The Autism studies/research thread

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A new study published in Autism Research reveals that autistic individuals possess unique mental imagery abilities, with some aspects being superior and others being similar to those of non-autistic individuals.

Mental imagery, which is the ability to visualize objects and scenarios in the mind without external stimuli, plays a crucial role in various cognitive functions such as remembering past events and making decisions. Previous research has suggested that autistic individuals often perceive the world differently and might have enhanced perceptual abilities, leading researchers to hypothesize that many aspects of mental imagery abilities could also be superior.

Led by Clara Bled from the Université Toulouse Jean Jaurès in France, the study team sought to test this theory. The researchers recruited 44 autistic adults (aged 18 to 50 years old, 52% women) and 42 typical participants without a neurodevelopmental disorder (aged 21 to 47 years old, 52% women). They were subjected to four tasks designed to assess different stages of mental imagery: image generation, visual pattern maintenance, image scanning, and mental rotation.

In the image generation task, participants were asked to mentally generate a letter on a grid and determine if it passed over a specific point. Both autistic and typical individuals performed similarly in terms of accuracy and response time, indicating no significant difference in this aspect of mental imagery.

The visual pattern test, which assessed the ability to maintain visual patterns in short-term memory, revealed a notable difference. Participants were briefly presented with a matrix with some sections filled in black, and were instructed to reproduce this pattern to the best of their ability. Autistic participants demonstrated a significantly higher span, indicating better ability to hold mental images compared to their typical counterparts.

The image scanning test required participants to inspect mental images and determine if an arrow pointed to a previously seen dot. Specifically, a pattern of dots was presented, then removed and replaced with an arrow. Participants then indicated whether the arrow pointed to a location previously held by the dot. While typical participants’ response times varied with the distance to inspect, autistic participants were equally fast regardless of the distance.

Bled and colleagues concluded, “Our findings support the hypothesis of typical or superior mental imagery abilities among autistic individuals. In a broader context, these results are in line with previous studies. Indeed, a more accurate and less top-down influenced (i.e., context-dependent) perception has been demonstrated in autistic individuals … [whom] may integrate the inducing context of information to a lesser extent. Thus, mental representations (i.e., mental images) in autism, like perception, may be more precise and context-independent.”

However, limitations are to be noted. For example, the authors acknowledged that the complexity of the protocol required participants to be of average or above-average intellectual functioning, which does not capture the entire autism spectrum.

A new brain imaging study has concluded that autism likely isn't caused by faulty connections to the amygdala.

A prevailing hypothesis of autism spectrum disorder has held that people with the condition have poorer neural connections in certain brain regions, including the amygdala.

However, researchers found no evidence that people with autism had amygdala connections that differed substantially to those found in people without autism.

The amygdala is a small, almond-shaped structure in the brain that plays a key role in processing emotions and social cues, researchers explained.

For the study, researchers analyzed high-quality MRI brain scans from 488 people, including 212 with autism.

The team focused on the neural connections emanating from the amygdala when the participants were not actively engaged in any tasks.

Average variation in connectivity to the amygdala was similar in people with and without autism, results showed.

The results were the same when researchers looked at specific subregions of the amygdala, researchers added.

The new study was published in the American Journal of Psychiatry.

"It is important to note that we do not conclude that amygdala [connectivity] is generally typical in autism. Instead, we conclude that the evidence for atypical [connectivity] of the amygdala in autism is weak at best, and unreliable," concluded the researchers led by Dorit Kliemann, an assistant professor of psychological and brain sciences with the University of Iowa.

In a recent review article published in BMC Public Health, researchers discussed the association between environmental pollutants and the incidence of Autism Spectrum Disorder (ASD).

They concluded that specific pollutants, including nitrogen dioxide, copper, and certain phthalates, are significantly linked to ASD, highlighting the need to identify factors that increase risk to develop effective prevention strategies.

Background
Environmental pollutants can disrupt cellular metabolism, cause oxidative stress, and trigger brain inflammation, all of which may contribute to ASD. Pollutants can also cause genetic damage and epigenetic changes that affect brain development.

