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Autism increases to one in 54 children

Headlines have quieted down, but the numbers — and disagreements — march on

April 19, 2020 by Richard Moore

A decade ago — even five years ago — annual reports of ever higher numbers of autism in the American population were enough to launch a battery of headlines, as the nation’s families and schools braced for what they believed the exploding numbers foretold: a disorder of epidemic proportion in the United States and around the world.

In 2020, most of the major headlines are gone, but Autism Spectrum Disorder (ASD) is not. In fact, according to new numbers released last month by the Centers for Disease Control (CDC), ASD is still marching on.

The CDC report, released March 26, found that in 2016 ASD prevalence was 18.5 per 1,000 eight year olds, or one in 54. The CDC’s surveillance program monitors and provides estimates of ASD among eight 

year olds in 11 sites in the U.S., including one in Wisconsin. The numbers are released every two years and reflect the eight-year-old population four years earlier.

The one in 54 number represents 1.9% of all U.S. eight year old children, an increase of 8.4% over the previous two years and a new record. In 2018, the number was one in 59. 

In 2000, the prevalence rate was one child in 150; in 2004, one in 125; in 2008, one in 88; and in 2012, one in 69.

The one thing as consistent as the rise in numbers is the debate about the cause of ASD.

On the one side there are those, armed with reams of scientific studies, who assert that ASD is driven by genetic anomalies and predispositions. Alison Singer, the founder of the Autism Science Foundation, put it this way to the Wall Street Journal: “Autism is a genetic disorder. The only thing the parents do wrong is have the wrong genes.”

On the other side are those who believe environmental factors play a huge role, whether as the sole cause or in some combination with genetics. These advocates — oftentimes backed with peer-reviewed studies of their own — point to a host of potential causes, from pesticides to heavy metals to vaccines to an accumulation of all of the above.

For example, one leading researcher at the University of California-Davis, Dr. Irva Hertz-Picciotto, has delved into links between an increased risk of autism spectrum disorders following exposure to substances commonly used in everyday life.

“Tens of thousands of chemicals are on the market for which we cannot say that they are safe for fetuses and small children, either individually or in combination,” Hertz-Picciotto told Scientia Magazine in 2017.

In recent years there has been an emerging scientific consensus that both genetics and the environment play a role. Within that consensus, though, there is a large spectrum of thought on how nature and nurture actually interact.

“First, there is no single cause of ASD, and few if any cases of ASD results from one factor acting alone,” Hertz-Picciotto wrote in the Orange County Register in 2013. “Second, both genes and environment play substantial roles. Most genes probably increase susceptibility. Here, environment may act in concert with the underlying susceptibility or may contribute to it, by altering which genes are expressed (i.e., turned ‘on’).”

And, Hertz-Picciotto stressed, that environment is broad.

“It includes diet and nutrition; bacteria, viruses, medical procedures and medications; and environmental chemicals (naturally occurring and man-made) in air, food, water, soil and everyday household and personal care products used for cleaning homes or on our bodies or hair,” she wrote. “In short, environment covers anything not inherited in our DNA code.”

In 2019, a turn

While most research has been consistent in attributing causation to both genetics and environment, a quiet turn has taken place now that most of the headlines are gone. In much of the new research, the environment’s role has been relegated to secondary status while genetics has been elevated to primary causation.

In a 2019 study, “Association of Genetic and Environmental Factors With Autism in a 5-Country Cohort,” Dr. Dan Bai and his colleagues reported analyzing a population-based, multinational cohort study, including full birth cohorts of children from Denmark, Finland, Sweden, Israel, and Western Australia born between Jan. 1, 1998, and Dec. 31, 2011, and followed up to age 16 years. 

The data was analyzed between September of 2016 and February 2018.

Across five countries, the study stated, models were fitted to estimate and describe the total variance in risk for ASD occurrence owing to additive genetics, maternal, and shared and nonshared environmental effects.

The study included more than 2 million people, of which 22,156 were diagnosed with ASD. The study found that median ASD heritability was 80.8% for country-specific point estimates, ranging from 50.9% in Finland to 86.8% in Israel. Maternal effects were minimal.

“Based on population data from five countries, the heritability of ASD was estimated to be approximately 80%, indicating that the variation in ASD occurrence in the population is mostly owing to inherited genetic influences, with no support for contribution from maternal effects,” the study stated.

