1. Amso D, Haas S, Tenenbaum E, Markant J, Sheinkopf SJ. {{Bottom-Up Attention Orienting in Young Children with Autism}}. {J Autism Dev Disord}. 2013 Sep 1.
We examined the impact of simultaneous bottom-up visual influences and meaningful social stimuli on attention orienting in young children with autism spectrum disorders (ASDs). Relative to typically-developing age and sex matched participants, children with ASDs were more influenced by bottom-up visual scene information regardless of whether social stimuli and bottom-up scene properties were congruent or competing. This initial reliance on bottom-up strategies correlated with severity of social impairment as well as receptive language impairments. These data provide support for the idea that there is enhanced reliance on bottom-up attention strategies in ASDs, and that this may have a negative impact on social and language development.
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2. Anderson KA, Shattuck PT, Cooper BP, Roux AM, Wagner M. {{Prevalence and correlates of postsecondary residential status among young adults with an autism spectrum disorder}}. {Autism}. 2013 Aug 30.
This study examined the prevalence and correlates of three living arrangements (with a parent or guardian, independently or with a roommate, or in a supervised setting) among a nationally representative sample of postsecondary young adults with an autism spectrum disorder. We assessed living arrangements since leaving high school. Compared with young adults with other disability types (learning disabilities, intellectual disabilities, or emotional disturbances), those with an autism spectrum disorder were more likely to have lived with a parent or guardian and least likely ever to have lived independently since leaving high school. Members of the autism spectrum disorder group were less likely to have ever lived elsewhere and more likely to live under supervision since leaving high school compared to persons with emotional disturbances and learning disabilities. Group differences persisted after controlling for functional ability and demographic characteristics. Correlates of residential independence included being White, having better conversation ability and functional skills, and having a higher household income. Further research is needed to investigate how these residential trends relate to the quality of life among families and young adults.
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3. Egawa J, Watanabe Y, Endo T, Someya T. {{Association of rs2129575 in the tryptophan hydroxylase 2 gene with clinical phenotypes of autism spectrum disorders}}. {Psychiatry and clinical neurosciences}. 2013 Sep;67(6):457-8.
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4. Ey E, Torquet N, Le Sourd AM, Leblond CS, Boeckers TM, Faure P, Bourgeron T. {{The Autism ProSAP1/Shank2 Mouse Model Displays Quantitative and Structural Abnormalities in Ultrasonic Vocalisations}}. {Behavioural brain research}. 2013 Aug 27.
Mouse ultrasonic vocalisations have been often used as a paradigm to extrapolate vocal communication defects observed in patients with autism spectrum disorders (ASD). The role of these vocalisations as well as their development, structure and informational content, however, remain largely unknown. In the present study, we characterised in depth the emission of pup and adult ultrasonic vocalisations of wild-type mice and their ProSAP1/Shank2-/- littermates lacking a synaptic scaffold protein mutated in ASD. We hypothesized that the vocal behaviour of ProSAP1/Shank2-/- mice not only differs from the vocal behaviour of their wild-type littermates in a quantitative way, but also presents more qualitative abnormalities in temporal organisation and acoustic structure. We first quantified the rate of emission of ultrasonic vocalisations, and analysed the organisation of vocalisations sequences using Markov models. We subsequently measured duration and peak frequency characteristics of each ultrasonic vocalisation, to characterise their acoustic structure. In wild-type mice, we found a high level of organisation in sequences of ultrasonic vocalisations, suggesting a communicative function in this complex system. Very limited significant sex-related variations were detected in their usage and acoustic structure, even in adult mice. In adult ProSAP1/Shank2-/- mice, we found abnormalities in the call usage and the structure of ultrasonic vocalisations. Both ProSAP1/Shank2-/- male and female mice uttered less vocalisations with a different call distribution and at lower peak frequency in comparison with wild-type littermates. This study provides a comprehensive framework to characterise abnormalities of ultrasonic vocalisations in mice and confirms that ProSAP1/Shank2-/- mice represent a relevant model to study communication defects.
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5. Granovetter M. {{Let’s talk therapy: treatments for children with autism}}. {Lancet}. 2013 Aug 31;382(9894):753.