The timing of exposure to these pollutants is crucial, as early exposure during prenatal and early postnatal periods can significantly impact neurodevelopment.

However, reviews of these links have limitations, often focusing on air pollutants and using restricted search criteria, potentially overlooking important evidence. Further research into these associations can lead to a better understanding of how pollutants affect ASD risk.

About the study
his systematic review and meta-analysis examined the relationship between ASD and various environmental pollutants. After screening individual 5,780 studies, researchers included 27 articles in the systematic review and used 22 in their meta-analysis.

The included studies involved nearly 1.3 million individuals, mostly children, with a smaller number of adolescents. The studies collectively investigated the impact of 129 different pollutants, including air pollutants and toxic substances.

Individual pollutants considered risk factors
Several pollutants were frequently studied, including nitrogen dioxide, particulate matter (PM 2.5 and PM 10), ozone, and various phthalates and polychlorinated biphenyls (PCBs). The studies showed significant associations between certain pollutants and an increased risk of ASD.

Pollutants such as monobutyl phthalate, nitrogen dioxide, mono-3-carboxypropyl phthalate, copper, and one PCB were notably linked to ASD. For instance, nitrogen dioxide exposure was associated with a 20% increase in the risk of ASD, although this finding had high heterogeneity between studies.

Conversely, copper exposure showed a smaller but significant association with ASD, with low variability among the studies.

Categories of pollutants
The meta-analysis also revealed a significant association between ASD and several pollutants when grouped by categories. Carbon monoxide, metals like iron and molybdenum, and nitrogen oxides were positively linked to ASD.

Conversely, carbamates and organophosphates, a type of pesticide, were negatively associated with ASD, indicating that higher exposure to these compounds was linked to a lower likelihood of ASD, though these findings had high variability.

Sensitivity and robustness checks
Sensitivity analyses, which tested the robustness of the results, confirmed the significant associations between nitrogen dioxide, copper, and certain phthalates with ASD.

These results held consistent even when considering different methods for diagnosing or screening for ASD. However, one PCB could not be included in these analyses due to a lack of sufficient studies.

Conclusions
This systematic review, including a meta-analysis, explored how environmental pollutants and ASD are linked in adolescents and children. The findings showed that being exposed to certain pollutants, such as copper, nitrogen dioxide, specific phthalates, and PCBs, increases ASD risk.

Further analyses also linked exposure to metals, nitrogen oxides, and carbon monoxide with a higher risk of ASD development.

The study's results align with previous research on pollutants like PCBs and carbon monoxide but showed some differences regarding nitrogen dioxide and certain phthalates, likely due to variations in study designs and pollutant exposure times.

While these findings suggest that environmental pollutants may be associated with an increased risk of ASD, the certainty of the evidence was rated as low to very low. This was primarily due to inconsistencies between studies, such as differences in how the pollutants were measured and the varying designs of the studies.

The researchers also noted a potential risk of publication bias, where studies showing significant results might be more likely to be published than those without significant findings.

In summary, this study highlights a potential link between exposure to certain environmental pollutants and ASD development risk, particularly pollutants like nitrogen dioxide, copper, and certain phthalates and PCBs. The study's strengths include a comprehensive search strategy and a focus on high-quality studies, but limitations such as variability in exposure times and detection methods were noted.

The researchers emphasize the need for standardized methods in future studies to improve the understanding of how environmental pollutants contribute to ASD and to develop effective prevention strategies. Further research with more consistent study designs and measurements is needed to strengthen these conclusions and improve the certainty of the evidence.

The diagnostic criteria for autism have evolved several times, in part to recognize a broader range of presentations. But two trends have persisted across studies: a higher prevalence in boys relative to girls and a substantially high heritability. This prevalence difference highlights that sex is one of the most important predictors of autism. It also suggests that the biology underlying this sex ratio could reveal mechanisms of this condition.

