Researchers have determined that of the over 100 autism genes that exist, all act on early developmental functions and lead to diverse, overlapping outcomes, including psychiatric disorders, autism, and related conditions. Some genetic influences, while rare, can help define the mechanisms that lead to brain cells in autism developing over time. Although a link has been established connecting environmental influences to this same spectrum of conditions, few studies have successfully defined their interaction. These findings have implications for interventions and could lead to strategies for mitigating symptoms.

Given the comorbidity of mental health disorders with autism spectrum disorder, it should come as no surprise that new research reveals that ASD relevant genes act in fundamental ways that may influence multiple outcomes, ranging from ASD to schizophrenia, to ADHD27-30, neurodevelopmental disorders and intellectual disability31-33. Genes that act on such early and fundamental brain pathways have downstream effects on a number of brain functions, ASD being one of them. This might explain why there are so many ASD genes and why they are pleiotropic, meaning they have different functions. In fact, the list of genes associated with ASD keeps growing, as larger studies and better technology have revealed over 150 ASD associated genes34.   Infant siblings of children with autism also show rare and common gene variants in ASD genes that can aid in a diagnosis9.  

In addition, the presence of certain genetic mutations in ASD relevant genes can produce profound disabilities, which alone work to explain an ASD diagnosis. These mutations, referred to as rare genetic variants, are important to the community because their discovery has led to the creation of Patient Advocacy Groups that provide support and resources for focused research, as well as offer pathways to better understanding the basic circuitry of certain ASD behaviors35. Scientists are studying these rare genetic forms of ASD to understand all forms of ASD, particularly gene expression in the brain36,37. When compared to studies of the brains of people with bipolar disorder and schizophrenia, studies of brain tissue in people with ASD reveal overlapping genetic activity in genes that control synaptic signaling, neurotransmitter release, and immune response.36,37. The abnormal immune signaling in the brain might result in cell damage, as evidenced by accumulation of T-cells in brain tissue38. Studying the brains of people with ASD is the best way to understand the basic cellular and molecular basis of ASD, and is only possible through families who decide at the most difficult time to make the decision to donate. If you would like to learn more about the Autism BrainNet, which made these studies possible, visit www.takesbrains.org/signup

While genetic factors are incredibly important in the diagnosis and presentation of symptoms of ASD, understanding the role of environmental factors in both the diagnosis and presentation of symptoms of ASD is crucial. One of the most studied environmental factors in ASD is exposure to air pollution during pregnancy. This year, ancillary evidence taken from additional locations via different methodologies shows a particular effect for a component in air pollution called PM (particulate matter) 2.5 (2.5 microns)39.  Air pollution exposure may interact with maternal diabetes, which also increases the probability of ASD40.  Air pollution also seems to influence an ASD diagnosis more strongly in boys41. It is important that public health policy address established, scientifically based environmental factors to address even smaller, but preventable, environmental factors. 

There have been spurious reports of other environmental factors, but rather than look at factors in isolation, it is crucial to understand how these factors collectively influence brain development and interact with genetic susceptibility, either rare genetic or polygenic influences36. Another area of convergence of environmental and genetic factors is epigenetics, often called the “second genome”. The epigenome is a multitude of chemicals and tags on the DNA genome that is responsive to environmental factors that can turn on or turn off DNA expression, as early as when the embryo is formed. ASD risk genes identified in genetic studies can also work epigenetically42-46The next generation of research will hopefully focus on understanding the multifactorial influences of an ASD diagnosis, how these factors affect symptoms and influence long term trajectories across neuropsychiatric diagnoses, including ASD.

The high rate of mental health disorders in both children and adults with ASD means that a large percentage of this population and their families are burdened with enormous challenges Training community providers to deliver mental health interventions shows promise for alleviating these comorbidities. Clinicians need to be on the lookout for these psychiatric issues so people with autism receive the much-needed services they deserve.

