Violeta R. Manolova and Stoyan R. Vezenkov
Center for applied neuroscience Vezenkov, BG-1582 Sofia, e-mail: info@vezenkov.com
For citation: Manolova V.R. and Vezenkov, S.R. (2026) Autism as an Ecosystem Error: The Consequences of Misdiagnosed Screen Addiction. Nootism 2(4), 30-56, https://doi.org/10.64441/nootism.2.4.2
Abstract
The prevalence of diagnosed autism spectrum disorder (ASD) has increased significantly over the past two decades, yet its diagnosis remains predominantly behavioral and developmental, lacking a validated biomarker to independently confirm the condition. The present report examines the hypothesis that conditions currently diagnosed as autism represent manifestations of screen addiction – including early screen addiction and screen trauma – whose impact on regulation, learning, communication, attachment, and social development – when coupled with inadequate therapies and interventions – produces an autistic phenotype. Consequently, the central problem under consideration is not solely autism, but a potential ecosystemic fallacy: once developmental dysfunction induced by screen addiction is classified as autism, the diagnosis reorganizes subsequent understanding, scientific research, therapy, familial behavior, institutional responses, and social identity around the presumed irreversibility of the condition.
The report analyzes the mutually reinforcing diagnostic, medical, scientific, therapeutic, familial, technological, institutional, economic, social, and cultural mechanisms that may perpetuate this error. It is argued that the failure to recognize screen addiction as a potential causal and maintaining factor diverts children and families toward symptom management, thereby leaving the underlying screen exposure and addictive structure intact.
The proposed framework calls for a systemic differential assessment of screen addiction in individuals presenting with autistic symptomatology, as well as a direct investigation into whether the elimination of screen exposure, combined with targeted therapy for screen addiction, can alter the developmental trajectory. Should this hypothesis be corroborated, a subset of conditions currently classified as irreversible autism may in fact represent preventable and potentially reversible, environmentally induced impairments. This would necessitate a fundamental paradigm shift in the diagnosis, research, and treatment of autism.
Keywords: Autism Spectrum Disorder (ASD), screen addiction, screen trauma, ecosystemic fallacy, diagnostic expansion, therapeutic chronification, tertiary gain, familial co-addiction, technoference, Munchausen Syndrome by proxy
- Introduction
Initial epidemiological research on autism, undertaken in Europe and the U.S. throughout the 1960s and 1970s, established prevalence rates on the order of 2 to 4.5 per 10,000 children. These early findings gave rise to the long-standing clinical paradigm that conceptualized autism as a strictly rare childhood disorder. (Lotter, 1966; Treffert, 1970). Lotter’s pioneering study in Middlesex yielded an overall prevalence of 4.5 per 10,000. Subsequently, in the late 1970s, Wing and Gould applied a broader diagnostic definition to a cohort of 35,000 children in Camberwell, establishing a prevalence of approximately 21 per 10,000 across the entire behavioral spectrum, of which roughly 5 per 10,000 met the criteria for 'classic' Kanner's syndrome. (Wing & Gould, 1979). A comprehensive review of 23 epidemiological studies published between 1966 and 1998, encompassing over 4 million subjects, established a median prevalence of 5.2 per 10,000; for the eleven studies published after 1989, the median was 7.2 per 10,000, while the minimum estimate for all pervasive developmental disorders in the late 1990s stood at 18.7 per 10,000 (Fombonne, 1999). Therefore, at the baseline of the period under review – approximately 1990 – the prevalence of diagnosed autism was quantified in mere fractions of a percent: below 0.1% under strict diagnostic criteria and below 0.2% within the broadest spectrum definition. Against this historical baseline, data spanning the past two decades demonstrate a robust and substantial surge in identified autism, a trend no longer restricted to a singular developmental stage, demographic cohort, or geographic region. The most extensive standardized longitudinal series – conducted by the CDC’s ADDM Network – originated in 2000 with a baseline rate of 6.7 per 1,000 (1 in 150 children), escalating to 32.2 per 1,000, or 1 in 31 (3.2%), among 8-year-olds by 2022. This constitutes an approximate 4.8-fold escalation over a 22-year span (CDC, 2025; Shaw et al., 2025). This upward trajectory is remarkably consistent, recording prevalence rates of 8.0 per 1,000 in 2004, 9.0 in 2006, 11.3 in 2008, 14.7 in 2010, 16.8 in 2014, 18.5 in 2016, 23.0 in 2018, 27.6 in 2020, and reaching 32.2 in 2022. This constitutes an approximate 303% escalation strictly within the timeframe between 2004 and 2022. (CDC, 2025). When juxtaposed with baseline estimates from the early 1990s (5–7 per 10,000), the contemporary prevalence of 320 per 10,000 signifies an approximate 45- to 60-fold escalation. Admittedly, this comparison conflates diagnostic criteria – the restrictive 'autistic disorder' versus the modern broad spectrum – however, this methodological amalgamation constitutes an intrinsic component of the phenomenon under investigation, rather than a mere exogenous variable to be adjusted for. Crucially refuting the thesis that this growth is exhaustively accounted for by the inclusion of milder presentations: the 2022 data indicate that over one-third (39.6%) of the identified 8-year-old cohort exhibit comorbid intellectual disability (IQ < 70), whereas the prevalence of cases with an IQ > 85 has demonstrated a sustained downward trend across the preceding six reporting cycles, dropping to 36.1% (Shaw et al., 2025).
This upward trend is not restricted to the traditional ADDM cohort of 8-year-olds. A comprehensive investigation published in JAMA Network Open evaluated electronic health records (EHR) and insurance data across 12 prominent U.S. healthcare systems between 2011 and 2022. Within the overall study population, the rate of a registered ASD diagnosis escalated from 2.3 to 6.3 per 1,000, constituting a 175% surge over an eleven-year span (Grosvenor et al., 2024).
This escalation is particularly pronounced within the early childhood cohort (ages 0–4), surging from 6.4 per 1,000 in 2011 to 28.8 per 1,000 in 2022 (a 352% increase, or roughly 4.5-fold). Correspondingly, the 5–8 age bracket experienced a 207% increase, while the 9–12 cohort saw a 143% rise. The highest relative growth is documented among young adults: an approximate 452% surge in the 26–34 demographic and 338% among 35–44-year-olds. While these adult figures likely reflect, at least partially, historical underdiagnosis and enhanced clinical recognition – and thus cannot be construed as a true four- to five-fold epidemiological increase – they underscore the rapid expansion of the population to which the diagnostic criteria are now applied. Parallel to this, the gender distribution is undergoing a significant shift: diagnosis rates among girls climbed by 305% compared to 185% among boys, while in women, the increase was 315% against 215% for men (Grosvenor et al., 2024).
Data from the United Kingdom mirror this dynamic, exhibiting an even steeper growth curve. A population-level study drawing on the Clinical Practice Research Datalink (CPRD – which grew from 6.8 million registered patients in 1998 to 9.6 million in 2018) established a 787% exponential surge in the recorded incidence of autism over the 1998–2018 period (R² = 0.98). This escalation was accelerated in females and peaked among adults; the authors interpret this specific demographic configuration as indicative of expanded diagnostic recognition (Russell et al., 2022). The administrative peak is observed in Northern Ireland: according to data from the national school census, 5.9% of school-aged children (ages 4–15) held an autism diagnosis during the 2024/25 academic year – representing a nearly fivefold increase over 16 years (Department of Health Northern Ireland, 2025). By 2025/26 this rate reached 6.2%, compared with 1.2% - approximately 3,300 children – in 2008/09, an increase of over 300% across 15 years, with boys identified 2.3 times more frequently and prevalence 38% higher in the most deprived decile relative to the national average (Department of Health Northern Ireland, 2026). One methodological caveat applies to the series as a whole: because the basis of data collection shifted from the special educational needs register to the electronic medical register, figures from 2018/19 and earlier are not directly comparable with current years.
Scandinavian registries add the critically important distinction between phenotype and registration. In Sweden, the annual prevalence of the autistic symptom phenotype, measured via validated parental interviews in national population samples, remained stable over a ten-year period, while the prevalence of registered clinical diagnoses in the National Patient Register increased monotonically and statistically significantly (Lundström et al., 2015). A subsequent Swedish national cohort of 2.7 million individuals born between 1985 and 2020 and followed to 2022 documents the other side of the same divergence: age-specific diagnostic incidence rose in every successive calendar period and birth cohort, amounting to an approximately tenfold increase over the follow-up period – among 10–14-year-olds, from 56.5 to 564.1 cases per 100,000 person-years between 2000 and 2022. By 2022 the cumulative male-to-female ratio by age 20 had fallen to 1.2, indicating a substantial catch-up in the historical underdiagnosis of girls and women (Fyfe et al., 2026). In Denmark, an estimated 60% of this surge can be attributed to methodological shifts in reporting practices: approximately one-third is driven by the diagnostic transition from ICD-8 to ICD-10, and the remainder by the incorporation of outpatient diagnoses into the national registry. Crucially, this still leaves roughly 40% of the increase unaccounted for (Hansen et al., 2015). Furthermore, a systematic review encompassing 13 registry-based and national studies documents a descriptive escalation in prevalence across all Nordic and Scandinavian countries with available data, a trend observed across both age groups and birth cohorts (Jensen de López & Møller, 2024).
Israel exemplifies a delayed-onset yet significantly steeper trajectory. National prevalence estimates for 8-year-olds escalated from 0.12% in 2005 and 0.3% in 2008 to 0.65% in 2015, reaching 1.3% by 2018. Concurrently, between 2017 and 2021, the aggregate number of formally diagnosed pediatric cases (ages 1–17) doubled from 14,914 to 32,222. Notably, the 2–3 age bracket experienced a 4.4-fold surge, rising from 0.27% to 1.19% (Dinstein et al., 2024).
Evidence from East Asia indicates that this epidemiological phenomenon is not confined to Western diagnostic paradigms. In Japan, utilizing data from the national health insurance claims database, the cumulative incidence by age five was recorded at 2.75% for cohorts born between 2009 and 2014. This demonstrated robust longitudinal growth across birth cohorts – climbing from 2.23% for the 2009 cohort to 3.26% for the 2014 cohort – with significant geospatial variance across prefectures, ranging from 0.9% to 7.9%. Globally, this represents the highest medically diagnosed cumulative incidence rate on record (Sasayama et al., 2021). South Korea introduces the opposite methodological extreme: the inaugural total-population screening study (encompassing roughly 55,000 children aged 7–12) assessed the prevalence at 2.64%, or 1 in 38 children. Strikingly, two-thirds of these identified individuals were previously undiagnosed and unserved by the healthcare system (Kim et al., 2011; Pantelis & Kennedy, 2016).
An identical upward trend is evident in other global regions possessing longitudinal data. The Australian national disability survey documented 290,900 individuals diagnosed with autism (1.1% of the total population) in 2022, marking a 41.8% surge from 205,200 (0.8%) in 2018. Notably, prevalence stood at 3.1% for cohorts under the age of 25, contrasted against a mere 0.3% for the 25+ demographic; within the 5–14 age bracket, the rate escalated to 4.3% (compared to 3.2% in 2018 and a baseline of 0.4% in 2009) (Australian Bureau of Statistics, 2024). In Canada, national estimates climbed from 1 in 66 (1.5%) among the 5–17 age group in 2015 to 1 in 50 (2.0%) for the expanded 1–17 demographic in 2019 (Public Health Agency of Canada, 2018, 2022). Similarly, in Kazakhstan over the 2016–2022 period, diagnoses of childhood autism surged by nearly a factor of five, while atypical autism quadrupled (p < 0.01); specifically in Astana, registered prevalence peaked at 263.7 per 100,000 children (Nukeshtayeva et al., 2025). These geospatial variances powerfully illustrate that the steep phase of the epidemiological curve is triggered during different decades in different countries.