Many factors could contribute to the sex difference. For example, the presentation or development of autism traits may vary across sex, or girls and women may be more adept at camouflaging signs of autism. These and other nuances, coupled with biased gender expectations, may delay or reduce the recognition of autism in girls.

Nonetheless, because the etiology of autism is primarily genetic, with about 80 percent heritability, behavioral differences alone are unlikely to account for the observed disparity in prevalence across the sexes. Examining the heritability of autism by sex is therefore important for understanding how genetic factors that lead to autism may affect people differently.

We have developed modeling approaches that allow for sex-specific heritability estimation. Unlike past work, which assumed that both sexes share equal variance in genetic liability—and therefore equal heritability—our results show that autism is 10 to 12 percent more heritable in men and boys than in women and girls.

These findings point to several implications and provide guidance for future research. First, although autism is highly heritable in both sexes, there are measurable sex differences in its heritability. Second, researchers need to account for heritable influences and sex when studying the biology of autism, including in future studies that examine the condition’s severity, co-occurring conditions or age at diagnosis. Simply put, to understand autism’s roots, we need to understand relevant sex differences and whether causes might differ in boys and girls.

We used data from one of the world’s most extensive epidemiological registers to examine the relationship of sex to the heritability of autism among sibling and cousin pairs. Our cohort study included 1,047,649 Swedish children, forming 456,832 families.

By age 19, some 12,226 people—or 1.17 percent of our cohort—were diagnosed with autism. This group comprised 8,128 boys and 4,098 girls. As in previous research, we observed a high heritability for autism, with 87 percent heritability in boys and 75.7 percent heritability in girls. Higher male heritability persisted even after adjusting for factors such as birth year, gestational age and parental age.

Of course, variables other than additive genetic factors could influence the likelihood of an autism diagnosis. These variables—which we labeled as the “residual,” rather than the narrower term, “environment”—could have greater sway in girls.

The residual could include effects of the physical environment or environmental exposures, cultural differences affecting diagnosis, non-additive genetic factors such as rare or de novo variants, or a distinct presentation of autism in girls. But a series of sensitivity analyses indicated that these factors are unlikely to fully account for the difference in autism prevalence between sexes.

Altogether, our analyses suggest that additive genetic factors account for the majority of variance in autism occurrence and exert greater influence in boys than in girls. This conclusion supports a model in which men and boys are more susceptible to additive genetic influences that predispose people to autism.

Our findings align with the idea that there is greater variance of genetic liability for autism in boys. As such, these findings contrast with expected observations for the female protective effect (FPE), a prevailing theory for sex differences in autism prevalence.
The FPE generally emphasizes a higher genetic threshold for autism in girls. That theory usually assumes equal variance in genetic liability across sex. Other studies also fail to align with the FPE theory. For example, in a previous population registry study from our group, the children of women with autistic siblings did not show a greater likelihood of autism than the children of men with autistic siblings.

Although our observations do not exclude a female protective effect in autism, they suggest that other mechanisms may also explain sex differences in autism prevalence. For example, future investigations could explore gene-environment interactions that increase male susceptibility. Those factors could play out at the level of hormones, reflect effects of the Y chromosome or involve sex-differential regulatory effects by non-sex chromosomes.

Additionally, an alternative model of higher additive genetic variance in males (GVM) versus females warrants greater consideration. Underpinnings of a potential GVM effect could be explored by identifying autism endophenotypes that are more heritable in boys and emerge early in development, prior to the consolidation of the condition.

Given inconsistent evidence for the FPE, the possibility that higher additive genetic variance in boys contributes to the skewed sex ratio in autism should be given greater consideration. In that way, findings can inform future mechanistic studies to refine the assessment of autism likelihood and advance toward personalized targets for intervention.

In our new research, we looked at how genetic testing could support how people in New Zealand are diagnosed.

Genetic screening of 201 autistic individuals, as well as 101 non-autistic family members, found almost 13% of autistic participants had a clearly identified genetic variant. An additional 16% had a DNA change that likely explained their autism.