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6. Gu F, Chauhan V, Kaur K, Brown WT, Lafauci G, Wegiel J, Chauhan A. {{Alterations in mitochondrial DNA copy number and the activities of electron transport chain complexes and pyruvate dehydrogenase in the frontal cortex from subjects with autism}}. {Translational psychiatry}. 2013;3:e299.
Autism is a neurodevelopmental disorder associated with social deficits and behavioral abnormalities. Recent evidence suggests that mitochondrial dysfunction and oxidative stress may contribute to the etiology of autism. This is the first study to compare the activities of mitochondrial electron transport chain (ETC) complexes (I-V) and pyruvate dehydrogenase (PDH), as well as mitochondrial DNA (mtDNA) copy number in the frontal cortex tissues from autistic and age-matched control subjects. The activities of complexes I, V and PDH were most affected in autism (n=14) being significantly reduced by 31%, 36% and 35%, respectively. When 99% confidence interval (CI) of control group was taken as a reference range, impaired activities of complexes I, III and V were observed in 43%, 29% and 43% of autistic subjects, respectively. Reduced activities of all five ETC complexes were observed in 14% of autistic cases, and the activities of multiple complexes were decreased in 29% of autistic subjects. These results suggest that defects in complexes I and III (sites of mitochondrial free radical generation) and complex V (adenosine triphosphate synthase) are more prevalent in autism. PDH activity was also reduced in 57% of autistic subjects. The ratios of mtDNA of three mitochondrial genes ND1, ND4 and Cyt B (that encode for subunits of complexes I and III) to nuclear DNA were significantly increased in autism, suggesting a higher mtDNA copy number in autism. Compared with the 95% CI of the control group, 44% of autistic children showed higher copy numbers of all three mitochondrial genes examined. Furthermore, ND4 and Cyt B deletions were observed in 44% and 33% of autistic children, respectively. This study indicates that autism is associated with mitochondrial dysfunction in the brain.
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7. Johnson CR, Turner KS, Foldes E, Brooks MM, Kronk R, Wiggs L. {{Behavioral parent training to address sleep disturbances in young children with autism spectrum disorder: a pilot trial}}. {Sleep medicine}. 2013 Aug 27.
OBJECTIVES: A large percentage of children with autism spectrum disorders (ASD) have bedtime and sleep disturbances. However, the treatment of these disturbances has been understudied. The purpose of our study was to develop a manualized behavioral parent training (BPT) program for parents of young children with ASD and sleep disturbances and to test the feasibility, fidelity, and initial efficacy of the treatment in a small randomized controlled trial (RCT). PARTICIPANTS AND METHODS: Parents of a sample of 40 young children diagnosed with ASD with an average age of 3.5years were enrolled in our study. Participants were randomized to either the BPT program group or a comparison group who were given nonsleep-related parent education. Each participant was individually administered a 5-session program delivered over the 8-week study. Outcome measures of feasibility, fidelity, and efficacy were collected at weeks 4 and 8 after the baseline time point. Children’s sleep was assessed by parent report and objectively by actigraphy. RESULTS: Of the 20 participants in each group, data were available for 15 participants randomized to BPT and 18 participants randomized to the comparison condition. Results supported the feasibility of the manualized parent training program and the comparison program. Treatment fidelity was high for both groups. The BPT program group significantly improved more than the comparison group based on the primary sleep outcome of parent report. There were no objective changes in sleep detected by actigraphy. CONCLUSIONS: Our study is one of few RCTs of a BPT program to specifically target sleep disturbances in a well-characterized sample of young children with ASD and to demonstrate the feasibility of the approach. Initial efficacy favored the BPT program over the comparison group and suggested that this manualized parent training approach is worthy of further examination of the efficacy within a larger RCT.
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8. Jonsson L, Anckarsater H, Zettergren A, Westberg L, Walum H, Lundstrom S, Larsson H, Lichtenstein P, Melke J. {{Association between ASMT and autistic-like traits in children from a Swedish nationwide cohort}}. {Psychiatric genetics}. 2013 Aug 29.
