Increase In Prevalence Of Autism Spectrum Disorders Research Articles

Large increase in ASD prevalence in Israel between 2017 and 2021.

Accurate estimation of annual changes in autism spectrum disorders (ASD) prevalence is critical for planning the expansion of diagnostic, education, and intervention services at an adequate rate. Previous studies from Israel have reported that ASD prevalence among 8-year-old children has increased from estimates of 0.3% in 2008 to 0.65% in 2015 and 1.3% in 2018. Here, we analyzed data acquired from the National Insurance Institute of Israeli (NII), a governmental organization that approves and monitors all ASD children who receive welfare services in Israel, and Clalit Health Services (CHS), the largest Health Maintenance Organization in Israel that provides health services to ~52% of the population. Data from both sources included annual data files from 2017 to 2021 containing the number of ASD cases per year of birth for 1-17-year-old children. This allowed us to estimate annual ASD prevalence among 3.5 million children born between 2000 and 2020 in Israel. Both data sources revealed a nearly two-fold increase in ASD prevalence among 1-17-year-old children from 2017 to 2021. Estimated prevalence rates differed across age groups with 2-3-year-old (day-care) children increasing from 0.27% to 1.19% (>4 fold change), 4-6-year-old (pre-school) children increasing from 0.8% to 1.83%, and 8-year-old children increasing from 0.82% to 1.56% in NII data. These results demonstrate that autism prevalence continues to increase in Israel with a shift towards diagnosis at earlier ages. These findings highlight the challenge facing health and education service providers in meeting the needs of a rapidly growing autism population.

Factors in Infancy That May Predict Autism Spectrum Disorder.

The global increase in the prevalence of ASD (Autism Spectrum Disorder) is of great medical importance, but the reasons for this increase are still unknown. This study sought to identify possible early contributing factors in children who were later diagnosed with ASD. In this retrospective cohort study, postnatal records of 1105 children diagnosed with ASD were analyzed to determine if any signs of ASD could be found in a large database of births and well-baby care programs. We compared the recordings of typically developing children and analyzed the differences statistically. Rapid increases in weight, height, and head circumference during early infancy predict the development of ASD. In addition, low birth weight, older maternal age, and increased weight and height percentiles at six months of age together predict the development of ASD. At two years of age, these four parameters, in addition to impaired motor development, can also predict the development of ASD. These results suggest that the recent increase in ASD prevalence is associated with the "obesity epidemic" and with recommendations of supine sleeping to prevent Sudden Infant Death Syndrome, associated with atypical neural network development in the brain.

Beslenme Yaklaşımlarının ve Besin Takviyelerinin Otizm Üzerindeki Etkileri

ASDs (Autism Spectrum Disorders); is a neurodevelopmental disorder in which the symptoms and effects are different in each individual and there is an increase in prevalence worldwide. The increase in ASDs prevalence may be due to the increase in diagnostic criteria. The causes of ASDs are thought to be genetic, environmental and neurobiological factors. In recent years, studies have been conducted on the effect of dietary approaches on improving ASDs symptoms. Researchers are studying on dietary approaches based on the interaction between the brain and the gut. This review includes studies on the most popular dietary approach, the gluten-free and casein-free diet, and the effects of Omega 3, vitamin D, vitamin B12, folic acid and probiotic supplements on ASDs core symptoms. The results of the studies are evaluated according to special ASDs symptom criteria scores. The limited number of studies, the low number of participants in some studies and the lack of significant improvements are seen as limiting aspects of the studies.