Importantly, our analysis was successful in identifying autism-linked genetic variants for autistic New Zealanders regardless of neurological differences and other diagnoses such as ADHD. Many of these individuals were adults who grew up before autism was widely recognised.

Diagnosing autism
The challenge with diagnosing autism is that it often occurs along with other neurodevelopmental conditions or mental health challenges such as intellectual disability, ADHD, depression and anxiety.

An autism diagnosis typically involves meeting with an expert such as a developmental paediatrician or clinical psychologist. After diagnosis, some forms of genetic testing may be offered.

But there is interest in identifying the ever-growing genetic variations underlying autism to provide precise genetic answers for families.

For some, having a precise genetic answer marks the end of a long search for an accurate diagnosis. For others it has provided personalised clinical management for co-occurring conditions.

Having an accurate genetic answer can help people find community support. This personalised care can support an individual’s wide range of skills, interests and personalities.

A recent study from Canada found using genetic testing for the diagnosis of neurodevelopmental conditions can reduce time to diagnosis by more than half.

This has important implications for publicly-funded healthcare in Aotearoa New Zealand. But it also gives individuals and their families a chance to access support sooner and develop a tailored pathway of care for all aspects of their health needs.

Identifying the genetic variants
Our research participants ranged in age from two to 81, with a reported autism diagnosis. The majority were older children (six to 12 years). The participants had a wide range of neurological differences, reflecting the diversity of autistic individuals in New Zealand.

After collecting their DNA, we used a flexible genome-wide approach to screen the progressively expanding list of causative genes in autism.

Where we found variants in the DNA, we filtered them through key criteria: how often they appear in the population, the predicted consequence of the variant on protein function, and what role the gene has in neurodevelopment.

The variants were categorised as either “causal”, “likely causal” or a “candidate” (based on American College of Medical Genetics and Genomics guidelines and international databases such as the Simons Foundation Autism Research Initiative gene database).

Of our 201 research participants, 12.9% had a genetic variant identified as “causal”. A further 15.9% had variants defined as “likely causal”. An additional 13.9% had “candidate” variants, which require further evidence to establish their role in autism.

A “causal” or “likely causal” variant was more likely to be discovered in participants who also exhibited global developmental delay (when they are significantly delayed in two or more areas of development) or intellectual disability than those who did not.

Offering clarity
Our research demonstrates that comprehensive genome-wide genetic testing can provide precise genetic answers for individuals and their families, marking the end of a long search for an accurate diagnosis.

The genome-wide approach can enable expanded testing to newly discovered genes so participants can benefit without the need for repeated testing.

In addition to reducing costs in an already strained medical sector, genetic testing can offer clarity, and tailor customised support for autistic individuals and their families.

Children born to mothers with obesity both before and during pregnancy have an increased risk of neuropsychiatric and behavioral conditions, including autism spectrum disorder (ASD), and attention deficit hyperactivity disorder (ADHD), according to new research from the University of South Australia.

The paper is published in the journal Psychiatry Research.
Conducted in partnership with Curtin University, Monash University, SAHMRI and a team of national institutions, the systematic review and meta-analysis of more than 3.6 million mother-child pairs across 42 epidemiological studies found that obesity during pregnancy:

increases the risk of ADHD in children by 32%
doubles the risk of developing ASD in children (by 2.23 times)
increases the risk of conduct disorders by 16%

The study also found that maternal pre-conception obesity or overweight was linked with an increased risk of ADHD, ASD, conduct disorder and psychotic disorder as well as a 30% increased risk in both externalizing symptoms, and peer relationship problems.

"In this study, we examined maternal overweight and obesity before and during pregnancy, finding that both are significantly linked with psychiatric and behavioral problems in children later in life, specifically ASD, ADHD and peer relationship problems.

"Given the rising global obesity rates among women of reproductive age, and the growing numbers of children identified with neurodiverse conditions, it's important that we acknowledge the potential long-term consequences of maternal adiposity on child mental health."

