ICD-116A02	AUTISM SPECTRUM DISORDER (ASD) Autism spectrum disorder
ICD-10F84.0	Childhood autism
DSM-5-TRF84.0	Autism Spectrum Disorder

1. Definition and nosology

Autism spectrum disorder (ASD; ICD-11: 6A02; DSM-5-TR: F84.0 Autism Spectrum Disorder) is a neurodevelopmental disorder with onset in the early developmental period, accompanied by persistent deficits in two core domains:

1. Persistent deficits in social communication and social interaction — reciprocal social-emotional exchange, non-verbal communicative behaviour, and the development and maintenance of relationships.
2. Restricted, repetitive patterns of behaviour, interests, or activities — stereotyped motor movements or speech, adherence to fixed rituals and routines, restricted high-intensity interests, atypical reactivity to sensory stimuli.

In ICD-11, the diagnosis is specified with qualifiers: with/without intellectual developmental disorder; impairment of functional language (absent / mild-to-moderate / severe); overall persistent clinical course (stable, worsening, improving).

2. History

• Kanner L. (1943) — “early infantile autism” — observed social isolation, resistance to change, and language disturbances in 11 children.
• Asperger H. (1944) — “autistic psychopathy” — described deficits in social interaction with normal intelligence and language. (Asperger's history of collaboration with the Nazi regime has come to light in recent decades — Czech H. Mol Autism 2018.)
• Wing L., Gould J. (1979) — the “autistic spectrum” concept; the “triad of impairments” — social interaction, communication, imagination/behaviour.
• DSM-III (1980) → DSM-IV (1994): the Pervasive Developmental Disorders category — Autistic Disorder, Asperger's Disorder, Childhood Disintegrative Disorder, Rett's Disorder, and PDD-NOS as separate diagnoses.
• DSM-5 (2013) and ICD-11 (2019): all subtypes were merged into the single category of “Autism Spectrum Disorder”. The rationale: the evidence base for a reliable and valid separation of the subtypes was weak. In DSM-5, severity is divided into 3 levels (1 — requiring support; 2 — requiring substantial support; 3 — requiring very substantial support). In ICD-11, severity is not a separate qualifier — sub-specification is based on intellectual and language impairment.
• Childhood disintegrative disorder is preserved in ICD-11 with a separate code (atypical course qualifier).

3. Epidemiology

• Prevalence: CDC ADDM Network 2023 report (8-year-old children, 2020 data): 1/36 (2.8%) — increase recorded in recent decades (1/150 — 2000; 1/68 — 2012). Most of the increase is explained by expansion of diagnostic criteria, increased awareness, and application of screening.
• Sex: Males ~4:1 — but under-detection problem in females documented (female phenotype — social “camouflage”, fewer overt repetitive behaviors; Lai M.C., Baron-Cohen S. Lancet Psychiatry 2015).
• Comorbidity with intellectual disability: ~30–40% (CDC ADDM); approximately 30–35% IQ <70.
• Other comorbidities: ADHD ~30–50%, anxiety ~40%, depression in adolescence ~25%, epilepsy ~10–30% (increases with age), sleep disorders 50–80%, feeding problems, GI complaints.
• Mortality: Twice higher compared to the population — main causes: epilepsy, accidents (drowning, wandering incidents), suicide (in high-functioning ASD).

4. Aetiology and pathogenesis

4.1 Genetic factors (50–80% heritability)

• Heritability: Sandin S. et al. JAMA 2017 Swedish sibling and twin study n>2 mln: heritability ~80%; environmental factors account for ~20%.
• Association with genetic syndromes: Fragile X (~2–5% of ASD cases), Rett syndrome (almost always MECP2 mutation in females), tuberous sclerosis (~1–4%), 22q11.2 deletion, 16p11.2, Phelan-McDermid (22q13).
• De novo CNV and SNV mutations — identified in ~25% of cases; synaptic genes (SHANK3, NRXN1, NLGN3/4, CHD8, SCN2A) noted (Satterstrom F.K. et al. Cell 2020 — 102 risk genes).
• Polygenic risk architecture — hundreds of small-effect variants numerically; no single ‘autism gene’.
• Father's age > 40 — associated with new mutation risk.

