The relationship between autism spectrum disorder and screen time in children: a literature review

Abstract

Background:

Autism spectrum disorder (ASD) affects millions of children globally, significantly impacting their quality of life. Understanding factors that contribute to symptoms, is essential for improving outcomes. This review aims to explore the relationship between screen time and ASD and provide insights for targeted interventions.

Methods:

PubMed, Web of Science, and Google Scholar were searched for studies on the link between screen time and ASD symptoms.

Results:

The findings suggest a possible link between excessive screen time and increased ASD symptoms, including social withdrawal and communication challenges. Some studies propose a bidirectional relationship, where children with this disorder may prefer more screen time due to social isolation.

Conclusion:

Although there is evidence suggesting a link between screen time and ASD, the relationship remains unclear; further research is needed to better understand these connections and develop effective interventions for children with this disorder.

HIGHLIGHTS

• Autism spectrum disorder (ASD) impacts millions of children globally, affecting their quality of life.

• Findings suggest excessive screen time may worsen social withdrawal and communication issues in ASD.

• A possible bidirectional relationship is proposed, where children with ASD might prefer screen time due to social isolation.

Introduction

The phenomenon of screen time, denoting the duration individuals spend engaging with electronic or digital media, has evolved significantly since its inception in the 1950s with the introduction of television (TV) into households[1]. While home-based television viewing once predominated, contemporary screen-based devices, including computers, game consoles, and mobile digital devices, are now accessible to young children, fundamentally altering the landscape of screen time experiences[2]. The advent of mobile devices has diversified when and how children encounter screen time, encompassing solitary viewing, simultaneous device use, traditional TV content consumption on mobile devices, external viewing locations, and incorporation into early childhood education and care settings[3].

Guidelines established by the American Academy of Pediatrics (AAP) in 2016 advocated restricting screen time for children aged 2–5 years to 1 hour per day of high-quality programs, with a parallel recommendation for parents to regulate screen time for children aged 6 years and older[4]. The American Academy of Child and Adolescent Psychiatry (AACAP) recommends limiting screen time for children: until 18 months, only for video chatting with an adult; between 18 and 24 months, restricted to educational programming with a caregiver; for ages 2–5 years, cap noneducational screen time to about 1 hour per weekday and 3 hours on weekends; and for ages 6 years and older, advocate for healthy habits while limiting screen-related activities[5] (Fig. 1). It is crucial to note that these are guidelines, not strict rules, and emphasize the quality of screen time content. Longitudinal studies underscore a concerning escalation in screen time, particularly television viewing, as early as 1 year of age. Notably, children who initially experienced less than 1 hour of screen time per day at 14 months exhibited a noteworthy increase to over 2 hours per day by the age of 30 months[6]. A Japanese study further highlighted alarmingly high percentages of children, aged 18 months and 30 months, engaging in prolonged TV viewing[7].

Figure 1.

A comprehensive overview of screen time recommendations for children, illustrating age-specific guidelines (created with biorender.com).

The ubiquity of electronic screens plays a pivotal role as a socioeconomic factor in early childhood development. The effects of screen-based devices on cognitive abilities in children are dual-faceted, with the potential to enhance education and learning, as evidenced by the positive impact of electronic books and reading applications^[8-10^]. However, this potential benefit is often overshadowed by concerns about the content consumed and the context of screen use[8]. Despite the potential benefits offered by newer interactive screen-based devices, a well-documented association exists between excessive use of such devices in young children and adverse consequences. These consequences encompass cognitive and social/emotional delays, diminished physical activity, increased energy intake, compromised sleep quality, and a heightened risk of obesity^[11,12^]. Research has demonstrated the disruptive impact of screen time on sleep patterns and circadian rhythms, thereby influencing brain restoration and melatonin production[13]. The blue light emitted from screens can interfere with melatonin production, making it harder to fall asleep[14]. Additionally, screen time has been correlated with diminished or aberrant white matter brain integration and underdeveloped frontal lobes[15]. Individuals with elevated screen usage exhibit a twofold increase in the likelihood of being diagnosed with anxiety and depression compared to those with lower usage[16]. Moreover, heightened screen exposure is linked to elevated levels of psychiatric disturbances. Both the regulation of serotonin and alterations in amygdala function have been implicated in the context of screen time[17]. The amygdala plays a role in emotional processing, and disruptions to its function can contribute to anxiety and mood disorders[18].