"While further research is needed to explore the biological mechanisms underlying these associations, the findings do stress the need for health interventions that promote healthy living and weight among parents-to-be."

Since the start of the COVID-19 pandemic in 2020, there have been several reports on the health emergency’s impact on child development. However, a new study is debunking fears that pandemic-era babies may face a higher likelihood of developing autism.

The research, conducted by a team at Columbia University Irving Medical Center in New York City, challenges concerns that the stress of the pandemic or exposure to the SARS-CoV-2 virus during pregnancy might lead to increased rates of autism in children. The study published in JAMA Network Open examined nearly 2,000 toddlers born before and during the pandemic, looking for early signs of autism using a common screening tool called the Modified Checklist for Autism in Toddlers, Revised (M-CHAT-R). This parent-report questionnaire helps identify children who may benefit from a more comprehensive evaluation for autism spectrum disorder.

Contrary to expectations, the researchers found no significant difference in positive autism screenings between children born before the pandemic and those born during it. Even more intriguingly, children whose mothers contracted COVID-19 during pregnancy actually showed lower rates of positive autism screenings compared to those whose mothers hadn’t been infected.

“Autism risk is known to increase with virtually any kind of insult to mom during pregnancy, including infection and stress,” says Dani Dumitriu, an associate professor of pediatrics and psychiatry and senior author of the study, in a university release. “The scale of the COVID pandemic had pediatricians, researchers, and developmental scientists worried that we would see an uptick in autism rates. But reassuringly, we didn’t find any indication of such an increase in our study.”

The study focused on children between 16 and 30 months-old, a crucial period when early signs of autism often become apparent. The research team analyzed data from two groups: one consisting of 1,664 children whose M-CHAT-R scores were obtained from electronic health records and another of 385 children whose parents completed the screening as part of an ongoing research study.

While the overall rates of positive autism screenings were higher in this study compared to general population estimates, the researchers attribute this to the unique characteristics of their sample. The study population was predominantly living in urban areas, with a high percentage of Hispanic participants and families from lower-income backgrounds — all factors associated with higher rates of autism diagnoses or positive screenings.

“There has been broad speculation about how the COVID generation is developing, and this study gives us the first glimmer of an answer with respect to autism risk,” Dumitriu adds.

These findings contribute to a growing body of evidence suggesting that prenatal exposure to mild or moderate COVID-19 infection may not significantly impact early childhood development. However, the researchers caution that longer-term follow-up is necessary, as some neurodevelopmental effects may not become apparent until later in childhood.

The study also highlights the complex relationship between biological and environmental factors in child development. While the pandemic caused widespread stress and disruption, it also led to some positive changes, such as more time at home for many parents.

“Children who were in the womb early in the pandemic are now reaching the age when early indicators of autism would emerge, and we’re not seeing them in this study,” Dumitriu concludes. “And because it’s well-known that autism is influenced by the prenatal environment, this is highly reassuring.”

Study Limitations
The study has several limitations. All children, including those born before the pandemic, were assessed during the pandemic, which may have affected how parents reported their children’s behavior. The study relied on a screening tool rather than definitive autism diagnoses. Additionally, most COVID-19 cases in the study were mild, so the findings may not apply to severe infections. Lastly, unmeasured differences between exposed and unexposed groups could have influenced the results.

Funding & Disclosures
The study was funded by grants from the National Institute of Mental Health, the National Institute of Child Health and Human Development, and other sources. Some researchers reported receiving grants or fees from various pharmaceutical companies and foundations, but these were generally outside the scope of the submitted work. The funders had no role in the design, conduct, analysis, or reporting of the study.

A new study published in the Molecular Psychiatry scientific journal has revealed that 75 percent of the genes associated with autism spectrum disorder (ASD) are also linked to schizophrenia.

The paper notes that ASD is “one of the highly heritable neuropsychiatric disorders” and schizophrenia also “has high heritability estimates.”