Individuals with autism spectrum disorders often show low levels of melatonin, and it has been suggested that this decrease may be because of the low activity of the acetylserotonin O-methyltransferase (ASMT), the last enzyme in the melatonin-synthesis pathway. Also, genetic variants in ASMT have been associated with autism, as well as with low ASMT activity and melatonin levels, suggesting that the low ASMT activity observed in autism may partly be because of variations within the ASMT gene. In this study, we present a symptom-based approach to investigate possible associations between ASMT and autistic-like traits in the general population. To this end, continuous measures of autistic-like traits were assessed in a nationally representative twin cohort (n=1771) from Sweden and six single nucleotide polymorphisms (SNPs), and a duplication of exons 2-8 in ASMT were genotyped. Our results show a nominally significant association, in girls, between one single nucleotide polymorphism (rs5949028) in the last intron of ASMT and social interaction impairments. No significant association, however, was observed with traits related to language impairment or restricted and repetitive behavior. In conclusion, our results support the possible involvement of the ASMT gene in autism spectrum disorders, and our finding that only one of the three traits shows association suggests that genetic research may benefit from adopting a symptom-specific approach to identify genes involved in autism psychopathology.
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9. King IF, Yandava CN, Mabb AM, Hsiao JS, Huang HS, Pearson BL, Calabrese JM, Starmer J, Parker JS, Magnuson T, Chamberlain SJ, Philpot BD, Zylka MJ. {{Topoisomerases facilitate transcription of long genes linked to autism}}. {Nature}. 2013 Aug 28.
Topoisomerases are expressed throughout the developing and adult brain and are mutated in some individuals with autism spectrum disorder (ASD). However, how topoisomerases are mechanistically connected to ASD is unknown. Here we find that topotecan, a topoisomerase 1 (TOP1) inhibitor, dose-dependently reduces the expression of extremely long genes in mouse and human neurons, including nearly all genes that are longer than 200 kilobases. Expression of long genes is also reduced after knockdown of Top1 or Top2b in neurons, highlighting that both enzymes are required for full expression of long genes. By mapping RNA polymerase II density genome-wide in neurons, we found that this length-dependent effect on gene expression was due to impaired transcription elongation. Interestingly, many high-confidence ASD candidate genes are exceptionally long and were reduced in expression after TOP1 inhibition. Our findings suggest that chemicals and genetic mutations that impair topoisomerases could commonly contribute to ASD and other neurodevelopmental disorders.
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10. Kotagiri P, Chance SA, Szele FG, Esiri MM. {{Subventricular zone cytoarchitecture changes in autism}}. {Developmental neurobiology}. 2013 Sep 3.
Autism is thought to be a neurodevelopmental disorder with symptoms developing during neonatal neurogenesis in the subventricular zone (SVZ). Autism associated genes alter SVZ proliferation and cytoarchitecture, yet the response of the human SVZ in autism is unknown. Epilepsy drives neurogenesis in rodents, but it is uncear how epilepsy interacts with autism in SVZ responses. The striatal and septal SVZ derive from separate lineages in rodents and generate different interneuron types. Yet it is unclear if autism unevenly regulates the striatal and septal SVZ. The human SVZ was immunohistochemically examined post-mortem from individuals with autism (n=11) and controls (n=11). Autism showed a lower cell density in the septal, but not striatal, SVZ hypocellular gap only in the absence of epilepsy. There was a decline in septal hypocellular gap cells with age in autism, but no correlation with age in controls. In contrast, PCNA+ cell numbers increased only in autism with epilepsy both in the hypocellular gap and in the ependymal layer on the septal but not striatal side. Ependymal cells also became GFAP immunoreactive in autism irrespective of epilepsy co-morbidity, however this only occurred on the striatal side. In examining these questions we also discovered a subset of ependymal, astrocyte ribbon and RMS cells which express PCNA and Ki67, PLP, and alpha-tubulin. These results are the first example of a neuropsychiatric disease differentially affecting the the septal and striatal SVZ. Altered cell density in the hypocellular gap and proliferation marker expression suggest individuals with autism may follow a different growth-trajectory. (c) 2013 Wiley Periodicals, Inc. Develop Neurobiol, 2013.
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11. Ladd-Acosta C, Hansen KD, Briem E, Fallin MD, Kaufmann WE, Feinberg AP. {{Common DNA methylation alterations in multiple brain regions in autism}}. {Molecular psychiatry}. 2013 Sep 3.
