The Autism studies/research thread

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Stanford Medicine scientists investigating the neurological underpinnings of autism spectrum disorder have found that hyperactivity in a specific brain region could drive behaviors commonly associated with the disorder.

Using a mouse model of the disease, the researchers identified the reticular thalamic nucleus—which serves as a gatekeeper of sensory information between the thalamus and cortex—as a potential target for treatments.

Moreover, they were able to reverse symptoms similar to those of autism—including susceptibility to seizures, heightened sensitivity to stimulus, increased motor activity, repetitive behaviors and decreased social interactions—by giving the mice drugs that suppressed this area of the brain.

The same drugs are being studied for the treatment of epilepsy, highlighting where the processes underlying autism spectrum disorders and epilepsy may overlap in the brain and why they often occur in the same patients.

The findings are published in Science Advances. The senior author of the study is John Huguenard, Ph.D., professor of neurology and neurological sciences. The lead author is Sung-Soo Jang, Ph.D., a postdoctoral scholar in neurology and neurological sciences.

The neural circuitry connecting the thalamus and cortex has been implicated in autism in both humans and animal models, but the role of the reticular thalamic nucleus was not clear.

In the new study, the researchers recorded the neural activity of this brain region in mice while observing the animals' behavior. In mice that had been genetically modified to model autism (Cntnap2 knockout mice), the reticular thalamic nucleus showed elevated activity when the animals encountered stimuli like light or an air puff as well as during social interactions. The brain region also showed bursts of spontaneous activity, causing seizures.

Epilepsy is much more prevalent in people with autism than in the general population—30% versus 1%—though the mechanisms are not well understood. Recognizing this connection, the researchers tested an experimental seizure drug, Z944, and found that it reversed behavioral deficits in the autism mouse model.

With a different experimental treatment that genetically modifies neurons to respond to designer drugs, known as DREADD-based neuromodulation, the researchers could suppress overactivity in the reticular thalamic nucleus and reverse behavioral deficits in the autism mouse model. They could even induce these behavioral deficits in normal mice by ramping up activity in the reticular thalamic nucleus.

The most comprehensive quantitative review of research into complementary and alternative treatments for autism has found no strong evidence to support their use, and that the safety of these treatments was rarely assessed.

A new study from Paris Nanterre University, Paris Cité University and the University of Southampton, published in Nature Human Behaviour,assessed 248 meta-analyses, including 200 clinical trials involving over 10,000 participants.

Researchers were investigating the efficacy and safety of complementary, alternative and integrative medicines (CAIMs) to treat autism. They looked at 19 types of treatment, including animal-assisted interventions, acupuncture, herbal medicine, music therapy, probiotics and Vitamin D.

The team also created an online platform to make it easier for people to see the evidence they generated on different CAIMS.

Autistic people can find it hard to communicate, understand how people think or feel, be overwhelmed by sensory information, become anxious in unfamiliar surroundings and carry out repetitive behaviors.

All of this can interfere with their quality of life, and up to 90% report having used CAIMs at least once in their lifetime.

"Many parents of autistic children, as well as autistic adults, turn to complementary and alternative medicines hoping they may help without unwanted side effects," says Professor Richard Delorme, Head of the Child and Adolescent Psychiatry Unit at Robert Debré Hospital in Paris.

Researchers carried out an umbrella review—a type of study that pulls together evidence to give an overall "big picture" summary.

Dr. Corentin Gosling, Associate Professor at the Paris Nanterre University and first author of the study, explains, "Rather than looking at individual trials, we reviewed all the available meta-analyses, which are a compilation of many trials. This allowed us to evaluate the full body of evidence across different treatments.

"Importantly, we also developed a free and easy-to-use online platform, which we will continue to test. Ultimately, we hope this tool will support autistic people and practitioners in choosing together the best treatment."

While some treatments showed potential, most studies were supported by weak or poor-quality evidence, so the effects are not reliable. Concerningly, safety assessments were missing for most treatments, with less than half of CAIMs having had any evaluation of the acceptability, tolerability or adverse events.

Professor Samuele Cortese, NIHR Research Professor at the University of Southampton and co-senior author, concluded, "This study shows that when people want to know whether a treatment is effective, they shouldn't just look at one single study. It's essential to consider all the available evidence and how good that evidence is. Drawing conclusions from one low-quality study can be misleading."

Despite broad efforts in recent years to identify children with autism early, many continue to go undiagnosed for years. New research suggests that genetics may explain why.

Kids who receive an autism label earlier — generally before the age of 6 — have distinct genetic and developmental profiles compared to those who are diagnosed at older ages, according to findings published this month in the journal Nature.