While the core symptoms of ASD often lead to challenges in daily functioning, across the lifetime and spectrum of many individuals with ASD, co-occurring mental health conditions are a huge concern. Several older but smaller international studies provide a wide range of estimates of the prevalence of co-occurring conditions. A met- analysis and systematic review of these studies conducted in 2019 has helped to decipher the findings20. The findings revealed 28% comorbidity of ADHD (higher in kids than adults), 20% for anxiety disorders, 11% for depression and 9% for obsessive-compulsive disorder20. There is even overlap in brain based profiles of different diagnoses, both in terms of genetic activity21and structure22. These mental health issues, particularly anxiety, can lead to an acute crisis requiring hospitalization23. Unfortunately, clinicians have limited knowledge and understanding of the nature of these mental health conditions in ASD24, making intervention difficult. However, ASD researchers have had luck training community mental health providers to deliver interventions focused on addressing these mental health challenges25. Training community based providers is a move in a promising direction, allowing more people to receive services in a variety of settings, but the efficacy of these interventions still lags behind those delivered in clinics26. Understanding the high co-occurrence of mental health issues helps families and individuals both plan for later health care needs and anticipate potential mental health problems before they occur.

full reference list at: https://autismsciencefoundation.org/key-autism-research/https-autismsciencefoundation-org-key-autism-research-2019-the-year-of-preparing-for-the-future/

New technologies contribute to greater use of standardized measures in different community settings. At the same time, clinicians and scientists have developed new ways to use common records and tools, resulting in better identification of concerns at even earlier stages. Families and care providers should confidently screen early and often.

Biological based markers hold promise for even earlier detection of features, especially in those with a family history. However, to make predictions about not just a diagnosis but future expectations of needs as well, most care providers, physicians and clinicians rely on behavioral concerns. Right now, most families lack access to EEG machines and MRIs and expensive genetic testing is most often not covered by insurance. The reality of early detection of ASD in 2019 is that it occurs mostly in primary care settings, where physicians help to interpret results for the family.  In 2019, the AAP published an update to their 2007 guidelines for screening for autism and it continues to recommend autism-specific screening at 18 and 24 months12.  Researchers continue to explore new ways to make this tool more accessible via technology, such as electronic tablets, whereas scientists continue to refine and improve accuracy screening tools using machine learning13

One challenge of current screening practices (and in fact, in all of ASD research) is the disparity in screening and screening results amongst distinct racial and ethnic groups14. In order to address these differences, scientists are analyzing a variety of approaches fashioned to deal with these disparities and to increase access to screening tools. This includes remotely employing video based tools to capture ASD features to help identify and diagnosis ASD15-17. These video based tools help parents identify signs by providing real life examples of parent-child interactions18and by examining existing reports of developmental milestones from electronic medical records19, with the goal of identifying early signs of developmental concerns as soon as possible, in as many infants as possible, regardless of race or ethnicity . Doing so will increase early diagnosis, leading to earlier intervention and increased understanding of ASD, self-awareness of symptoms and long-term improvement of services.

Multiple studies this year have linked children’s symptoms and biology in infancy to later outcomes. Motor abilities, family history, brain connectivity all can independently contribute to how a child develops over time. These outcomes include an autism diagnosis, verbal ability, and cognition in adulthood. This sort of research can be used to help prepare families and customize interventions that focus on the most debilitating symptoms of ASD.

This year, to make predictions about future ASD features, more studies used a longitudinal study design. This design is critical to autism research because it follows a group comprised of individuals diagnosed with ASD and, at times, individuals without a diagnosis in order to determine how they are affected as adolescents and adults. Whereas a longitudinal study can be expensive, complex and does not produce immediate results, the nature of its design provides clinicians invaluable data, affording deeper insights that allow them to more fully educate families by managing expectations, identifying focus areas and providing coping strategies that serve to help those with ASD live their best lives.

Longitudinal studies help parents understand their child’s reality and manage future expectations, as well as help scientists refine interventions according to the variability of groups of people with ASD.  Multiple research studies have used data to group children based on trajectory, i.e. the progression from commencement, through adolescent development to adult functioning.  The composition of these groups consists of those who show fewer symptoms and continue to improve vs. those less functioning who continue to decline. This year, two longitudinal studies, one conducted in the United States and one in Canada, closely examined toddlers to pinpoint and study specific factors that influence outcomes, from childhood to adulthood. In these studies, two patterns emerged: those possessing lower levels of symptoms who improve vs. those with more profound symptoms who decline. 