That suggests that the mother’s life experience before birth — her weight, or diet, or whether she has an infection during pregnancy — does not contribute to autism. And because environmental causes are responsible for just 20% of the risk, either by themselves or in interaction with genetic influence, the environment, while statistically significant, becomes a bit player, not a co-star, in the major causes of autism.

“The contribution of the environment to autism spectrum disorder risk appears to be much smaller than the contribution of genetics,” Drs. Amandeep Jutla, Hannah Reed, and Jeremy Veenstra-VanderWeele of Columbia University wrote in an editorial about the Bai findings in the journal JAMA Psychiatry.

This frustrates those who think environmental factors are heavily involved and who wonder, if the disorder is primarily inherited, where all those people with inherited autism were in earlier generations. They believe an environmental trigger, whether individually specific or cultural in scope, is involved.

A pesticide of a different color

They also point to studies that don’t get the same headlines but have reached opposite conclusions nonetheless.

In a 2019 study published in BMJ, “Prenatal and infant exposure to ambient pesticides and autism spectrum disorder in children,” Dr. Ondine S. von Ehrenstein, an associate professor at the UCLA Fielding School of Public Health, and her colleagues examined associations between early developmental exposure to ambient pesticides and autism spectrum disorder.

They concluded an offspring’s risk of ASD increases following prenatal exposure to ambient pesticides within 2000 meters of their mother’s residence during pregnancy, compared with offspring of women from the same agricultural region without such exposure. Infant exposure also could further increase risks for autism spectrum disorder with comorbid intellectual disability, they wrote.

The study followed 2,961 people with a diagnosis of autism spectrum disorder based on the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, including 445 with intellectual disability comorbidity, as identified through records maintained at the California Department of Developmental Services and linked to their birth records, the researchers wrote. 

In the study, data from California state-mandated Pesticide Use Reporting were integrated into a geographic information system tool to estimate prenatal and infant exposures to pesticides, the researchers stated, and 11 high-use pesticides were selected for examination according to previous evidence of neurodevelopmental toxicity in vivo or in vitro.

The risk of ASD was associated with prenatal exposure to glyphosate, chlorpyrifos, diazinon, malathion, avermectin, and permethrin — all pesticide substances. For autism spectrum disorder with intellectual disability, they wrote, estimated odds ratios were higher by about 30% for prenatal exposure to glyphosate, chlorpyrifos, diazinon, permethrin, methyl bromide, and myclobutanil, and exposure in the first year of life increased the odds for the disorder with comorbid intellectual disability by up to 50% for some pesticide substances.

Other environmental concerns

A raft of other studies have pointed to active environmental causations in certain populations. A 2012 study, for example, out of the University of Aarhus in Denmark, located a small increased risk for ASD and infantile autism after the use of different antibiotics during pregnancy.

A 2010 review, “Environmental Risk Factors for Autism: Do They Help Cause De Novo Genetic Mutations That Contribute to the Disorder?” by Harvard’s Dr. Dennis Kinney acknowledged that advanced parental age at the time of conception is associated with increased risk for both autism and de novo mutations, but his team set out to investigate the hypothesis that other environmental factors associated with increased risk for autism might also be mutagenic and contribute to autism by causing de novo mutations. 

In a review of the literature, his team identified nine environmental factors for which increased pre-conceptual exposure appeared to be associated with increased risk for autism. Five of the factors — mercury, cadmium, nickel, trichloroethylene, and vinyl chloride — are established mutagens, the researchers reported, while another four, including residence in regions that are urbanized, located at higher latitudes, or experienced high levels of precipitation, are associated with decreased sun exposure and increased risk for vitamin D deficiency. 

The researchers also explored the role that heavy metals and other pollutants might play in higher autism rates and they found evidence of a strong correlation.

One study, for example, identified several pollutants associated with increased prevalence of autism spectrum disorders by comparing U.S. Environmental Protection Agency data on pollutant exposure with demographic data on 284 children with ASD and 657 controls in the San Francisco Bay Area, the Kinney researchers wrote. 

“Children from areas exposed to higher concentrations of three heavy metals and two chlorinated solvents had significantly higher rates of ASD than children residing in areas with low exposure,” Kinney wrote. “The substances for which higher exposure was most strongly correlated with increased ASD risk were mercury, cadmium, nickel, trichloroethylene, and vinyl chloride.”

