autism stats

Increased awareness of the symptoms of autism, now commonly referred to as Autism spectrum disorder (ASD), has resulted in frequent discussions in the media and society at large. In 2017, the World Health Organization estimated that the global prevalence of autism spectrum disorder in children is about 1 in 160. Even though reported prevalence varied substantially across various studies, there is no denying that epidemiological studies conducted over the past 50 years showed increasing prevalence of ASD and a sharp geometric rise over the last decade.

In the USA, economic impact of ASD based on direct and indirect medical cost as well as lower productivity reached $268 billion in 2015, and the burden is projected to rise to $461 billion by 2025. However, it is also possible that the disorder has not become more common, but rather the improvement, expansion and revisions in diagnostic criteria; better diagnostic tools, improved reporting and analysis methodologies that allowed higher accuracy in the identification and reporting of the condition.


Current & Projected Indirect ASD Medical Costs compared to Total Cost for Electricity Consumption in USA

[Source: AUTISM A GLOBAL FRAMEWORK FOR ACTION Report of the WISH Autism Forum 2016.  Kerim M Munir, Tara A Lavelle, David T Helm, Didi Thompson, Jessica Prestt, Muhammad Waqar Azeem]


In 2018, the Autism and Developmental Disabilities Monitoring Network (ADDM) examined educational records of children who had received a formal ASD diagnosis, and reported a prevalence rate in the USA of 1:59 from the results gathered. However, a study that used a different methodology where parents responded to online, mail or telephone survey, reported a rate as high as 1:40.   This high disparity could be due to how age is factored during analysis.




The apparent increase in autism in recent years can be partially attributed to a decrease in the age at diagnosis.  Changes in the age at diagnosis of autism over time can significantly impact changes in observed risks for a reported diagnosis of autism at different ages.  The important point is that shifting the age at diagnosis, especially the earlier diagnosis at younger ages, would artificially inflate the differences in the observed prevalence of autism in young children in the more recent cohorts compared with the cohort of the oldest children. Moreover, changes in the age at diagnosis may confound the observed increase in prevalence if there is insufficient follow-up to estimate the final prevalence rate.  It is therefore imperative that the length of follow-up be increased into adulthood when differences in prevalence between the cohorts would be decreased, and stabilization of prevalence could be more accurately determined.

An excellent example of this phenomenon is a 2018 study conducted in Denmark that revealed prevalence of ASD changed with age in the children studied.  The highest prevalence identified in that study was 1:35 in sixteen year olds born in 2000-2001.  The USA ADDM study that reported the 1:59 prevalence rate examined only 8 year olds whereas the study that reported prevalence of 1:40 examined children across different age ranges. Children missing cut off points also added to the disparity in the prevalence rates reported.

Figure: Cumulative Incidence of Autism Spectrum Disorder by Age Through 2016
in Denmark Among 1980-2012 Birth Cohorts

Each curve in the main body of the Figure corresponds to the autism spectrum disorder cumulative incidence through 2016 among persons in a 2-year birth cohort (beginning 1980-1981, bottom curve), except for the left-most curve that corresponds to the last cohort composed of a single birth year, 2012. The inset is a close-up view of the autism spectrum disorder cumulative incidence through age 5 years for each birth cohort, 1994-2012 (corresponding to births after the adoption of International Statistical Classification of Diseases and Related Health Problems, Tenth Revision autism spectrum disorder diagnostic criteria).

[Source: Cumulative Incidence of Autism Spectrum Disorder by Age Through 2016 in Denmark Among 1980-2012 Birth Cohorts, Diana E. Schendel, PhD1; Erla Thorsteinsson, MS1 JAMA. 2018;320(17):1811-1813. doi:10.1001/jama.2018.11328 ]

Autism spectrum disorder, ASD is a complex, multifactorial neurodevelopmental disorder defined by observed changes in social communication and interactions, including a range of restricted, repetitive behaviors and interests.  Many studies have also identified altered sensory perceptions. Sensory abnormalities are now included in the diagnostic criteria for ASD.  Co-existing psychiatric and cognitive symptoms include social anxiety disorder, oppositional defiant disorder, attention-deficit/hyperactivity disorder, and intellectual disability. Other frequently reported medical conditions include immune system abnormalities, gastrointestinal disorder, mitochondrial dysfunction, sleep disorders, and epilepsy.