Prenatal stress and fluoxetine exposure in mice differentially affect repetitive behaviors and synaptic plasticity in adult male and female offspring

Autism spectrum disorder (ASD) is characterized by social communication impairments with restricted and repetitive behaviors (RRBs). The increase in prevalence of ASD and the heterogeneity of symptom severity may arise from a complex interaction of environmental and genetic factors that alter synaptic plasticity. Maternal stress during pregnancy, which is linked to depression, may be one risk factor for an ASD phenotype in offspring. Selective serotonin reuptake inhibitor (SSRI) treatment can be effective in alleviating maternal depression but prenatal SSRI exposure itself may be a risk factor for autism in offspring. The present study investigated in C57BL/6J pregnant mice whether restraint stress (G4–18) and/or treatment with the SSRI fluoxetine (G8–18) affects autism-related behaviors and hippocampal synaptic plasticity in male and female offspring. The findings indicate that restraint stress reduces preference for sucrose reward in pregnant dams that is reversed by fluoxetine. In adult male offspring, combined prenatal stress and SSRI exposure increased self-grooming and impaired spatial reversal learning. In adult female offspring, the prenatal experiences did not affect self-grooming, but restraint stress alone or SSRI exposure alone impaired spatial reversal learning. Prenatal stress reduced anxiety-related behavior in male and female offspring. Further, LTP induced by theta-burst stimulation of Schaffer-commissural afferents in field CA1 was significantly reduced in female offspring exposed to prenatal stress alone or combination with fluoxetine. Together, these findings suggest that exposure to prenatal stress, SSRI treatment or the combination differentially affects male and female offspring in autism-like behaviors and synaptic plasticity.

Autism Spectrum Disorder.

1. Melissa Long, MD* 2. Kelly Register-Brown, MD, MSc† 1. *Division of General and Community Pediatrics 2. †Division of Psychiatry and Behavioral Health Sciences, Children’s National Hospital, Washington, DC * Abbreviations: AAP: : American Academy of Pediatrics ABA: : applied behavior analysis ADHD: : attention-deficit/hyperactivity disorder ASD: : autism spectrum disorder CBD: : cannabidiol CDC: : Centers for Disease Control and Prevention COVID-19: : coronavirus disease 2019 DSM-5 : : Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition EEG: : electroencephalogram FDA: : Food and Drug Administration ID: : intellectual disability MCHAT-R/F: : Modified Checklist for Autism in Toddlers, Revised, with Follow-up With autism spectrum disorder (ASD) prevalence rising and a shortage of specialists available for diagnosis and management, pediatricians will need to be increasingly comfortable 1) giving a provisional diagnosis of ASD to create access to critical early behavioral interventions, 2) managing the comorbidities that significantly affect quality of life, and 3) supporting families to navigate the increasingly complex web of ASD-related services. After completing this article, readers should be able to: 1. Appreciate the evolution in prevalence data over time and recognize the disparities that exist in diagnosis based on race and sex. 2. Recognize the heterogeneity of autism spectrum disorder (ASD) clinical presentation depending on the child’s age, sex, and developmental abilities. 3. Understand the diagnostic criteria for ASD. 4. Distinguish findings associated with ASD from those of isolated speech and language delay, intellectual disability, and profound hearing loss. 5. Determine age-appropriate screening for ASD and be prepared to discuss results and next steps with families. 6. Plan for appropriate management of core symptoms of ASD and identify the common medical and psychiatric comorbidities with ASD. 7. Recognize the complexity of care coordination required to support families of children with ASD and the importance of advocating for a pediatric medical home. Autism spectrum disorder (ASD) is a neurodevelopmental disability characterized by differences in social and communication functioning and by restricted and repetitive behaviors and interests. The increasing prevalence of ASD has been the subject of intense attention in the medical literature and lay press. In the United States, the Centers for Disease Control and Prevention (CDC) Autism and Developmental Disabilities Monitoring Network, which measures confirmed diagnoses of ASD, has found an increased prevalence of ASD among 8-year-old US children from 1 in 150 in 2000 to 2002 to 1 in 54 during 2016. (1) Reasons for the observed increase in ASD prevalence likely include increased screening …