Autism spectrum disorders (ASD) are increasingly common neurodevelopmental disorders defined clinically by a triad of features including impairment in social interaction, impairment in communication in social situations and restricted and repetitive patterns of behavior and interests, with considerable phenotypic heterogeneity among individuals. Although heritability estimates for ASD are high, conventional genetic-based efforts to identify genes involved in ASD have yielded only few reproducible candidate genes that account for only a small proportion of ASDs. There is mounting evidence to suggest environmental and epigenetic factors play a stronger role in the etiology of ASD than previously thought. To begin to understand the contribution of epigenetics to ASD, we have examined DNA methylation (DNAm) in a pilot study of postmortem brain tissue from 19 autism cases and 21 unrelated controls, among three brain regions including dorsolateral prefrontal cortex, temporal cortex and cerebellum. We measured over 485 000 CpG loci across a diverse set of functionally relevant genomic regions using the Infinium HumanMethylation450 BeadChip and identified four genome-wide significant differentially methylated regions (DMRs) using a bump hunting approach and a permutation-based multiple testing correction method. We replicated 3/4 DMRs identified in our genome-wide screen in a different set of samples and across different brain regions. The DMRs identified in this study represent suggestive evidence for commonly altered methylation sites in ASD and provide several promising new candidate genes.Molecular Psychiatry advance online publication, 3 September 2013; doi:10.1038/mp.2013.114.
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12. Mandelberg J, Frankel F, Cunningham T, Gorospe C, Laugeson EA. {{Long-term outcomes of parent-assisted social skills intervention for high-functioning children with autism spectrum disorders}}. {Autism}. 2013 Aug 30.
This study aims to evaluate the long-term outcome of Children’s Friendship Training, a parent-assisted social skills intervention for children. Prior research has shown Children’s Friendship Training to be superior to wait-list control with maintenance of gains at 3-month follow-up. Participants were families of children diagnosed with autism spectrum disorder who completed Children’s Friendship Training 1-5 years earlier. They were recruited through mail, phone, and email. Information collected included parent and child completed questionnaires and a phone interview. Data were collected on 24 of 52 potential participants (46%). With an average of 35-month follow-up, participants had a mean age of 12.6 years. Results indicated that participants at follow-up were invited on significantly more play dates, showed less play date conflict, improved significantly in parent-reported social skills and problem behaviors, and demonstrated marginally significant decreases in loneliness when compared to pre-Children’s Friendship Training.
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13. Marshall J, Hill RJ, Ziviani J, Dodrill P. {{Features of feeding difficulty in children with Autism Spectrum Disorder}}. {International journal of speech-language pathology}. 2013 Sep 3.
Parents of children with Autism Spectrum Disorders (ASD) commonly report concerns regarding feeding difficulties and poor nutrition. Feeding difficulties, in the form of undesirable mealtime behaviours and/or skill deficits, can cause parental concern and impact on family dynamics. Poor nutrition can have an impact on development and health outcomes. The purpose of this paper was to review recent research regarding feeding difficulties in children with ASD, in order to describe: (1) the most frequently reported undesirable mealtime behaviours and skill deficits; and (2) dietary intake and weight patterns as markers of nutrition. While the ASD population is a somewhat heterogeneous group, this literature review of 44 research studies identified a number of common issues for these children. Restricted dietary variety, food neophobia, food refusal, limiting diet based on texture, and a propensity towards being overweight were frequently reported. Gaining a better understanding of the common features of feeding difficulties experienced by children with ASD will assist in directing intervention studies. Findings from such studies have the potential to enhance developmental and nutritional outcomes for this group. Well-designed longitudinal research would be valuable in monitoring the impact of feeding difficulties for these children as they age.
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14. Plasschaert RN, Bartolomei MS. {{Autism: A long genetic explanation}}. {Nature}. 2013 Aug 28.
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15. Rhodes G, Jeffery L, Taylor L, Ewing L. {{Autistic traits are linked to reduced adaptive coding of face identity and selectively poorer face recognition in men but not women}}. {Neuropsychologia}. 2013 Aug 29.