Global epidemiological syntheses effectively round out this landscape. The systematic review conducted by Zeidan and colleagues identifies a median global prevalence of approximately 1% (100 per 10,000) – a marked increase from the 62 per 10,000 reported in the preceding global synthesis (Elsabbagh et al., 2012; Zeidan et al., 2022). A three-level meta-analysis of 79 studies spanning 1994 to 2019 quantifies this trajectory within the pooled literature itself: the global pooled point-prevalence of ASD rose consistently from 0.25% (95% CI = 0.12–0.42) in the 1994–1999 window to 0.99% (95% CI = 0.73–1.28) in the 2015–2019 window. This does not constitute a single global longitudinal series – the constituent studies differ by country, age band, diagnostic criteria, and case-ascertainment method, and statistical heterogeneity remained exceptionally high and largely unexplained by the moderators tested. Restricting the analysis to upper-middle- and high-income countries in Europe and North America for 2015–2019, with participant age and study design entered as moderators, yields an adjusted pooled prevalence of 1.18% (95% CI = 0.92–1.48) (Talantseva et al., 2023). The WHO currently utilizes this same benchmark, estimating approximately 1 in 100 children (WHO, 2025). Furthermore, the Global Burden of Disease (GBD) study estimates that 61.8 million individuals were on the autism spectrum in 2021, equating to 1 in every 127 people (an age-standardized prevalence of 788.3 per 100,000). The authors attribute this sharp escalation from the GBD 2019 estimate (1 in 271) to methodological revisions – namely, the exclusion of passive registry sources known to systematically underreport prevalence. Crucially, the GBD model detects no actual growth in standardized prevalence over a 15-year temporal window; this conclusion stands in direct contradiction to the U.S. and UK administrative data series (Charman, 2025; Santomauro et al., 2025). A derivative analysis of the same GBD 2021 database extends the series back to 1990 and reaches a convergent conclusion: prevalent cases rose from approximately 41.93 million in 1990 to 61.82 million in 2021 – a 47.4% increase – while age-standardized prevalence moved only from 773.25 to 788.34 per 100,000, or roughly 1.95%, with decomposition analysis identifying population growth as the principal driver of the rising absolute count. The regional picture, however, is not uniform: age-standardized prevalence rose across almost all 21 GBD regions, fastest in high-income Asia Pacific (EAPC = 0.25), while Oceania and the Caribbean recorded slight declines; in 2021 the highest national rates were recorded in Japan, South Korea, and Singapore, and the lowest in Bangladesh, Brazil, and Nepal (Zhu et al., 2025). The most recent cross-national synthesis, published by the OECD, reveals that the population of children and youth diagnosed with ASD has surged two- to fourfold over a mere 15-year span across member states, demonstrating an average annual growth rate of 6–10% in nearly all countries with available data. The organization interprets this trend as being predominantly driven by heightened detection and diagnostic capacity, rather than a true shift in baseline epidemiological prevalence (OECD, 2026).
These epidemiological data yield three overarching conclusions. First, the escalation in identified autism represents a robust, global, and systemic healthcare phenomenon rather than a uniquely American anomaly. Among the 8-year-old cohort, the CDC longitudinal series demonstrates an approximate 303% surge between 2004 and 2022; an independent analysis of healthcare systems confirms a 175% escalation from 2011 to 2022; and across all regions possessing longitudinal data – the UK, Northern Ireland, Scandinavia, Israel, Japan, Australia, Canada, and Kazakhstan – registered diagnoses routinely multiply by a factor of two to nine within a 10- to 20-year timeframe. In healthcare systems with the most expansive detection capacities, this rate now captures 3–6% of the pediatric population. From a macro-historical perspective, identified prevalence has expanded by two orders of magnitude over half a century – from isolated single-digit cases per 10,000 in the 1960s–1980s to 1–3% and beyond today – representing an approximate 20- to 60-fold escalation relative to the 1990 baseline, contingent upon the diagnostic criteria applied.
Second, this surge is not restricted by age demographic, sex, or geography. Within the US between 2011 and 2022, the growth rate reached 352% for the 0–4 age bracket, 207% for 5-8-year-olds, 143% for 9-12-year-olds, and 452% for 26–34-year-olds, with the acceleration being markedly steeper in females than in males (Grosvenor et al., 2024). Similarly, in Israel, the most precipitous growth is observed precisely within the 2–3-year-old cohort (Dinstein et al., 2024). Parallel to this, the onset of these growth waves manifests across different nations at varying temporal junctures – emerging earliest in the US and the UK, subsequently in Israel, and more recently in Central Asia. This specific configuration is equally consistent with the global diffusion of diagnostic practices as it is with the staggered introduction of corresponding environmental exposures; differentiating between these two hypotheses forms the focal point of the ensuing sections.
Third, while these statistics indisputably validate the rise in identified or diagnosed autism, they do not intrinsically determine what fraction of this surge constitutes a genuine biological increase in the developmental disorder. The interpretive debate remains fiercely contested on both fronts. Bolstering the detection hypothesis are: the stability of the symptom phenotype despite rising diagnostic rates in Sweden (Lundström et al., 2015); the quantitative assessment that methodological reporting shifts account for approximately 60% of the Danish increase (Hansen et al., 2015); the GBD global model indicating zero temporal prevalence growth (Santomauro et al., 2025); and the formal interpretation provided by the OECD (OECD, 2026). Conversely, challenging the premise that enhanced detection exhaustively explains the phenomenon are: the disproportionately rapid growth among early childhood cohorts; the sustained upward trajectory following the stabilization of DSM-5 diagnostic criteria in 2013; the steadily declining proportion of high-functioning presentations in the American series (Shaw et al., 2025); and active screening data demonstrating that the true behavioral pool still exceeds formally registered cases (Kim et al., 2011). Currently, no available longitudinal series tracks the behavioral phenotype independently of diagnostic frameworks over a sufficiently extended temporal window to definitively resolve this debate. This precise limitation underscores the paramount importance of the etiological question: confronting a proliferation of this magnitude, merely chronicling the statistical trend is inadequate. It is scientifically imperative to interrogate the underlying drivers, delineating precisely what proportion is attributable to shifting diagnostic parameters versus actual transformations in developmental phenotypes and environmental exposures.
The present paper explores a conceptual framework that frames autism as an environmentally induced disorder, emerging in the presence of complex predispositions as a consequence of functional alterations in the brain and central nervous system driven by screen addiction. Screen addiction is posited to possess the capacity to fundamentally rewire an individual's personality and physiology in a manner that precipitates autism, along with all its concomitant characteristics, in both children and adults. (Vezenkov & Manolova, 2025b, 2026b) Within clinical practice, encompassing the evaluation and therapeutic treatment of hundreds of children, every documented case of autism has been etiologically linked to screen addiction and its specific sub-forms, namely early screen addiction and screen trauma. (Manolova & Vezenkov, 2025c; Vezenkov & Manolova, 2025b, 2025c) Moreover, following the successful treatment of screen addiction and the complete remission of autistic symptoms, re-exposure to screens triggers an immediate relapse, often with greater symptom severity than prior to the initiation of therapy; continued screen exposure during treatment completely impedes recovery and clinical progress, in stark contrast to pediatric patients who undergo total screen abstinence (100% screen detox) during their screen addiction therapy. (Petrova et al., 2025; Vezenkov & Manolova, 2025e) The emergence of the diagnosis systematically and sequentially parallels the introduction of mass radio and television across diverse populations; consequently, the belief that autism existed prior to screens is naively erroneous. (Manolova & Vezenkov, 2025d)
The developmental trajectory is fundamentally compromised and redirected by screen addiction and its associated sub-phenomena, namely early screen addiction and screen trauma. The organism's regulatory and learning systems undergo severe functional distortion to subserve goals that diverge drastically from normative development. Consequently, survival supersedes developmental progression; a closed, stimulus-dependent loop replaces adaptation, variation, and enrichment; and localized hyper-abilities (hyper-connectivity) emerge in lieu of the systemic integration essential for the formation of personality and identity (Manolova & Vezenkov, 2025a; Vezenkov & Manolova, 2025e, 2025f, 2025d, 2026c). Characterized by its severe symptomatology, this condition is conventionally diagnosed as autism. The inherent 'spectrum' profile of autism is, in fact, a function of the chronological onset, intensity, and chronicity of screen addiction. Specifically, early screen addiction and screen trauma prior to 36 months of age precipitate severe autism (hallmarked by absent verbal communication, self-injurious behavior, and aggression). Conversely, later-onset forms generate a variable clinical picture with fluctuating severity. This symptomatology is subject to environmental modulation: adverse factors such as violence and neglect exacerbate the presentation, whereas protective factors – such as physical activity, musical engagement, and enriched interpersonal communication characterized by secure attachment to primary caregivers – mitigate the symptoms and provide a therapeutic milieu for partial rehabilitation. Crucially, however, no therapeutic modality achieves ultimate efficacy (total symptom eradication) in the absence of complete screen removal. Cases of total symptom remission in severe autism are documented strictly under protocols combining targeted screen addiction interventions with comprehensive screen detoxification (total abstinence) (Manolova & Vezenkov, 2025e; Vezenkov & Manolova, 2025b).
As evidenced by the extensive literature cited above, the clinical diagnosis of autism is fully reversible when subjected to targeted therapeutic interventions for screen addiction and screen trauma. For severe presentations of autism, the critical developmental window of reversibility spans up to 6 years of age, extending to 9 years in specific cases (Petrov, Dimova, et al., 2025; Vezenkov et al., 2026). Conversely, milder presentations remain reversible at any point in the lifespan, contingent upon appropriate intervention.
This paper endeavors to expose the intricate framework of misconceptions and flawed paradigms that precipitate and perpetuate the risk of individuals receiving an autism diagnosis in lieu of screen addiction. Such mischaracterization sets a profoundly erroneous trajectory regarding a patient's motivational drive, hope, belief systems, and sense of identity. It skews the pursuit of rehabilitation toward therapeutic modalities that fail to eliminate screen exposure – a critical oversight that renders many otherwise viable clinical practices entirely ineffective for autistic individuals. Furthermore, it entrenches the fragmentation of scientific inquiry, precluding a holistic examination of the individual seamlessly integrated with their environment and immediate interpersonal network.
This systemic fallacy – the persistent neglect of the etiological root cause in favor of treating fragmented, isolated symptomatology – is heavily subsidized by contemporary autism theory and praxis, culminating in a catastrophic reality for an immense number of individuals, children, and families. This error is fortified by a sophisticated apparatus that sustains the diagnosis, thereby calcifying its ecosystem into a hermetic, impenetrable mechanism defined by inevitability and immutability. Thus, parents, clinicians, researchers, and policymakers find themselves ensnared in a self-perpetuating loop of clinical error, one that offers no egress until the fundamental root cause of autism spectrum conditions is definitively addressed.
The architecture of this delusion is profoundly multifaceted, manifesting across diagnostic, genetic, methodological, medical, therapeutic, psycho-familial, technological, institutional, economic, social, and cultural domains. Dismantling these intertwined fallacies will afford humanity the unprecedented capacity to eradicate this crisis holistically. Firstly, it establishes that autism is a curable condition when its primary driver – screen addiction – is clinically resolved; and secondly, as a direct corollary to the preceding logic, it proves that the condition is entirely preventable.
- Ecosystemic Support of the Autism Fallacy
2.1. The Premise that Autism is Incurable.
According to leading health authorities, autism is not to be understood as a "disease" – in the traditional sense of a pathology that can be medically treated and eliminated – but rather as a neurodevelopmental condition or disorder rooted in divergences in brain development and functional architecture. The NHS formulates this most explicitly: being autistic "does not mean you have an illness or disease," but rather that the brain operates differently. Simultaneously, the agency underscores that autism is not a medical condition for which there is a "cure" (NHS, 2026). The WHO characterizes autism as a spectrum of conditions intrinsically linked to brain development (WHO, 2025), whereas the CDC and NIMH classify it as a neurological and developmental disorder that generally persists throughout the lifespan (CDC, 2026; NIMH, 2024). Therefore, the most precise conceptualization is that autism is inherently "incurable" in terms of fully resolving or eradicating ASD. Nevertheless, there are targeted therapies, interventions, and support frameworks capable of significantly improving the communication, adaptive skills, daily functioning, psychological well-being, and overall quality of life of the autistic person (CDC, 2026; WHO, 2025).
This constitutes not merely a clinical diagnosis, but a definitive verdict. Packaged with a veneer of 'specialness,' parents are placated with the assertion: 'Your child simply possesses a differently wired brain, and that is all.' Therapeutic interventions are proposed with the objective of achieving marginal improvements, yet with the explicit stipulation that autistic traits will permanently persist – ostensibly because this reflects the fundamental neurological architecture of the child. This pervasive mantra strips parents, the scientific community, and society at large of the imperative to seek and discover a definitive cure. As a direct consequence, the prospect of total rehabilitation is summarily dismissed from clinical discourse. Rebranding a pathological phenomenon not as a disease or a disorder, but as 'neurodiversity,' is a profound fallacy – one that unconditionally perpetuates the condition and facilitates its limitless expansion across time and demographics. Every pathology and disorder curable today was, at some historical juncture, deemed incurable; nevertheless, humanity persistently sought and ultimately devised treatments. Today, in the context of autism, this fundamental scientific drive has been inexplicably eradicated at its very root. Instead, parents are instructed that resistance is futile and that they are obligated to accept the diagnosis in its entirety. The prevailing clinical attitude chillingly mirrors the prognosis of a terminal illness.
2.2 "Everyone is a Little Autistic"
In discussions regarding the contemporary conceptualization of autism, Prof. Uta Frith highlights the problematic inflation of the "autism spectrum" construct. In her view, autism is increasingly less understood as a sharply demarcated "spectrum of disorders," but rather as a seamless continuum where neurodivergence gradually dissolves into neurotypicality. It is within this precise context that she articulates the proposition that “we can all be a little bit autistic” (Frith & Frith, 2024). This assertion, however, must not be misconstrued as a reductive popular generalization that "everyone is autistic." Instead, it serves as a profound critique of the excessive broadening of the concept's diagnostic and cultural application. Frith underscores that this erosion of boundaries between clinical autism, subclinical autistic traits, and normative human variability poses significant challenges for both clinical praxis and empirical research. By diluting the discriminative validity of the diagnosis, it obfuscates the identification of individuals who are in genuine need of specialized support and clinical services (Frith, 2026; Frith & Frith, 2025).