Phenotypic overlap between atopic dermatitis and autism

BackgroundAutism, a childhood behavioral disorder, belongs to a large suite of diseases, collectively referred to as autism spectrum disorders (ASD). Though multifactorial in etiology, approximately 10% of ASD are associated with atopic dermatitis (AD). Moreover, ASD prevalence increases further as AD severity worsens, though these disorders share no common causative mutations. We assessed here the link between these two disorders in the standard, valproic acid mouse model of ASD. In prior studies, there was no evidence of skin involvement, but we hypothesized that cutaneous involvement could be detected in experiments conducted in BALB/c mice. BALB/c is an albino, laboratory-bred strain of the house mouse and is among the most widely used inbred strains used in animal experimentation.MethodsWe performed our studies in valproic acid (VPA)-treated BALB/c hairless mice, a standard mouse model of ASD. Mid-trimester pregnant mice received a single intraperitoneal injection of either valproic acid sodium salt dissolved in saline or saline alone on embryonic day 12.5 and were housed individually until postnatal day 21. Only the brain and epidermis appeared to be affected, while other tissues remain unchanged. At various postnatal time points, brain, skin and blood samples were obtained for histology and for quantitation of tissue sphingolipid content and cytokine levels.ResultsAD-like changes in ceramide content occurred by day one postpartum in both VPA-treated mouse skin and brain. The temporal co-emergence of AD and ASD, and the AD phenotype-dependent increase in ASD prevalence correlated with early appearance of cytokine markers (i.e., interleukin [IL]-4, 5, and 13), as well as mast cells in skin and brain. The high levels of interferon (IFN)γ not only in skin, but also in brain likely account for a significant decline in esterified very-long-chain N-acyl fatty acids in brain ceramides, again mimicking known IFNγ-induced changes in AD.ConclusionBaseline involvement of both AD and ASD could reflect concurrent neuro- and epidermal toxicity, possibly because both epidermis and neural tissues originate from the embryonic neuroectoderm. These studies illuminate the shared susceptibility of the brain and epidermis to a known neurotoxin, suggesting that the atopic diathesis could be extended to include ASD.

Prevalence and cumulative incidence of autism spectrum disorders and the patterns of co-occurring neurodevelopmental disorders in a total population sample of 5-year-old children

BackgroundsWhether there is a true increase in autism spectrum disorder (ASD) frequency or not remains unclear. Additionally, the rates of co-existing neurodevelopmental disorders (NDD) in a total population sample has not been fully examined before. Therefore, using a total population sample in Japan, we aimed to estimate the prevalence and cumulative incidence of autism spectrum disorder (ASD) annually, to determine whether there is a true increase in ASD prevalence by estimating the cumulative incidence of ASD annually, and to examine the rates of co-existing neurodevelopmental disorders (NDD).MethodIn this cross-sectional sequential design study, all 5-year-old children in the catchment area underwent the screening annually from the year 2013–2016. Screen-positive children were invited to participate in a comprehensive assessment, including child and parent interview, behavioral observation, and cognitive and motor function testing. All cases were reviewed by a multidisciplinary research team.ResultsCaregivers of 3954 children returned the screening, among which 559 children underwent the assessment with 87 children receiving an ASD diagnosis. Adjusted ASD prevalence was 3.22% (95% confidence interval (CI) 2.66–3.76%). The male to female ratio of the crude prevalence was 2.2:1. The cumulative incidence of ASD up to 5 years of age for the total study years was 1.31% (95% CI 1.00–1.62%). A generalized linear model revealed no significant linear trends in 5-year cumulative incidence over the study years. Only 11.5% of children had ASD alone; the remaining 88.5% were found to have at least one co-existing NDD.LimitationsModest sample size for a total population study.ConclusionsOur findings demonstrate the stability of the 5-year cumulative incidence of ASD, implying no true rise in ASD incident cases over the 4-year study period in the study catchment area. High rates of co-existing NDDs reflect the importance of investigating broad developmental challenges in children with ASD.