Though ASD is apparent in early childhood while the onset of schizophrenia happens in adulthood, clinical reports indicate that the two conditions co-occur at rates higher than in the general population. In addition, there is some overlap of symptoms in the realm of impaired social interaction.

Previous studies that examined the genetic connection between the two disorders have identified only a few shared genes.

The new findings reveal a much larger quantity of shared genes, and this is a very significant breakthrough in research,” said Prof. Shani Stern from the Sagol Department of Neurobiology at the University of Haifa, who led the study.

The researchers’ analysis provides additional support to the assertion that people with ASD may have an increased risk of schizophrenia.

Stern’s students, in cooperation with Prof. Ahmad Abu-Akel from the university’s School of Psychological Science, conducted a quantitative meta-analysis that examined a series of genetic research studies over the past decade.

The researchers also utilized meta-analysis to identify the shared phenotypes (observable traits, such as height, eye color and blood type) found in the nerve cells of people with ASD.

After analyzing the findings, the researchers discovered that 75% of the genetic variants that were attributed to ASD are also associated with the genes expressed in schizophrenia. Further analysis of the strongly associated common genes revealed that 45% of the variants are shared between both disorders.

ne of the most significant genes shared by the two disorders is CACNA1C, which is responsible for providing instructions for making one of several calcium channels. It is often associated with bipolar disorder and schizophrenia.

The other two major genes in common are TCF4, which provides instructions for the protein involved in developmental processes, and SORCS3, which codes for the protein that suppresses cytokine signaling.

According to new research from the Geisinger College of Health Sciences in Pennsylvania, risk factors for autism may be linked to the Y chromosome.

"A leading theory in the field is that protective factors of the X chromosome lower autism risk in females," Matthew Oetjens, an assistant professor at Geisinger's Autism & Developmental Medicine Institute, said in a statement.

However, Oetjens and his team at Geisinger College wanted to investigate whether the Y chromosome may also play a role.

To test this, the team analyzed a cohort of individuals with an abnormal number of X and Y chromosomes, a condition known as sex chromosome aneuploidy. These chromosomes, known as sex chromosomes, are the main factors in determining our sex, with XX usually resulting in females and XY usually resulting in males. However, roughly 1 in 450 newborns are born with more than two of these chromosomes, allowing the researchers to study their relative impacts on autism.

The study, published in the journal Nature Communications, explored the prevalence of autism spectrum disorders in 350 individuals with different variations of sex chromosome aneuploidy. What they found was that individuals with an extra X chromosome saw no change in their autism risk, whereas those with an additional Y chromosome were twice as likely to receive a diagnosis.

Decades of studies have described how difficulties in attention and impulse control underpin ADHD. Meanwhile, difficulties with switching attention and flexibility of thinking have been proposed to underpin autism.

As a result, different supports and interventions developed for different neurodevelopmental conditions target these skills. It sets up a system where a diagnosis is made first, then a set of supports is provided based on that diagnosis.

But our recent study, published in Nature Human Behavior, shows executive function problems are similar across all neurodevelopmental conditions. Understanding these common needs could lead to better access to supports before waiting for a specific diagnosis.

Our study found more similarities than differences
We looked at 180 studies, over 45 years, that compared executive function skills across two or more neurodevelopmental conditions.

We brought the research together for all neurodevelopmental conditions that have been defined by diagnostic manuals, including ADHD, Tourette's syndrome, communication disorders and intellectual disabilities.

Surprisingly, we found most neurodevelopmental conditions showed very similar delays in their executive skills.

Children with ADHD showed difficulties with attention and impulse control, for example, but so did children with autism, communication and specific learning conditions.

There were very few differences between each neurodevelopmental condition and the type of executive function delay.

This suggests executive function delay is best considered as a common difficulty for all children with neurodevelopmental conditions. All of these children could benefit from similar supports to improve executive skills.

But supports have become siloed
For decades, research has failed to integrate findings across conditions. This has led to siloed research and practices across the education, health and disability sectors.