4.2 Prenatal and perinatal risk factors

• Parental valproate use (during pregnancy) — increases the risk of autism spectrum disorder ~2.9-fold (95% CI 1.7–4.9) and of childhood autism ~5.2-fold (95% CI 2.7–10.0); absolute risk 4.42% and 2.50% (1.53% and 0.48% in the population) — Christensen J. et al. JAMA 2013; FDA and EMA warning.
• Preterm birth — at 22–27 weeks increases the risk ~3.7–4.2-fold (Crump C. et al. Pediatrics 2021), at 22–31 weeks ~2.3-fold (Persson M. et al. PLOS Med 2020); pooled ASD prevalence among preterm children is 7% (95% CI 4–9) at a median gestation of 28 weeks (Agrawal S. et al. Pediatrics 2018).
• Low birth weight, perinatal hypoxia.
• Parental diabetes, severe obesity, gestational hypertension — indicated as risk factors.
• Maternal viral infections during pregnancy (rubella, cytomegalovirus) — high risk.

4.3 Neurobiological mechanisms

• Atypical pattern of early brain growth — acceleration at 2–4 years, then normalization (Courchesne E. et al. JAMA 2003).
• Disregulation in synaptic formation and pruning processes — excitatory/inhibitory imbalance.
• Atypical pattern of interregional functional connectivity in the brain — local hyperconnectivity, long-range hypoconnectivity (Just M.A. et al. Brain 2004; later mixed evidence).
• Social cognition network (medial prefrontal, temporal-parietal junction, amygdala) and mirror neuron system show atypical activation patterns.

4.4 Environmental risk factors

• Air pollution (PM2.5, NO2) during pregnancy and early childhood — moderately increases risk (Volk H.E. et al. JAMA Psychiatry 2013).
• Maternal folate deficiency (during the periconceptional period) — risk reduced with folate supplements (Surén P. et al. JAMA 2013).

5. Clinical features

5.1 Social communication and interaction deficits

• Reciprocal social-emotional exchange deficit — atypical social proximity, reduced reciprocal conversation, restricted shared interests.
• Non-verbal communicative behavior deficits – atypical use of eye contact, reduced coordination of gestures and facial expressions.
• Difficulty forming and maintaining relationships — paucity of age-appropriate friendships, lack of imaginative role play.

5.2 Restricted, repetitive behavior patterns

• Stereotyped or repetitive motor movements, object use, or speech (echolalia, idiosyncratic phrases).
• Insistence on sameness, inflexible adherence to routines, or ritualized patterns of behavior (clothing, food, route).
• High intensity or focused limited interests (complex knowledge of a specific topic — “intense passion”).
• Atypical reactivity to sensory input — hyperreactivity (sound, touch), hyporeactivity (pain), or atypical sensory interests (examining surfaces, visual stimulation).

5.3 Developmental trajectory

Early signs — reduced social attention, lack of response to name calling, reciprocal smiling, non-verbal communication (12–18 months). In some children developmental regression (loss of acquired language and social skills over 12–24 months) is noted — ~30% of cases (CDC).

In adulthood — social “camouflage” in females and high-functioning individuals (Hull L. et al. J Autism Dev Disord 2017) — leads to exhaustion and secondary psychiatric comorbidity (anxiety, depression) by concealing difficulties.

6. Diagnosis

6.1 Unified diagnostic criteria (DSM-5-TR · ICD-11 · NICE CG170 consensus points)

A. Persistent deficits in social communication and social interaction — The following three areas in all:

1. Social-emotional reciprocal exchange.
2. In social reciprocity, nonverbal communicative behavior;
3. Development, maintenance, and understanding of relationships.

B. Restricted, repetitive patterns of behavior, interests, or activities — At least two of the following four:

1. Stereotyped or repetitive motor movements, object use, speech;
2. Insistence on sameness, adherence to routine, ritualized behavior or speech;
3. High intensity, focused limited interests;
4. Hyper- or hyporeactivity to sensory input, or atypical sensory interests.