Researchers analyzed longitudinal data from children with autism in the U.K. and Australia to assess whether the age of diagnosis was associated with different behavioral trajectories. They also evaluated genetic data from more than 45,000 individuals with autism in Europe and the U.S., looking at sets of thousands of variants that are responsible for certain traits.

“We found that, on average, individuals diagnosed with autism earlier and later in life follow different developmental pathways, and surprisingly have different underlying genetic profiles,” said Xinhe Zhang, a researcher at the University of Cambridge who led the study.

Children diagnosed with autism earlier in life were more likely to have behavioral challenges and issues with social interaction from a young age, the study found.

By contrast, those diagnosed later often exhibited social and behavioral difficulties during adolescence, the findings indicated. They were also at increased risk for depression and other mental health conditions.

Meanwhile, the genetic data showed distinct profiles for those diagnosed earlier versus later with little overlap. In fact, the researchers said that the average genetic profile of individuals diagnosed later is more similar to those with ADHD and mental health conditions than children with autism who were diagnosed at younger ages.

“Our findings suggest that the timing of autism diagnosis reflects more than just differences in access to healthcare or awareness, important as these are,” Zhang said. “However, it is important to note that these are average differences on a gradient, so earlier and later diagnosed autism are not valid diagnostic terms.”

The researchers said that their findings have broad implications for how autism is viewed and studied and for how those with the condition are supported.

“The term ‘autism’ likely describes multiple conditions,” said Varun Warrier from the University of Cambridge, a senior author of the study. “Understanding how the features of autism emerge not just in early childhood but later in childhood and adolescence could help us (recognize), diagnose and support autistic people of all ages.

emple Grandin, PhD, is likely the most well-known, living autistic individual—both nationally and internationally. As Distinguished Professor of Animal Science at Colorado State University, she is equally famous as an astute observer and researcher of animal science and behavior, especially in designing humane livestock-handling systems. As a stellar scientist and educator driven by scientific inquisitiveness, Dr. Grandin extended her writings and research toward an improved understanding of autism, including how her own journey and insights could provide testable hypotheses about its neurobiological underpinnings.

Growing up in the 1940s through the 1960s, Dr. Grandin battled misperceptions about autism, which sparked her first writings about coping strategies (Grandin, 1983). She then asked more fundamental scientific questions about the neurobiology of autism, which moved toward personal speculations about brain–behavior relationships and the autism spectrum (Grandin, 2009a, 2009b; Ratey et al., 1992). In these later publications, Dr. Grandin wrote about how she processes sounds and visual stimuli, speculating on how differences in brain organization and connectivity may relate to autistic features. When lecturing about autism, Dr. Grandin routinely discussed how she “thinks in pictures, not words.”

In this personal quest, knowing how important a unique case study can be in medicine and psychology, Dr. Grandin underwent magnetic resonance imaging (MRI) of her brain, working with investigators at the University of Utah, the University of Wisconsin–Madison (UW), and Brigham Young University (BYU), who had formed the Interdisciplinary Science to Learn about Autism collaborative research program. These extensive MRI studies involved both structural and functional MRI, which included state-of-the-art quantitative neuroimaging analyses as well as a battery of neuropsychological tests. Current advances in quantitative neuroimaging, combined with neuropsychological assessment findings, now permit a more comprehensive understanding of brain–behavior relations by directly examining brain MRIs.

In a case study published in the Journal of Pediatric Neuropsychology, Erin David Bigler and colleagues summarize the initial neuroimaging investigations involving brain morphometrics and Dr. Grandin’s functional neuroimaging. These studies integrated her brain-imaging data with her neurocognitive profile, derived from standard methods of neuropsychological assessment. This article is the first of a series showing how advanced neuroimaging can provide unique insights potentially relevant to understanding variation in autistic adults.

A comprehensive scientific platform synthesizing evidence from over 400 clinical trials (25,000+ participants) to support informed decision-making about autism interventions across the lifespan.

A sweeping international review of nearly 250 analyses has found that popular complementary and alternative treatments for autism lack strong scientific support, and their safety is rarely evaluated.

The largest and most detailed analysis of alternative and complementary autism treatments has found little reliable evidence that these methods are effective, and noted that their safety is seldom evaluated.

In a study published in Nature Human Behaviour, researchers from Paris Nanterre University, Paris Cité University, and the University of Southampton reviewed 248 meta-analyses, which together included 200 clinical trials and more than 10,000 participants.

The research examined how well complementary, alternative, and integrative medicines (CAIMs) work in treating autism, as well as their safety. The team analyzed 19 different approaches, such as animal-assisted therapy, acupuncture, herbal remedies, music therapy, probiotics, and Vitamin D.

In a recent study, scientists discovered a link between autism and evolution.

The study showed that layer 2/3 of intratelencephalic excitatory neurons, also known as the outer layers of human brain cells, change more quickly than in non-human primates.