Research shows that attention-deficit/hyperactivity disorder, ADHD, and ASD frequently overlap, and possibly even have a shared basis in neural dysfunction.  ADHD was first included in the DSM-II category by the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders in 1968. It was subsequently revised from DSM-2 to DSM-5 in 2013. The DSM-5 broadly defines ASD by two categories: 1) Impaired social communication and/or interaction. 2) Restricted and/or repetitive behaviors. DSM-5 also consolidated all subcategories of the condition into one umbrella diagnosis of autism spectrum disorder (ASD). As a result of that consolidation, Asperger’s Syndrome is no longer considered a separate condition. Although there are many differences between Asperger’s Syndrome and ASD, since 2013, doctors have been instructed to diagnose Asperger’s and autism both as autism spectrum disorders.

Despite extensive research performed in the field, the genetic etiology for at least 70% of cases of ASD remains unknown. Environmental factors have also been implicated in all stages of development, from prenatal to postnatal.  For example, in mouse models, maternal infection has been demonstrated to affect deficits in social interaction and language, as well as the presence of restricted and stereotyped patterns of behavior.  Other environmental risks in neonatal periods such as decreased neurotrophic factors that support growth, differentiation and survival of neurons also may contribute to development of ASD.  Severity of autism-related symptoms have been associated with physiological vulnerability to environmental influences, especially the burden of organic pollutants.  The evidence of epigenetic causes of ASD is currently derived only from animal models.

In 1908, the term ‘autism’ was part of the ‘four A’s (Associations, Affectivity, Ambivalence, and Autism) used by Swiss psychologist Paul Eugen Bleuler in 1908  to describe a small group of schizophrenic patients showing symptoms of withdrawal and “self-absorption”.  However, the documentation of symptoms similar to those associated with ASD found in a court petition filed in 1748 involving the eighteenth-century aristocrat Hugh Blair of Borgue (b. 1708) led scientists to conclude that ASD existed by implication even long before eighteenth-century Britain and Europe.

Since the 1940s the work of Hans Asperger, Director of the Vienna University Hospitals and Leo Kanner separated the term ‘autism’ from schizophrenia. Hans Asperger’s famous work in 1944, “Autistic Psychopathy in Childhood”, found that children he identified with ‘autistic psychopathy’ were socially isolated, physically clumsy, lacked nonverbal communication skills, and showed no empathy with their peers. However, Asperger also believed those individuals were capable of exceptional achievement and original thought later in life. In 2013, along with ADHD, Asperger’s syndrome was officially incorporated into the DSM-5 category in the Diagnostic and Statistical Manual of Mental Disorders for ASD.

The most cited literature on autism in the twentieth century was published in 1943 by Leo Kanner, M.D.  His paper, “Autistic Disturbances of Affective Contact” marked the defining moment for infantile autism.  The understanding of childhood autism was further developed by Dr. Bernard Rimland who published the ground-breaking book titled “Infantile Autism: The Syndrome and Its Implication for a Neural Theory of Behavior.” in 1964  Dr. Rimland’s insights provided enormous guidance on the understanding and treatment of individuals with ASD. Dr. Rimland’s own son, Mark was autistic.

More than half a century has passed since the publication of Dr. Rimland’s book.  Although the understanding and treatment for ASD has improved significantly, from the use of LSD and other biologic treatments that included electroconvulsive therapy, sub-shock insulin, amphetamines, as well as antidepressants in the 1960s, to current day therapies that aim to minimize the impact of common features and deficits of ASD, while maximizing functional independence as well as quality of life. Treatments employed today include applied behavioral analysis (ABA), occupational therapy, speech therapy, physical therapy, detoxification protocols and pharmacological therapy.

Even though ASD is not a ‘modern’ disease, there is no doubt that changes in our environment contribute to the observed increase in prevalence of ASD, notwithstanding the changes and improvements in diagnostic and analytic methodologies.

While a heated debate over vaccination as one of the causes of increased ASD prevalence continues, the herbicide glyphosate, has also been implicated as the cause for increased ASD prevalence.  Yet one of the most obvious connections between modern diseases and ASD prevalence has not been duly noticed; and that is diabetes.