Recent investigations, including a study examining the impact of the COVID-19 pandemic on adolescents with autism spectrum disorder, have disclosed a significant surge in both weekday and weekend screen time[19]. Autism spectrum disorder (ASD), a disorder characterized by impaired social skills, affects one in 44 children, with a higher prevalence among boys^[20,21^]. While no singular cause of autism has been conclusively identified, a complex interplay of genetic and environmental factors is suggested[22]. Research into the role of environmental factors, including screen time, in the development or exacerbation of ASD symptoms is ongoing[23].

This literature review seeks to examine the current body of knowledge on the association between screen time and ASD. Additionally, it aims to evaluate the methodologies employed in extant literature, critically analyzing its limitations, and providing recommendations for future studies. The review also addresses the essential measures that healthcare practitioners should undertake to enhance understanding and contribute to improvements in this field. It’s important to investigate not just how much screen time is used, but what type of content is being consumed, and how it is being used (e.g., passively watching vs. actively engaging).

Methods

An extensive literature search was conducted across PubMed, Web of Science, and Google Scholar to identify studies examining the relationship between screen time and ASD symptoms. The search employed a range of keyword combinations, including “autism spectrum disorder,” “screen time,” “digital media,” “child development,” and “neurodevelopmental disorders.” The inclusion criteria focused on studies published up to December 2023, specifically investigating the impact of screen time on ASD symptoms. No restrictions were placed on the study design to allow for a comprehensive selection of relevant literature. Each study was carefully reviewed, with methodologies and findings critically evaluated to extract information aligned with the research objectives. The most relevant results were incorporated into the review to provide a nuanced understanding of the potential associations between screen time exposure and ASD symptoms.

Possible mechanism

Mechanism of ASD

Mutations linked to the Wingless-Related Integration Site (WNT) signaling pathway, including genes like Catenin Beta-1 (CTNNB1) and Chromodomain Helicase DNA Binding Protein 8 (CHD8), are implicated in ASD. Additionally, disruptions in Ras and Mechanistic Target of Rapamycin (MTOR) signaling pathways of mRNA translation lead to an increase in protein synthesis, resulting in a change in synaptic plasticity associated with ASD. Moreover, abnormalities in transcriptional regulators such as MECP2 are also associated with ASD[24]. MECP2 regulates transcription by interacting with both transcriptional activators and chromatin. Mutations in this gene lead to Rett syndrome, which predominantly affects females and manifests with symptoms of autism spectrum disorder[25]. Mutations in Myocyte Enhancer Factor 2 (MEF2), Forkhead Box O (FOXO), Nuclear Factor of Activated T Cells (NFAT), Voltage-Gated Calcium Channel 1.2 (Ca(v)1.2), and cAMP Response Element-Binding Protein (CREB) genes are linked to Timothy syndrome, which is also associated with ASD^[26,27^]. Mutations in the Tuberous Sclerosis Complex 1/2 (TSC1/2) complex lead to tuberous sclerosis, a condition associated with intellectual deficits and ASD. The TSC1/2 complex, comprising TSC2, a Guanosine Triphosphatase (GTPase) activating protein, and TSC1, a regulator of TSC2, is responsible for inhibiting protein synthesis. Disruption of this regulatory mechanism results in uncontrolled protein synthesis and unchecked cell growth^[28,29^]. In mice, autism spectrum disorder is associated with mutations in the SH3 and Multiple Ankyrin Repeat Domains 3 (SHANK3 gene), which codes for scaffolding proteins in the postsynaptic membrane[30].