C. Symptoms must be present in early developmental period (may not fully manifest until social demands increase).

D. Functional impairment — in social, academic, or other important areas.

E. Exclusions — Not fully explained by intellectual developmental disorder or global developmental delay (comorbidity possible).

6.2 Source-specific clarifications

• DSM-5-TR (F84.0): Three severity levels (1-3) are separately assigned for both domains — based on the intensity of support need. Qualifiers: intellectual disability, language impairment, known medical/genetic condition, another neurodevelopmental disorder, with catatonia.
• ICD-11 (6A02): Subspecifications — with intellectual developmental disorder (6A02.0/.1)/without (6A02.2/.3); degree of functional language impairment (absent / mild-moderate / severe). The 1–3 severity system in DSM is not officially adopted.
• NICE CG170 (Autism spectrum disorder in under 19s: support and management, 2013): the diagnosis should be made by a multidisciplinary team (pediatrician/psychiatrist + speech-language pathologist + clinical psychologist); ADOS-2 and ADI-R considered diagnostic gold standard.
• AAP 2020 (Hyman S.L., Levy S.E., Myers S.M. Pediatrics 2020;145(1)): At 18 and 24 months universal autism screening Recommended (M-CHAT-R/F); positive screening → specialist evaluation.
• AACAP Practice Parameter (Volkmar F. et al. J Am Acad Child Adolesc Psychiatry 2014): diagnostic algorithm, comorbidity assessment, treatment recommendations.

6.3 Diagnostic algorithm

1. Parent and caregiver interview — developmental history, early social and communicative signs.
2. Screening: 18 and 24 months (M-CHAT-R/F); follow-up questionnaire if positive.
3. Specialist assessment — pediatrician / developmental pediatrician / psychiatrist / clinical psychologist.
4. Gold standard diagnostic tools: ADOS-2 (Autism Diagnostic Observation Schedule) — structured play-based observation; ADI-R (Autism Diagnostic Interview, Revised) — parent interview.
5. Intellectual assessment (WISC-V, Stanford-Binet 5, non-verbal options — Leiter-3, Mullen).
6. Speech-language and adaptive behavior assessment (Vineland-3).
7. Hearing and vision tests.
8. Medical and genetic assessment — chromosomal microarray (CMA), Fragile X (FMR1), selective trio exome; EEG when seizure suspicion exists; MRI in clinical suspicion (microcephaly, regression).
9. Comorbidity screening: ADHD, anxiety, depression, OCD, sleep, eating, GI.

6.4 Differential diagnosis

7. Examination and assessment

7.1 Clinical diagnostic tools

• Screening: M-CHAT-R/F (16–30 months), SCQ (4+ years, parent questionnaire), SRS-2 (Social Responsiveness Scale).
• Diagnostics: ADOS-2 (toddler-adult modules), ADI-R (1.5+ years, parent).
• Intellect and cognition: Mullen Scales of Early Learning, Bayley-III/IV (young age), WISC-V, Leiter-3 (non-verbal).
• Adaptive behaviour: Vineland-3, ABAS-3.
• Speech and language: PLS-5, CELF-5, CCC-2 (pragmatic).
• Sensory profile: Sensory Profile-2 (Dunn).
• Comorbidity: Conners for ADHD, SCARED for anxiety, PHQ-9 adaptations for depression.

7.2 Laboratory investigations

First-line (AAP 2020 / AACAP 2014): Chromosomal microarray analysis (CMA — diagnostic yield ~10–20%); Fragile X (FMR1).

Selective: trio exome sequencing (WES — diagnostic yield of 25–40% if CMA is negative); MECP2 (for suspected Rett syndrome in females); metabolic (lactate, ammonia, amino acids — if regression is present); lead level; TSH.

7.3 Instrumental investigations

• EEG — in case of seizure, regression, bizarre behavior episodes.
• Brain MRI — focal neurological signs, micro/macrocephaly, regression.
• Hearing test — mandatory in all cases (audiometry, ABR).