Our ability to discriminate and recognize thousands of faces despite their similarity as visual patterns relies on adaptive, norm-based, coding mechanisms that are continuously updated by experience. Reduced adaptive coding of face identity has been proposed as a neurocognitive endophenotype for autism, because it is found in autism and in relatives of individuals with autism. Autistic traits can also extend continuously into the general population, raising the possibility that reduced adaptive coding of face identity may be more generally associated with autistic traits. In the present study, we investigated whether adaptive coding of face identity decreases as autistic traits increase in an undergraduate population. Adaptive coding was measured using face identity aftereffects, and autistic traits were measured using the Autism-Spectrum Quotient (AQ) and its subscales. We also measured face and car recognition ability to determine whether autistic traits are selectively related to face recognition difficulties. We found that men who scored higher on levels of autistic traits related to social interaction had reduced adaptive coding of face identity. This result is consistent with the idea that atypical adaptive face-coding mechanisms are an endophenotype for autism. Autistic traits were also linked with face-selective recognition difficulties in men. However, there were some unexpected sex differences. In women, autistic traits were linked positively, rather than negatively, with adaptive coding of identity, and were unrelated to face-selective recognition difficulties. These sex differences indicate that autistic traits can have different neurocognitive correlates in men and women and raise the intriguing possibility that endophenotypes of autism can differ in men and women.
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16. Schaaf RC, Benevides TW, Leiby BE, Sendecki JA. {{Autonomic Dysregulation During Sensory Stimulation in Children with Autism Spectrum Disorder}}. {J Autism Dev Disord}. 2013 Aug 31.
Autonomic nervous system (ANS) activity during sensory stimulation was measured in 59 children with autism spectrum disorder (ASD) ages 6-9 in comparison to 30 typically developing controls. Multivariate comparisons revealed significant differences between groups in the respiratory sinus arrhythmia (parasympathetic measure) vector of means across sensory stimuli (p = 0.02) and in change from domain to domain (p = 0.01). Sympathetic activity, measured by pre-ejection period, did not differ significantly between groups, although it was higher in ASD participants. Findings suggest that participants with ASD demonstrated a different pattern of parasympathetic activity during sensory stimulation. Findings are discussed in relation to the biological mechanisms of sensory processing in autism, insight into the autism phenotype, and the utility of ANS activity as an outcomes marker.
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17. Schneider D, Slaughter VP, Bayliss AP, Dux PE. {{A temporally sustained implicit theory of mind deficit in autism spectrum disorders}}. {Cognition}. 2013 Aug 28;129(2):410-7.
Eye movements during false-belief tasks can reveal an individual’s capacity to implicitly monitor others’ mental states (theory of mind – ToM). It has been suggested, based on the results of a single-trial-experiment, that this ability is impaired in those with a high-functioning autism spectrum disorder (ASD), despite neurotypical-like performance on explicit ToM measures. However, given there are known attention differences and visual hypersensitivities in ASD it is important to establish whether such impairments are evident over time. In addition, investigating implicit ToM using a repeated trial approach allows an assessment of whether learning processes can reduce the ASD impairment in this ability, as is the case with explicit ToM. Here we investigated the temporal profile of implicit ToM in individuals with ASD and a control group. Despite similar performance on explicit ToM measures, ASD-diagnosed individuals showed no evidence of implicit false-belief tracking even over a one-hour period and many trials, whereas control participants did. These findings demonstrate that the systems involved in implicit and explicit ToM are distinct and hint that impaired implicit false-belief tracking may play an important role in ASD. Further, they indicate that learning processes do not alleviate this impairment across the presentation of multiple trials.
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18. Toma C, Torrico B, Hervas A, Valdes-Mas R, Tristan-Noguero A, Padillo V, Maristany M, Salgado M, Arenas C, Puente XS, Bayes M, Cormand B. {{Exome sequencing in multiplex autism families suggests a major role for heterozygous truncating mutations}}. {Molecular psychiatry}. 2013 Sep 3.