Epigenetic modifications, including DNA methylation and histone acetylation, are also connected to ASD. Elevated methylation of the oxytocin receptor gene (OXT), or the MECP2 receptor is linked to ASD. In addition to DNA methylation, ASD is connected to changes in histone acetylation[31]. Exposure to valproate during prenatal development increases the likelihood of ASD in children, potentially through its involvement in inhibiting histone deacetylases and promoting histone acetylation.[32].

Noncoding mRNA, such as microRNA (miRNA), plays a role in post-transcriptional modifications of protein synthesis, and disturbances in these miRNAs are associated with ASD. Dysregulation of miR-664a-3p, miR-424-5p, miR-197-5p, and miR-500a-5p is observed in children with autism spectrum disorder and these miRNAs have the potential to serve as readily accessible biomarkers for ASD. A diagnostic molecular test, testing for miR-197-5p and miR-500a-50 en bloc would yield the highest specificity and sensitivity[33]. Addressing dysfunctional miRNAs through miRNA-based therapy, which seeks to decrease the activity of these malfunctioning miRNAs, holds promise as a potential treatment approach for autism spectrum disorder[24].

The intricate interplay of genetic factors associated with ASD disrupts the fragile equilibrium between excitatory and inhibitory (E/I) neurotransmission at the cellular level, leading to dysfunction in circuits across multiple brain regions[34]. Heightened excitability observed in the brains of individuals with ASD is linked to increased signaling through glutamate receptors[35]. Additionally, imbalances between E/I processes can result from developmental abnormalities in inhibitory circuits, including γ-aminobutyric acid (GABA) receptors, GABAergic synaptic transmission, and the maturation of GABAergic interneurons[36]. Examinations of post-mortem samples from individuals diagnosed with ASD reveal constricted minicolumns and modified neuropil space, indicating disruptions in inhibitory circuits[37]. Magnetic Resonance Spectroscopy (MRS) studies demonstrate diminished levels of GABA in the sensorimotor areas of individuals with ASD, correlating with indicators of inhibited behavior[38].

The transition from depolarizing to hyperpolarizing GABA during brain maturation is overseen by oxytocin and involves changes in the expression of Sodium-Potassium-Chloride Cotransporter 1 (NKCC1) and Potassium-Chloride Cotransporter 2 (KCC2), resulting in a gradual reduction in intracellular chloride concentration in GABA-sensitive neurons[39]. Investigations in autism spectrum disorder animal models suggest persistent excitatory effects of GABA and irregularities in NKCC1 and KCC2 in specific brain regions, such as the hippocampus, revealing immature characteristics of GABA signaling[40]. Elevated levels of glutamate in the blood and platelets of individuals with ASD suggest heightened excitation, though a direct impairment of glutamatergic transmission cannot be dismissed[41]. Disrupted expression of the glutamate transporter-1 (GLT-1) and compromised glutamate uptake contribute to the disorder’s pathogenesis, with the absence of GLT-1 resulting in synaptic over-excitability and pathological behaviors[42].

The manifestation of ASD symptoms coincides with synaptic maturation, underscoring the significance of synaptic connections in the disorder’s pathophysiology. Both human and animal research have confirmed that autism spectrum disorder is characterized by arrested synaptic development, as evidenced by an increased prevalence of slender, disrupted, and immature dendritic spines. Additionally, individuals with ASD exhibit elevated mutation rates in genes governing synaptic structure and function[35].

Metabolic disorders, such as depletion of pyridoxal-5-phosphate and phenylketonuria, have an impact on GABAergic and glutamatergic transmission[36]. Immune dysfunctions, characterized by increased autoantibodies against brain-specific proteins (e.g., human myelin basic protein, glial fibrillary acidic protein, neuro-axon filament protein, etc.), abnormal levels of immunoglobulins, and maternal immune activation, contribute to neuroinflammation in autism spectrum disorder. ASD is marked by a pro-inflammatory cytokine pattern, with heightened levels of Interleukin-1 (IL-1) and IL-6 associated with regression, and elevated levels of IL-5 and IL-17[43]. The pro-inflammatory pattern is also influenced by molecules related to the oxidative stress response, mitochondrial system function, and gastrointestinal pathways^[44,45^].