8. Treatment

8.1 General principles (NICE CG170 · AAP 2020 · AACAP 2014 consensus)

1. ASD cannot be ‘cured’ — individual development, adaptation, and quality of life are improved. Claims of “cure” and “full recovery” are not scientifically based; the goal is functional skills, communication, independence, quality of life.
2. Early, intensive, individual behavioral intervention First-line — effect greatest between ages 18 months to 6 years (Reichow B. et al. Cochrane 2018, EIBI/ESDM meta-analysis).
3. Naturalistic Developmental Behavioral Interventions (NDBI) — based on the principles of behavior-development in play and daily contexts; more flexible than the classical discrete-transition version of ABA. Included in this group:
   • Early Start Denver Model (ESDM)
   • Joint Attention, Symbolic Play, Engagement, and Regulation (JASPER)
   • Pivotal Response Treatment (PRT)
   • Enhanced Milieu Teaching (EMT)
   • Paediatric Autism Communication Therapy (PACT)
   Detailed description of methods — in the ‘Treatment methodologies’ section.
4. Parent-mediated approach — Hanen “More Than Words”, PACT (Pickles A., Green J. et al. Lancet 2010, 2016 follow-up — 6-year effect sustained), PRT parent version. Most cost-effective approach in resource-limited settings.
5. Social skills groups — for older children and adolescents; PEERS program (UCLA, Laugeson E.A.) — also effective in adults.
6. Structured educational environment — TEACCH (Treatment and Education of Autistic and related Communication-handicapped Children, Schopler E. North Carolina); IEP / EHCP individual education plan.
7. Communication support — In minimally verbal patients — Augmentative and Alternative Communication (AAC) — PECS (Picture Exchange Communication System), speech-generating devices, tablet-based applications.
8. Comorbidity treatment — ADHD (stimulants, Cortese 2018), anxiety (CBT modification — Storch E.A. RCTs), depression (CBT, SSRIs), epilepsy (standard antiepileptic), sleep (sleep hygiene, melatonin — RCT evidence Goldman S.E. J Clin Sleep Med 2014).
9. Pharmacotherapy only for comorbid symptoms — There is no FDA-approved medication for the core symptoms of ASD. For behavioral aggression and irritability — risperidone (5–16 years, FDA approval 2006) and aripiprazole (6–17 years, FDA approval 2009). Both are evidence-based (McCracken J.T. et al. NEJM 2002 RCT — risperidone), but the side effect burden is significant (metabolic, EPS). Behavioral intervention is first-line.

8.2 Source-specific clarifications

• NICE CG170 (2013, 2021 update): diagnosis by a multidisciplinary group; social communication interventions are first-line; parent programs are superior; antipsychotics only when behavioral interventions fail; caution against claims of actual “treatment”.
• AAP Clinical Report 2020 (Hyman et al.): 18 and 24 months universal screening; early intervention (<3 years); integrated medical and behavioral management.
• AACAP Practice Parameter 2014 (Volkmar): emphasis on diagnosis-specific educational placement, comorbidity treatment, family support.
• WHO Caregiver Skills Training (CST): resource-limited parent training program for low and middle income countries; widely adapted across countries (Salomone E. et al. Autism 2019).