While all groups showed improvement in daily living skills, those who presented less severe symptoms in toddlerhood and showed marked progression during adolescence also had the highest adaptive abilities as adults2.   Although most participants showed improvement in social communication with age, improvement varied, based on individual language ability as toddlers. Social communication impairments in 19 year olds was found to correlate with differences in language ability as early as age two. As speech improved, so did this core symptom of ASD3: those with early minimal language ability showed the greatest functioning impairments as adults. Likewise, fine motor skills in infancy4is a predictor of language at age 19, in that better fine motor skills in early childhood is a predictor of better command of language in adulthood. Together, these findings demonstrate that poor early motor skills and decreased language function are related to later ASD symptoms. This is a crucial identification, considering that both fine motor skills and language are target areas of early intervention and that intervention may improve ASD through adulthood. 

The study of early motor function is not only vital to further understanding how it affects those diagnosed, it also offers insight pre-diagnosis in terms of how early motor function may predict a later ASD diagnosis. The Baby Siblings Research Consortium (BSRC) is a group of researchers that studies initial features of ASD in siblings of children with ASD as young as 6 weeks of age. Siblings of children with ASD have a 15x greater probability of having ASD themselves than do other children.  Similar to previously mentioned studies, BSRC also concludes that fine motor abilities at 6 months can predict an ASD diagnosis in siblings and expressive language ability in younger siblings at 3 years6,7

Another factor BSRC researchers have employed to estimate the probability of diagnosis in children is number of siblings previously diagnosed with ASD. Those with at least 2 older siblings with ASD were found to have a higher probability of a diagnosis, as well as increased severe cognitive disabilities8. Based on family history, this  information is vital in helping families better understand the probability of an ASD diagnosis in future children, as well as predicting strengths and limitations future children may face.

In addition to identifying behavioral markers, the past decade of research has revealed a blossoming of early biological factors that may serve as additional predictors of diagnosis, ranging from genetic tests9, salivary hormone markers and other reflections of altered development. Studies of brain structure, activity and connectivity have also proven valuable; when measured non-invasively, identified changes in activity in the frontal lobe of the brain during the first year of life have served to predict an ASD diagnosis in infant siblings10. Because brain wavelengths vary, identifying and monitoring changes in the size of each different type of wavelength over the course of a year serves as valuable information in terms of not just determining an ASD diagnosis but also for further understanding brain fluctuations during that time period10.

Complementary to brain activity, previous studies from the Infant Brain Imaging Network (IBIS) revealed different approaches to more accurately predicting ASD diagnosis by using measurements of brain structure and connectivity, in addition to mathematical algorithms based on the shape and function of different brain regions, as potential predictors of a later diagnosis. This year, the analysis of early brain based ASD markers has afforded scientists more precision in determining an association with brain connectivity in critical ASD brain regions, as well as an insistence on sameness and stereotyped behaviors at 12 – 24 months11. Not only do these biological based markers aide in predicting later diagnosis and identifying features of ASD within a diagnosis, they have the potential to serve as objective ways to help determine specific interventions, both medical and behavioral.

(for the full list of references, visit http://www.autismsciencefoundation.org)

Reprinted with permission from Matthew Belmonte, PhD.

Dr. Belmont is a Visiting Researcher at the Com DEALL Trust, Bangalore, 
India, and Reader in Psychology at Nottingham Trent University in the 
UK.  This article represents his personal views.

With the academic term finished I’m just catching up on all that I ought to have written about the annual meeting of the International Society for Autism Research 2-4 May in Montreal. For me the high point was Alison Singer‘s brilliantly delivered speech at the morning Special Interest Group on Clinical Strategies for Including Severely Affected Individuals in Neuroscience Studies: https://www.ncsautism.org/…/including-severe-autism-in-neur… . Alison and colleagues pointedly described the weariness that so many of us feel after opening yet another front in a conflict that we thought that we had put behind us.

The first front has been the fight for justice: All my life I have witnessed the battle against governments, local authorities, schools and other institutions for appropriate education and participation in society. In the 1970s, long before the Individuals with Disabilities Education Act 1990 and before even the Education for All Handicapped Children Act 1975, my mother set up a Montessori classroom in the basement because no school would take my elder brother. I remember the household litter of PECS cards and sign-language manuals. I remember my brother’s shoelace-tying practice board made from old trainers, the secret thrill of finding it and mastering it before he did. I remember my father’s absences at breakfast and supper during his long drives back and forth to board meetings and hearings at the state capital. I remember learning helplessness in the face of my father’s rage and my mother’s sobs, in the throes of a marriage overstressed by autism without respite. I remember finding out so belatedly that this family life actually was not what other children experienced and was not normal. And I have looked on from a distance as my sister with her daughter has fought and re-fought these same battles. I’ve witnessed my brother dashing in the opposite direction from the door of his locked institution, a year before we finally figured out that what he was trying to tell us, without speech, is that he was being beaten daily. I’ve witnessed my parents’ guilt at having sent him there.