Mechanism of excessive screen time

Examining the hereditary patterns and molecular mechanisms associated with prolonged screen time is crucial for comprehending its impact on brain development. The genetic basis of preferences for screen time lacks comprehensive documentation in the current literature, emphasizing the need for a thorough investigation into the genes involved and their influence on the molecular processes responsible for excessive screen time. Despite this gap, we present some existing literature findings that aim to elucidate the connection between the heritable aspects of prolonged screen time and its presence within families.

In behavioral genetics research, assessing the similarity between twins aids in estimating the heritability of certain behavioral traits[46]. This method helps establish that the resemblances observed between individuals are more likely attributable to genetic factors rather than environmental ones, though environmental factors are not entirely disregarded. For instance, the heritability of text message frequencies in twins has been reported as 53% in one sample and 50% in another, challenging the common assumption that consumer behavior, exemplified by mobile phone use in this case, is solely shaped by cultural and environmental factors, with no consideration of genetic contributions[47].

Prolonged screen time has a substantial impact on brain development, influencing neurotransmitter release and function, modifying synaptic plasticity, and causing disturbances in neural connectivity. Nuclear imaging results underscore the connection between internet addiction and irregularities in brain dopaminergic systems, indicating that dysregulation of the prefrontal cortex might play a role in the uncontrollable behaviors linked to excessive internet use. This functional change mirrors patterns seen in substance abuse and manifests in brain regions crucial for cognitive control in maintaining a balance between sensitivity to rewards and punishments[48]. Functional magnetic resonance imaging studies indicate structural changes in individuals with internet gaming disorder, reflecting reduced gray matter volume in regions crucial for attention, motor coordination, and executive function. Moreover, lower white matter measures impact serotonin and dopamine-dependent decision-making, behavioral inhibition, and emotional regulation[49].

The dysregulation of neurotransmitter systems, particularly dopamine, is evident in individuals experiencing addiction to digital media, as evidenced by significantly elevated peripheral blood dopamine levels observed in adolescents with internet addiction[50]. Additionally, reward-related circuitry associated with digital addiction affects dopamine pathways in the brain. Concurrently, deficiencies in vitamin D and melatonin, brought about by prolonged digital exposure, disrupt serotonin regulation[48]. Studies on urban left-behind children addicted to the internet reveal deficiencies in several neurotransmitters, including dopamine, acetylcholine, GABA, and serotonin, leading to a range of abnormal behavioral patterns[51]. Ultimately, this neurotransmitter imbalance contributes to issues such as obesity, sleep problems, depression, anxiety, and addiction, resulting from altered reward sensitivity and disturbed circadian rhythms[52].

Repetitive use of touchscreens brings about changes in the processing of sensations in fingertips and consistently molds cortical processing through digital media engagement. Concerns arise regarding potential adverse effects on face recognition and processing due to the competition for cortical space. Extensive use of digital media in early childhood is linked to poorer microstructural integrity of white-matter tracts, diminished executive functions, and literacy abilities[53]. Furthermore, digital media usage is associated with reduced functional connectivity within the language network, suggesting heightened strain on the language network due to visual stimuli. Intensive engagement with social media is correlated with alterations in gray matter in brain regions involved in addictive behavior. Prolonged screen time, especially on social media, diminishes connectivity among subcortical, frontal, and parietal areas, impacting attentional networks and impulse regulation. These abnormalities in neural circuitry are connected with attention problems and difficulties in regulating impulses, underscoring the profound and multifaceted impact of excessive screen time on the developing brain[54].

Commonalities and interactions

Understanding the shared genetic factors and molecular pathways connecting autism spectrum disorder and a proclivity for excessive screen time is crucial for elucidating the developmental interactions between ASD and excessive screen time. By investigating these missing connections, it becomes possible to identify potential dual risks and disruptions in neurobiological pathways that contribute to ASD development within the framework of screen time. The genetic foundation of autism spectrum disorder involves a network of genes, including brain-derived neurotrophic factor (BDNF), Methyl CpG Binding Protein 2 (MECP2), GABA, and RING Finger Protein 2 (RFN2). During infancy, a period marked by rapid brain development, external factors such as light stimulation, microwave irradiation, and low- or high-frequency electrical stimulation can activate receptors associated with these genes. The stimulation of these receptors is implicated in the manifestation of symptoms of ASD[55].