Treatment methods

1. Applied Behavior Analysis (ABA) — Learning method based on behavioral principles; shaping social, communicative, and adaptive skills, reducing challenging behavior. Applied in discrete trial training (DTT) or naturalistic format. Part of adult autistic community criticizes classical form of ABA (autonomy, distress).
2. Early Intensive Behavioral Intervention (EIBI) — Structured intensive intervention based on ABA at early age (25–40 hours per week); target — social, communicative, and adaptive skills. Evidence: Reichow B., Hume K., Barton E.E., Boyd B.A. Cochrane 2018 — small-to-medium effect on IQ, language, and adaptive behavior; current claims should be approached with caution.
3. Early Start Denver Model (ESDM) — Rogers S., Dawson G — Naturalistic developmental behavioral intervention for 12–48 months; learning within the context of play and daily activities. Evidence: Dawson G. et al. Pediatrics 2010 RCT n=48 — significant improvement in IQ, language, and adaptive behavior, diagnosis change at age 6 (Dawson G. et al. JAACAP 2012 follow-up). Parent version (P-ESDM) Rogers S.J. et al. JAACAP 2012.
4. Joint Attention, Symbolic Play, Engagement, and Regulation (JASPER) — Kasari (Kasari C.) — Intervention targeting joint attention and symbolic play development; 12–60 months. Evidence: Kasari C. et al. JAMA Pediatr 2014, J Consult Clin Psychol 2010 — significant improvement in joint attention and expressive language.
5. Paediatric Autism Communication Therapy (PACT) — Pickles (A.), Green (J.) — Parent-coordinated communication intervention; ages 2–11. Video-based analysis and expansion of parent-child interaction. Evidence: Pickles A. et al. Lancet 2016 — n=152, 6-year follow-up — sustained improvement in autism severity and parent synchronization. Adapted for resource-limited settings.
6. Pivotal Response Treatment (PRT) — Koegel (Koegel R.L., Koegel L.K.) — focusing on “Pivot” behaviors (motivation, response to multiple signals, self-regulation, self-initiation) — when learned, change spreads to multiple areas. In naturalistic format, based on child's choices.
7. Treatment and Education of Autistic and related Communication-handicapped Children (TEACCH) — Schopler E. — Structured visual educational environment — ‘structured teaching’ — visual schedules, work systems, individual transitions; in home, school, and community contexts. Originated in North Carolina, spread worldwide.
8. Picture Exchange Communication System (PECS) — Bondy, Frost — Picture exchange-based communication training for minimal-verbal patients — in 6 stages. Evidence: Howlin P. et al. J Child Psychol Psychiatry 2007 RCT — increase in communication.
9. Program for the Education and Enrichment of Relational Skills (PEERS) — Laugeson (Laugeson E.A., UCLA) — Structured social skills group for adolescents and young adults with ASD; 16 weeks, with parental support. Evidence: Laugeson E.A. et al. J Autism Dev Disord 2012, 2015.
10. Hanen “More Than Words” — 8 group sessions + 3 individual home visits for parents of children with ASD aged 2–5. hanen.org.
11. WHO Caregiver Skills Training (CST) — WHO's limited-resource parent training for low- and middle-income countries; for ASD and developmental delays; implemented by non-specialist trainer-facilitators working in the community.
12. EEG Neurofeedback — Neurofeedback training, based on real-time monitoring of brainwave patterns, aimed at enabling the user to regulate their own brain activity. In ASD, the evidence base for an effect on core symptoms is limited; Holtmann M. et al. Dev Med Child Neurol 2011 — modest in ADHD, specific evidence in ASD is weak. Not first-line, adjunct status; the limited evidence base should be explained to the patient and the family.
13. Autism Diagnostic Observation Schedule (ADOS-2) and Autism Diagnostic Interview-Revised (ADI-R) — Diagnostic gold standard tools — ADOS-2 structured play-based observation (5 modules, toddler-adult); ADI-R standardized parent interview (1.5+ years, ~2 hours).

9. Prognosis

Good prognostic factors

• Early diagnosis (<3 years) and early intensive intervention.
• Intellectual function preserved (IQ >70).
• Acquisition of functional language by age 5.
• Management of comorbid disorders.
• Stabil family support and community resources.

Poor prognostic factors

• Comorbid intellectual disability (severe-profound).
• Absence of functional language by age 5.
• Epileptic seizures — additional risk increase in adulthood.
• Severe behavioral disturbances, self-harm.
• Late initiation of diagnosis and intervention.

Follow-up targets

• Comorbid psychiatric conditions (ADHD, anxiety, depression, OCD) screening — annual.
• Epilepsy monitoring — especially during adolescence.
• Sleep, food, gastrointestinal tract, motor disturbance screening.
• Late adolescence planning (16–18 years) — career, independent living, employment.
• In adult patients, the emotional burden of social camouflage, anxiety, and depression — active screening.
• Respite support for family, peer support, psychoeducation.
• Neurodiversity approach — strengthening the patient's strengths, no claim of ‘full cure’.