647 Basis for the link between atopic dermatitis and autism

A subset of patients with autism spectrum disorders (ASD) have a prior history of atopic dermatitis (AD). Moreover, the prevalence of ASD increases dramatically as AD phenotypes worsen. In a standard ASD animal model (parenteral administration of valproic acid [VPA] to second trimester pregnant mice), we explored the basis for the baseline association, and second, for the AD phenotype-dependent increase in ASD prevalence. At birth, VPA-treated mice demonstrated extensive neuro- and epidermal cytotoxicity, but no evidence of inflammation. Yet, by one-day post-partum, cutaneous inflammation became apparent, while in contrast, neuroinflammation did not appear until approximately 4 days post-partum. These histopathologic changes were paralleled by alterations in cutaneous, as well as brain lipid content and ultrastructural morphology, which mimicked comparable, well-known abnormalities in AD. The initial emergence of cytotoxicity was paralleled by elevated levels of TNFα, IL-17 and IFNγ in both tissues, but Th2 markers appeared initially in skin, and only later in brain, suggesting a skin⇒brain putative sequence. We conclude first, that the parallel susceptibility in both the brain and epidermis of VPA-induced cytotoxicity reflects their shared origin in the primitive neuroectoderm. Second, that the AD phenotype-‘driven’ increase in ASD prevalence reflects the prior development of Th2 inflammation in the skin, linking the additional, superimposed burden of xeric stress that occurs at birth, further amplifying cutaneous cytokine production. These studies could also explain why evidence of AD (1-3 months) precedes the earliest evidence of ASD (≥ 6 months). Finally, if ASD represents another end-point of the ‘atopic march;’ then it is possible that early treatment of subjects at risk for AD could prevent/mitigate the downstream development of ASD.

Annual trends in prevalence and incidence of autism spectrum disorders in Manitoba preschoolers and toddlers: 2004-2015.

Autism spectrum disorders (ASD) are among the leading causes of disabilities in children. We examined the annual prevalence and incidence rate of ASD between 2004 and 2015 in children aged 1 to 5years residing in Manitoba. A population-based study was conducted using the Manitoba Population Research Data Repository. The study included children aged 1 to 5years residing in Manitoba between 2004 and 2015. Standard identification algorithm was used to identify ASD cases from hospital abstracts and medical claims. Annual prevalence and incidence rates were calculated for the overall population and then stratified according to sex, region, and socio-economic status (SES). Multivariable negative binomial regression models, adjusted for sex, region, and SES, were used to examine changes in prevalence and incidence over study years. Among children aged 1 to 5years, 1685 ASD cases were diagnosed between 2004 and 2015. The crude ASD prevalence increased from 0.46% in 2004 to 0.97% in 2015 (p = 0.002). The crude incidence rate increased from 0.16% in 2004 to 0.39% in 2015 (p = 0.002). The increase in ASD prevalence and incidence was observed in all subgroups based on sex, region, and SES. The adjusted negative binomial model showed an annual relative risk increase, since 2004, for both prevalence and incidence of 1.69 (95% CI 1.56-1.83) and 1.84 (95% CI 1.62-2.09), respectively. During the period from 2004 to 2015, both prevalence and incidence rates of diagnosed ASD in preschoolers and toddlers residing in Manitoba increased significantly.

Prevalence and Treatment Patterns of Autism Spectrum Disorder in the United States, 2016

Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder. Previous surveys have reported a steady increase in ASD prevalence in US children over the past decades. Several behavioral therapies and medications have been developed to treat the symptoms of ASD; however, little is known about the current status of treatment usage for children diagnosed as having ASD. To estimate the prevalence and treatment patterns of ASD among US children using nationally representative data. This study used data from the 2016 National Survey of Children's Health, a nationwide, population-based, cross-sectional survey. We included 43 032 children aged 3 to 17 years. Data were collected through questionnaires completed by a parent or guardian. Data were analyzed from February 2018 to March 2018. Outcome variables included ASD diagnosed by a physician or health professional and the use of behavioral treatment or medication treatment among children with ASD. Of the 43 032 included participants, 22 072 (51.3%) were male, and the mean (SD) age was 10.7 (4.4) years. The weighted prevalence of ever-diagnosed ASD and current ASD were 2.79% (95% CI, 2.46-3.12) and 2.50% (95% CI, 2.21-2.79), respectively. The state-level prevalence of ever-diagnosed ASD varied from 1.54% (95% CI, 0.60-2.48) in Texas to 4.88% (95% CI, 2.72-7.05) in Florida. Nationally, about 70% of children with current ASD (70.5%; 95% CI, 65.1-75.8) were treated; 43.3% (95% CI, 37.4-49.2) received behavioral treatment only, 6.9% (95% CI, 3.7-10.1) received medication treatment only, and 20.3% (95% CI, 16.5-24.1) received both behavioral and medication treatments. The remaining 29.5% (95% CI, 24.2-34.9) of children with current ASD did not receive either behavioral or medication treatment. This study showed that the prevalence of ASD in the United States was relatively high, and it varied substantially across US states. Almost 30% of US children with ASD did not receive behavioral or medication treatment, which calls for a critical need to understand and address the barriers for those children to receive appropriate treatments.

The medical home for children with autism spectrum disorder: an essential element whose time has come.

The purpose of this review is to describe the role of the medical home in children with autism spectrum disorder (ASD). A high-quality medical home is essential, given the increase in prevalence of ASD and the array of services, community partners, specialists, therapists, and healthcare team members needed to care for this population. Providing care through the medical home model results in fewer unmet needs. Care coordination and integration are the aspects of the medical home currently most lacking. Navigating the healthcare landscape for children with ASD may be enhanced with patient navigators, integration of physical and behavioral health, and telehealth services. Children with ASD have an increased number of medical and mental health needs. Obtaining care via a medical home has been shown to decrease unmet healthcare needs. However, they are less likely to receive care through the medical home model compared with other children with special healthcare needs. Barriers identified by families include a lack of early identification, limited knowledge on educational plans, and unknown community resources. Barriers identified by providers include lack of time, training, and resources. Providing care coordination and family-centered care in a medical home model are essential for children with ASD.

Redesign of the autism spectrum screening and diagnostic process for children aged 12 to 36 months.

Diagnosing autism spectrum disorder (ASD) is challenging, resource-intense and time-consuming due to clinical and etiologic heterogeneity. With the rapid increase in prevalence of ASD, higher demand for diagnostic assessment often means long waitlists for families, and limited access to specialized intervention and support. In 2013, the Alberta Children's Hospital-Autism Spectrum Disorder Diagnostic Clinic (ACH-ASDC) experienced a significant waitlist in the 12 to 36 months' population. A Quality Improvement Project was started in 2014; one program aim was to create an efficient, sustainable and evidence-based ASD diagnostic evaluation process. The redesigned diagnostic process included: 1) pre- and postassessment parent information sessions, 2) a screening appointment and 3) standardized clinical appointment pathways. Within its first year, the new process reduced wait times to under a month without an increase in resources, leading to an efficient diagnostic process being sustained since its implementation.

Incompatibilities and seclusion of patients with an autism spectrum disorder detained in high-secure psychiatric care

Purpose Whilst individuals with an autism spectrum disorder (ASD) represent a relatively small proportion of patients detained in high-secure psychiatric care (HSPC), previous research suggests that such individuals present with difficulties and needs significantly different from non-ASD patient groups. However, to date, there has not been any formal examination of how individuals with an ASD are represented in records of key risk management actions (i.e. seclusions and incompatibilities with other patients). The paper aims to discuss these issues. Design/methodology/approach An observation of hospital data examining two key risk management actions for a group of individuals with an ASD is detained in one HSPC hospital. These include the number of formal incompatibilities with other patients and the number of, and hours in, seclusion. Both actions require extra staff and security provisions and can decelerate the rehabilitation and recovery process. Findings In addition to suggesting an overall increase in the general prevalence of ASD within the hospital compared to previous estimates, individuals with an ASD appear to have a disproportionately higher number of incompatibilities with other patients compared to those patients without an ASD and experience more and longer periods of seclusions. Originality/value Although the methodological limitations of the study are acknowledged, explanations for the findings are discussed along with future research and recommendations as to how ASD patients might be best managed in the hospital. It is argued that the findings add further support for a specialist ASD service within HSPC.