Being autistic has become fashionable. It affords privileges, sympathy, understanding, and systemic support. Consequently, the premise that everyone exhibits some autistic traits holds true only to the extent that everyone currently exhibits some degree of screen addiction. The deliberate obfuscation of diagnostic boundaries serves to popularize and normalize the disorder, thereby disarming societal resistance to its alarming proliferation. Crucially, however, as of 2026, there are virtually no living individuals within the civilized world who remain completely unexposed to screen influence. Where, then, lies the baseline for comparison?
2.3. The Symptomatic Diagnosis of Autism.
The diagnosis of autism is fundamentally clinical and symptomatic, predicated on the evaluation of developmental trajectories, behavior, social communication, sensory processing anomalies, repetitive behavioral paradigms, and the extent of functional impairment in daily life. Standard diagnostic protocols generally entail acquiring a detailed anamnesis from caregivers or the patient, assessing early developmental milestones, conducting behavioral observations in clinical or naturalistic settings, applying standardized psychometric instruments, and evaluating symptoms against DSM-5/DSM-5-TR or ICD-11 criteria. The CDC explicitly acknowledges the absence of any medical pathology test – such as serological testing – to diagnose autism, reaffirming that the diagnosis is contingent upon developmental and behavioral assessments. Concordantly, the CDC specifies that diagnostic instruments rely predominantly on two qualitative sources: caregiver-reported developmental histories and professional behavioral observation.
Consequently, autism is characterized by the conspicuous absence of a validated diagnostic biomarker that can independently and reliably substantiate or negate the diagnosis. Although genetic, metabolic, immunological, neurophysiological, and neuroimaging markers are extensively investigated within the scientific literature, they remain entirely unintegrated into routine diagnostic standards. Comprehensive reviews underscore that, despite presumed genetic underpinnings and intensive biomarker research, autism remains exclusively behaviorally defined and diagnosed. Furthermore, prominent clinical guidelines maintain that contemporary biomarker data lack the requisite evidentiary validity for routine clinical implementation.
A critical methodological omission is the exclusion of routine neuroimaging from the diagnostic paradigm. While MRI, CT, EEG, or other neurodiagnostic modalities may be indicated for specific clinical red flags – such as suspected epilepsy, underlying neurological pathology, genetic syndromes, developmental regression, anatomical malformations, or to establish a differential diagnosis – they do not "confirm" autism and fall outside standard diagnostic confirmation protocols. NICE explicitly recommends against the routine administration of medical investigations during autism diagnostic assessments in pediatric and adolescent populations, advising that such procedures be considered strictly on the basis of physical examinations, clinical discernment, and individual clinical profiles.
This dynamic can therefore be encapsulated as follows: autism is classified as a neurodevelopmental diagnosis, yet it is adjudicated through behavioral and developmental metrics rather than direct biological quantification of the brain. The clinical paradox lies in diagnosing a condition whose biological substrate is the brain, without directly examining the organ itself for diagnostic verification. Instead, the clinician retrospectively infers the neurodevelopmental profile via observable behavioral manifestations, historical developmental narratives, and adaptive deficits. Herein lies the core methodological vulnerability and epistemic tension: the diagnosis purports to delineate a neurodevelopmental anomaly, yet in clinical praxis, it is almost entirely phenotype-driven – reliant on visible patterns of behavior, communication, and adaptation – completely devoid of a definitive biological assay, neuroimaging marker, or laboratory benchmark to serve as objective confirmation.
No definitive biomarkers have been isolated. Neuroimaging modalities remain systematically unutilized. An organ – the brain – is diagnosed without ever being objectively examined. This epistemic void generates profound latitude for diagnostic subjectivity and obscures any precise understanding of the underlying impairment, effectively paralyzing the pursuit of restorative pathways. Since when is a structurally healthy brain no longer the norm?
2.4. Parental Exhaustion as a Systemic Variable.
Parents of autistic children frequently exist in a state of protracted psychological and existential distress that vastly exceeds normative parenting stress. The scientific literature systematically documents elevated baseline levels of stress, anxiety, depressive symptomatology, and compromised quality of life within this demographic. This vulnerability is tethered not exclusively to the diagnosis per se, but to the cumulative burden of daily caregiving, compounded by behavioral and communicative deficits, sensory meltdowns, sleep dysregulation, financial strain, social isolation, pervasive stigma, and the systemic dearth of adequate clinical services (Demirpençe Seçinti et al., 2024, 2024; Ni’matuzahroh et al., 2022; Yesilkaya & Magallón-Neri, 2024).
The meta-analysis conducted by Hayes and Watson (2013), which systematically juxtaposed parents of children with and without autism, revealed not merely a statistically significant divergence, but a large effect-size discrepancy in parental stress. Crucially, this variance remains robust even when compared to parents of children with other neurodevelopmental or physical disabilities, underscoring that the heightened stress cannot be attributed solely to the presence of special needs (Hayes & Watson, 2013). The systematic review and meta-analysis by Schnabel et al. (2020), encompassing 31 studies and 9,208 parents, translated this phenomenon into clinical prevalence rates: the median frequency of depressive disorders among these parents stands at 31%, and anxiety disorders at 33%, albeit with substantial inter-study heterogeneity (Schnabel et al., 2020). Furthermore, the cohort study by Warreman et al. (2023), surveying 3,354 caregivers from the Dutch Lifelines population-based cohort, provides the critical comparative baseline lacking in most literature: caregivers of autistic individuals report significantly higher caregiver burden not only against non-caregiving controls but also relative to caregivers of individuals with other chronic conditions – manifesting simultaneously across psychological, behavioral, and somatic domains (Warreman et al., 2023). It is imperative to note, however, that the correlation between child behavior and parental distress is non-linear and bidirectional: the meta-analysis by Yorke et al. (2018) established that the child’s emotional/behavioral challenges and the parent’s psychological distress are mutually reinforcing. Thus, the parental psychological state acts concurrently as a consequence of the caregiving environment and an operative agent within the family ecology (Yorke et al., 2018).
Immersed in this dynamic, the parent is routinely forced to simultaneously inhabit the roles of primary caregiver, clinical therapist, service coordinator, institutional advocate, behavioral interpreter, and emotional container for the child’s crises. In the context of chronic systemic neglect, this multifaceted role routinely precipitates profound exhaustion, clinical parental burnout, learned helplessness, guilt, disorientation, and the erosion of personal perspective (Kütük et al., 2021; Myers et al., 2009).
The multicenter case-control study by Kütük et al. (2021) is notable for operationalizing burnout as a distinct psychological construct rather than a mere proxy for stress, identifying concurrently elevated depressive symptomatology and exacerbated emotional exhaustion relative to a matched control cohort. Complementing this quantitative data, the qualitative investigation by Myers, Mackintosh, and Goin-Kochel (2009) illuminates the internal phenomenological experience: through thematic analysis of parental narratives, the authors reveal that the caregiving experience is anchored not by isolated clinical symptoms, but by a fundamental restructuring of their entire life architecture – spanning daily routines, long-term trajectories, and core self-concept.
Ultimately, empirical data confirm that for a subset of parents and caregivers, this unrelenting psychological load can culminate in severe clinical depression and suicidal ideation. This risk is particularly acute when exorbitant caregiving demands converge with impoverished social support, chronic anxiety, future-oriented uncertainty, and the profound realization of systemic abandonment (Akram et al., 2019; Demirpençe Seçinti et al., 2024; Shtayermman & Zhang, 2022).
The investigation by Akram, Batool, and Bibi (2019) is particularly illuminating as it not only establishes an association between caregiver burden and maternal suicidal ideation, but also identifies perceived social support as a moderating variable in this dynamic. This implies that psychological distress is not a fixed function of the child’s clinical severity, but is heavily contingent upon the exogenous support the family receives. Furthermore, Marsack-Topolewski and Graves (2020) articulate the specific manifestation of future-oriented uncertainty among aging parents of adult children on the spectrum: the pervasive anxiety regarding "what will happen to them after I am gone" emerges as an autonomous and persistent source of distress – one that exacerbates rather than attenuates with the passage of time (Marsack-Topolewski & Graves, 2020).
Therefore, parental psychological distress must not be misconstrued as a personal vulnerability or a deficit in parental affection; rather, it is the predictable systemic consequence of protracted caregiving amidst profound uncertainty, institutional neglect, and chronic emotional mobilization. In the vast majority of cases, these families are fundamentally under-supported by the system (Ni'matuzahroh et al., 2022; Yesilkaya & Magallón-Neri, 2024; Warreman et al., 2023).
This psychological erosion is rarely contained within the individual psyche of the mother or father; it progressively restructures the entire familial architecture. Rearing an autistic child frequently demands such an exorbitant expenditure of time, vigilance, financial capital, physical stamina, and emotional bandwidth that parents suffer profound depletion – as autonomous individuals, as intimate partners, and as parents to their neurotypical offspring. Empirical literature on family functioning in the context of autism consistently reports elevated tension, fractured family dynamics, and pronounced systemic dysfunction wherever the child's care requirements are severe and coping resources are sparse (DESQUENNE GODFREY et al., 2024; Warreman et al., 2023).
The systematic review conducted by Godfrey et al. (2024), which synthesized 62 quantitative studies published between 1980 and 2021 utilizing validated psychometric measures of family functioning, concluded that systemic functioning in families raising an autistic child is demonstrably more compromised than in non-autism control families. Crucially for the present thesis, these functional deficits correlate positively with caregiving burden and inversely with available support resources. This statistical relationship is paramount, as it proves that familial disintegration is not a mechanistic byproduct of the diagnosis itself, but rather a direct consequence of the disproportionate ratio between systemic demands placed upon the family and the resources provisioned to it.
Operating under such exorbitant strain, the marital dyad is subjected to relentless pressure. Core relational elements – intimacy, communicative exchange, sexuality, leisure, and shared future trajectories – are systematically usurped by therapeutic regimens, behavioral crises, financial triage, chronic sleep deprivation, and reciprocal blame. Academic reviews examining couple dynamics among parents of autistic children chronicle this exact phenomenon: an amplified risk of marital conflict, a precipitous decline in relationship satisfaction, and the pervasive fear of dissolution, even if epidemiological data regarding definitive divorce rates remain equivocal (DESQUENNE GODFREY et al., 2024; Saini et al., 2015).
The one most prominently cited population-based study addressing this specific metric arrive at diametrically opposed conclusions, effectively demarcating the epistemic limits of what can be definitively claimed. Hartley et al. (2010), employing a survival analysis model on a cohort of 391 parents of children on the spectrum alongside a matched control sample, reported a divorce prevalence of 23.5%, compared to 13.8% among controls. Significantly, this heightened vulnerability persists unabated across the child’s childhood, adolescence, and early adulthood – a stark deviation from normative demographic patterns, wherein divorce risk typically inversely correlates with marital duration and child age (Hartley et al., 2010).
When primary caregivers fail to sustain this exorbitant burden alone, caregiving responsibilities are frequently reallocated to the extended family – grandparents, aunts, and other relatives. While these individuals emerge as critical emotional, financial, and practical pillars, this systemic shift dictates that the entire familial network becomes fundamentally organized around the diagnosis and the chronic deficit of formal support (Baena et al., 2026; Li et al., 2025; Prendeville & Kinsella, 2019).
Prendeville and Kinsella (2019) conceptualize this role through the framework of family systems theory, illustrating that grandparents function concurrently as emotional anchors for the parents, auxiliary caregivers, and systemic mediators between the nuclear and extended family. Consequently, their active integration can substantially fortify the broader familial system. Conversely, the qualitative investigation by Baena, Jiménez, Bejarano, and Hidalgo (2024), encompassing 17 grandparents of children and adolescents on the spectrum, illuminates the collateral cost of this dynamic: the grandparents independently report profound emotional fatigue, persistent anxiety concerning both the grandchild's future and their own cognitive/physical decline, and severely unmet needs for clinical information and support. These deficits are systematically ignored by formal service provisions, which remain myopically designed around the nuclear family model. Thus, the systemic failure to provide adequate support is not simply absorbed by the extended family; rather, the psychological toll is outsourced to a demographic that remains fundamentally invisible to the healthcare system.
The collateral impact on siblings is particularly poignant. Typically developing (TD) children within these households systematically receive diminished parental bandwidth, assume caregiving responsibilities prematurely, routinely witness severe behavioral crises, and constantly calibrate their own behavior to accommodate the autistic child. Consequently, they are frequently ensnared in a process of "parentification" – the premature and developmentally inappropriate assumption of adult responsibilities (Nuttall et al., 2018; Shivers et al., 2019; Tomeny et al., 2017).