10. Myths and misconceptions

10.1 Aetiology myths

Myth 1: “Vaccines (especially MMR) cause autism”

Why it is widespread: Wakefield A.J. et al. Lancet 1998 — claimed association of MMR vaccine with bowel disorder and autism based on 12 children. Subsequently, Brian Deer's journalistic investigation and the General Medical Council inquiry revealed Wakefield's financial interest and data manipulation; article fully retracted in 2010; Wakefield stripped of medical license.

Clinical and biological rationale: Autism clinically manifests at 12–18 months — temporal correlation with typical MMR vaccination period may lead to misinterpretation as a ‘cause’. Pathogenesis is genetic and early neurodevelopmental-based (hereditability 80%, prenatal and perinatal factors) — not vaccine-dependent.

Evidence: Taylor L.E., Swerdfeger A.L., Eslick G.D. Vaccine 2014 meta-analysis n>1.2 million children — between MMR and autism there is no relation; Madsen K.M. et al. NEJM 2002 Danish study n>537,000; Jain A. et al. JAMA 2015 US study. CDC, WHO, NICE, AAP hold the same position.

Real clinical step: Present evidence calmly, respectfully to family; explain the risk of vaccine refusal for child and community health (2018–2019 measles epidemic in Madagascar, 1200+ child deaths).

Myth 2: “Microplastics, heavy metals, chemical food additives are the main cause of autism”

Why it is widespread: “Natural / chemical-free” movement exaggerated in mass media; out-of-context use of microplastic research.

Clinical and biological rationale: Primary etiology of autism. is genetic (heritability 80% — Sandin JAMA 2017). Environmental factors are investigated as risk factors (PM2.5 air pollution — Volk JAMA Psychiatry 2013; prenatal valproate — Christensen JAMA 2013), but there is no evidence base for microplastics or heavy metals as a “primary cause”.

Evidence: Hertz-Picciotto I. Environ Health Perspect 2018 review — some neurotoxins (especially valproate, alcohol) are considered risk factors; heavy metal exposure has not been proven as a direct etiology of autism.

Real clinical step: Provide family with realistic risk factors (valproate during pregnancy, limiting air pollution) and realistic protective steps (periconceptional folate).

Myth 3: “‘Cold mother’ (Bettelheim's ‘Refrigerator Mother’ theory)”

Why it is widespread: Bruno Bettelheim in his 1967 work “The Empty Fortress” attributed autism to maternal emotional coldness; dominant belief until the 1970s.

Clinical and biological rationale: autism Is a neurodevelopmental disorder — Related to genetics and early brain development; parental behavior does not cause autism.

Evidence: Rimland B. (1964) “Infantile Autism” — argument for biological etiology; Folstein S., Rutter M. Nature 1977 — twin study demonstrated genetic inheritance. APA, AAP, AACAP — “refrigerator mother” concept has been discarded.

Real clinical step: Support and psychoeducation to family instead of blaming; parent-coordinated interventions (PACT, ESDM, Hanen).

10.2 Harmful or dangerous “treatment” methods

Myth 4: “Chelation therapy removes heavy metals and cures autism”

Why it is widespread: “Heavy metal autism” false theory; marketing by alternative clinics.

Evidence and risk: AAP 2010 and FDA warning — a 5-year-old child died from cardiac arrest due to calcium deficiency during chelation procedure (2005). Chelation is indicated only for confirmed heavy metal poisoning (high lead), not for autism. AAP, AACAP — absolute contraindication.

Myth 5: “Hyperbaric oxygen chamber (HBOT) cures autism”

Evidence: Cochrane (Xiong T. et al. 2016) review of n=1 RCT — no evidence of efficacy for autism. Risks: pneumothorax, ear barotrauma, fire (oxygen + static).

Myth 6: “MMS / ‘Miracle Mineral Solution’ (chlorine dioxide) cures autism”

Evidence: FDA 2019, EMA warnings — chlorine dioxide is caustic, liver and kidney damage, deaths reported. All clinical use is prohibited. Worse — “treatment” recommending it as an anal cleansing agent is child torture.

Myth 7: Stem cell injections cure autism

Evidence: ISSCR (International Society for Stem Cell Research) and FDA — no approved stem cell therapy for autism. In illegal clinics — infections, brain tumors, deaths have been reported (Berkowitz NEJM 2016).