Les relations entre le bisphénol A et les troubles du spectre autistique se précisent : la sérotonine est-elle le lien manquant ?

The etiology of autism spectrum disorders (ASD) is believed to be multifactorial and to involve genetic and environmental components. Environmental chemical exposures are increasingly understood to be important in causing neurotoxicity in fetuses and newborns. Recent data from the Centers for Disease Control and Prevention in the United States suggest a substantial increase in ASD prevalence, only partly explicable by factors such as diagnostic substitution. Bisphenol A (BPA) is an ubiquitous xenoestrogen widely employed in a variety of consumer products including plastic and metal food and beverage containers, dental sealants and fillings, medical equipment and thermal receipts. Therefore, most people are exposed almost continuously to BPA in industrialized countries. Sources of BPA exposure are predominantly diet, but also through inhalation or dermal absorption. BPA can be measured in many human fluids and tissues including saliva, serum, urine, amniotic fluid, follicular fluid, placental tissue and breast milk. There is concern that BPA exposure may influence human brain development and may contribute to the increasing prevalence of neurodevelopmental and behavioural problems. Epigenetic mechanisms are suggested by a mouse study that demonstrated that BPA exposure during gestation had long lasting, transgenerational effects on social recognition. Previous epidemiological studies suggested a relationship between maternal BPA exposure and ASD. A recent study of 46 children with ASD and 52 controls found for the first time a direct association between children with ASD and BPA exposure and demonstrated that BPA is not metabolized well in children with ASD. The metabolomic analyses showed a correlation between ASD and essential amino acid metabolism pathways. Essential amino acids are precursors of neurotransmitters, for example tryptophan for serotonin. Fetal and prenatal BPA exposure was suggested to perturb the serotonergic system in rat and mice models. On the other hand, hyperserotonemia was reported in approximately one-third of autistic patients and also in relatives. Moreover, neuroimaging studies revealed two fundamentally different types of serotonin synthesis abnormality in children with autism compared to age-matched nonautistic children, a difference in whole-brain capacity and focal abnormalities. Finally, decreased serotonin transporter and serotonin receptor binding have been reported in both children and adults with autism. So, the link between BPA and autism could be a defect of the normal in utero or perinatal serotonergic system development. In France, BPA was banned in baby bottles in 2010 and in any food or beverage packaging since January 2015. Therefore, there is an urgent need to find safe alternatives in the use of BPA in the manufacture of industrial products.

Trends in the Prevalence of Autism Spectrum Disorder, Cerebral Palsy, Hearing Loss, Intellectual Disability, and Vision Impairment, Metropolitan Atlanta, 1991–2010

This study examined the prevalence and characteristics of autism spectrum disorder (ASD), cerebral palsy (CP), hearing loss (HL), intellectual disability (ID), and vision impairment (VI) over a 15–20 year time period, with specific focus on concurrent changes in ASD and ID prevalence. We used data from a population-based developmental disabilities surveillance program for 8-year-olds in metropolitan Atlanta. From 1991–2010, prevalence estimates of ID and HL were stable with slight increases in VI prevalence. CP prevalence was constant from 1993–2010. The average annual increase in ASD prevalence was 9.3% per year from 1996–2010, with a 269% increase from 4.2 per 1,000 in 1996 to 15.5 per 1,000 in 2010. From 2000–2010, the prevalence of ID without ASD was stable; during the same time, the prevalence of ASD with and without co-occurring ID increased by an average of 6.6% and 9.6% per year, respectively. ASD prevalence increases were found among both males and females, and among nearly all racial/ethnic subgroups and levels of intellectual ability. Average annual prevalence estimates from 1991–2010 underscore the significant community resources needed to provide early intervention and ongoing supports for children with ID (13.0 per 1,000), CP, (3.5 per 1,000), HL (1.4 per 1,000) and VI (1.3 in 1,000), with a growing urgency for children with ASD.