Autism is a severe neurodevelopmental disorder, the aetiology of which remains mainly unknown. Family and twin studies provide strong evidence that genetic factors have a major role in the aetiology of this disease. Recently, whole exome sequencing (WES) efforts have focused mainly on rare de novo variants in singleton families. Although these studies have provided pioneering insights, de novo variants probably explain only a small proportion of the autism risk variance. In this study, we performed exome sequencing of 10 autism multiplex families with the aim of investigating the role of rare variants that are coinherited in the affected sibs. The pool of variants selected in our study is enriched with genes involved in neuronal functions or previously reported in psychiatric disorders, as shown by Gene Ontology analysis and by browsing the Neurocarta database. Our data suggest that rare truncating heterozygous variants have a predominant role in the aetiology of autism. Using a multiple linear regression model, we found that the burden of truncating mutations correlates with a lower non-verbal intelligence quotient (NVIQ). Also, the number of truncating mutations that were transmitted to the affected sibs was significantly higher (twofold) than those not transmitted. Protein-protein interaction analysis performed with our list of mutated genes revealed that the postsynaptic YWHAZ is the most interconnected node of the network. Among the genes found disrupted in our study, there is evidence suggesting that YWHAZ and also the X-linked DRP2 may be considered as novel autism candidate genes.Molecular Psychiatry advance online publication, 3 September 2013; doi:10.1038/mp.2013.106.
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19. Wei H, Alberts I, Li X. {{Brain IL-6 and autism}}. {Neuroscience}. 2013 Aug 27.
Autism is a severe neurodevelopmental disorder characterized by impairments in social interaction, deficits in verbal and non-verbal communication, and repetitive behavior and restricted interests. Emerging evidence suggests that aberrant neuroimmune responses may contribute to phenotypic deficits and could be appropriate targets for pharmacologic intervention. Interleukin (IL)-6, one of the most important neuroimmune factors, has been shown to be involved in physiological brain development and in several neurological disorders. For instance, findings from postmortem and animal studies suggest that brain IL-6 is an important mediator of autism-like behaviors. In this review, a possible pathological mechanism behind autism is proposed, which suggests that IL-6 elevation in the brain, caused by the activated glia and/or maternal immune activation, could be an important inflammatory cytokine response involved in the mediation of autism-like behaviors through impairments of neuroanatomical structures and neuronal plasticity. Further studies to investigate whether IL-6 could be used for therapeutic interventions in autism would be of great significance.
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20. Williams ME, Fink C, Zamora I, Borchert M. {{Autism assessment in children with optic nerve hypoplasia and other vision impairments}}. {Developmental medicine and child neurology}. 2013 Sep 3.
AIM: This study examined the utility of standard autism diagnostic measures in nine children (aged 5-9y) with severe vision impairment and a range of social and language functioning. METHOD: The Autism Diagnostic Observation Schedule (ADOS) and the Autism Diagnostic Interview, Revised (ADI-R) were systematically modified and used to assess symptoms of autism in children with vision less than or equal to 20/800, the majority of whom had optic nerve hypoplasia. The results of the assessments, including analysis of symptom patterns, were compared with expert autism diagnoses. RESULTS: Modified autism measures demonstrated good agreement with clinical diagnoses. Symptoms found to be most and least reliable in discriminating autism from behaviors common to most children with congenital vision impairment are described. Comparisons of current behavior with parent-reported behaviors from a younger age suggested that some symptoms of autism in very young children who are congenitally blind may improve with age. INTERPRETATION: The ADOS and ADI-R are useful for clinical assessment and for advancing research efforts to understand autism symptoms in children with vision impairment. However, some autistic symptoms in very young children may change over time, and developmental changes should be closely monitored.
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21. Winburn E, Charlton J, McConachie H, McColl E, Parr J, O’Hare A, Baird G, Gringras P, Wilson DC, Adamson A, Adams S, Le Couteur A. {{Parents’ and Child Health Professionals’ Attitudes Towards Dietary Interventions for Children with Autism Spectrum Disorders}}. {J Autism Dev Disord}. 2013 Sep 1.
Parents of children with autism spectrum disorders (ASD) use a wide range of interventions including poorly evidenced dietary interventions. To investigate parents’ and professionals’ experience of dietary interventions and attitudes towards a proposed trial to evaluate the gluten free casein free diet (GFCFD). Survey of UK parents of children with ASD, and professionals. 258 parents and 244 professionals participated. 83 % of children had received a range of dietary manipulations; three quarters of professionals have been asked for advice about GFCFD. Respondents identified an inadequate evidence base for dietary interventions in ASD and suggested modifications to a proposed trial design. Both parents and professionals supported the need for further evaluation of dietary interventions in ASD.