The polygenic risk score (PRS) is a method that helps elucidate the genetic susceptibility to neurodevelopmental disorders in infancy arising from prolonged screen exposure. PRS serves as a genetic tool facilitating associations among genes associated with different traits, behaviors, and diseases, indicating potential dual-risk relationships[56]. The PRS for ASD (ASD–PRS) has demonstrated a link with both moderate and extended screen time in children. In simpler terms, children at a higher risk for autism spectrum disorder tend to spend more time in front of screens. While this does not necessarily imply that screen time causes autism, it highlights the genetic connection between the two, suggesting that excessive screen time may serve as an early indicator for autism spectrum disorder. This information can be valuable in developing robust diagnostic protocols for ASD[57].

Both oxytocin and the serotonin 1b receptor gene are identified as susceptibility loci for ASD. Oxytocin levels are linked to social impairments in individuals with autism[58]. Additionally, the decrease in serotonin binding in the anterior and posterior cingulate cortices is associated with impaired social cognition in individuals with ASD. A notable correlation exists between repetitive or obsessive behaviors and interests and the reduction of serotonin transporter binding in the thalamus[59]. Children diagnosed with autism spectrum disorder display lower serum vitamin D and higher serotonin levels in their blood compared to healthy children[60]. It is theorized that the vitamin D hormone (calcitriol) activates the transcription of the serotonin-synthesizing gene tryptophan hydroxylase 2 (TPH2) in the brain at a vitamin D response element (VDRE) and represses the transcription of Tryptophan Hydroxylase 1 (TPH1) in tissues outside the blood-brain barrier at a distinct VDRE, providing an explanation for these levels[61]. Deficiencies in serotonin levels have also been observed with excessive screen time, attributed to reduced daylight activity. This interplay between oxytocin and serotonin in the context of both excessive screen time and ASD suggests that excessive screen time may exacerbate neurotransmitter abnormalities in children with ASD.

In summary, the shared neurobiological pathways seen in both ASD and excessive screen time, involving alterations in oxytocin and serotonin, are preliminary evidence that ASD and excessive screen time are interrelated. This highlights the necessity for a more in-depth exploration of the complex interplay among genetic and molecular predispositions, environmental influences, and the impact of prolonged screen time in the context of ASD.

Rapid review of existing studies

To rapidly review the existing literature on the association between autism in children and screen time, extensive research of relevant studies was conducted via PubMed, Web of Science, and Google Scholar databases. The search strategy was set to retrieve studies published within the last two decades. The keywords “Screentime, Autism, Children with Autism symptoms about Screentime, Screen usage among children, children, and screentime, hours children spend watching screens, guidelines for screentime for children, recent analysis on the use of screentime among children” and Boolean operators of “and, or, ‘’, ()” were utilized to enhance precision. Initial title and abstract screening were conducted to identify studies that meet the inclusion criteria, which included original studies primarily focusing on Autistic children and screen time use. Subsequently, full-text articles corresponding to the selected studies were retrieved for further critical evaluation. The present review has established specific exclusion criteria to ensure the integrity of the study. These criteria comprise studies that are irrelevant to the scope of the review as well as those that are not published in the English language. The rigidity of these criteria is intended to preserve the accuracy and credibility of the study’s findings. Table 1 summarizes key studies investigating the relationship between screen time and autism spectrum disorder symptoms across various populations and study designs.

Table 1.