Parental Age and Autism Spectrum Disorders Among New York City Children 0-36 Months of Age.

We examined trends in autism spectrum disorders (ASD) and the association of ASD with parental age among young New York City (NYC) children. Children born in NYC to resident mothers from 1994-2001 were identified through vital statistics records (N = 927,003). Records were linked to data from NYC Early Intervention (EI) Program through 2004. The independent parental age-specific odds of having an ASD before 36 months of age were estimated using multiple logistic regression controlling for risk factors. The increase in ASD attributable to changes in parental age at birth was examined. Births to mothers and fathers 35 years or older increased 14.9 and 11.5 %, respectively, between 1994 and 2001. ASD prevalence in EI increased significantly from 1 in 3,300 children born in 1994 to 1 in 233 children born in 2001. Children born to mothers ages 25-29, 30-34 and 35 or older had significantly greater odds of being diagnosed with ASD than children of mothers younger than 25 years (OR 1.5, 1.6, and 1.9, respectively). Children born to fathers ages 35 or older (OR 1.4) had greater odds of ASD than children of fathers younger than 25. The change in parental age accounted for only 2.7 % of the increase in ASD prevalence. Older paternal age and maternal age were independently associated with increased risk of ASD. However, while parental age at birth increased between the 1994 and 2001 birth cohorts in NYC, it did not explain the increase in number of ASD cases.

Changes in prevalence of autism spectrum disorders in 2001-2011: findings from the Stockholm youth cohort.

In a record-linkage study in Stockholm, Sweden, the year 2011 prevalence of diagnosed autism spectrum disorders (ASD) was found to be 0.40, 1.74, 2.46, and 1.76% among 0-5, 6-12, 13-17, and 18-27 year olds, respectively. The corresponding proportion of cases with a recorded diagnosis of intellectual disability was 17.4, 22.1, 26.1 and 29.4%. Between 2001 and 2011, ASD prevalence increased almost 3.5 fold among children aged 2-17 years. The increase was mainly accounted for by an eightfold increase of ASD without intellectual disability (from 0.14 to 1.10 %), while the prevalence of ASD with intellectual disability increased only slightly (from 0.28 to 0.34%). The increase in ASD prevalence is likely contributed to by extrinsic factors such as increased awareness and diagnostics.

Research round-up

Research round-up

Élévation du glucuronide de bisphénol A (BPA) urinaire au cours du syndrome des ovaires polykystiques