Although the reason is unclear, research suggests that this development in humans is related to critical thinking and learning or language capacity.

L2/3 IT neurons are crucial for cortical processing. They form connections across different parts of the cortex, playing a key role in supporting cognitive functions such as language, abstract reasoning and other complex cognition.

The study combined single-celled RNA sequencing datasets from humans and non-human primates to examine how L2/3 IT neurons influence different brain regions. Specifically, it focused on how gene expression varies between species.

The study revealed that human-accelerated regions are sections of the genome that have been sequenced by natural selection in other mammals and have evolved rapidly in humans. It was also found that individuals with autism and schizophrenia have an excess of genetic variants.

Scientists tested collections of genes that are associated with autism and discovered that L2/3 IT neurons are expressed at lower levels compared to chimpanzees. This occurred due to positive natural selection acting on genes through changes in gene regulatory regions.

The rapid evolution of autism-linked genes may have provided a fitness advantage by slowing down postnatal brain development or creating space for language capacity.

The additional time during early childhood for brain development was beneficial to human evolution because it led to more complex thinking.

Autism is often stigmatized and misunderstood

Research that supports the idea of autism developing humans’ complex thinking skills humanizes the disorder and shows that humans have evolved in various ways to support growth and survival.

Ultimately, research suggests that autism and schizophrenia are beneficial to humans because both stimulate complex thinking and enhance language capacity, making humans more neurodiverse.

Despite these discoveries, more research must be done to look at why these traits occur in individuals with these disorders and understand why fitness is reduced.

Abstract
Accounts of emotional dysregulation in autism and ADHD are typically based on external adult observations anchored in neurotypical notions of appropriate emotional responses1. These often fail to account for neurodivergent people’s efforts to regulate in the context of the upsetting experiences they face, and to explore how neurodivergent young people manage emotional burden or find effective strategies to reduce distress and increase resilience. We interviewed 57 adolescents (11-15 years; 19 females) with diagnoses of ADHD (n=24), autism (n=21) or both (n=12), about their experience of upsetting events using a codesigned semi-structured interview schedule. We analysed data using reflexive thematic analysis which generated shared themes with diagnostic nuances. Three themes were found: What helps prevent experiences from becoming upsetting, Managing emotional responses during periods of upset and Leveraging own strengths. Participants highlighted the importance of consistent, neurodivergent-affirming environments, flexible supports, and being genuinely accepted. Autonomy in choosing self-regulation strategies, co-regulation and expressing distress without stigma were key to emotional wellbeing. These findings underscore the value of stable, trusting relationships and the need for predictable routines. Results offer actionable insights for educators, caregivers, and professionals aiming to foster inclusive, emotionally supportive environments for neurodivergent youth.

Exposure to specific components of fine particulate air pollution during pregnancy may raise a child’s risk of developing autism, according to Canadian researchers.

They have found that fine particulate matter, particularly its sulphate and ammonium components, is linked to increased autism spectrum disorder (ASD) diagnoses in early childhood, with the second and third trimesters emerging as critical periods of vulnerability.

The researchers said their study added to growing evidence that air pollution, particularly its chemical makeup, could influence neurodevelopmental outcomes.

Their findings have met mixed reactions from experts around the world, including in Australia, some of whom warn the findings show correlation, not causation.

Sulphate typically originates from industrial and power generation sources, while ammonium stems from agriculture, sewage and vehicle emissions.

The population-based study, published in JAMA Network Open, analysed more than 2.1 million births in Ontario between 2002 and 2022, linking detailed air pollution estimates with administrative health data.

The researchers found that prenatal exposure to sulphate and ammonium – key chemical components of fine particulate matter (PM 2.5) – was associated with a statistically significant increase in ASD diagnoses by age five years.

The findings held even after accounting for total PM 2.5 levels and postnatal exposure.

Children whose mothers were exposed to higher concentrations of sulphate and ammonium during the second and third trimesters were more likely to be diagnosed with ASD, suggesting these periods are particularly sensitive to environmental insults, the researchers wrote.

Postnatal ozone (O₃) exposure was also linked to elevated risk, although the association with prenatal ozone disappeared after adjustment for early-life exposure.

“Fine particulate matter (PM 2.5) is a well-established air pollutant linked to a wide range of adverse health outcomes,” the researchers wrote.

“Despite regulatory advances, PM 2.5 exposure remains a public health concern, particularly in urban areas with substantial industrial and vehicular emissions.

“Prenatal and early postnatal exposure to PM 2.5 is of particular concern, as it has been associated with neurodevelopmental outcomes, including autism spectrum disorder (ASD).

“Clinical and animal studies suggest several biological pathways through which PM 2.5 may influence neurodevelopment, including epigenetic modifications, pro-inflammatory responses, and oxidative stress.

