed after the age of 6 months. The theoretical implications of the findings are considered, and the policy implications are noted.

Psychopathology and Development

Abstract: The childhood antecedents of psychiatric disorder in adult life are reviewed with regard to four groups of conditions that show sharply contrasting patterns of linkage between childhood and adult life. For emotional disorders the links are weak and the mechanisms largely unknown. About half of schizophrenic psychoses are preceded by non-psychotic abnormalities of behaviour in childhood; the processes involved are probably largely constitutional. Affective disorders only infrequently begin in childhood and the behavioural percursors of adult depression do not constitute a clearly recognisable pattern. However, adverse experiences in childhood may create a vulnerability to later depression. The child-adult linkages are strongest with conduct disturbance in childhood and adult personality disorder, the mechanisms in this continuity are probably both constitutional and environmental.

Policy and practice implications from the English and Romanian adoptees (ERA) study: forty five key questions

Abstract: The English Romanian Adoptees (ERA) study is a remarkable exploration of the experiences of children whose early lives in Romanian institutions were unimaginably poor and who were then adopted into English families with all the material, emotional and social advantages that this brings. This publication focuses on the policy and practice implications of this internationally known study. Initiated in 1992 because of the major uncertainties about what would happen to children adopted by UK families from extremely depriving Romanian institutions, the ERA study has been reported on, at initial and then follow-up stages, over the past 17 years, with the most recent findings published in 2009. To be able to follow these children longitudinally over so many years, and to track their progress and understand the influence and interaction of both their poor start and their later advantage, has transformed the understanding of child and adolescent development. This book considers the policy and practice implications of what has been learned through this longitudinal study. Rather than focusing on the research findings as such, which have been reported upon elsewhere, this publication tackles those questions most often posed by practitioners and policy makers, including the following: * Does the removal from institutions and the adoption into well functioning families bring about recovery for these children? * What are the challenges for the children and for the adopting families? * What are the effects on the young people of leaving institutional care? * What are the effects of deprivation on physical development and psychological functioning? * What are the service implications of these? The book begins with the necessary introduction to the ERA study, proceeds to answer 45 key questions, and ends with overall conclusions. It will be of great interest, both in the UK and internationally, to practitioners, policy makers, adoptive families, academics and all others interested in the outcomes for children adopted into the UK from institutions overseas.