The second front has been the fight for beneficence: I’ve witnessed and then myself fought the battle against scientists and physicians hamstrung by ideology and prejudice. I’ve heard, in her weaker moments, the self-criticism and despair of a mother who was lectured by a physician, a psychiatrist who had read Bettelheim, “Mrs Belmonte, don’t you feel *guilty*?” I’ve seen my brother and my parents contort their lives to follow research protocols that advance scientific careers more than scientific understanding. I’ve seen families’ reports of disrupted sleep, gastrointestinal distress, and immune disease ignored for decades because autism was a disorder of social cognition. I’ve seen families spend desperate money on bullshit therapies from auditory training to immunoglobulin infusion because science was ignoring them. I’ve seen families’ stories of heightened affective empathy dismissed because people with autism are impaired at (cognitive) empathy. I’ve seen case reports of independent keyboard communication dismissed because people with autism, whose cognitive, perceptual and motor dyscontrol mean that they can’t look and think and do at the same time, “aren’t even looking at the keyboard”, because proponents of typing methods don’t trust scientists, and because scientists haven’t consulted autistic people and their families and teachers and therapists about how to test. I’ve watched, every September when I was in graduate school, a queue of students enter the medical school office through one door and emerge through the other wielding a white coat, a stethoscope, and an attitude.

The third and perhaps least intractable front has been the fight for knowledge: For half my life I have been fighting the battle to understand the biomedical causes of autism in ways that lead to evidence-based, targeted treatments, and may in future lead to prevention or even cure. It’s been a long time coming, but with subtyping in terms of behaviour, neurophysiology and genetics, and informed by syndromic associations, the field at long last is zeroing in to be able to provide something more than the perennial ABA and PECS.

Never did I anticipate, though, that I would end up fighting a fourth battle, for respect for persons, against so-called ‘self-advocates’ and their fellow travellers, about the very definition and status of autism as the disease condition that it is. After the 1970s’ ignorant “Oh my child is very artistic too”, by the late twentieth century, thanks in no small part to the publicity efforts of parent-driven organisations such as Cure Autism Now (on whose Scientific Review Council I’m proud to have served) and the National Alliance for Autism Research (which, by funding my doctoral research, prevented me from dropping out of graduate school) people finally knew autism: People knew- or at least knew about- people who couldn’t speak, or who otherwise couldn’t connect thoughts and intentions to behaviours and actions flexibly and in the moment. People also knew a lot of their family members who, like me, were socially and motorically maladroit and fascinated with sensory, sensorimotor and cognitive patterns and relationships. Some of this latter group began receiving the label ‘Asperger syndrome’; more of us simply recognised in ourselves the broader phenotype described by Joe Piven and others. We all had some autistic traits. But none of us went around labelling ourselves ‘autistic’, any more than, say, a talented artist with schizoid traits would label herself ‘schizophrenic’. To do so, to appropriate that label, would have been patently absurd because our petty deficits were of a nature and degree that could be worked around. Yes, we didn’t get picked when the class was choosing kickball teams, we didn’t get party invitations, we didn’t get girlfriends and boyfriends, and time after time in the working world our social deficits and executive and affective dyscontrol lost us the very same jobs that our technical skills and intensity of focus had gained us. Life was lonely and often Sisypheanly hard- but you know what? Life is hard for a lot of people, indeed for everyone to some degree or other, because that’s life. And you don’t need to appropriate a label because life is hard. Instead you just need to get on with it, changing those aspects of the world that you can change but living with those that won’t budge.