“These mechanisms are thought to contribute to structural and functional changes in the developing brain.

“However, most epidemiological studies have focused on total PM2.5 mass, often overlooking potential variability in toxic effects among its chemical components.”

The cohort included more than two million mother-infant pairs with complete residential and health insurance data. ASD diagnoses were identified using a validated administrative algorithm with a follow-up period extending to five years of age. About 0.8% of children in the study were diagnosed with ASD, with boys affected roughly three and a half times more often than girls.

The associations were strongest among urban populations and more pronounced in lower-income and racially diverse neighbourhoods, underscoring persistent environmental inequities.

The authors acknowledged several limitations, including potential exposure misclassification due to reliance on residential postal codes and limited sensitivity of ASD case identification. Nevertheless, the large sample size, long follow-up, and fine temporal resolution of exposure estimates lent weight to the findings, they said.

“These findings underscore the potential importance of early-life environmental exposures and reinforce the need for public health strategies to reduce air pollution, particularly in urban and socioeconomically disadvantaged communities,” the researchers concluded.

Among the experts unattached to the research who weighed in on the findings was Dr Rachel Moseley, principal academic in Psychology at Bournemouth University in the UK.

“This paper shows a correlation between prenatal exposure to sulphate and ammonium components and childhood autism diagnoses,” she said.

“There is absolutely no evidence within the paper to suggest that the former caused the latter.

“It could potentially cause great worry to the general population if they thought this paper demonstrated a causal effect, having already been exposed to inaccurate claims around Tylenol and vaccines as causes of autism.

“Reports like this contribute to the very harmful myth that autism is increasing in prevalence: robust evidence from many studies indicates that this is not the case, but rather more autistic people, especially women and adults, are being recognised and diagnosed (which is an excellent thing, both on a personal level but also on a socioeconomic one, since late diagnosis is associated with poorer health and suicidality).

The wording and framing of the article, talking about ‘autism risk’, also contributes to harmful narratives in which autism is presented such as a disease, something negative to be eradicated or avoided; we know that these kind of messages are felt as deeply detrimental by autistic people and their families, who feel they’re living in a world where they’re unwanted and unacceptable.

“It is deeply disappointing that authors continue to contribute to these harmful narratives rather than following responsible guidelines in the way they speak about autism – thus harming the community they’re studying.”

Professor Anne-Louise Ponsonby, division head for Early Brain Science and head of the Neuroepidemiology Research Group at the Florey Institute for Neuroscience and Mental Health in Melbourne, said the paper highlighted “the importance of early life environment in autism”.

“Autism is often a multifactorial condition, where multiple factors, both environmental and genetic combine to cause the condition,” she said.

She said an important next step would be to look at the combined effect of multiple air pollutant chemicals, including those generated inside the home.

“Further, this work reinforces the importance of considering manufactured chemicals more generally to consider the combined effect of total chemical load,” Professor Ponsonby said.

“Consideration needs to be given that chemicals are not only inhaled but absorbed through the skin and also ingested. If chemicals are leading to similar biological effects in the body, then their additive or supra-additive effects will be important to consider.”

“We are investigating these issues in neurodevelopmental work at the Florey Institute, together with other Australian collaborating organisations.

“A key focus is the possible contribution of plastic chemicals in early life, and this work is supported by the Minderoo Foundation. Our work indicates it is important to consider not only combined chemical effects but also child genetic vulnerability to these environmental exposures.”

Dr Chloe Brimicombe, a climate scientist and public engagement manager at the Royal Meteorological Society in the UK, said the study showed correlation between air pollution exposure and potential cognitive development towards neurodivergence and autism.

“This study is not confirming air pollution exposure causes autism in children. This is because we do not know the biological pathways where air pollution could change neurodevelopment in this way,” she said.

“We do know that negative impacts on cognitive function are associated with air pollution exposure but most of this research is for an older age category.

“The study highlights important next steps around introducing socioeconomic variables alongside air pollution to suggest why an individual might be neurodiverse vs neurotypical, another approach is called life course analysis where we model air pollution over different phases of life.”

A large study from Massachusetts found that babies whose mothers had COVID-19 while pregnant were slightly more likely to have a range of neurodevelopmental diagnoses by age 3. Most of these children had speech or motor delays, and the link was strongest when the mother was infected late in pregnancy and in boys.

The increase in risk was small for any one child, but because millions of women were pregnant during the pandemic, even a small increase matters. The study doesn't prove that COVID-19 infection during pregnancy causes autism or other brain conditions in the fetus, but it suggests that infections and inflammation during pregnancy can affect how a baby's brain grows, something scientists have seen before with other illnesses. It's reason to help pregnant women avoid COVID-19 and to keep a close eye on children who were exposed in the womb.