Overview of key studies investigating the relationship between screen time exposure and autism spectrum disorder symptoms

Author	Title	Type of study	Study design	Conclusion
Sadeghi et al (2023)	Associations between symptom severity of autism spectrum disorder and screen time among toddlers aged 16 to 36 months	Cross-sectional study	Study focus: Analyzing sociodemographic variables through correlation analyses (Pearson’s correlations and multiple regression analyses) within the initial 36 months of life.	The study suggests that heightened screen time is associated with decreased social interaction, resulting in an elevated likelihood of children displaying symptoms associated with autism spectrum disorder.
			Sample size: 68 Iranian toddlers aged up to 36 months.
			Screen time Variables: investigated the impact of foreground, background, and overall social interaction on screen time.
Geng et al 2023	Association between screen time and suspected developmental coordination disorder in preschoolers: A national population-based study in China	Retrospective cohort study	Utilizing the Chinese National Cohort of Motor Development’s national retrospective cohort design, the study involved a stratified population sample of 188 814 children. Motor performance was assessed using a concise developmental coordination disorder questionnaire.	The study has identified a negative correlation between screen time and motor control, with the most significant connection observed when individuals are exposed to screens before bedtime.
Takahashi et al (2023)	Screen time at age 1 year and communication and developmental delay at 2 and 4 years	Prospective cohort study	The study, conducted from July 2013 to March 2017 at the Tohoku Medical Megabank Project, gathered prospective data from 50 prenatal clinics involving 7097 mother–child pairs.	There was an association between increased screen time for children at 1 year of age with problem-solving abilities in communication and developmental delays at 2 and 4 years of age.
Al Hosani et al (2023)	Screen time and speech and language delay in children aged 12–48 months in UAE: a case–control study	Case-control study	The study involved 227 children with language delay and 227 typically developing peers, aged 12–48 months, in a UAE preschool. Language delay was assessed using the Receptive Expressive Emergent Language Test (RELT).	The study concluded that usage of electronic devices and screens at 12–24 months leads to language delays.
				It also added that watching television and the mother’s level of education were less likely interlinked.
McArthur et al (2022)	Screen time and developmental behavioral outcomes for preschool children	Observational cohort study	The study comprises 1994 Canadian children and their parents. At 36 months, maternal reports were utilized to assess children’s screen time (hours per day), behavior problems, developmental milestones, and vocabulary acquisition. Socio-demographic factors and baseline performance at 24 months were considered.	The study concluded that there is an association between children’s screen time duration and poor child developmental, language, and behavioral outcomes.
Kushima et al (2022)	Association between screen time exposure in children at 1 year of age and autism spectrum disorder at 3 years of age. The Japan Environment and Children’s Study	Observational cohort study	The study utilizes a birth cohort design in Japan to explore the link between early childhood autism, screen exposure, and autism spectrum disorder-specific brain changes. Data are sourced from the Japan Environment and Children’s Study, involving 84 030 mother–child dyads. Following WHO and American Academy of Pediatrics guidelines, 15 regional centers collaborate to assess screen exposure from age 1 and Autism development by age 3. Methods involve questionnaire scoring based on ages and stages.	The study concludes that screen time exposure at an early stage can lead to progressive autism spectrum disorder at year 3 with prevalence among boys.
Lu et al (2022)	The association between autistic traits and excessive smartphone use in Chinese college students: The chain mediating roles of social interaction anxiety and loneliness. Research in Developmental Disabilities.	Cross-sectional study	Study was done in Guangdong province in southern China from November 2020 to January 2021. recruited 1103 college students and after providing their informed consent, the participants were asked to complete an anonymous self-report questionnaire that measured the degrees of autistic traits, social interaction anxiety, loneliness, and excessive smartphone use.	Study suggests that more autistic traits were correlated with higher levels of social interaction anxiety and higher levels of loneliness that were found to be associated with excessive smartphone use.
Chen et al (2021)	Screen time and autistic-like behaviors among preschool children in China	Observational cohort study	Utilizing data from the 2017 Longhua Child Cohort Study in Shenzhen, China, the study involves 29 461 child–caregiver pairs. Data collection relies on questionnaires, encompassing sociodemographic variables, screen time exposure details, and Autism Behavior checklist for measuring autism behaviors. Covariates are also incorporated into the dataset.	Electronic screen time causes a higher risk of autism spectrum disorder-like behaviors.