The meta-analysis by Shivers, Jackson, and McGregor (2019) comprehensively synthesizes the quantitative literature, confirming demonstrably more adverse social, emotional, behavioral, and psychological trajectories for these siblings relative to normative control cohorts. Lovell and Wetherell (2016) introduce a critical psychophysiological dimension, documenting elevated depressive symptomatology among siblings of autistic children; crucially, this vulnerability is directly predicted by the severity of the autistic child's behavioral deficits and inversely mitigated by the availability of exogenous social support (Lovell & Wetherell, 2016). Nuttall, Coberly, and Diesel (2018) empirically document the direct caregiving roles imposed during childhood, demonstrating a strong longitudinal correlation with future adult caregiving intentions – indicating that this parentified role is never truly terminated, but perpetually carried forward. Tomeny et al. (2017) explicitly classify this specific familial dynamic as parentification, definitively correlating it with elevated psychological distress and compromised sibling relationship quality.
Ultimately, the concept of a "robbed childhood" transcends mere emotional metaphor; it captures a tangible, systemic clinical risk. The family architecture forcibly centers one child due to their profound pathology, inadvertently conditioning the typically developing sibling to remain perpetually silent, to defer, to assist, to suppress their own demands, and to internalize profound guilt whenever they experience autonomous needs of their own (Shivers et al., 2019; Watson et al., 2021).
The systematic review conducted by Watson, Hanna, and Jones (2021) comprehensively synthesizes the qualitative literature, demonstrating that cohabiting with a sibling on the autism spectrum profoundly impacts the identity formation, personal development, emotional phenomenology, and coping mechanisms of the typically developing (TD) child. This indicates that the ramifications transcend quantifiable clinical symptoms, fundamentally altering the trajectory of personality development. Through qualitative interviews with 21 adult siblings of individuals with autism and comorbid intellectual disability, Tozer, Atkin, and Wenham (2013) reveal that this familial obligation does not terminate at the threshold of adulthood. Rather, it calcifies into a long-term assumption of caregiving responsibility that remains systematically unacknowledged by both formal service providers and the family unit itself.
In the most severe clinical presentations – especially those characterized by pronounced behavioral meltdowns, aggression, self-injurious behavior (SIB), profound intellectual comorbidity, or the onset of puberty, when the child's physical strength eclipses the family's capacity for containment – a subset of parents is compelled to resort to residential care or out-of-home institutional placement. The empirical literature consistently identifies aggressive and destructive behaviors as primary catalysts for out-of-home placement; yet parents overwhelmingly experience this transition not as a "liberation," but as a tragic necessity compounded by profound guilt, grief, and the agonizing sensation of ambiguous loss – effectively mourning a living child (Baker & Blacher, 2002; Friedman et al., 2014; Jackson & Roper, 2014; Kanne & Mazurek, 2011; Quetsch et al., 2023).
Investigating a cohort of 1,380 children and adolescents on the spectrum, Kanne and Mazurek (2011) established that aggression constitutes a clinically significant challenge for a substantial demographic, and notably, it is not reliably predicted by the core severity of autistic symptomatology alone. Quetsch et al. (2023) corroborate this clinical picture through direct comparative analysis with a non-autistic normative sample, longitudinally tracking the trajectory of aggressive behaviors across childhood. A clinical report issued by the Council on Children with Disabilities of the American Academy of Pediatrics (2014, reaffirmed in 2024) delineates the etiologies, systemic barriers, and psychosocial consequences of out-of-home placement. It emphatically underscores that such a decision is virtually never a first-line choice, but rather the culmination of a protracted period characterized by the total depletion of familial resources. Baker and Blacher (2002) longitudinally examined post-placement family dynamics, demonstrating that institutionalization does not automatically precipitate relief; instead, it necessitates a complex restructuring of caregiving paradigms and intra-familial relationships. Furthermore, in investigating parents of children with severe and profound developmental disabilities, Jackson and Roper (2014) articulate the complex amalgamation of guilt, profound sorrow, fear, and gradual adaptation that ensues following such a decision. Crucially, it is this emotional crucible – not a sense of liberation – that predominantly characterizes and dominates parental narratives.
2.5. Factitious Disorder Imposed on Another (FDIA) / Munchausen Syndrome by Proxy
Munchausen syndrome by proxy (MSBP) – predominantly classified in contemporary diagnostic nomenclature as Factitious Disorder Imposed on Another (FDIA) or conceptualized as a form of medical child abuse – represents a pathological caregiving dynamic wherein the primary caregiver fabricates, exaggerates, maintains, or actively induces symptoms in a dependent child. This mechanism ensures the child is relegated to a chronic state of illness, helplessness, and perpetual reliance on care. The etiology of this syndrome is rarely rooted in mere ignorance or parenting deficits; rather, it is driven by the profound psychological imperatives of the adult. These include a pervasive need for control, attention, and validation; an identity rigidly anchored in the persona of the "sacrificial" or "exceptionally devoted" parent; a pathological fear of the child's individuation; severe emotional enmeshment; or the unconscious secondary gains derived from preserving the child's dependence and symptomatology. Consequently, this syndromic cycle can be perpetuated indefinitely: the child's pathology becomes the organizing principle of the adult’s life, rationalizing their behavior, solidifying their social role, and insulating the family system from confronting underlying systemic conflicts, psychological deficits, or domestic abuse.
The insidious nature of this threat lies in its clinical presentation: superficially, this dynamic masquerades as hyper-vigilant care, parental anxiety, and profound devotion. Functionally, however, it precipitates symptom chronicity, excessive and invasive medicalization, gratuitous clinical interventions, severe social isolation, developmental regression, iatrogenic addiction, the deliberate sabotage of therapeutic progress, and the systematic dismantling of the child's autonomy (Sanders & Bursch, 2020; Wang et al., 2026). When applied to pediatric populations carrying diagnoses such as ASD and/or ADHD, the risk of this underlying mechanism remaining undetected is the same. In such cases, severe behavioral, communicative, and self-regulatory deficits are easily and exclusively misattributed to "neurodevelopmental differences," precluding any critical investigation into the familial milieu, chronic screen overstimulation, latent neglect, emotional enmeshment, or active therapeutic sabotage.
It is within this precise theoretical framework that we hypothesize the MSBP syndromic logic operates beyond the classical fabrication or direct induction of physiological illness. Instead, it manifests insidiously through the active maintenance of the child's symptomatology via chronic screen exposure, the staunch denial of its neurodevelopmental toxicity, the active concealment of screen-time data from clinicians, and the abrupt termination of therapeutic interventions precisely at the juncture of clinical improvement (Manolova et al., 2025). Ultimately, this phenomenon transcends individual parental psychopathology to constitute a profound diagnostic hazard: the clinical system successfully identifies the child's diagnosis, yet remains entirely blind to the toxic environment that systematically amplifies, perpetuates, and exploits it.
The concepts of narcissism by proxy and Munchausen syndrome by proxy describe two distinct yet partially overlapping forms of psychological abuse in which the child is instrumentalized within a disturbed relational system. Whereas in narcissism by proxy the parent utilizes the child as a vehicle to extract admiration, prestige, and symbolic superiority, in FDIA the objective is to garner sympathy, attention, and medical legitimacy through the fabrication or induction of illness and vulnerability. Although their motivational profiles diverge – one being organized around grandiosity and validation, the other around suffering and caregiving – both phenomena share a profound underlying logic: the child is stripped of their status as an autonomous subject with independent needs and is transformed into an external regulator of parental deficits, identity, and coercive control. In the context of contemporary family conflicts, these dynamics may coexist, alternate, or be transmitted transgenerationally, rendering the child a proxy through whom the unresolved traumas and battles of the adults are enacted (Manolova et al., 2025; Vezenkov & Manolova, 2026a).
2.6. Tertiary Gain
Parallel to the classical formulation of Munchausen syndrome by proxy, a broader clinical dynamic of tertiary gain may be observed within a subset of family systems navigating an autism diagnosis. This phenomenon does not necessarily equate to conscious deception or a formal psychiatric pathology; rather, it constitutes a systemic configuration wherein the child's clinical condition begins to generate profound psychological, social, relational, or material dividends for the adult caregiver. Consciously or unconsciously, these dividends serve to perpetuate the child's addiction, symptomatology, and enduring status as a "severe clinical case." In foundational psychodynamic and medical literature, "tertiary gain" delineates the interpersonal, social, or material advantages procured by a third party – such as a parent or caregiver – as a direct consequence of the patient's illness (Fishbain, 1994). emphasize the indispensability of this construct for comprehending illness behavior, while simultaneously cautioning against its reductive conflation with overt malingering or moral culpability (Fishbain et al., 1995). Within the context of autism, this pathogenic dynamic can operationalize across multiple domains: financial gain via child support, state welfare, disability pensions, philanthropic funds, therapeutic subsidies, or material extraction from the co-parent and extended family; social gain through the monopolization of attention, sympathy, public visibility, social media platforms, and the cultivation of an identity rooted in sacrificial or heroic parenting; relational gain enacted by tethering the partner to the relationship via guilt, fear, pity, or moral coercion; and existential gain, wherein the perpetual care of the child provides the parent with an existential scaffolding – furnishing a defining role, a mission, and a profound sense of exceptionalism. It is imperative to explicitly state that the provision of financial support is inherently legitimate and functionally critical: families raising autistic children face demonstrably higher economic burdens, and systemic frameworks such as the US SSI program are explicitly engineered to support children with severe functional impairments and economically vulnerable families (Social Security Administration, 2026). It should be stated plainly that financial support is in itself legitimate and often essential: families of autistic children do incur substantially higher costs and resource demands, and public programmes such as Supplemental Security Income (SSI) in the United States were designed precisely for children with severe functional limitations in low-income households. Access, however, is not automatic. Diagnosis alone does not suffice: the regulation requires both medical documentation of the relevant deficits and "extreme limitation of one, or marked limitation of two" of four areas of mental functioning, established through "objective medical evidence from an acceptable medical source" (20 C.F.R. pt. 404, subpt. P, app. 1, §§ 112.10, 112.00C1).
The clinical problem arises not from receiving assistance but from a structural coupling that the regulator states directly: "the more extensive the support you need from others… the more limited we will find you to be" (§ 112.00F3d). Correspondingly, a child's capacity to function in a structured setting is expressly not taken as evidence of age-appropriate functioning (§ 112.00C6b), and entitlement remains subject to periodic continuing-disability review (20 C.F.R. § 416.994a). Recognised severity is, in short, a function of required support.
Precision is obligatory here, because the claim is easily overstated. The same text contains an explicit safeguard: "We will not find that you function age-appropriately solely because you have a period(s) of improvement (remission)" (§ 112.00F4a). The system does not penalise episodic recovery.
The clinical pathology emerges not from the receipt of necessary aid, but at the precise juncture where financial assistance, social validation, or identity consolidation become strictly contingent upon the child remaining maximally impaired, chronically dependent, clinically "unsalvageable," or perennially exhibited in the public sphere.
Diagnostically, this dynamic is exceptionally insidious, as it frequently camouflages itself beneath the socially sanctioned veneer of profound devotion, self-sacrifice, and fierce advocacy. The caregiver may eloquently articulate their systemic struggles, orchestrate fundraising efforts, cultivate extensive online communities, and posture as a tireless systemic crusader or a paradigm of "success against all odds." In this process, the autistic child is effectively transfigured into symbolic capital – a unique relational asset that elevates and distinguishes the parent from peers possessing normative markers of success, such as corporate or academic achievements. Sociological research on digital networks corroborates that parents of children with special needs actively leverage Facebook groups and digital communities to source information, aggregate support, and mitigate perceived societal judgment. While this function is fundamentally adaptive, the very same digital architecture can easily commodify the child's clinical suffering, transforming it into a public narrative that reliably yields attention, peer recognition, and a robust social identity for the adult (Ammari et al., 2014). Concurrently, literature examining the positive psychosocial sequelae of raising an autistic child confirms that many caregivers derive profound meaning, post-traumatic growth, relational depth, and resilience from the experience. While intrinsically healthy, this adaptive process can metastasize into pathological enmeshment, wherein the caregiver's core identity becomes inextricably fused with the child's clinical diagnosis (Curley et al., 2025). Ultimately, the systemic hazard is not the acquisition of parental support, meaning, or societal recognition; rather, it is the latent, unconscious instrumentalization of the child as a reliable conduit for capital, social currency, moral authority, interparental control, or performative exceptionalism. Within such a deeply inverted family system, any genuine clinical improvement in the child paradoxically constitutes an existential threat. Should the child attain greater autonomy, exhibit diminished symptomatology, demonstrate substantive therapeutic progress, or should the public narrative forfeit its dramatic urgency, the parent stands to lose not merely their financial subsidies, but the very foundation of their identity, their social platform, their relational leverage, and their organizing life purpose.