Our data showed a gradual shift in the type of conditions that have been studied since 1980. In the earlier days, as a percentage, there were a far greater proportion of studies conducted on tic disorders, such as Tourette's syndrome. In the past ten years, autism has been of greater focus.

This means research and practice is also siloed, based on the focus on funding and interest in the community. Some groups miss out from good science and practice when they become less visible in the political landscape.

This has led to a skewed support system where only children with a specific diagnosis can be offered certain interventions. It also reduces access to supports if families can't access diagnostic services, which can be particularly difficult in regional and rural communities.

Due to these diagnosis-driven research practices, there are now assessment services, guidelines and treatments that are recommended for autism. These are usually independent from and not offered to children with ADHD, Tourette's syndrome, communication disorders or intellectual disabilities despite a significant overlap in children's needs.

How does this affect access to support?
Families often find it hard to get the help they need. They often describe the assessment and support process as confusing, with long wait times and lots of barriers.

We have previously shown caregivers often attend assessment and support services with a broad range of needs, but leave with many needs unaddressed.

Recent national child mental health, autism and ADHD guidelines call for more integrated supports for children. But most services are not well set up to do this. It will take time to drive such system change if this is to be achieved.

Why we need integrated research
More integrated research will lead to more cohesive support systems across education, health and disability for all children in need.

Studies show, for example, that many risk factors (genetic and environmental) are common to all neurodevelopmental conditions. These include a broad overlap of risk genes that are the same between conditions, and common environmental factors that influence development in the womb, such as the use of certain drugs, stress and a significant immune response.

Other studies show how most children diagnosed with one neurodevelopmental condition will also be diagnosed with others.

But gaps remain. While we know certain stimulant medications can work well for ADHD, for example, we have less information about how they might help children with other neurodevelopmental conditions who have attention difficulties.

Unlike our knowledge about social supports for children with autism, we don't have much research on how we can help children with ADHD with their social needs.

We should take a wider view of children's needs
It's important for families to be aware that if their child meets criteria for one neurodevelopmental condition, it is very likely that they will meet criteria for other neurodvelopmental conditions. They will likely have many needs relevant to other conditions.

It is worth asking clinical services about broader needs beyond a diagnosis. This should include developmental, mental and physical health needs.

It is also important to consider that many common interventions may have potential to support all children with neurodevelopmental conditions.

This is an important issue for government. Reviews are under way for supporting the needs of people with autism, intellectual disability and ADHD.

It's time to establish more integrated systems, supports and strategies for all people with neurodevelopmental conditions for their home, school, play and work.

Lyndsay A. Avalos, Ph.D., M.P.H., from Kaiser Permanente Northern California in Pleasanton, and colleagues examined the association between maternal cannabis use in early pregnancy and ASD in children in a population-based retrospective birth cohort study. The study cohort included 178,948 singleton pregnancies among 146,296 unique pregnant individuals, 4.7 percent of whom screened positive for cannabis use. The researchers found that 3.6 percent of children were diagnosed with ASD. Maternal prenatal cannabis use was not associated with child ASD after adjustment for maternal characteristics. After confounder adjustment, no statistically significant associations were observed when self-reported frequency of cannabis use was assessed.

In a second study, Avalos and colleagues examined associations between maternal prenatal cannabis use in early pregnancy and child early developmental delays in a cohort study involving 119,976 children born to 106,240 unique individuals followed up to age 5.5 years or younger. Maternal prenatal cannabis use was documented in 5.6 percent of pregnancies. The researchers observed no association between maternal prenatal cannabis use and child speech and language disorders, global developmental delays, or motor delays. The frequency of maternal prenatal cannabis use was not associated with child early developmental delays.

"Additional studies are needed to evaluate cannabis use throughout pregnancy, mode of administration and product strength, as well as potential factors that may mitigate adverse associations and neurodevelopmental outcomes that may emerge later in childhood," Avalos and colleagues write in the second study.

One author of the second study disclosed receiving grants from the Gerber Foundation.