Kinney said a complementary ecological study investigated autism prevalence as a function of proximity to industrial and power plant sources of environmental mercury in 1,040 Texas school districts and found higher rates of autism. 

“After controlling for socioeconomic factors and urbanicity, Palmer et al. found that autism prevalence increased 2.6% for every 1,000 pounds of mercury released in the vicinity of the geographical center of a given district, and 3.7% with nearby power plant emissions,” he wrote.

What’s more, Kinney observed, a meta-analysis of prevalence studies around the world found that significantly increased risk for autism was associated with urban vs. rural residence, and he said several studies had reported that a significantly higher autism prevalence was associated with residence in geographic regions at higher latitudes.

A study published in 2014, “Urbanicity and Autism Spectrum Disorders,” corroborated the increased risk in urban areas.

“We found a dose-response association with greater level of urbanicity and risk of ASD,” the study stated. “This association was found for residence at birth as well as residence during childhood. Further, we found an increased risk of ASD in children who moved to a higher level of urbanicity after birth.”

As for higher prevalence rates in northern locations, Kinney wrote, two studies conducted by the Centers for Disease Control found that when prevalence rates of ASD were compared across different U.S. states that had used the same ascertainment procedures, autism prevalence was significantly higher in New Jersey than in any of the nine other, more southern states. 

A 2016 review upheld those geographical findings. More northern states — including Minnesota, Iowa, Missouri, Illinois, Indiana, Maine, New Hampshire, Massachusetts, Connecticut, and New Jersey — were more likely than southern states to have prevalence rates above 3%.

Indeed, Florida was the only southern state to reach a 3% ASD prevalence rate in the survey.

A parallel reason for increase; a parallel failure of reason

In addition to the causes of autism, debate continues to flare about whether there has been a true increase in autism prevalence or whether increasing numbers merely reflect better diagnosis and awareness.

In the early days of skyrocketing autism numbers, those who rejected an environmental link argued that better diagnosis and awareness of the disorder accounted for sharply increasing ASD numbers. 

The counter was (and is) that, while some increases could undoubtedly be chalked up to better awareness and diagnosis, those factors alone could not possibly account for the astronomical increase in ASD from one in 10,000 children to one in 54. Troops on the ground — both parents and teachers — also reported the rise of a real and new disorder based on behaviors they were observing.

The “better-diagnosis” argument persists, though with less credibility — every doctor is aware of ASD these days — but now a parallel argument has emerged to explain the latest rise in numbers, that is, better screening at a younger age is catching more ASD cases early, and the new numbers merely reflect earlier diagnosis.

For example, a report on early identification of ASD among children aged four years, published by the CDC to accompany the new prevalence figures on eight year olds, shows a much higher incidence of early diagnosis at age four.

“In 2016, the overall prevalence of ASD in the Early ADDM Network using DSM-5 criteria (15.6 per 1,000 children aged 4 years) was higher than the 2014 estimate using DSM-5 criteria (14.1 per 1,000),” the report stated. “Children born in 2012 had a higher cumulative incidence of ASD diagnoses by age 48 months compared with children born in 2008, which indicates more early identification of ASD in the younger group.”

Some who say autism numbers aren’t really higher have interpreted that to mean the increase in autism diagnoses at eight years of age only reflects an uptick in autism diagnosis at four years of age.

“An accompanying report on 4-year-old children suggests that more autistic children are being identified earlier,” says a March 26 report in Spectrum News. “If the trend continues, experts say, the prevalence among 8-year-olds will continue to rise.”

Spectrum News is associated with the Simons Foundation, which has long contended that autism is genetically based and has long contested the notion that higher prevalence rates are anything other than better awareness and diagnosis.

On the other hand, a higher diagnosis of autism at age four might merely mean those children are being diagnosed then rather than at age six or seven, which would not affect the eight-year-old count every two years, which is the basis for the official CDC numbers.

However, another development in this year’s numbers might challenge whether the new numbers represent a real rise in prevalence. For the first  time, the discrepancy between prevalence rates for whites and blacks virtually disappeared.

It has long been suspected that autism in blacks has been undercounted because of a variety of socioeconomic factors, and many say the new numbers show that the government’s effort to increase inclusion of the black population in its monitoring has paid off.

That could be true, but, if it is, that merely means autism prevalence rates were higher than previously reported.

Richard Moore is the author of the forthcoming “Storyfinding: From the Journey to the Story” and can be reached at richardmoorebooks.com.

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