Myth 8: “Chelyabinsk remedy” and similar unregulated medical preparations

Evidence: no ‘alternative’ agents approved by any confirmed regulatory body (FDA, EMA, EU) for autism treatment — risk high, benefit unproven.

10.3 Ineffective methods or those delaying primary intervention

Myth 9: “Facilitated Communication (FC) and Rapid Prompting Method (RPM) reveal the inner world of minimally verbal individuals with autism”

Why it is widespread: Emotionally engaging narratives — children who “start to talk” with facilitator assistance.

Evidence: ASHA Position Statement 2018 (update): independent reviews have shown that messages come from the facilitator (ideomotor effect), not the patient. This evidence has been confirmed in multiple RCTs (Schlosser R.W. et al. Augment Altern Commun 2014). Clinical outcome: false belief for the family; the patient's true authentic communication (PECS, AAC devices) is delayed; public harm — false ‘testimony’ incidents in legal issues.

Real clinical step: Evidence-based AAC tools for minimally verbal patients — PECS, tablet-based communication programs (Proloquo2Go, TouchChat).

Myth 10: “Gluten-free / casein-free diet cures autism or significantly improves it”

Evidence: Hyman S.L. et al. (AAP 2020 Clinical Report) — effect of special diets on autism symptoms not proven; diet is medically indicated if gastrointestinal symptoms or celiac disease present. Broad dietary restriction leads to nutritional deficiencies and eating disorders in children. Karagas M.R. et al. JAMA Pediatr 2018 — risks of broad dietary restriction.

Myth 11: “EEG Neurofeedback cures core symptoms of autism”

Evidence: Holtmann M. et al. Dev Med Child Neurol 2011 review — modest effect in ADHD; specific evidence for autism weak. Adjunct status, not first-line. Must be clearly explained to the patient and the family.

Myth 12: “Auditory Integration Training (AIT) cures autism”

Evidence: ASHA Position Statement 2004; AAP 1998 — experimental status, no evidence of effect.

Myth 13: “Vitamin B6 / magnesium or other mega-dose vitamin therapy”

Evidence: Cochrane (Nye C., Brice A. 2005) — no evidence for efficacy of B6/magnesium combination for autism. Vitamin mega-doses may lead to side effect burden (B6 neuropathy).

Myth 14: “Patterning” (Doman-Delacato)

Evidence: AAP 1968 and 2010 Statements — no evidence of effect, excessive burden on family; delays children from evidence-based interventions.

Myth 15: “Cranio-Sacral Therapy, reflexotherapy, homeopathy”

Evidence: systematic reviews (Cochrane and others) — no evidence of effect for autism. NICE CG170 — warning against complementary interventions.