Diabetes mellitus (DM) is one of the most prevalent diseases worldwide. The global prevalence has increased from about 180 million in 1980 to about 425 million as of last year.  This number greatly surpassed an estimate made in 2010 where scientists projected diabetes to increase from 285 million in 2010 to  439 million people by the year 2030. We are now at 425 million and we will achieve the target of 439 million in 2 years at the current rate of increase.

Type 2 diabetes  represents about 85%–95% of the total cases in DM. The two main characteristics of T2D is hyperglycemia, which is caused by insulin resistance in the peripheral metabolic tissues; and impaired insulin secretion from β cells in pancreatic islets. However, due to the complexity of the disease, there is currently a lack of true understanding in how and why this disease is expanding so quickly.

In the USA, more than 100 million U.S. adults have diabetes or are prediabetic, according to a report released in 2017 by the CDC. Centers for Disease Control and Prevention. The report found that as of 2015, 30.3 million Americans or 9.4 percent of the U.S. population, have diabetes.  


Number and Percentage of US Polulation
with Diagnosed Diabetes, 1958-2015

[Source: Long-term Trends in Diabetes April 2017 CDC’s Division of Diabetes Translation. United States Diabetes Surveillance System available at]

In 2011, Michael Stern of Rice University, Texas, linked autism to insulin signaling pathways; and that gestational diabetes increases the incidence of autism.  The hypothesis being maternal diabetes is able to increase fetal insulin secretion, leading to hyperactivation of the fetal PI3K/Tor pathway.  In neurons, the PI3K/Tor signaling pathway affects a form of synaptic plasticity that has been implicated in autism. Interestingly, a study observed improvement in children with ASD using ketogenic diets which suppress insulin secretion.

An impressive list of studies conducted in the past several years all showed increased ASD risk with maternal diabetes and/or obesity.  A large retrospective longitudinal cohort study involving 322,323 children born in 1995-2009 at Kaiser Permanente Southern California (KPSC) hospitals showed a 42% risk increase for ASD when gestational diabetes was diagnosed by 26 weeks.

A Boston Birth Cohort study involving 2,734 children showed obese mothers with diabetes three to four times more likely to have child with ASD. A Cincinnati Children’s Hospital study involving 38,810 control children, 503 children with ASD, and 1,533 children with developmental delay in the Cincinnati, Ohio, area showed mothers with obesity or gestational diabetes were 1.5 times more likely to have a child with ASD than controls. Having both diabetes and obesity doubled the ASD risk.

Compare the steep rise in diabetes since 1997 to the rise in ASD prevalence in 0-4 years in 1997 in the state of California, USA.


[Source: The Rise in Autism and the Role of Age at Diagnosis Irva Hertz-Picciotto and Lora Delwiche  Epidemiology. 2009 Jan; 20(1): 84–90. doi: 10.1097/EDE.0b013e3181902d15


Would it be simplistic to assume that the continued exponential growth of diabetes and obesity will see a concomitant increase in ASD prevalence?  Or should we attribute the cause for increased prevalence to vaccines, environmental pollutants like glyphosate, or even genetic mutation? Even though changes in over 1,000 genes have been reported to be associated with ASD, a large number of these associations have not been confirmed.

Many common gene variations are thought to affect the risk of developing ASD, but not all people with the gene variation will be affected. In addition, the specific ways that changes in the genes affect the development of ASD are also currently unknown. With all our impressive achievements in research and development in the medical field, we seem to be at a loss in our attempts to halt the progression of ASD and diabetes.

That begs the question, are we really trying? What sacrifices might be necessary for a truly serious effort? As technology pervades modern life, it may be time to begin looking more critically at the assumption that anything not shown by double blind studies to be toxic, doesn’t slowly but surely have tragic adverse effects on humans. In the USA at least, we live in a capitalist society where critically important health issues are decided based on profitability and not societal health. Both science and government have been captured by our corporations and this makes it very difficult to peer into the true causes of autism.

For hundreds of years the Roman empire was the greatest power on earth. And yet it collapsed. It can happen to us too. The economic costs of the surging autism epidemic will eventually force us to look deeper at its roots. But, will it be too little, too late? The human race is now faced with the most challenging crossroads. Our choices today will affect not only our health, but those of future generations.



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