2.7. Medical Vacuum, Unproven Interventions, and Exploitation
The powerlessness of medicine in the face of autism – namely, the fact that there is no "cure" in the sense of a complete recovery, no single proven etiology for all cases, and no universal therapy that eradicates the core characteristics of the condition – creates a distinct therapeutic vacuum wherein many parents are left in a chronic search for a solution (CDC, 2026; NHS, 2026). Official medical sources emphasize that the causes of ASD are multifactorial and, for many children, remain unknown. Furthermore, current interventions aim to support development, behavior, communication, and quality of life, rather than to "cure" autism as such (CDC, 2026; NIMH, 2024). It is precisely from this point that the phenomenon described as intervention decision-making and information-seeking originates: parents navigate a multitude of specialists, centers, therapies, schools, methodologies, and "alternative" practices, frequently vacillating between hope, guilt, despair, and the fear of missing out on the sole opportunity for improvement (Gosling et al., 2025; Höfer et al., 2017). While some of these interventions are legitimate and evidence-based, others fall into the domain of complementary, alternative, and integrative medicine (CAIM). The most comprehensive available synthesis of evidence regarding CAIM in autism was published in 2025, fundamentally altering the premise upon which this topic can be discussed. The umbrella review by Gosling and colleagues (2025) encompasses 53 meta-analytical reports, from which 248 individual meta-analyses covering 19 types of interventions were extracted, synthesizing over 200 controlled clinical trials and more than 10,000 autistic participants. The methodological quality of each meta-analysis was assessed using AMSTAR-2, and the certainty of evidence was evaluated via an algorithmic version of the GRADE framework. The conclusion is unequivocal: there is no high-quality evidence supporting the efficacy of any of the investigated methods, neither in relation to the core symptoms of autism nor its co-occurring conditions. The only intervention to reach at least a moderate level of evidence for any outcome was oxytocin, albeit with a small effect size limited to repetitive behaviors in adults (SMD 0.404, 95% CI 0.166–0.643). Several methods – such as music therapy, animal-assisted interventions, transcranial stimulation, physical activity, and melatonin – demonstrated large and statistically significant effects; however, all of these were systematically underpinned by very low-quality evidence attributable to small sample sizes, wide confidence intervals, and a high risk of bias in the primary trials (Gosling et al., 2025; Höfer et al., 2017).
Two findings from this review hold greater significance for the present argument than the efficacy assessments themselves. The first relates to safety: the authors established that safety was rarely evaluated at all, with fewer than half of the identified interventions possessing any assessment of acceptability, tolerability, or adverse events. Thus, the issue is not merely that these methods lack efficacy, but rather that for the majority of them, no one has investigated potential harms, despite their widespread use and a median prevalence rate reaching 54% (Höfer et al., 2017; Gosling et al., 2025). The second finding concerns the very literature upon which parents and clinicians rely: out of 72 meta-analytical reports meeting the inclusion criteria, the authors were compelled to exclude 19 – seven lacked sufficient information to reproduce their calculations, and twelve contained actual or probable analytical errors. Consequently, approximately one in four meta-analyses in this field proved to be either irreproducible or flawed. Therefore, the vacuum is not solely therapeutic but also epistemic: in the very domain where families seek guidance, the secondary literature itself is unreliable in a substantial proportion of cases (Gosling et al., 2025).
In this context, the child may be subjected to an endless succession of therapies, diets, supplements, injections, "detox" regimens, hyperbaric oxygen therapy, chelation, experimental protocols, stem cell therapies, or other complex, painful, costly, and risky procedures. The American Academy of Pediatrics emphasizes that pharmacological agents do not alter the core symptoms of ASD, but rather manage specific co-occurring conditions, while the FDA warns that approved stem-cell products exist solely for limited hematopoietic indications, and not as a treatment for autism (Hyman et al., 2020). Regarding stem cells in particular, the literature remains cautious: available reviews and meta-analyses indicate insufficient evidence for efficacy and safety, unknown mechanisms of action, undefined critical periods, and the risk posed by commercial clinics peddling hope outside the purview of well-controlled clinical trials (FDA, 2024; Saisa et al., 2025; Zhang et al., 2026). Concurrently, despair can drive the family entirely outside the medical realm – towards clairvoyants, folk healers, energy healers, hypnotists, "bioresonance" practitioners, miracle regimens, and other fraudulent promises – because where science states, "we do not fully know" and "we cannot cure," the market of hope frequently asserts, "we can" (Doherty et al., 2025; Gosling et al., 2025). The clinical danger lies in the child gradually becoming not a subject in need of stability, development, and protection, but rather an object of perpetual experimentation, wherein parental hope, guilt, and panic can override the principle of primum non nocere – first, do no harm (Hyman et al., 2020).
Three caveats protect this analysis from oversimplification. First, the mechanism of perceived improvement must not be overlooked: the placebo response in autism trials is systematically documented and substantial (Siafis et al., 2020), which explains why a parent might, in good faith, observe progress following an ineffective intervention. This perception is not indicative of gullibility, but rather a predictable outcome of the assessment structure itself. Second, the underreporting of adverse events is not exclusive to alternative medicine; it has also been identified in mainstream intervention research involving young autistic children (Bottema-Beutel et al., 2021). Consequently, the dichotomy of "conventional versus alternative" does not equate to "safe versus risky." Third, the impetus for this pursuit should not be attributed entirely to objective medical limitations. Research on parental decision-making highlights a combination of personal values, the perceived inefficacy of conventional approaches, and genuine barriers to accessing and implementing them (Carlon et al., 2013; Edwards et al., 2018; Shepherd et al., 2018). Tellingly, parents themselves frame their need not as a quest for a miracle, but as a demand for a reliable and accessible resource to help them navigate the contradictory literature (Smith et al., 2020) – a need directly addressed by the aforementioned umbrella review through the open-access platform developed by its authors.
2.8. Beyond „virtual autism“
Dr. Anne-Lise Ducanda has described clinical cases of very young children, typically under three years of age, in whom intensive early screen exposure is accompanied by autism-like symptoms – absent or delayed speech, diminished eye contact, social withdrawal, stereotypies, and regulatory and behavioral disturbances – and in whom the cessation of screen exposure, replaced by live human interaction, play, and structured care, leads to significant and occasionally near-complete developmental recovery. A similar framework underlies the work of the Romanian psychologist Marius Teodor Zamfir, who coined the term "virtual autism" for an autism-like syndrome in children aged 0–3 years with a history of more than four hours of daily exposure to a virtual environment; in his data, children with this history demonstrated greater DQ/IQ gains following therapeutic intervention and reduced exposure than children without it (Marcelli et al., 2018; Zamfir, 2018). In both approaches, however, the intervention remains multifaceted: screen elimination proceeds alongside conventional developmental therapies – psychological counseling, occupational and sensory integration therapy, speech therapy, behavioral and family interventions – which makes it difficult to isolate screen cessation as the operative therapeutic factor (Barreto et al., 2024; Heffler et al., 2020, 2024; Heffler, Frome, Garvin, et al., 2022; Heffler, Frome, & Gullo, 2022; Heffler & Oestreicher, 2016; Zamfir, 2018).
Our clinical material introduces a more radical distinction – one the term "virtual autism" cannot carry. In children up to approximately 30 months of age, when screen addiction is still in its early stages and has not yet consolidated into screen trauma, full recovery following screen cessation is observed in nearly half of the cases. For the remaining children, and for older cohorts, outcome depends on the age of onset, the intensity and duration of exposure, the quality of in-person caregiving, the extent of linguistic and social deprivation, and related developmental factors (Ivanova et al., 2025; Manolova & Vezenkov, 2025c, 2025a; Petrova et al., 2025; Vezenkov & Manolova, 2025e).
The present framework allows this split to be stated functionally rather than merely statistically. The detox-responsive presentation corresponds to cue-bound closure (C1): the artificial source still regulates the child from outside, the criterion of reality remains externally anchored, and removal of the source destabilizes the system – which is precisely why eliminating it and restoring a human-mediated regulatory source in its place can suffice. The non-responders are children in whom screen trauma and reversed development have already reorganized regulation: developmental anchors – pathological reflexes, vestibular and sensory distortions, cortical fragmentation – hold the system in phylogenetically older survival modes, and, at the deepest tier, the criterion of reality migrates inward (C2, sealed inversion). In C2 the closure is self-referential: the state is stable without any external source; the child may present favorable autonomic indices while access to the shared world remains minimal (autonomic-relational dissociation); and there is, strictly speaking, nothing left to remove. Screen prohibition is here a category error. What is required is the re-anchoring of the reality referent through protected inclusion windows, on the principle that regulation precedes meaning. The dynamics of the learning systems complete the picture: in both closed states learning is not absent but inverted – the systems continue to operate efficiently, yet toward closure – which is why the untreated condition deepens over time rather than plateauing (Manolova & Vezenkov, 2025e; Vezenkov & Manolova, 2026c, 2026b).
From this perspective, "virtual autism" is not "autism caused by screens," nor a unitary syndrome, but the name of the reversible surface tier of a continuum. The heterogeneity of outcomes reflects depth along that continuum – the degree of trauma, the direction of development, the regulatory state – rather than the presence or absence of some "true" underlying autism in a given child. Herein lies the conceptual cost of the term. By defining the phenomenon through its resemblance to autism, it tacitly preserves the classical paradigm as the explanatory frame and leaves open the notion of another, "conventional" autism from which these children merely borrow their symptoms. The difficulty is not the acknowledgement that primary neurodevelopmental conditions exist – our claim concerns a subgroup – but the direction of explanation: even when screens are recognized as a causal or maintaining factor, intervention continues to be conceptualized through the classical autism paradigm rather than through a model of early screen addiction. The clinically operative questions, however, are no longer "which autism?" They are: at what depth of the continuum is this child – addiction, trauma, reversed development; in which regulatory state – C1 or C2; and in which direction are the learning systems currently running? These questions, unlike the term, determine both prognosis and the therapeutic sequence.
2.9. High-Functioning Autistic Individuals
In high-functioning autistic adults, a diagnosis may carry not only clinical significance but also identity-related, social, legal, and occasionally material value. Once established, the diagnosis can begin to function as a stable framework through which the individual contextualizes their past, difficulties, social failures, professional conflicts, sensory vulnerability, trauma resulting from masking, and the pervasive sense of having always been "different." Research on late-diagnosed autistic adults indicates that the diagnosis frequently provides validation, a sense of belonging, a new identity, access to a community, enhanced self-acceptance, and a vocabulary through which the individual can request understanding and accommodations (Cooper et al., 2021; Davies et al., 2024).
It is precisely here that the potential for secondary gain emerges: the diagnosis can secure access to educational, occupational, social, or institutional accommodations; lower expectations regarding specific social, emotional, or professional behaviors; offer moral shielding against criticism; transform personal hardship into a recognized group identity; and pave the way for a public role as a spokesperson, activist, "first-person" expert, or representative of neurodiversity. In this regard, a subset of high-functioning autistic adults may have a vested interest in the diagnosis being treated as irrefutable and definitive. Any questioning thereof may be experienced not merely as a diagnostic revision, but as an assault on their identity, biography, sense of belonging, acquired accommodations, and the social legitimacy of their distress.
This phenomenon is particularly pronounced within the context of the neurodiversity movement, where autism is increasingly conceptualized not solely as a clinical disorder, but as a social identity and a natural variant of human neurological diversity. This process can engender a rigid identity construct, wherein the diagnosis ceases to be a working clinical hypothesis and metamorphoses into an almost inviolable personal status. Consequently, any discussion of potential misdiagnosis, overdiagnosis, comorbidity, trauma, personality organization, screen addiction, depression, social anxiety, or alternative etiologies may be readily dismissed as "ableism," "gaslighting," or the invalidation of one's identity.
In such scenarios, the secondary gain is not necessarily financial or consciously manipulative; rather, it can be far more subtle. It may manifest as protection from shame, absolution from guilt, an explanatory framework for life's setbacks, integration into a community, assuming a moral stance of vulnerability, and asserting the right to demand environmental accommodations without a reciprocal expectation for personal change. The inherent clinical risk is that the diagnosis may begin to confine the individual within a rigid identity, rather than serving as a dynamic tool for understanding, development, and enhanced overall functioning.
In the spirit of the Orwellian critique of that brand of ideological thinking which loves the oppressed less than it constructs its identity through hatred of the "privileged," a segment of the radicalized discourse surrounding autism can be interpreted not as a defense of the weakest, most dependent, and most severely impaired autistic individuals, but as the production of a moral identity through opposition to the "neurotypical," the mentally healthy, and the functional. Although Orwell himself did not verbatim coin the popular adage that socialists "do not love the poor, but hate the rich," in The Road to Wigan Pier he critiques precisely the elitist, moralizing, and frequently disdainful activism that purports to speak on behalf of the working class without genuinely belonging to it or comprehending it (Orwell, 1937).
Similarly, within a subset of contemporary neurodiversity rhetoric, the autism diagnosis transcends its role as a mere clinical category, morphing into a social identity, a minority status, and a political language of recognition. While this serves a crucial anti-stigmatizing function, it can concurrently lead to strategic essentialism, the flattening of internal heterogeneity within the autism spectrum, and the framing of autism as an almost indisputable identity immune to clinical revision (Ellis, 2023). Within such a framework, the individual does not merely articulate difficulties but may assume the position of a victim – a bearer of a distinct authenticity and moral vulnerability – while the "normal" or "neurotypical" individual is construed as privileged, oppressive, insensitive, or culpable. Consequently, the diagnosis begins to confer not only an explanatory model and support but also insulation from criticism, public legitimacy, community belonging, and, occasionally, moral superiority (Cooper et al., 2021; Davies et al., 2024).