L’étiologie des troubles du spectre autistique (TSA) est multifactorielle et un nombre croissant d’arguments suggère l’implication d’interactions entre l’environnement et le génome d’individus physiologiquement vulnérables. Le système nerveux en développement chez le fœtus et le jeune enfant est particulièrement sensible aux effets délétères de substances neurotoxiques de notre environnement, parmi lesquelles nous retrouvons des perturbateurs endocriniens comme le bisphénol A (BPA). Il est suspecté depuis longtemps que le BPA est lié d’une façon ou d’une autre à l’autisme chez l’enfant, sans qu’il soit possible de le documenter de façon précise. Une étude publiée début 2015 montre pour la première fois chez les enfants atteints de TSA un mauvais métabolisme du BPA et une corrélation entre le BPA urinaire total et le métabolisme des acides aminés essentiels, parmi lesquels le tryptophane précurseur de la sérotonine. D’autre part, différentes études ont montré sur des modèles animaux que le BPA perturbe le système sérotoninergique et, d’autres, que les taux urinaires de sérotonine sont élevés chez les autistes ainsi qu’une altération de la transmission sérotoninergique chez les enfants et adultes autistes. Ainsi, le lien entre le BPA et les TSA pourrait être un défaut de développement du système sérotoninergique in utero ou en période périnatale.The etiology of autism spectrum disorders (ASD) is believed to be multifactorial and to involve genetic and environmental components. Environmental chemical exposures are increasingly understood to be important in causing neurotoxicity in fetuses and newborns. Recent data from the Centers for Disease Control and Prevention in the United States suggest a substantial increase in ASD prevalence, only partly explicable by factors such as diagnostic substitution. Bisphenol A (BPA) is an ubiquitous xenoestrogen widely employed in a variety of consumer products including plastic and metal food and beverage containers, dental sealants and fillings, medical equipment and thermal receipts. Therefore, most people are exposed almost continuously to BPA in industrialized countries. Sources of BPA exposure are predominantly diet, but also through inhalation or dermal absorption. BPA can be measured in many human fluids and tissues including saliva, serum, urine, amniotic fluid, follicular fluid, placental tissue and breast milk. There is concern that BPA exposure may influence human brain development and may contribute to the increasing prevalence of neurodevelopmental and behavioural problems. Epigenetic mechanisms are suggested by a mouse study that demonstrated that BPA exposure during gestation had long lasting, transgenerational effects on social recognition. Previous epidemiological studies suggested a relationship between maternal BPA exposure and ASD. A recent study of 46 children with ASD and 52 controls found for the first time a direct association between children with ASD and BPA exposure and demonstrated that BPA is not metabolized well in children with ASD. The metabolomic analyses showed a correlation between ASD and essential amino acid metabolism pathways. Essential amino acids are precursors of neurotransmitters, for example tryptophan for serotonin. Fetal and prenatal BPA exposure was suggested to perturb the serotonergic system in rat and mice models. On the other hand, hyperserotonemia was reported in approximately one-third of autistic patients and also in relatives. Moreover, neuroimaging studies revealed two fundamentally different types of serotonin synthesis abnormality in children with autism compared to age-matched nonautistic children, a difference in whole-brain capacity and focal abnormalities. Finally, decreased serotonin transporter and serotonin receptor binding have been reported in both children and adults with autism. So, the link between BPA and autism could be a defect of the normal in utero or perinatal serotonergic system development. In France, BPA was banned in baby bottles in 2010 and in any food or beverage packaging since January 2015. Therefore, there is an urgent need to find safe alternatives in the use of BPA in the manufacture of industrial products.

Do aluminum vaccine adjuvants contribute to the rising prevalence of autism?

Autism spectrum disorders (ASD) are serious multisystem developmental disorders and an urgent global public health concern. Dysfunctional immunity and impaired brain function are core deficits in ASD. Aluminum (Al), the most commonly used vaccine adjuvant, is a demonstrated neurotoxin and a strong immune stimulator. Hence, adjuvant Al has the potential to induce neuroimmune disorders. When assessing adjuvant toxicity in children, two key points ought to be considered: (i) children should not be viewed as “small adults” as their unique physiology makes them much more vulnerable to toxic insults; and (ii) if exposure to Al from only few vaccines can lead to cognitive impairment and autoimmunity in adults, is it unreasonable to question whether the current pediatric schedules, often containing 18 Al adjuvanted vaccines, are safe for children? By applying Hill's criteria for establishing causality between exposure and outcome we investigated whether exposure to Al from vaccines could be contributing to the rise in ASD prevalence in the Western world. Our results show that: (i) children from countries with the highest ASD prevalence appear to have the highest exposure to Al from vaccines; (ii) the increase in exposure to Al adjuvants significantly correlates with the increase in ASD prevalence in the United States observed over the last two decades (Pearson r = 0.92, p < 0.0001); and (iii) a significant correlation exists between the amounts of Al administered to preschool children and the current prevalence of ASD in seven Western countries, particularly at 3–4 months of age (Pearson r = 0.89–0.94, p = 0.0018–0.0248). The application of the Hill's criteria to these data indicates that the correlation between Al in vaccines and ASD may be causal. Because children represent a fraction of the population most at risk for complications following exposure to Al, a more rigorous evaluation of Al adjuvant safety seems warranted.