During the past decade and a half or so, though, the logic of many newly and lately diagnosed Asperger or broader-phenotype individuals seems to have gone thus:
1. I am autistic. (false)
2. My condition is not a disease. (true)
3. Therefore autism is not a disease. (false)

This logic has been lately abetted by the DSM-5’s elimination of Asperger syndrome as a diagnostic term distinct from autism- as though when we see red we ought to think ‘violet’ because after all, light is a continuous spectrum! And it doesn’t help matters that this rhetoric is being driven by a population who tend to view distinctions in black and white rather than shades of colour. So we are back to a situation where people in general don’t know autism- except worse, because they *think* that they do know it. They have listened to those mildly affected and often very talented individuals who have appropriated the label. They have listened to the artists and authors and engineers who have clothed themselves in autism chic. These people are listened to because they can speak. I remember the moment when I first saw this public misperception taking hold. I was a postdoctoral scientist at Cambridge giving a public engagement talk. To augment the science with a personal connection I spoke a bit about my brother. I mentioned that he’d never spoken. A woman in the audience looked puzzled. “What,” she spluttered, “you mean, he has nothing to say?” Seriously. She actually didn’t get it. That’s the moment when I knew where we were headed, and that was sixteen years ago. And this change of climate has reached such a fever pitch that now, in last month’s Autistica Discover conference at the University of Reading, mainstream scientists apparently felt compelled to adopt this celebratory rhetoric of autism. That conference culminated in a panel none of whose members were authors and bloggers with autism such as Jonathan Mitchell who advocate treating autism as the problem that it is.

I want to share two letters of mine. One is ten years old, a reply to _Newsweek’s_ story about Ari Ne’eman and the ‘self-advocacy’ movement which was not selected for publication. The other is a few weeks old, a plea to a prominent scientist (whose name I’ve removed because his reply was a thoughtful one and I don’t want him tarred and feathered by the Internet) who spoke at the Autistica Discover meeting.


Date: Sun, 24 May 2009 16:25:22 -0400 (EDT)
From: Matthew Belmonte
To: Letters@newsweek.com
Subject: letter for publication
Cc: Claudia Kalb


Claudia Kalb’s 25 May article “Erasing Autism” describes Ari Ne’eman as a “master networker,” “sociable,” with a “well-timed sense of humor.” These characteristics are exactly why Mr Ne’eman is no more qualified than you or I to speak for people with autism.

There are many of us who as children had trouble with loud sounds, were fascinated by sensory patterns, lined up our toys in order of size or colour, had a nervous habit of hand-flapping, couldn’t immediately recognise new faces, felt anxious looking into others’ eyes, spoke too softly or too loudly, shied away from flexible social interaction, and spent most of our time gazing at railway cars, poring over science books, or programming computers. I know: I was one of them. I’m convinced that the same genetic susceptibility that made me a scientist is what made my brother and my niece autistic. BUT THIS MILD SIMILARITY DOESN’T MEAN THAT I HAVE AN AUTISM SPECTRUM CONDITION – and mis-applying that label, as so many detail-focused and mildly socially awkard “geeks” now seem wont to do, devalues the diagnosis for those people who really _are_ severely impaired.

Here’s the difference: My brother cannot speak, and is lucky to get out a couple of hundred words in an hour of painstaking pointing at a keyboard. (Many of those words are devoted to how frustrated he feels and how he’d like to have a cure.) My niece has speech, but can’t use it for flexible social communication. Both of them have such trouble controlling their own behaviours and bodies that, absent a miracle, they’ll never be able to live independently.

We families want that miracle, and we will not allow Mr Ne’eman to take it away from us by blurring the important distinction between severe autism, which is a disease to be cured, and milder forms of autism spectrum condition, which need not be treated as disease.

Mr Ne’eman makes an important point about the need for societal acceptance and accommodation of Asperger syndrome and autism. (Two huge unmet needs are augmentative technologies for communication and supported or sheltered places of employment.) Fundamentally, though, one has to live in the world, and like it or not, the world is defined by the majority. Being unable to speak, or to use speech communicatively, or to control one’s behaviour places a person at severe disadvantage – and that is the real tragedy.

Much of the rancour surrounding the prospect of a cure for autism stems from confusion over what we mean by “cure.” To me as an autism researcher, a cure is a treatment that augments and does not take away. A cure is something that confers on people with autism the social and communicative capacities that allow their unique insights to be shared with the rest of the world. It is not something that deletes those insights.


From: Matthew Belmonte
Subject: Re: Autistica Discover Conference
Date: Mon, 1 Jul 2019 16:46:55 +0100

Dear Professor *****

At this past Thursday’s Autistica Discover Conference in Reading I was dismayed to hear you- of all people!- question whether autism were something that ought to be prevented. That moment has stuck in my mind during these past days. I didn’t stand up at the end of your talk to take issue with your position, because I was so literally dumbfounded, that someone who’s devoted so much time and scholarship to work that has demonstrated potential to ameliorate- and indeed perhaps in borderline cases to prevent- autism.