The core issue does not lie in acknowledging the genuine distress, discrimination, and need for accommodations experienced by autistic individuals, nor does it reside in the social model of disability, which rightfully demonstrates that the environment can engender suffering through inaccessibility and stigma (Pellicano & den Houting, 2022). The problem arises when advocacy is supplanted by ressentiment: instead of deliberating on how the most severely affected – the non-verbal, the highly dependent, the self-injurious, the aggressive, and the institutionalized – along with their exhausted families, might receive tangible assistance, a symbolic bubble is constructed. Within this bubble, the diagnosis serves simultaneously as a shield, an identity, a moral privilege, and a weapon against mental health, normalcy, and functionality (Ellis, 2023; Frith, 2026; Ortega, 2009).
2.10 Clinical and Societal Misunderstandings of Addiction Contribute to the Misunderstanding of Autism
One of the reasons screen addiction remains poorly recognized is that humanity, as a whole, understands addictions incompletely, inconsistently, and often retrospectively. Historically, addiction has long been conceptualized primarily through substances – alcohol, opiates, nicotine, and stimulants – making it more difficult for culture, medicine, and institutions to recognize addictions that lack an external chemical agent, where the object of addiction is a behavior, an environment, an experience, or a technological interface. Even today, behavioral addictions are approached with caution: gambling disorder is officially recognized in the DSM-5, and gaming disorder is included in the ICD-11, but many other forms of compulsive digital behavior remain in a gray area between habit, poor parenting, anxiety, depression, ADHD, autism, social isolation, and addiction (American Psychiatric Association, 2022; WHO, 2019). This conceptual lag makes screen addiction particularly difficult to delineate: it does not resemble classical intoxication; there is no needle, bottle, or smell of alcohol; and it is frequently socially normalized, technologically encouraged, and even presented as education, entertainment, socialization, or a source of "calm" for the child. It is precisely for this reason that the pathological use of screens can be masked as modern childhood, digital literacy, or parental convenience, whereas in reality, it fulfills functions remarkably similar to other addictions: rapid soothing, avoidance of frustration, dopamine-seeking stimulation, loss of control, withdrawal-like irritability upon interruption, narrowing of interests, and the gradual displacement of live human connection, play, physical embodiment, and language (Brand et al., 2019; Fineberg et al., 2018; Radesky et al., 2023; Vezenkov et al., 2026).
Even the AAP explicitly prefers the term PMU over "addiction" to avoid „stigmatizing“ youth, acknowledging that online platforms utilize "sticky" design features to hold attention and that media use has both risks and „benefits“. The American Academy of Pediatrics (AAP) defines Problematic Media Use (PMU) not by the number of hours a child spends online, but by the resulting physical, emotional, social, or functional impairments, such as sleep deprivation, academic decline, or relying on digital media as a primary emotional regulator (American Academy of Pediatrics, 2025).
The problem is exacerbated by the fact that medicine and psychotherapy are generally not particularly successful in treating addictions. Even for well-recognized addictions, treatment is often protracted, unstable, and marked by relapse, high comorbidity, and a strong reliance on motivation, environment, family, access to services, and the quality of the therapeutic alliance. The U.S. National Institute on Drug Abuse emphasizes that addiction is a chronic, relapsing disorder in which returning to use is a common feature of the clinical picture, rather than merely a "failure of willpower"(McLellan et al., 2000). If systemic frameworks struggle to manage alcohol, substance, or gambling addictions in adults, it is significantly more challenging to recognize and treat an addiction that begins in early childhood – a period when self-regulation, language, attachment, and symbolic play are still in their formative stages. For a young child, a screen is not simply a "bad habit"; it can become the primary regulator of the nervous system. It soothes, feeds attention, substitutes for human connection, structures waking hours, suppresses crying, abolishes boredom, and provides the child with potent, easily accessible stimulation that the real world struggles to rival.
Within paediatrics the screen addiction has been named „screen dependency disorder” and argued onto the child-neurological agenda (Sigman, 2017), yet it carries no operational criteria, no instrument in routine developmental surveillance, and no diagnostic code. A clinician who suspects it has no category in which to record the suspicion.
Therefore, the cessation of screen time in an addicted child is not merely a disciplinary measure; it can precipitate a severe crisis of regulation, manifesting as irritability, aggression, crying, insomnia, refusal to play, sensation-seeking, regression, and an inability to engage in live interaction. If a therapist does not conceptualize this dynamic in terms of addiction and withdrawal, they may erroneously interpret it as "autistic rigidity," a "behavioral problem," or a reflection of the "severity of the diagnosis," rather than as an acute reaction to the disruption of a digital regulator. In this sense, the issue is not solely that screen addiction is a novel phenomenon; the core problem is that it emerges within a civilization that already possesses systemic vulnerabilities in recognizing addiction as such, struggles to treat those who are addicted, and frequently prefers to re-label addiction as a symptom, a diagnosis, a character trait, a choice, or a cultural norm. Thus, the deficiency in understanding addictions translates directly into a diagnostic deficiency regarding screen addiction, ultimately facilitating the perpetuation and misapplication of the "autism" diagnosis.
2.11. "Screens Are Not the Problem; They Are the Solution for Autistic Individuals"
The premise that "autistic individuals communicate best through screens" can readily devolve into a dangerous rationalization. The screen is not a solution to the communicative deficit; rather, it is often the very mechanism that engenders, exacerbates, or perpetuates it. The child does not develop robust social capabilities through the screen, but instead becomes fixated on an environment characterized by high predictability, instantaneous stimulation, low demands for reciprocity, and minimal somatic frustration.
This mode of "communication" is not equivalent to the development of language, symbolic play, empathic attunement, cognitive flexibility, tolerance for the real other, and active participation in a human community; rather, it constitutes a addiction to a highly controllable digital environment. Even when a child presses buttons, selects images, responds to algorithms, or interacts via templated digital signals, this does not evidence mature social communication – the very same rudimentary forms of selection, signaling, and instrumental interaction can be mastered by non-human primates.
However, the ultimate goal of child development is not the acquisition of minimal operant communication, but rather the cultivation of a healthy, functional, autonomous, and socially capable human being. Consequently, the screen must not be romanticized as an "alternative homeland" for the autistic child, as doing so merely introduces yet another factor that perpetuates the diagnosis.
2.12 The General Rise in Mental Disorders
The rise in autism does not occur in isolation, but rather against the backdrop of a much broader expansion of psychiatric, neurodevelopmental, and behavioral diagnoses in contemporary societies. Global data indicate that mental disorders are among the leading sources of health burden, and following COVID-19, anxiety and depression increased by an additional 25% during the first year of the pandemic (GBD 2019 Mental Disorders Collaborators, 2022; GBD 2023 Mental Disorder Collaborators, 2026; WHO, 2022).
When virtually all categories of mental distress – anxiety, depression, ADHD, addictions, eating disorders, behavioral problems, and learning disabilities – are increasing statistically and culturally, sensitivity to the specific rise of autism diminishes. It begins to appear as merely one component of a general "epidemic" of mental disorders, rather than a distinct phenomenon requiring independent etiological, diagnostic, and social explanation. A critical observation is that, even concerning these other mental health conditions, the role of screen addiction and problematic digital use frequently remains insufficiently acknowledged. The literature already links the problematic use of the internet, social media, gaming, and smartphones with depression, anxiety, psychological distress, and disruptions in attention, sleep, and socio-emotional functioning. However, these factors are predominantly regarded as comorbid or secondary, rather than as potential causal, maintaining, or exacerbating mechanisms (Brand et al., 2019; Eirich et al., 2022; Fineberg et al., 2022; Munzer et al., 2026; Vasconcellos et al., 2025; Xiao et al., 2025).
Thus, a normalizing effect emerges: if all disorders are increasing, then autism is "naturally" increasing as well. If society has become more informed, more inclined toward diagnosis, and more tolerant of psychiatric categories, then any statistical increase can be conveniently attributed to better recognition, broadened diagnostic criteria, and reduced stigma. While this explanation is partially valid, it can also function as a defense mechanism against a more challenging question: whether, alongside this diagnostic expansion, there exist tangible environmental, familial, technological, and developmental factors that are actively producing a new type of pathology.
In this sense, the overall surge in mental disorders diminishes the sense of alarm regarding the rise of autism. Concurrently, the inadequate understanding of screen addiction allows it to be subsumed under other diagnoses – such as anxiety, ADHD, depression, behavioral disorders, or ASD – instead of being rigorously investigated as a potential independent and perpetuating factor in contemporary psychopathology.
2.13. Screen-Addicted Adults
Here, another crucial layer of the problem can be articulated: screen addiction in children develops within an environment that is already screen-addicted. Parents, teachers, therapists, and institutions who themselves operate in a mode of constant screen stimulation frequently exhibit an elevated tolerance for screens and a diminished sensitivity to their addictive potential. In parents, this phenomenon is described by the concept of technoference – the interference of technology in the parent-child relationship, wherein a phone or screen disrupts attention, emotional availability, synchrony, and responsiveness to the child. Systematic reviews and meta-analyses link parental device use to lower interaction quality, increased child screen time, and adverse psychosocial outcomes in young children (Coyne et al., 2025). Thus, the adult does not merely "permit" the screen, but models it as a normative environment of existence: the child observes an adult who self-regulates via a phone, avoids boredom through scrolling, interrupts social contact for notifications, and utilizes the screen as a rapid means of soothing. In such a culture, the child's screen addiction is difficult to recognize because it reflects the addiction of the environment itself (Mallawaarachchi et al., 2024; Manolova & Vezenkov, 2025b; Petrov, Manolova, et al., 2025; Vezenkov & Manolova, 2025a, 2025c).
This also serves a protective psychological function. If it is acknowledged that screens can be a causal, maintaining, or exacerbating factor for regression, language delay, social withdrawal, sensory dysregulation, and autism, then the adults surrounding the child must admit their own complicity – not merely as bystanders, but as individuals who provided, tolerated, normalized, or even utilized the screen as a substitute for live caregiving. This admission exacts a heavy toll: guilt, responsibility, the necessity to alter familial routines, restriction of one's own use, addiction therapy, and the reorganization of the educational and therapeutic environment. Therefore, the diagnosis of "autism" is convenient because it shifts causality from the environment to the child: the problem is now located "in the child's brain," rather than in the screen ecology, parental absence, pedagogical passivity, or therapeutic blindness. This logic is further reinforced by the fact that for children with ASD, screens are frequently present both in daily life and in rehabilitative and educational practices, creating an additional risk that excessive use will be disguised as "assistive technology," "education," "communication," or "regulation" (Ophir et al., 2023; Vanderloo et al., 2025).
Thus, a vicious cycle takes shape: addicted adults raise, educate, and treat addicted children; their own addiction renders them less capable of perceiving the addiction in the child; and the "autism" diagnosis stabilizes the system by absolving adults of the painful questions regarding causality, complicity, and change. In this sense, screen addiction is not solely an individual pediatric issue, but rather a familial-pedagogical-therapeutic phenomenon: it is maintained by adults who are frequently as attached to screens as the child is. The clinical question, then, is not merely "how many hours does the child spend in front of a screen," but rather "who within the system has a vested interest in the screen remaining normative, invisible, and blameless" (Petrov, Dimova, et al., 2025; Vezenkov et al., 2026). It is precisely here that the strongest resistance emerges: if the screen is recognized as a factor, it is no longer sufficient for the child to simply attend speech therapy, occupational therapy, or psychological counseling. The adults must alter their own behavior, bear the burden of guilt, restore live connection, and undergo treatment alongside the environment they have created.
2.14. The Structural Economics of the Lifelong Patient
In the therapeutic field surrounding autism, there exists a potential structural conflict of interest that is rarely addressed directly: the more the diagnosis expands, the more the market for associated services expands alongside it. Official medical sources emphasize that current interventions for ASD aim to mitigate symptoms that interfere with daily functioning and quality of life, rather than to "cure" autism as such (CDC, 2024). This engenders a distinct model of a chronic therapeutic economy: the diagnosis is lifelong, there are no biomarkers, a definitive "endpoint" of recovery is frequently ill-defined, and therapies can continue for years in various forms – speech therapy, occupational therapy, behavioral interventions, sensory integration, social skills training, parental counseling, and educational support. Although evidence-based practices exist, the report by the National Clearinghouse on Autism Evidence and Practice delineates 28 evidence-based practices rather than a singular restorative therapy with a universal criterion for completion (Hume et al., 2021). Furthermore, major systematic reviews highlight that the evidence for early interventions is uneven, that effects are contingent upon study quality, and that under more stringent methodological criteria, some of the reported effects diminish (Sandbank et al., 2023). This does not imply that therapies are futile; rather, it signifies that in the absence of clear, measurable, and publicly verifiable outcome criteria, a space emerges for prolonged therapy with low accountability.