Fridberg et al 2021	watching videos and television is related to a lower development of complex language comprehension in young children with autism	Observational cohort study	Utilizing a language therapy app, data from 3,225 children aged 6 months or older is analyzed. Five orthogonal measures are assessed through various checklists every three months, including the Autism Treatment Evaluation Checklist and Screen Time Assessment. Testing involves evaluations of expressive and receptive language, as well as video and television watching time.	This study found that children with autism spectrum disorder who watch TV have more severe receptive language symptoms and show improvement in expressive language, but this difference was not significant at 36 months.
Alrahili et al (2021)	the association between screen time exposure and autism spectrum disorder-like symptoms in children	Cross-sectional study	The study assesses the association between screen time and social skill development using a 40-item parent-reported scale, the Arabic version of the Social Communication Questionnaire. The population comprises 306 children aged 4 to 6 years, with exclusions for non-Arabic speakers or those with existing autism. The SCQ demonstrates good sensitivity (0.796), specificity (0.966), and reliability (Cronbach’s alpha, 0.916).	The study found a positive correlation between daily device use and autism spectrum disorder-like symptoms (SCQ score > 15).
Dong et al (2021)	Screen time and autism: current situation and risk factors for screen time among preschool children with autism spectrum disorder	Cross-sectional study	The study recruited 193 children with autism spectrum disorder, collecting sociodemographic and screen time data through questionnaires. Autism core symptoms and developmental quotient were assessed using the Autism Behavior Checklist, Childhood Autism Rating Scale, Autism Diagnostic Observation Schedule-Second Edition, Griffiths Development Scales-Chinese Language Edition, and Chinese Children’s Parent–Child Relationship Questionnaire. Correlations between autism spectrum disorder children’s screen time and assessment scores (ABC, CARS, ADOS, GDS-C DQs, CPCIS) were analyzed.	Excessive screen time is related to autism spectrum disorder-like symptoms, DQ, and decreased parent–child interaction
Subir pal et al (2021)	Delayed speech in toddler associated with increase screen time	Observational cohort study	This study was conducted for the children attending the outpatient Department in private chamber for consultation in West Bengal during December 2015 to December 2020. The children of 18 months to 30 months with delayed speech were included in this study. Daily mobile media used by the kids and the parents were noted. Normal speech development and red flags were assessed and diagnostic evaluation including audiometry and additional tests if needed.	The study concludes that there is a significant association between the use of electronic devices and delayed speech.
Dong et al (2021)	Correlation between screen time and autistic symptoms as well as development quotients in children with autism spectrum disorder	Cross-section study	This study compares screen time of 101 children with autism spectrum disorder and 57 typically developing (TD) children. A correlation analysis was done to enunciate the correlation between the screen exposure time and the autism spectrum disorder-related scale scores and DQ of the Gesell Developmental Schedules (GDS) of autism spectrum disorder children. autism spectrum disorder group was further into subgroups according to their age, screen time and analyzed.	The screen time is associated with autism-like symptoms and with developmental quotient. The longer the screen time, the more severe is autistic spectrum disorder. (especially sensory symptoms), and the developmental delay, especially in autism spectrum disorder children with longer screen time and younger age, particularly in the language domain.
Heffler et al (2020)	Association of Early-life social and digital media experiences with development of autism spectrum disorder-like symptoms	Observational cohort study	The study explores correlations between early screen exposure, parental engagement, perinatal, and demographic factors with Autism risk using data from the National Children’s Study. The population sample comprises children born between 1 October 2010, and 31 October 2012. Utilizing a public archive dataset, study factors were evaluated at 12 and 18 months, with Autism measured through a Modified Checklist for Autism in Toddlers.	Excessive screen exposure early in life is associated with autism spectrum disorder like symptoms.
Hill et al 2020 al., 2020)	Screen time in 36-month-olds at increased likelihood for autism spectrum disorder and ADHD	Cross-sectional study	The study examines children with a family history of Autism, potentially at risk for developmental delays, following American Academy of Pediatrics guidelines. Ethical approval and participant consent were obtained for a cross-sectional analysis involving 120 children at 36 months, categorized by diagnostic status. Methodologies encompass parent-reported screen time hours, Mullen scales of early learning, and Autism Diagnostic Observation Schedules.	Children with autism spectrum disorder had intermediate screen time levels, while those with elevated ADHD symptoms spent more time on screens than the Comparison group.
Engelhardt et al (2013)	Media use and sleep among boys with autism spectrum disorder, ADHD, or typical development	Observational comparative study	The study compared the impact of pronouns on children with Autism (49 participants) to neurotypical children (79 participants out of 128 males). Data collection involved demographic, history, and social communication questionnaires focusing on autism spectrum disorder-related symptoms.	The findings suggest that media may play a crucial role in sleep disturbances among children with autism spectrum disorder.