I did later scribble out what I wanted to say, and during the question time at the end of the conference’s closing panel I raised my hand to say it, but alas was not called on. Here it is:

I am brother and uncle to two people with autism.

I’m also a neuroscientist studying autism, and have served on the Scientific Review Council of Cure Autism Now.

My brother and I always have thought in similar ways and been fascinated by the same sorts of stimuli, and I always have held the thought that I could have been he, or he I.

My brother can’t speak. On a good DAY he can laboriously and haltingly type a few tens of words. In a bad YEAR, he was beaten daily because when he would run away from the ‘training centre’ where this was happening, nobody stopped to understand what he was trying to say.

The reason I want to cure autism is that I want him and people like him to be able to share their unique insights with the rest of the world. I don’t at all want to delete those insights. I’ve made this point in my public speech for the past two decades.

It’s very hard to fight for scientific and social understanding of autism whilst simultaneously fighting all the people who equate prevention and cure with eugenicism and genocide. I wish that you wouldn’t fuel that rhetoric and that false narrative.

Very sincerely,
Matthew Belmonte

You can read this post here: https://www.facebook.com/Matthew.K.Belmonte/posts/1245483425630265

From Alycia Halladay, PhD, CSO of the Autism Science Foundation:

There has been some back and forth about a brand of early intense behavioral intervention for ASD called Early Start Denver Model, or ESDM, in the past few weeks.  Unfortunately a valid and important scientific debate has crept into the mainstream calling question into the use of early intensive behavioral interventions, period.  That’s nonsense.  I am very afraid that the result of these scientific debates on type and brand and magnitude of effect, will lead to a distrust in early intervention for symptoms of ASD.  I think during all the back and forth on may be clouding the message to families about the importance of early intervention.  The magnitude of the effects are variable, they may not be monumental, but early behavioral intervention is important.  Now after reading this, I’ve got you curious and you might be thinking: what is going on?  I’ll explain.



In 2010, a research group published the first randomized control trial of an early intervention for kids who had been diagnosed with ASD between 1 ½ years of age to 2 ½ years of age1.  The intervention was Early Start Denver Model, or ESDM, but as I will mention later, it falls into a larger collection of naturalistic developmental behavioral interventions.   These interventions have things in common: they are implemented in natural settings, involve shared control between child and therapist, utilize natural contingencies, and use a variety of behavioral strategies to teach developmentally appropriate and prerequisite skills.  They use principles of ABA, which helps the child know when to respond and when the clinician should provide feedback.   There are several of these now, thankfully, because very few existed before 2010. Others  (but not all) that fall into this category are called JASPR or  Joint Attention, Symbolic Play, Engagement, and Regulation, or SCERTS which stands for Social Communication Emotional Regulation and Transactional Support.  There is also a Canadian version of naturalistic developmental behavioral interventions called the Social ABCs in Canada.  What brand you receive may depend on what you have access to in your community or research going on in your area.  Since 2010, these types of interventions have also shown to be effective using randomized clinical trials.   I’m not saying these interventions are identical, because they are different in what they emphasize and how they are trained to be delivered. Some of these interventions mostly target social and communication skills, whereas other, such as ESDM, target all domains of skills, including things like fine motor skills.   It’s good to have choices.  I am not speaking on behalf of the researchers, but I don’t believe any one of the clinician researchers who study these interventions went into the research thinking that any one particular named intervention should be the only one used by everyone.    I would be thrilled if my daughter had access to any one of these named interventions.   Many of them have been adapted to be parent-delivered, which is incredibly important because let’s face it, 2  year old kids spend most time at home with their parents and it’s important for parents to at least learn what they could be doing in the home and in different settings to promote different behaviors and redirect other behaviors.  Getting these home-based models to work has been more challenging, because parents sometimes say, and I get it, I don’t come to your job and tell you what to do so don’t come to my home and tell me what to do.  But generally, they are well liked.  Without going into too much detail about these, I really hope you have the time to read a more comprehensive discussion of these interventions here.  The link is to an article that is open access, so enjoy.

