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      Good social skills despite poor theory of mind: exploring compensation in autism spectrum disorder

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          Abstract

          Background

          It is proposed that some individuals with Autism Spectrum Disorder (ASD) can ‘compensate’ for their underlying difficulties (e.g. in theory of mind; ToM), thus demonstrating relatively few behavioural symptoms, despite continued core cognitive deficits. The mechanisms underpinning compensation are largely unexplored, as is its potential impact on mental health. This study aimed to estimate compensation patterns in ASD, by contrasting overt social behaviour with ToM task performance, in order to compare the characteristics of ‘Low’ and ‘High’ Compensators.

          Methods

          A total of 136 autistic adolescents, from the ongoing Social Relationships Study, completed a range of cognitive tasks, the Autistic Diagnostic Observation Schedule (ADOS) and a self‐report anxiety questionnaire. Participants were assigned compensation group status; High Compensators demonstrated good ADOS scores despite poor ToM performance, while Low Compensators demonstrated similarly poor ToM, accompanied by poor ADOS scores.

          Results

          High Compensators demonstrated better IQ and executive function (EF), but greater self‐reported anxiety, compared with Low Compensators. Such differences were not found when comparing individuals who had good versus poor ADOS scores, when ToM performance was good. Other core autistic characteristics (weak central coherence, nonsocial symptoms) did not differentiate the High and Low Compensators.

          Conclusions

          IQ, EF and anxiety appear to be implicated in the processes by which certain autistic young people can compensate for their underlying ToM difficulties. This tendency to compensate does not appear to reflect the severity of ‘hit’ for ASD per se , suggesting that well‐compensated individuals are not experiencing a milder form of ASD. The construct of compensation in ASD has implications for research and clinical practice.

          Abstract

          Read the Commentary on this article at doi: 10.1111/jcpp.12989

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          Most cited references25

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          Quantifying and exploring camouflaging in men and women with autism

          Autobiographical descriptions and clinician observations suggest that some individuals with autism, particularly females, ‘camouflage’ their social communication difficulties, which may require considerable cognitive effort and lead to increased stress, anxiety and depression. Using data from 60 age- and IQ-matched men and women with autism (without intellectual disability), we operationalized camouflaging in adults with autism for the first time as the quantitative discrepancy between the person’s ‘external’ behavioural presentation in social–interpersonal contexts (measured by the Autism Diagnostic Observation Schedule) and the person’s ‘internal’ status (dispositional traits measured by the Autism Spectrum Quotient and social cognitive capability measured by the ‘Reading the Mind in the Eyes’ Test). We found that the operationalized camouflaging measure was not significantly correlated with age or IQ. On average, women with autism had higher camouflaging scores than men with autism (Cohen’s d = 0.98), with substantial variability in both groups. Greater camouflaging was associated with more depressive symptoms in men and better signal-detection sensitivity in women with autism. The neuroanatomical association with camouflaging score was largely sex/gender-dependent and significant only in women: from reverse inference, the most correlated cognitive terms were about emotion and memory. The underlying constructs, measurement, mechanisms, consequences and heterogeneity of camouflaging in autism warrant further investigation.
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            Heritability of Autism Spectrum Disorder in a UK Population-Based Twin Sample.