Role of health care personnel

Children with autism spectrum disorder engage with various health professionals, such as physicians, psychiatrists, psychologists, occupational therapists (OTs), and speech-language therapists (SLTs), each playing distinct roles in addressing the intricate challenges faced by individuals with ASD[62]. Collaboration among specialists is common throughout the diagnostic process. This coordination facilitates a comprehensive assessment and emphasizes the importance of a multi-disciplinary approach to cater to the unique needs of children with ASD (Fig. 2) ^[63,64^].

Figure 2.

A summarized framework depicting the role of healthcare professionals in managing autism spectrum disorder and regulating screen time in children (created with Microsoft PowerPoint and flaticon.com).

The collaborative efforts of healthcare professionals further enhance program efficacy and consistency, ensuring a holistic approach to language development that minimizes the dependence on screen-based communication in children.

Implementing these strategies for regulating screen time in children presents several challenges. One challenge lies in overcoming the diverse contributing factors identified, such as lower parental education, limited oversight, and the use of screens as a parenting tool. Collaborative planning involving a multidisciplinary team requires effective communication and coordination among healthcare professionals, which can be challenging to achieve consistently. Moreover, ensuring parents’ active participation in educational programs and sustaining their commitment to screen time limitations at home requires ongoing support and reinforcement. Balancing the goal of reducing screen time while promoting creativity, connection, and engagement introduces complexities that necessitate careful consideration and strategy adjustments.

Figure 2 illustrates strategies for regulating screen time in children.

Conclusion

The increasing prevalence of screen time and its intersection with ASD in children presents a complex challenge with multiple dimensions. This situation highlights the dual nature of screen time, offering educational advantages while posing risks for adverse developmental outcomes. Certain research suggests a connection between prolonged screen time exposure and the emergence of symptoms associated with ASD in children. Conversely, other studies propose a reciprocal influence, indicating that children with autism spectrum disorder might be predisposed to isolation, leading to an elevated amount of time spent on screens.

To unravel this intricate relationship, future investigations should concentrate on establishing precise associations, including causal relationships, between genetic, molecular, and environmental factors that influence both screen usage and ASD exacerbation. This approach is crucial for developing targeted interventions that harness the positive aspects of screen time while minimizing potential risks. A balanced perspective on screen time in the context of ASD is urgently needed. Recognizing the potential benefits of digital media is essential, but equal attention must be given to preventing its excessive use. Implementing strategies to ensure that children’s screen time contributes to their overall development and well-being is of paramount importance.

Ethical approval

Ethics approval was not required for this review.

Consent

Informed consent was not required for this review.

Sources of funding

None.

Author contributions

The authors confirm contribution to the paper as follows: study conception and design: A.A., A.D.; data collection: A.D., A.A., C.S.S., M.H.K., F.M., Y.M., P.K.S., A.V., A.A.; analysis and interpretation of results: A.D., A.A., C.S.S., M.H.K., F.M., Y.M., P.K.S., A.V., A.A.; draft manuscript preparation: A.D., A.A., C.S.S., M.H.K., F.M., Y.M., P.K.S., A.V., A.K.S., A.A.. All authors reviewed the results and approved the final version of the manuscript.

Conflicts of interest disclosure

None.

Guarantor

Anum Akbar.

Research Registration Unique Identifying Number (UIN)

Not applicable.

Provenance and peer review

Not applicable.