It is precisely here that the critical problem arises: the child with autism can become an ideal long-term client – a patient with a lifelong diagnosis, anxious parents, an uncertain prognosis, multiple co-occurring needs, and frequently, third-party financing from the state, a municipality, insurers, the school system, funds, or donors. Within health economics, it is well-documented that the fee-for-service model introduces a risk of overuse, as the provider is compensated for a higher volume of services rather than necessarily for better outcomes. Publications on medical overuse note that financial incentives and specialty bias can promote unnecessary services, particularly when clear accountability for outcomes is lacking (Sandbank et al., 2024; Wagenschieber & Blunck, 2024). A similar logic applies to the therapeutic services surrounding autism: if progress is described using vague phrases such as "there is improvement," "they are calmer," "we are working on regulation," or "they engage better," without specific timeframes, functional indicators, and criteria for terminating or modifying the therapy, virtually any ongoing intervention can be framed as indispensable. NICE recommends organized multidisciplinary support for children and young people with autism; however, the very fact that assistance is coordinated across health, educational, and social services illustrates how easily autism transforms into a long-term institutional domain, rather than a brief therapeutic episode.
This structure now possesses a pronounced market dimension. Industry analyses in the U.S. describe autism services, particularly ABA therapy, as a rapidly expanding market driven by the increasing prevalence of the diagnosis, expanded insurance coverage, and growing provider capacity. A consulting analysis by L.E.K. estimates the U.S. ABA market at approximately $25–35+ billion, with an annual growth rate of 10–13% (Vig & Kadar, 2025). Other reports note the substantial influx of private equity into autism services, warning that when a sector is underwritten by stable public or insurance reimbursements, it becomes highly attractive to investors, which can engender tension between the quality of care and the pursuit of financial returns (Batt et al., 2021). Recent investigations and public data further reveal that Medicaid expenditures for autism therapy in the U.S. have surged, and in some states, issues have been identified concerning excessive billing, questionable therapy hours, and weak quality regulation (Weaver et al., 2026). Consequently, the critique is not that all therapists act in bad faith – many operate competently and with genuine care – but rather that the system surrounding autism intrinsically produces an objective incentive for the diagnosis to be expanded, chronified, and rarely revised. When there is no clear norm for recovery, no established timeframes, and no penalties for ineffective therapy; when payment is sourced from a third party; and when the therapist concurrently accrues income and the social status of a "savior," the autistic child is at risk of being retained in the role of an eternal patient. This is not necessarily the result of a conspiracy, but rather the convergence of economics, professional prestige, parental desperation, and diagnostic ambiguity.
2.15. Institutional Preservation through Diagnostic Authority
Psychiatry participates in this system not as an entirely neutral external observer, but as an institution that holds diagnostic authority, professional prestige, and economic interest. In the case of autism, the diagnosis is typically established clinically – through parental history, behavioral observation, and comparison with DSM/ICD criteria – given the absence of any biomarker, laboratory test, or neuroimaging study capable of confirming the condition in the manner by which many somatic diseases are confirmed (CDC, 2025, 2026; Frith, 2026). This renders psychiatric expertise simultaneously necessary and authoritative: the specialist does not merely describe symptoms, but frequently acts as the gatekeeper to resource support, therapies, social services, pharmacological monitoring, educational accommodations, financial assistance, and institutional recognition. In this sense, the diagnosis begins to function as an administrative and economic key, with psychiatry positioned as the profession holding the exclusive right to issue it (Penner et al., 2018).
The critical literature on the DSM and psychiatric diagnosis has long warned that the expansion of diagnostic categories can lead to the medicalization of normal variations, diagnostic inflation, and a growing dependence on expert authority (Conrad, 2007; Fitzgerald, 2011; Fombonne, 2023). For autism, this risk is particularly pronounced because, once assigned, the diagnosis is often perceived as a lifelong framework, and any subsequent improvement may be interpreted not as grounds for diagnostic revision, but rather as "good adaptation in autism." Thus, a system is created wherein the psychiatric diagnosis generates revenue through assessments, follow-up consultations, expert evaluations, medication management, expert opinions, and administrative documentation, while also conferring prestige: the psychiatrist assumes the role of the supreme interpreter of child development and the entry point to an entire network of services.
The issue is not that every psychiatrist acts in bad faith, but rather that the system creates a structural incentive for the diagnosis to be assigned, maintained, and rarely revised, because an ecosystem of funding, professional authority, institutional rights, and therapeutic markets is organized around it. If, instead, the question were raised regarding screen addiction, screen trauma, family environment, deprivation, therapeutic sabotage, or reversible developmental breakdown, then the focus would shift from a lifelong diagnosis to causality, responsibility, environmental modification, and the potential for recovery. This shift threatens not only the established clinical narrative but also the economy and the prestige of the system that thrives on its stability.
2.16. Additional Harm from Autism Therapy
When autism establishes itself as the sole explanatory framework, young professionals – psychologists, speech therapists, occupational therapists, special education teachers, and behavioral therapists – are trained exclusively within its parameters. They are taught to perceive the child through the lexicon of "autistic deficits," "lack of social skills," "sensory dysregulation," and "behavioral problems," rather than through the vocabulary of early screen addiction, withdrawal, screen trauma, and inverted development. Consequently, a child who ought to be treated for screen addiction and reintegrated into live human connection, play, physical embodiment, speech, and genuine social interaction is instead treated as having a lifelong autistic condition.
Instead of eliminating the root cause, the system begins to train the symptoms: conditioning the child to sit, imitate, follow instructions, vocalize words on command, suppress meltdowns, and appear socially acceptable. This does not constitute recovery, but rather behavioral drilling. It produces external manageability, but not internal development; obedience, but not health; adaptation to the diagnosis, but not liberation from the addiction.
Thus, parents, teachers, and therapists, convinced that they are treating autism, inadvertently exacerbate the impairment. They do not treat the screen addiction, nor do they restore the live human environment; rather, they discipline the consequences of its absence. The child remains addicted, regressed, and fundamentally misinterpreted, while the system registers "progress" simply because the child has become more convenient for the adults.
2.17. The Fragmentation of Scientific Research
One of the fundamental methodological problems in autism research is the fragmentation of scientific knowledge: various disciplines investigate distinct components of the same child, yet relatively rarely is the child itself examined as a unified, developing biological, psychological, and social system. Genetics searches for genetic variants and hereditary mechanisms; neuroscience focuses on the structural and functional characteristics of the brain; immunology investigates inflammatory and autoimmune processes; gastroenterology and microbiome research examine intestinal dysbiosis and the gut-brain axis; metabolic studies explore mitochondrial function, oxidative stress, folate, and other biochemical pathways; nutritional research focuses on micronutrient deficiencies; and psychology and psychiatry investigate behavior, communication, and symptomatology.
Each of these approaches may establish genuine and significant associations; however, when the results remain siloed within individual disciplines, a risk arises of conflating the part with the whole. Consequently, stereotypic behavior is investigated in isolation from sleep, sleep in isolation from nutrition, nutrition in isolation from the microbiome, the microbiome in isolation from the nervous system, the nervous system in isolation from attachment and the social environment, and all of these in isolation from the daily screen-and-technology environment in which the child actually develops.
Thus, science accumulates a vast repository of data regarding isolated mechanisms, yet struggles significantly more to answer the integrative question: what has occurred within the specific child as a holistic, developing system, in what sequence did the disruptions emerge, and how do the various biological, environmental, behavioral, and relational factors interact over time? It is precisely this dearth of sufficient longitudinal, interdisciplinary, and systemic research that engenders a paradox wherein genetic associations, immune deviations, metabolic characteristics, gastrointestinal issues, sleep disturbances, sensory dysregulation, and differences in brain function can all be described simultaneously, without clarity as to which is the cause, which is the consequence, which is a compensatory reaction, and which is a co-occurring phenomenon.
2.18. The Genetic Theory of Autism as the Tip of the Iceberg
The genetic theory is one of the strongest pillars supporting the understanding of autism as a lifelong, inevitable, and inherently unpreventable neurodevelopmental condition. The problem lies not in the existence of a genetic contribution, but in its transformation into genetic determinism: from the establishment of heritability and genetic associations, there is a shift toward a much stronger public implication that the cause is inherent within the child, that the condition cannot be prevented, and that the sole task of medicine and the family is adaptation. Thus, the genetic argument ceases to be merely a scientific hypothesis regarding a fraction of the causality and begins to fulfill a crucial legitimizing function – it closes the question of "what caused this?" while simultaneously validating the answer that "nothing could have been done."
High heritability, however, is synonymous neither with inevitability nor with independence from the environment. It describes a statistical variation within a specific population and environment, rather than an individual destiny. Genetic vulnerability may dictate which children are more susceptible to a given environmental factor, without that factor being genetic in itself. This is precisely why the "genes versus environment" dichotomy is misleading: biological vulnerability and environmental impact can participate in the very same causal chain. If genetics is presented as the definitive explanation, the search for preventable environmental factors practically concludes before it has even begun.
This same limitation applies to twin studies. Monozygotic twins share not only genetic material but also a substantial portion of their prenatal, familial, and early developmental environment. Consequently, high concordance is a compelling argument for a genetic contribution, but it does not intrinsically prove that environmental causality is negligible. Still less can it exclude factors that are systematically shared within a single household, including caregiving practices and the digital environment.
The most substantial problem facing a strictly genetic explanation is the dynamic nature of the phenomenon itself. The genome of human populations does not change at the rate at which the recorded prevalence of autism has changed in recent decades. While a portion of this increase can undoubtedly be attributed to the expansion of diagnostic criteria, improved recognition, and changes in diagnostic practices, the genetic argument alone does not account for the remainder, nor does it negate the necessity of searching for changing environmental factors.
There are genetic syndromes and variants in which autistic symptomatology is part of a clearly established biological pathology. Their existence, however, does not permit this same causal model to be automatically extrapolated across the entire broad and heterogeneous spectrum, particularly to cases lacking an established syndromic etiology or diagnostic biomarker. When conditions of disparate origins are grouped under a single behavioral label, the evidence for strong genetic causality in certain cases can illegitimately begin to serve as an explanation for all others.
Thus, the overemphasis on genetics has a consequence that transcends genetics itself: it normalizes the perception of autism as inevitable, unpreventable, and irreversible, thereby diminishing both public and scientific pressure to search for modifiable causal factors. For the layperson, the message becomes straightforward: the child was born this way, no one could have prevented it, and nothing can alter the underlying condition. It is precisely this reductionism that constitutes the problem. Genetics must be part of causal research, but when it morphs into a universal answer, it no longer opens a scientific inquiry; it closes it. And closing the question of causality simultaneously stabilizes all three fundamental tenets of the current paradigm: that autism is incurable, that its onset is inevitable, and that its prevention is impossible.
Genetics is an exceedingly complex and highly specialized field, the critical comprehension of which requires expertise typically lacking in the general public, parents, psychologists, and even physicians without a specialization in medical genetics. Consequently, the genetic conclusions presented to them are frequently accepted on faith, without any genuine opportunity to independently evaluate their methodological limitations, their degree of uncertainty, or the boundaries of their causal inferences.
3. Discussion
The described mechanisms do not operate in parallel but rather form a pathological ecosystem in which medical pessimism, genetic determinism, familial exhaustion, screen addiction, secondary gain, therapeutic chronification, diagnostic identity, and economic incentives mutually legitimize one another. The system's strength lies not in isolated factors, but in their symbiosis: one engenders the conditions for another, the second masks the first, and the third transforms the cumulative outcome into novel evidence validating the system itself. Thus, the cause can be normalized as the environment, the symptom diagnosed as a disease, the adaptation to the symptom presented as treatment, and the persistence of the condition utilized as evidence of its biological immutability. The fundamental ecosystemic fallacy, therefore, is a self-validating system that interprets its own consequences as independent evidence.
3.1. Incurability – Despair – Screen – Familial Co-Addiction
The medical premise of lifelong chronicity, the genetic explanation, the absence of etiological treatment, parental burnout, pediatric screen addiction, and adult screen addiction constitute the first closed symbiosis. Medicine informs the family that the condition cannot be cured; genetics lends biological credibility to this finality; the parent gradually substitutes the goal of recovery with the lesser objective of rendering the child manageable. The screen simultaneously resolves two problems: it regulates the child and liberates the exhausted adult from the perpetual necessity of regulating them, whereby the addiction of one party becomes functionally advantageous to the addiction of the other. Thus, medical pessimism lowers the therapeutic benchmark, familial exhaustion increases screen exposure, the screen deepens familial co-addiction, and the ensuing symptomatology reaffirms the initial premise of a severe and immutable disorder.
This configuration possesses a distinct stabilizing mechanism: the more poorly the child functions without a screen, the more indispensable the screen appears; the more indispensable the screen becomes, the lower the probability that the system will evaluate the child's functioning in its absence. Parental technoference further normalizes the digital environment, as the adult struggles to recognize behavior in the child as pathological when that same behavior is pervasive in their own daily life. The family gradually adapts not to the child, but to the addiction: feeding, traveling, soothing, leisure time, and communication begin to be organized around the device. The screen is no longer merely a stimulus within the environment; it becomes the very infrastructure of familial functioning.