What the study found
Researchers at Massachusetts General Hospital examined medical records from more than 18,000 mothers and their children born between March 2020 and May 2021, before vaccines were widely available. Because everyone giving birth during that period was tested for COVID, the team could clearly see which pregnancies were exposed.

About 5% of those mothers had COVID while pregnant. Their children were modestly more likely to be diagnosed with a neurodevelopmental condition by age 3 than those whose mothers weren't infected, even after accounting for differences in maternal age, race, insurance status, and preterm birth.

The link appeared strongest when infection occurred in the third trimester and among boys. Still, the vast majority of children in both groups showed typical development.

"This was a very clean group to follow," said Dr. Andrea Edlow, a maternal-fetal medicine specialist at Mass General and one of the study's authors. "Because of universal testing early in the pandemic, we knew who had COVID and who didn't."

Experts say COVID, which causes a powerful immune response in some people, fits the biological pattern seen with other infections in pregnancy. Dr. Alan Brown, a professor of psychiatry and epidemiology at Columbia University, who studies maternal infection and brain development, explained, "COVID would be a very strong candidate for it to happen because the amount of inflammation is very extreme."

How might infection affect brain development?
Scientists are still piecing together how various types of infections in pregnancy affect fetal development. Severe illness can cause inflammation that disrupts brain growth or trigger preterm birth, which carries its own risks.

"There's a long history of evidence showing that maternal infection can slightly raise the risk for many neurodevelopmental disorders," said Dr. Roy Perlis, the vice chair for research in psychiatry at Massachusetts General Hospital and co-author of the new study.

Edlow's lab is investigating how infection and inflammation may interfere with brain development. In a healthy brain, immune cells help shape developing neural circuits by trimming away extra or unnecessary connections, a process known as "synaptic pruning," which sculpts the brain's wiring. When a mother's immune system is activated by infection, inflammatory molecules can reach the fetal brain and alter the pruning process.

Animal studies support Edlow's hypothesis. When scientists trigger inflammation in pregnant mice, their offspring often show changes in how brain cells grow and connect, changes that can alter learning and behavior.

Why late pregnancy and why boys?
In Edlow and Perlis' study, the link between COVID and developmental delays was strongest when infection occurred late in pregnancy, during the third trimester. That's also when the fetal brain is growing most rapidly, forming and refining millions of neural connections.

"When we think of organ development, we think earlier in pregnancy, but the brain is an exception in this regard, where there's a massive amount of brain development in the third trimester. And that continues after birth," said Perlis. "It is entirely plausible that the third trimester is a period of vulnerability specifically for brain development."

But not everyone agrees the third trimester is uniquely vulnerable. Dr. Brian Lee, a professor of epidemiology at Drexel University, cautioned that because most mothers in the study were tested at delivery, there were simply more late-pregnancy infections to analyze. "That gives the study more power to find a difference in the third trimester," he said. "It doesn't prove earlier infections aren't important."

The study also found stronger effects in boys. That pattern is familiar: boys are generally more likely than girls to have speech or motor delays and to be diagnosed with autism. Researchers suspect that male fetuses may be more sensitive to stress and inflammation before birth, though the biology isn't fully understood.

What the study can and can't show
Edlow and Perlis are careful to say the study shows an association, not proof that COVID infection in pregnancy causes developmental problems. Many other factors could explain the link.

Mothers who get sick with COVID may also have other health issues, like obesity, diabetes or mental health conditions, that increase the risk of developmental delays in children. "Persons with mental disorders are much more likely to get COVID. Women with mental disorders are much more likely to have kids with neurodevelopmental problems," Lee said. "Mothers with worse physical health are also at higher risk of having children with neurodevelopmental problems."

Lee's research has shown that even infections before or after pregnancy can be linked to autism, suggesting that shared genetics or environment, rather than the infection itself, could be at play. That's why experts say much larger, longer studies are needed to understand the extent of any risk from the infection.

Edlow, Perlis and their team plan to follow the children in their study as they grow older to see whether early differences persist or fade. They're also studying how inflammation during pregnancy affects the placenta and fetal brain, and how to counteract those effects.

What about vaccination?
Because this study followed pregnancies from early in the pandemic, before vaccines were widely available, it doesn't answer whether vaccination changes the risk. But other research offers reassurance.

"Vaccination is a short spike… your immune system revs up, then it goes back to normal," said Edlow. "COVID [infection] is much more prolonged, unpredictable, and people can get… a dysregulated immune phenomenon that really doesn't exist in vaccine responses."