Untitled design (12)This first randomized clinical trial compared the progress of kids offered ESDM to kids who received whatever was available in the community prior to 2010. It used both therapists and parents. Remember,  it was  published in 2010, so the work was done earlier to 2010.  The results  of this study showed that, after two years of intervention, children who received ESDM made larger gains in IQ, language, and adaptive behavior compared to kids who received whatever was offered in the community at the time.  In addition, some kids changed from an autism to a PDD-NOS diagnosis, which means they gained some skills in social and cognitive ability1.   The study was relatively small, but it did, and does, show that ESDM intervention delivered early resulted in gains for young kids with ASD.  The team then took their findings a step further by showing that brain function was changed to look more like typical children compared to those receiving community based intervention after two years2.   They kept following up these families and showed that improvements were sustained 2 years after the intervention, when the kids were now 6 years old 3.  In fact, other groups have replicated their findings (just the behavioral findings, not everyone has access to brain activity, or EEG monitors).  This includes improvement cognitive function in young children 4,5.   Because of these gains, the cost of autism services in kids who had received ESDM was lower after they left the ESDM study6.  Studies outside the US have also shown ESDM to be effective.  All of these things are good news even if the gains are not what  some people would consider “drastic”, functioning was  improved in the short and long term, and it corresponds to how the brain functions.

Just recently, as in a few weeks ago, another study looking at ESDM was published by the same authors that published the 2010 study.  This time, the age was pushed down a few months, and it included three sites7.  This was great.  These changes from the first study increased the number of children involved in the study, and diversified out who was getting the intervention.  It added a parent coaching phase at the beginning since the parents are so involved in the intervention.  This parent coaching component had been refined by the team for years and was found to really help parents.  The pre-defined primary endpoint was a standardized test of language ability rather than cognitive ability or adaptive function, although those things were included. Some things that make it an example of a well-designed clinical trial are:    The treatment was manualized. Therapists were trained and monitored for fidelity of implementation.  Outcome assessments were conducted by examiners naive to group assignment.  Data were managed and analyzed independently by a data coordinating center with strong expertise in clinical trial methodology. Investigators had no access to the data.   So, what did they find the second time around, almost 10 years later and with small changes in the protocol?

There were greater improvements in expressive and receptive language in the children who received ESDM, compared to the community group, however, this effect was only seen at 2 out of the 3 sites.  Also, unlike the 2010 study, there was no difference in the improvements in cognitive ability, adaptive behavior and autism severity between the two treatments. In fact, in these areas, everyone showed an improvement, regardless of treatment group.   Everyone showing an improvement with no differences between groups is a good thing.

A scientific magazine which is read by the community pointed out the criticisms of the latest trial.  The article itself calls into question the required size of an improvement in skills that is meaningful.  Is an only “mild” improvement not clinically significant?  Who makes that judgement?  That was left for the reader to decide.  There was a greater than expected chance that language ability was more improved in the ESDM group compared to treatment as usual, and both groups had cognitive and adaptive behavior gains across the time periods studied over the course of the 2 years.  Cognitive function is measured differently across time, measuring it just in toddlers shows different trajectories8.   A finding of improvement in both groups but lack of difference on all measures is an unfair criticism.  Kids in both groups received about the same number of hours of intervention.  Researchers including Elizabeth Berry-Kravitz who works in community-based settings, have noticed that more and more, knowledge and skill are being brought into the community and this is leading to better community-based treatment.  This is likely why there may not have been an effect – the community interventions got better since the original study.  That’s something to celebrate.  Of course, not all families live in communities that provide high levels of early intervention. We have a lot more work to do to make sure that all children in all communities get access to evidence-based early intervention.

As a parent of a young child with autism, don’t be dissuaded from this particular controversy.  Have faith that behavioral interventions have improved over the years, if you get the opportunity to enroll your child in a program or study that examines one of these named interventions, take it, and realize that your participation  will improve the long-term gains that your child will make in the short and the long term. Parents and family members who read about this controversy should not be dissuaded from enrolling their children in ESDM programs or any other naturalistic developmental behavioral intervention program.