3.2. The Diagnosis as an Alibi for the Environment
Symptomatic diagnosis, the lack of a biomarker, genetic determinism, the concept of an innate neurodevelopmental disorder, and parental guilt forge a second, more profound symbiosis: the diagnosis not only defines the child but also absolves the environment from the necessity of explaining itself. If the impairment is predetermined in the brain and genes, the daily environment transitions from a potential cause to a neutral background; the screen evolves from a causal candidate into a mere preference of the "autistic child." Thus, the very same behavior alters its causal meaning following the diagnosis: social withdrawal becomes a symptom of autism, screen fixation – a special interest, withdrawal meltdown – rigidity, and the return of the device – regulation.
This creates a diagnostic loop of self-validation: the symptoms prove the diagnosis, the diagnosis explains the symptoms, and the explanation obviates the need to investigate the environment that sustains them. The more comprehensively a behavior is interpreted through the lens of autism, the less room remains for causal analysis. In this sense, the diagnosis can function as an etiological closure: it provides a label precisely where an explanation is required.
3.3. The Cause Becomes a Therapeutic Tool
Screen addiction, the autism diagnosis, digital communication, sensory regulation, special education, and symptomatic therapy form a paradoxical configuration in which the putative causal factor is reintroduced into the child's life as a means of support. The screen soothes the child, communicates on their behalf, educates them, rewards their behavior, and fills the intervals between therapies; its functional utility thus masks its pathological role. The system compensates for the deficit through the very same environment that the report identifies as a factor in its genesis.
This extends beyond a conventional therapeutic contradiction. A closed causal-compensatory loop is generated: exposure creates a deficit, the deficit legitimizes the diagnosis, the diagnosis legitimizes the adaptation, and the adaptation reintroduces the exposure. The more dependent the child becomes on the adaptation, the more convincing the assertion appears that it is necessitated by the autism. The cause and the treatment gradually become indistinguishable.
3.4. Medical Vacuum and Therapeutic Hypertrophy
The absence of a causal treatment does not lead to therapeutic moderation, but rather to its exact opposite: the proliferation of symptomatic therapies. The medical vacuum, parental despair, speech therapy, behavioral therapies, sensory interventions, dietary regimens, medications, supplements, and alternative methods constitute a market that expands precisely because the central causal problem remains unresolved. Each specialist treats a different manifestation; therefore, the lack of an overarching outcome does not discredit the system, but instead engenders the need for yet another intervention.
Here, a distinct therapeutic hydra-mechanism emerges: every unresolved symptom spawns a new specialist, and every new specialization further fragments the child. Failure does not terminate the therapy, as it is pre-emptively explained by the condition's incurability; partial success also does not terminate it, because it proves that the therapy "works." Thus, both success and failure can lead to the identical outcome – the perpetuation of therapeutic dependency.
3.5. The Child's Illness as a Resource for the Family System
Secondary gain, parental burnout, social benefits, public sympathy, the caregiver identity, familial control, and Munchausen-like mechanisms forge a distinct pathological symbiosis: the addiction of the child begins to fulfill functions for the adult. These functions may be material, social, psychological, or relational, and do not necessarily imply conscious deception. The more the adult's life is organized around the illness, the more the child's recovery demands a reorganization not merely of caregiving, but of the family's identity, income, relationships, and social standing.
It is precisely here that the absence of a medical standard for a healthy relationship with a diagnosed child becomes systemically significant. If there is no clear demarcation between necessary support and the perpetuation of addiction, between adaptation and overprotection, or between care and pathological enmeshment, then self-sacrifice easily acquires the status of an absolute good. Medicine evaluates the child's symptoms, but far less frequently evaluates whether the familial organization enhances the child's autonomy or impedes it. Thus, the most problematic addiction can remain concealed precisely behind the facade of the most intensive care.
3.6. Factitious Disorder Imposed on Another (Munchausen by Proxy) and Institutional Blindness
In its most extreme form, secondary gain, pathological enmeshment, medical ambiguity, parental control over information, and the social reward of the sick role can intersect with Factitious Disorder Imposed on Another (FDIA). The literature notes the difficulty of diagnosis, the manipulation of the medical narrative, and the necessity of carefully documenting discrepancies. The specific risk with a non-verbal or highly dependent child is information asymmetry: the individual describing the symptoms to the system may simultaneously be the individual controlling the environment, the treatment, and access to the child.
Thus arises an epistemic addiction of the medical system upon the guardian. The more dependent the child is, the more the system must rely on the adult; the more it relies on the adult, the more difficult it becomes to recognize the pathological involvement of that same adult. If material gain, the social prestige of the sacrificial parent, and the pre-existing conviction that autism is lifelong are added to this dynamic, deterioration may be interpreted as the natural trajectory of the condition, rather than as a signal necessitating an environmental analysis.
3.7. The Lifelong Patient as the Intersection of Multiple Interests
The chronic diagnosis aligns the interests of the family, the therapeutic professions, social services, educational structures, administrative systems, and the market. The family receives support through the diagnosis; the therapeutic system secures a long-term patient; institutions organize services around categorical membership; specialists accumulate practice and expertise; and the market acquires sustained demand. None of these interests independently proves abuse, but their convergence creates a structural preference for a stable diagnosis over diagnostic revision.
The most substantial conflict emerges when recovery begins to dismantle the resources generated by the illness. At that point, clinical success translates into an economic loss for segments of the system. No overt coordination is required: it is sufficient for each structure to rationally defend its own continuation in order to yield a collective outcome wherein chronicity possesses more institutional allies than recovery.
3.8. The Adult Patient: Diagnosis, Identity, and Secondary Gain
In high-functioning adults, medical ambiguity intersects with a different type of secondary gain. The diagnosis can simultaneously explain one's biography, diminish personal guilt, and provide a sense of belonging, accommodations, social legitimacy, and a special status. In the absence of a biomarker and amidst a broad phenotypic spectrum, medicine possesses a limited capacity to differentiate autism from overlapping manifestations of anxiety, trauma, ADHD, addiction, social isolation, or personality traits.
Here, an asymmetry emerges: the diagnosis can be relatively easily affirmed socially, yet it is psychologically and institutionally difficult to revoke. Once it becomes an identity, its re-evaluation begins to be perceived as an invalidation of personal experience, rather than as a standard diagnostic procedure. Social acceptance, therefore, can devolve into diagnostic inertia, and diagnostic inertia into a defense against clinical revision.
3.9. From Neurospecificity to Neurodiversity: When the Description Becomes the Norm
A particularly potent symbiosis arises among the broad spectrum, the identity model, late-stage diagnosis, and the discourse on neurodiversity. The difference in neurological functioning may be genuine, without it necessarily following that every form thereof constitutes a healthy variant that ought not to be altered. The critical distinction lies between neurospecificity as the description of a condition, and the normative conclusion that this condition necessarily represents an equivalent variant of health.
When this boundary is obliterated, the therapeutic goal shifts: from normalizing the impaired function to adapting the world to the impairment. In severely affected individuals, this contradiction becomes especially conspicuous, because the loss of speech, self-injurious behavior, the incapacity for autonomy, or severe dysregulation can scarcely be reduced to a neutral difference. For high-functioning individuals, however, social identity can render the very striving for a functional norm suspicious. Thus, diagnostic expansion produces identity, identity protects the expansion, and neurodiversity discourse provides the moral framework that closes the cycle.
3.10. Diagnostic Expansion and the Halo of the Diagnosis
The expansion of the spectrum, self-identification, social networks, late-stage diagnosis, and neurodiversity advocacy can engender a cultural environment wherein the diagnosis acquires an aura of inviolability. Clinical doubt begins to be interpreted as stigmatization, and diagnostic revision – as the denial of identity. This impedes medicine in fulfilling one of its primary functions: not only to assign diagnoses, but also to reject them when the criteria or the causal model are insufficiently compelling.
The result is a system with a low threshold for inclusion and a high threshold for exclusion. Every new diagnosis expands the social visibility of the category; expanded visibility normalizes more borderline manifestations; normalization increases the demand for diagnosis; more diagnosed adults bolster public advocacy for the category. Thus, social validity begins to amplify medical validity, rather than the two remaining independent.
3.11. Scientific Fragmentation as a Mechanism for the Loss of Causality
Genetics, neuroscience, immunology, gastroenterology, metabolism, psychiatry, and psychology can simultaneously discover real characteristics while entirely missing their overarching causal architecture. Fragmentation transforms a single developmental process into multiple, distinct scientific objects: sleep becomes a separate comorbidity, nutrition a separate problem, social isolation a diagnostic symptom, screen fixation a behavioral characteristic, and family burnout a parental issue. The overarching temporal sequence disappears.
This creates a paradox: the more consequences are discovered, the more complex the disease appears, and the less likely the search for a common organizing factor becomes. The complexity of the outcome begins to be utilized as an argument for the complexity of the cause. Scientific specialization can thus inadvertently transform the multiple manifestations of a single process into evidence of multiple independent processes.
3.12. Genetics as an Amplifier of Diagnostic Finality
Genetic association, high heritability, familial clustering, and neurodevelopmental theory endow the diagnosis with biological weight; however, the risk arises when predisposition morphs into predestination. At that point, genetics does not merely explain individual susceptibility but begins to invalidate the question of what activates, amplifies, or maintains that susceptibility. The environment becomes secondary precisely because the biological vulnerability is real.
This logic is exceptionally convenient for the other components of the ecosystem: it absolves parents from analyzing the environment, relieves medicine from the necessity of finding a modifiable causal factor, justifies the lifelong nature of the condition to the therapeutic system, and provides a biological foundation for the identity model. Genetic determinism, therefore, functions as a central ideological stabilizer of a system in which almost all other participants benefit from causal finality.
3.13. The Overarching Pathological Symbiosis
Taken together, these mechanisms form not a linear causal chain, but a network characterized by multiple positive feedback loops. Medicine declares the condition incurable; genetics provides finality; the parent loses the expectation of recovery and seeks palliation; the screen regulates the child and liberates the parent; parental burnout and their own digital addiction normalize the exposure; the symptoms intensify; the diagnosis reinterprets them as manifestations of an innate condition; the screen is reintroduced as a therapeutic and educational tool; therapies manage the isolated symptoms; and the lack of full recovery ultimately confirms the incurability.
Around this primary cycle, a secondary one is constructed. The diagnosis unlocks therapies, social services, financial assistance, and accommodations; the family, therapists, and institutions gradually organize their functioning around it; secondary material, psychological, and social benefits increase the cost of recovery; and the lack of a standard for healthy autonomization allows addiction and dependency to be framed as care. For adults, the same mechanism undergoes a transformation: the diagnosis provides identity and belonging, and the social protection of this identity increases the cost of diagnostic revision.
A third cycle protects the first two on a cultural and scientific level. Neurodiversity transforms pathological neurospecificity into normative difference; diagnostic expansion increases the number of bearers of this identity; and their social visibility further legitimizes the expansion. Meanwhile, scientific fragmentation distributes the manifestations across multiple disciplines, thereby hindering the reconstruction of the overarching causal sequence.
Thus, a pathological symbiosis emerges among the family, medicine, the therapeutic market, institutions, culture, and science, wherein each system compensates for the weaknesses of the others. Medicine cannot cure, but the therapeutic sector can manage; therapy cannot achieve full recovery, but genetics explains why; the family cannot break the addiction, but the diagnosis explains why the child requires adaptation; the diagnosis lacks a biomarker, but social identity grants it cultural resilience; identity does not prove causality, but neurodiversity renders the very question of causality morally sensitive.
This is the profound essence of the ecosystemic fallacy: the weakness of each individual component is compensated by another component, as a result of which the system as a whole becomes more resilient than the evidentiary strength of its constituent parts.
4. Conclusion
In the model under consideration, the central problem is not merely the misidentification of screen addiction, but rather the system of symbioses that renders this misidentification resilient. The screen serves both the child and the parent; the diagnosis serves medical certainty and the familial absolution from causal guilt; chronicity serves the therapeutic and social infrastructure; the sick role can serve familial and individual secondary gains; genetic determinism serves the premise of immutability; the neurodiversity discourse protects the diagnosis as an identity; and scientific fragmentation impedes the reconstruction of the overarching causal picture.
Consequently, the unit of analysis cannot be solely the child. It must encompass the child–family–screen–medicine–therapy–institutions–culture continuum, because the pathological equilibrium emerges precisely at their intersection. Altering a single component allows the others to restore the previous state; lasting recovery, therefore, necessitates the simultaneous disruption of several mutually reinforcing cycles.
The most profound conclusion is that a system can be comprised of well-intentioned actors and nevertheless produce a pathological outcome. No overarching design or conspiracy is required when interests, beliefs, and adaptations naturally align in a single direction. The true ecosystemic fallacy emerges when the cause is normalized as the environment, the symptom is institutionalized as an identity, the addiction is rebranded as an adaptation, and the system's inability to restore the individual is utilized as definitive evidence that they are fundamentally beyond recovery.
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