            Most evidence to date highlights the importance of genetic influences on the liability to autism and related traits. However, most of these findings are derived from clinically ascertained samples, possibly missing individuals with subtler manifestations, and obtained estimates may not be representative of the population. To establish the relative contributions of genetic and environmental factors in liability to autism spectrum disorder (ASD) and a broader autism phenotype in a large population-based twin sample and to ascertain the genetic/environmental relationship between dimensional trait measures and categorical diagnostic constructs of ASD. We used data from the population-based cohort Twins Early Development Study, which included all twin pairs born in England and Wales from January 1, 1994, through December 31, 1996. We performed joint continuous-ordinal liability threshold model fitting using the full information maximum likelihood method to estimate genetic and environmental parameters of covariance. Twin pairs underwent the following assessments: the Childhood Autism Spectrum Test (CAST) (6423 pairs; mean age, 7.9 years), the Development and Well-being Assessment (DAWBA) (359 pairs; mean age, 10.3 years), the Autism Diagnostic Observation Schedule (ADOS) (203 pairs; mean age, 13.2 years), the Autism Diagnostic Interview-Revised (ADI-R) (205 pairs; mean age, 13.2 years), and a best-estimate diagnosis (207 pairs). Participants underwent screening using a population-based measure of autistic traits (CAST assessment), structured diagnostic assessments (DAWBA, ADI-R, and ADOS), and a best-estimate diagnosis. On all ASD measures, correlations among monozygotic twins (range, 0.77-0.99) were significantly higher than those for dizygotic twins (range, 0.22-0.65), giving heritability estimates of 56% to 95%. The covariance of CAST and ASD diagnostic status (DAWBA, ADOS and best-estimate diagnosis) was largely explained by additive genetic factors (76%-95%). For the ADI-R only, shared environmental influences were significant (30% [95% CI, 8%-47%]) but smaller than genetic influences (56% [95% CI, 37%-82%]). The liability to ASD and a more broadly defined high-level autism trait phenotype in this large population-based twin sample derives primarily from additive genetic and, to a lesser extent, nonshared environmental effects. The largely consistent results across different diagnostic tools suggest that the results are generalizable across multiple measures and assessment methods. Genetic factors underpinning individual differences in autismlike traits show considerable overlap with genetic influences on diagnosed ASD.
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              Cognitive, language, social and behavioural outcomes in adults with autism spectrum disorders: a systematic review of longitudinal follow-up studies in adulthood.

              Although increasing numbers of children diagnosed with Autism Spectrum Disorders (ASD) are now entering adolescence and adulthood, there is limited research on outcomes post childhood. A systematic review of the existing literature was conducted. PsycINFO, PubMed, MedLine and CINAHL were systematically searched using keywords related to ASD and adolescent and adult outcomes. Studies of individuals diagnosed with ASD in childhood and followed up into adulthood were identified and reviewed. Only studies with samples sizes >10, mean age at outcome >16 years and at least one previous assessment in childhood (<16 years) were included. Twenty-five studies meeting criteria were identified. Reported outcomes in adulthood were highly variable across studies. Although social functioning, cognitive ability and language skills remained relatively stable in some studies, others reported deterioration over time. Adaptive functioning tended to improve in most studies. Diagnosis of autism or ASD was generally stable, although severity of autism-related behavioural symptoms was often reported to improve. Childhood IQ and early language ability appeared to be the strongest predictors of later outcome, but few studies examined other early variables associated with adult functioning. Implications of the findings are discussed in relation to methodological challenges in longitudinal outcome research and future research directions. Copyright © 2013 Elsevier Ltd. All rights reserved.
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                Author and article information

                Contributors
                lucy.livingston@kcl.ac.uk
                Journal
                J Child Psychol Psychiatry
                J Child Psychol Psychiatry
                10.1111/(ISSN)1469-7610
                JCPP
                Journal of Child Psychology and Psychiatry, and Allied Disciplines
                John Wiley and Sons Inc. (Hoboken )
                0021-9630
                1469-7610
                26 March 2018
                January 2019
                : 60
                : 1 ( doiID: 10.1111/jcpp.2019.60.issue-1 )
                : 102-110
                Affiliations
                [ 1 ] Social, Genetic and Developmental Psychiatry Centre Institute of Psychiatry, Psychology and Neuroscience King's College London London UK
                [ 2 ] Department of Child and Adolescent Psychiatry Institute of Psychiatry, Psychology and Neuroscience King's College London London UK
                Author notes
                [*] [* ] Correspondence

                Lucy Anne Livingston, Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, De Crespigny Park, London SE5 8AF, UK; Email: lucy.livingston@ 123456kcl.ac.uk

                Article
                JCPP12886
                10.1111/jcpp.12886
                6334505
                29582425
                3dd98a38-2763-4d3a-8360-7655b51f7145
                © 2018 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 26 January 2018
                Page count
                Figures: 1, Tables: 2, Pages: 9, Words: 7172
                Funding
                Funded by: Medical Research Council
                Categories
                Original Article
                Original Article
                Custom metadata
                2.0
                jcpp12886
                January 2019
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.5.4 mode:remove_FC converted:16.01.2019

                Clinical Psychology & Psychiatry
                autism spectrum disorder,compensation,compensatory mechanisms,adaptation,remediation,theory of mind,executive function,camouflaging

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