What this means for parents and clinicians
Since late 2020, there's been widespread confusion and misinformation about the safety of COVID vaccination during pregnancy. Some women have hesitated to get vaccinated out of fear it might harm their baby. But the evidence since then has been clear: the COVID vaccine is safe in pregnancy. The American College of Obstetricians and Gynecologists strongly recommends COVID vaccination to protect both mother and child.

Experts say the broader lesson is that pregnancy is a period of vulnerability, and prevention matters, not only for COVID, but other infections as well.

Dr. Janet Currie, a professor of economics at Yale University, said these risks remain "underappreciated," despite decades of evidence. "Even though the flu vaccine is recommended for pregnant women, very few pregnant women get it," she said. "Physicians seem to be reluctant to vaccinate pregnant women."

As Dr. Gil Mor, scientific director of the C.S. Mott Center for Human Growth and Development at Wayne State University, put it, "Protecting the mother is protecting the long-term health of the offspring. … The best intervention is vaccination."

A century-old echo
The idea that what happens in the womb can shape life after birth began with studies of famine, like the Dutch Hunger Winter in the final months of World War II. Between 1944 and 1945, as German forces blockaded the western Netherlands, rations fell to just a few hundred calories a day. Thousands died of starvation, and women who were pregnant during that period gave birth to babies who later faced higher risks of heart disease, diabetes and schizophrenia. The episode became a cornerstone of the "fetal origins" idea, that deprivation or stress in pregnancy can have lifelong effects.

The 1918 flu pandemic broadened that idea to infection. Babies exposed to influenza in utero later showed small but lasting differences in education and earnings, one of the first signs that illness during pregnancy could affect brain development. Research in Taiwan, Sweden, Switzerland, Brazil, and Japan found similar impacts. Some argued that those findings reflected the disruptions of World War I, not the flu itself. But later studies, including those from the United Kingdom and Finland, have strengthened the case for a biological effect, reinforcing that the infection itself, not wartime upheaval, was the key driver.

"It isn't simply influenza that can alter fetal neurodevelopment," Dr. Kristina Adams Waldorf, a professor of obstetrics and gynecology at UW Medicine, explained. "Many types of infections… in the mother can be transmitted as a signal to the fetus, which can alter its brain development."

A century later, the same question has returned with COVID: could infection during pregnancy subtly shape how children grow and learn? The new Massachusetts General Hospital study offers an early look at the answer.

A multi-institutional team including Health Canada researchers has found that prenatal air exposure to specific particulate matter components and early-life ozone is associated with autism spectrum disorder in Ontario children.

Fine particulate matter has been linked to adverse health outcomes, with prenatal and early postnatal exposure associated with neurodevelopmental outcomes including autism spectrum disorder.

Most previous work has focused on fine particulate matter of airborne particles with a diameter of 2.5 micrometers or less (PM2.5), leaving uncertainty about variation in toxic effects among various chemical components and timing of exposure related to sensitive points in pregnancy. A large Southern California cohort study reported associations for several components, including sulfate, and a follow-up study also noted nitrate.

In the study, "Prenatal Exposure to Fine Particulate Matter Components and Autism Risk in Childhood," published in JAMA Network Open, researchers conducted a population-based retrospective cohort study to examine associations between prenatal and first-year-of-life exposure to specific PM2.5 components, nitrogen dioxide, and ozone with autism diagnoses, and to identify potentially sensitive gestational windows.

Looking at birth through the first five years in Ontario, covering approximately 20 years, yielded 2,183,324 children after exclusions and 19,569 children who received an autism diagnosis.

Postal code modeling
Exposure assessment assigned prenatal concentrations by maternal postal code at delivery. Weekly nitrogen dioxide and ozone and biweekly PM2.5 mass and components were estimated from conception to age 36 weeks, with first-year exposures as annual postal code–level averages weighted by time at each address.

Components included black carbon, dust, ammonium, nitrate, organic matter, sulfate, and sea salt. Models integrated satellite data, chemical transport modeling, land-use regression, and ground monitoring data.

What the data show
Prenatal PM2.5 mass was associated with increased risk when adjusted for first-year averages (HR 1.15), and window-specific signals were driven by sulfate during weeks 23–36 (HR 1.11) and ammonium during weeks 21–34 (HR 1.11), after which PM2.5 mass was no longer associated with autism.

First-year ozone exposure was associated with autism risk with HR 1.09. Weekly models indicated significant windows for PM2.5 during gestational weeks 14 to 32, sulfate during weeks 23 to 36, ammonium during weeks 21 to 34, and ozone during weeks 26 to 30, with reported window-specific HRs of 1.12 for PM2.5, 1.11 for sulfate, 1.11 for ammonium, and 1.03 for ozone.

Black carbon, organic matter, dust, sea salt were not significant after adjustments, suggesting that specific chemical and not general PM2.5 exposure associations.