  1. Dawson G, Rogers S, Munson J, et al. Randomized, controlled trial of an intervention for toddlers with autism: the Early Start Denver Model. Pediatrics. 2010;125(1):e17-23.
  2. Dawson G, Jones EJ, Merkle K, et al. Early behavioral intervention is associated with normalized brain activity in young children with autism. J Am Acad Child Adolesc Psychiatry. 2012;51(11):1150-1159.
  3. Estes A, Munson J, Rogers SJ, Greenson J, Winter J, Dawson G. Long-Term Outcomes of Early Intervention in 6-Year-Old Children With Autism Spectrum Disorder. J Am Acad Child Adolesc Psychiatry. 2015;54(7):580-587.
  4. Touzet S, Occelli P, Schroder C, et al. Impact of the Early Start Denver Model on the cognitive level of children with autism spectrum disorder: study protocol for a randomised controlled trial using a two-stage Zelen design. BMJ Open. 2017;7(3):e014730.
  5. Vivanti G, Dissanayake C, Victorian AT. Outcome for Children Receiving the Early Start Denver Model Before and After 48 Months. J Autism Dev Disord. 2016;46(7):2441-2449.
  6. Cidav Z, Munson J, Estes A, Dawson G, Rogers S, Mandell D. Cost Offset Associated With Early Start Denver Model for Children With Autism. J Am Acad Child Adolesc Psychiatry. 2017;56(9):777-783.
  7. Rogers SJ, Estes A, Lord C, et al. A Multisite Randomized Controlled Two-Phase Trial of the Early Start Denver Model Compared to Treatment as Usual. J Am Acad Child Adolesc Psychiatry. 2019.
  8. Henry L, Farmer C, Manwaring SS, Swineford L, Thurm A. Trajectories of cognitive development in toddlers with language delays. Res Dev Disabil. 2018;81:65-72.


The rate of under or unemployment in the autism community is high, and many


Neil Barnett

solutions for improving opportunities for people with ASD are being tested.  One of them is called the Autism@Work Employer Roundtable.  Neil Barnett at Microsoft helped create this program for helping people with autism become employed at companies including, but not limited to, Microsoft.  This program has been featured on many news outlets and has gotten a lot of attention.  Neil was gracious to answer some questions for me about the program and what is aimed to do.

Describe the Autism @ Work Employer Roundtable.  How did it get started, and what is it really?

The Autism @ Work Employer Roundtable is a growing group of employers, across industry and size, that have committed to hiring individuals with Autism, in a programmatic manner.  The goal was to bring these diverse employers together to share best practices and help each other with the goal to hire more individuals on the spectrum, given that 80% of people on the autism spectrum are unemployed or underemployed. We came together as a resource to help other employers looking to start programs. Recently, we’ve come together and collaborated with the University of Washington Information School to develop an Autism @ Work Employer Roundtable Playbook, a resource aimed at providing programmatic guidance for organizations looking to start their inclusive hiring journey.

Who are currently members?  Are other businesses invited to attend?

You can find the most current members on the our website. The Employer Roundtable includes a diverse range of organizations, including Microsoft, Ford, EY, JP Morgan Chase, SAP, Cintas, IBM, Travelers, and Rising Tide Car Wash. This last year, the Employer Roundtable grew from 5 to 15 organizations. We also welcome any company, who has been running an organized program to hire people on the spectrum for over a year, to join the Autism @ Work Employer Roundtable.

Why do these companies participate?

Each organization participates because they want to learn from other employers on their journey and share what they are experiencing in order to empower more people to be successful in the workplace. This is a space where companies do not compete. We are all looking to hire talent from this community and change the unemployment rate for people on the autism spectrum.


What can someone expect after they fill out the application?

The interview and hiring process for any candidate differs by employer. Through the Autism Hiring Programat Microsoft, we use a cohort model where we invite candidates to come to our campus and participate in a skills assessment program, gain feedback via mock interviews, and meet with hiring managers. We also offer each hire an immersive onboarding process with a comprehensive set of services to support the transition to working at Microsoft.

It is important to keep in mind that every company culture and process is slightly different. You can check out the Employer Roundtable website that gives examples of the opportunities that are available and to start the process.

What kind of background is the Roundtable looking for? In other words, who is most likely to be matched with an  opportunity?

Although we welcome all types of backgrounds, we commonly see experience in IT, testers, cybersecurity, and developers, but there is also a wide range of non-technical roles where employers are looking to hire great talent.

How does the roundtable partner with other organizations which help people with autism get jobs?

We partner with universities, non-profit organizations, and service providers to spread awareness of our programs and that we are hiring and looking for talent. We come together to see how we can help other employers start similar programs as we see disability as a strength, and we are always looking for partners to help.

Where can I find more information about the roundtable? 

The Autism @ Work Employer Roundtable websitehas all the important information and includes a job listing board for anyone interested in applying for available positions within each program.


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