11. Sources

1. WHO. ICD-11 for Mortality and Morbidity Statistics. 6A02 Autism spectrum disorder. 2024.
2. American Psychiatric Association. DSM-5-TR. Washington DC: APA Publishing; 2022.
3. NICE Clinical Guideline 170. Autism spectrum disorder in under 19s: support and management. 2013, 2021 update.
4. Hyman S.L., Levy S.E., Myers S.M.; AAP Council on Children with Disabilities. Identification, Evaluation, and Management of Children With Autism Spectrum Disorder. Pediatrics 2020;145(1):e20193447.
5. Volkmar F., Siegel M., Woodbury-Smith M., King B., McCracken J., State M. AACAP Practice Parameter for the Assessment and Treatment of Children and Adolescents With Autism Spectrum Disorder. J Am Acad Child Adolesc Psychiatry 2014;53(2):237–257.
6. Centers for Disease Control and Prevention (CDC). Prevalence and Characteristics of Autism Spectrum Disorder Among Children Aged 8 Years — Autism and Developmental Disabilities Monitoring Network. MMWR Surveill Summ 2023;72(2):1–14.
7. Sandin S., Lichtenstein P., Kuja-Halkola R. et al. The Heritability of Autism Spectrum Disorder. JAMA 2017;318(12):1182–1184.
8. Satterstrom F.K. et al. Large-Scale Exome Sequencing Study Implicates Both Developmental and Functional Changes in the Neurobiology of Autism. Cell 2020;180(3):568–584.
9. Taylor L.E., Swerdfeger A.L., Eslick G.D. Vaccines are not associated with autism: an evidence-based meta-analysis. Vaccine 2014;32(29):3623–3629.
10. Madsen K.M., Hviid A., Vestergaard M. et al. A population-based study of measles, mumps, and rubella vaccination and autism. NEJM 2002;347(19):1477–1482.
11. Christensen J., Grønborg T.K., Sørensen M.J. et al. Prenatal valproate exposure and risk of autism spectrum disorders. JAMA 2013;309(16):1696–1703.
12. Surén P., Roth C., Bresnahan M. et al. Association between maternal use of folic acid supplements and risk of autism spectrum disorders in children. JAMA 2013;309(6):570–577.
13. Volk H.E., Lurmann F., Penfold B. et al. Traffic-related air pollution, particulate matter, and autism. JAMA Psychiatry 2013;70(1):71–77.
14. Dawson G., Rogers S., Munson J. et al. Randomized, Controlled Trial of an Intervention for Toddlers With Autism: The Early Start Denver Model. Pediatrics 2010;125(1):e17–e23.
15. Reichow B., Hume K., Barton E.E., Boyd B.A. Early intensive behavioral intervention (EIBI) for young children with autism spectrum disorders (ASD). Cochrane Database Syst Rev 2018;(5):CD009260.
16. Pickles A., Le Couteur A., Leadbitter K., Salomone E., Cole-Fletcher R., Tobin H., Gammer I., Lowry J., Vamvakas G., Byford S., Aldred C., Slonims V., McConachie H., Howlin P., Parr J.R., Charman T., Green J. Parent-mediated social communication therapy for young children with autism (PACT): long-term follow-up of a randomised controlled trial. Lancet 2016;388(10059):2501–2509.
17. Kasari C., Gulsrud A., Paparella T., Hellemann G., Berry K. Randomized comparative efficacy study of parent-mediated interventions for toddlers with autism. J Consult Clin Psychol 2015;83(3):554–563.
18. McCracken J.T., McGough J., Shah B. et al. Risperidone in children with autism and serious behavioral problems. NEJM 2002;347(5):314–321.
19. Xiong T., Chen H., Luo R., Mu D. Hyperbaric oxygen therapy for people with autism spectrum disorder. Cochrane Database Syst Rev 2016;(10):CD010922.
20. ASHA Position Statement: Facilitated Communication. American Speech-Language-Hearing Association; 2018. asha.org/policy/PS2018-00352.
21. Goldman S.E., Adkins K.W., Calcutt M.W. et al. Melatonin in children with autism spectrum disorders. J Clin Sleep Med 2014;10(8):871–882.
22. Laugeson E.A., Frankel F., Gantman A., Dillon A.R., Mogil C. Evidence-based social skills training for adolescents with autism spectrum disorders: the UCLA PEERS program. J Autism Dev Disord 2012;42(6):1025–1036.
23. Lai M.C., Baron-Cohen S. Identifying the lost generation of adults with autism spectrum conditions. Lancet Psychiatry 2015;2(11):1013–1027.
24. Berkowitz A.L., Miller M.B., Mir S.A. et al. Glioproliferative lesion of the spinal cord as a complication of “stem-cell tourism”. NEJM 2016;375(2):196–198.
25. Bondy A., Frost L. The Picture Exchange Communication System. Behav Modif 2001;25(5):725–744.
26. Koegel R.L., Koegel L.K. Pivotal Response Treatments for Autism. Baltimore: Brookes, 2006.
27. Mesibov G.B., Shea V., Schopler E. The TEACCH Approach to Autism Spectrum Disorders. New York: Springer, 2005.
28. Storch E.A., Arnold E.B., Lewin A.B. et al. The effect of cognitive-behavioral therapy versus treatment as usual for anxiety in children with autism spectrum disorders: a randomized, controlled trial. J Am Acad Child Adolesc Psychiatry 2013;52(2):132–142.