Patterns found across places and groups
Urban settings showed larger estimated effects for PM2.5, sulfate, and ammonium compared with rural areas. Sex-stratified results indicated larger estimates for male children, with sulfate the only pollutant significantly associated among female children.

Neighborhood patterns suggested more pronounced estimated risks in lower-income and middle-income areas and in areas with higher proportions of racialized and newcomer populations.

Authors conclude that prenatal exposure to specific PM2.5 components, particularly sulfate and ammonium, was associated with autism risk, with sensitive periods in the second and third trimesters.

Postnatal ozone exposure in the first year of life was also associated with risk. Findings point to the potential importance of early-life environmental exposures.

In a recent article in the journal Nutrients, researchers examined the differences in dietary habits and gut microbiota between children with autism spectrum disorder (ASD) and their non-ASD family members.

While gut microbial diversity appeared to be remarkably similar between the two groups, distinct dietary patterns emerged. Children with ASD ate fewer vegetables and more sweets, suggesting that in this cohort and design, ASD behaviors could shape the microbiome rather than vice versa.

Alongside its core symptoms, ASD is often associated with gastrointestinal problems, selective eating, anxiety, and immune irregularities, which together reduce quality of life.

Gut-Brain Axis and Microbiome Research Challenges
These comorbidities have drawn attention to the gut-brain axis, a bidirectional system through which gut microbes communicate with the brain via metabolic, immune, and neural pathways.

Animal studies suggest that gut microbiota may affect behavior, but human research has produced inconsistent results, likely due to factors such as diet and geography.

Although some clinical studies indicate that prebiotic or probiotic interventions may modestly relieve gastrointestinal symptoms, their behavioral benefits remain unproven. Consequently, it is unclear whether microbial changes in ASD are a cause or an effect of dietary selectivity and behavioral differences.

Methods: Microbiome Sequencing and Dietary Assessment
Fecal samples were collected to analyze bacterial and fungal communities, while detailed seven-day food diaries provided dietary data.

Using a within-family design minimized differences in genetics and shared environment. Stool samples were stored at −80 °C and processed using standardized protocols.

Deoxyribonucleic acid (DNA) was extracted, amplified, and sequenced, targeting bacterial and fungal regions.

Resulting sequences underwent quality control, taxonomic classification, and normalization. Microbial diversity was assessed using Shannon and Simpson indices for α-diversity and Bray–Curtis and UniFrac metrics for β-diversity.

PERMANOVA on Bray–Curtis dissimilarities yielded low, non-significant R² values, reinforcing the absence of between-group microbiome differences.

Dietary intake was categorized into eight food groups, and dietary diversity was calculated from food-frequency data. Statistical analyses employed non-parametric tests, such as the Kruskal–Wallis test and the Wilcoxon test, as well as linear mixed-effects models that accounted for family clustering.

Multiple comparisons were corrected using false discovery rate adjustments. The study adhered to established guidelines to ensure methodological transparency and was approved by an institutional ethics committee, with informed consent obtained from all participants.

Microbiome Diversity Shows Minimal Differences
The analysis showed no significant link between gut microbiome composition and autism diagnosis. Bacterial diversity, measured through both α-diversity and β-diversity, was similar among children with ASD, their siblings, and their parents.

Heatmaps and principal component analyses revealed that microbial community structures and species abundances were broadly comparable across all groups. Similarly, the fungal (mycobiome) analysis found no significant group differences. Only two fungal species showed statistical variation, and these differences were between children and parents rather than between ASD and non-ASD siblings.

Dietary Patterns Strongly Linked to ASD Behaviors
In contrast, clear group-level distinctions emerged in dietary patterns. Children with ASD consumed significantly more sweets and sugary foods and fewer vegetables than both siblings and parents. This finding aligns with the statistical results. No differences were found between siblings and parents.

Smaller differences were also seen in fruit and processed food intake, but these mainly distinguished parents from children.

However, the authors note that some of these dietary associations weakened or lost statistical significance when more complex linear mixed-effects models were applied to account for family clustering, likely due to the small sample size.

They also emphasize that the absence of significant microbiome differences may partly reflect limited statistical power rather than a definitive lack of effect.

Overall, the findings suggest that dietary preferences, rather than gut microbial composition, differentiated children with ASD from non-ASD family members, highlighting selective eating behaviors as a defining feature of the ASD group.

Interpretation and Study Limitations
This study found that dietary habits, not gut microbiome composition, best explained group differences in children with ASD. Both bacterial and fungal communities showed minimal variation across participants, indicating that prior inconsistencies in ASD–ASD microbiome studies may stem from small sample sizes, diverse methods, and unaccounted dietary factors.

Children with ASD showed strong preferences for sweet foods and limited vegetable intake, consistent with selective eating behaviors often seen in autism. These habits may contribute to nutritional deficiencies and metabolic issues.

The study’s strengths include its within-family design and integration of bacterial, fungal, and dietary analyses. However, limitations such as the small sample size, cross-sectional nature, and lack of metabolomic data restrict causal interpretation. Differences between child and adult diets also complicate comparisons.

Overall, the findings support a behavior-to-diet-to-microbiome pathway in this cohort; however, causality cannot be inferred from the cross-sectional data. The authors further conclude that larger, multi-omic studies with greater statistical power are required to confirm whether subtle microbiome differences might emerge under more robust analytical conditions.

A new analysis of Kaiser Permanente Northern California mothers and children adds to evidence that maternal blood sugar metabolism in pregnancy could play a role in the likelihood a child has of being diagnosed with a neurodevelopmental disorder.

The study of 4,546 mother-child pairs did not find a significant link between gestational diabetes and risk of autism spectrum disorder or developmental delay in the children analyzed as one group. But when the researchers broke the data down by child sex and other factors, they found an elevated risk associated with gestational diabetes among girls only, and in children of both sexes whose mothers were diagnosed with gestational diabetes early in pregnancy (before 24 weeks gestation).

A separate, less serious form of metabolic disorder, known as impaired glucose intolerance, was associated with increased risk of developmental delay. The study was published in JAMA Network Open.

Maternal blood sugar metabolism is one of many health factors being studied for their potential role in children’s development of autism. These findings, while statistically significant and in a large, well-designed study, add to the evidence around the complex question of how gestational diabetes might relate to autism. But they are not intended to prompt any changes in clinical advice to pregnant patients, said lead author Luke Grosvenor, PhD, a research fellow with the Kaiser Permanente Division of Research.

“Based on this research, we would not say that gestational diabetes causes autism, or conclude that it is caused by other factors related to treatment of gestational diabetes, such as medication or lifestyle changes,” Grosvenor said. “But this study provides some important areas for future research, such as why there may be a difference in likelihood of autism by sex of the baby, and why we saw greater likelihood of developmental delays in girls if the mother had a milder version of metabolic disorder in early pregnancy.”

Of the total 4,546 mothers, 403 had gestational diabetes and 64 had elevated blood glucose levels but no diagnosis, which the researchers defined as sub-clinical impaired glucose tolerance (IGT). Of the children, 683 had an autism spectrum disorder diagnosis, and 2,054 had a developmental delay diagnosis. These children were compared to 1,809 children who did not have either diagnosis. All the children were born between 2011 and 2018 and followed through 2023.

The analysis found the strongest link between early gestational diabetes and autism in both genders. It also found a strong association between impaired glucose tolerance and developmental delays in girls.

The study also identified an increased likelihood of developmental delay in girls whose mothers’ gestational diabetes was diagnosed late. However, this subgroup of children was relatively small, so further research is needed, the authors said.

While the findings might suggest more focus on diagnosing gestational diabetes in early pregnancy, the reality in practice is more complicated. Gestational diabetes screening usually takes place between 24 and 28 weeks gestation, and a positive screening can lead to major lifestyle changes in activity and diet, blood sugar monitoring several times a day, and potential use of medication.

Doctors weigh the burden of treating diabetes during pregnancy with any potential benefit in outcomes, such as avoiding pregnancy and birth complications. A growing body of research suggests that early gestational diabetes diagnosis (before 24 weeks) may not make a difference in infant outcomes such as large-for-gestational age baby, caesarean section, preterm birth, or NICU admission.

Some health systems, such as Kaiser Permanente Northern California, are reducing the emphasis on early screening for gestational diabetes (a condition that occurs only during pregnancy) and ensuring that patients at risk for chronic diabetes (a lifetime condition) are screened early in pregnancy. There are different medical tests for gestational diabetes and chronic (type 2) diabetes.

Blood sugar’s relationship to autism spectrum disorder and developmental delays adds another factor into the complex mix. If further research suggests early screening for metabolic disorders could make a difference in likelihood of autism, that would be another thing for doctors and patients to consider, said senior author Lisa Croen, PhD, a senior research scientist with the Division of Research.

“Blood sugar metabolism is an important area for future research in neurodevelopmental disorders, and I expect future research will provide greater insights to help guide treatment,” Croen said.

She noted that the potential causes of autism spectrum disorder are broad and complex, extending to genetics, environmental exposure, infections, fevers, and other maternal health conditions.

If future research supports the findings in this study, Grosvenor said, pregnant patients with mild glucose metabolism issues might benefit from lifestyle changes during pregnancy involving diet and movement.

The study was funded by the National Institute of Child Health and Human Development.

Summary A new study shows that autism symptom severity, rather than a formal diagnosis, aligns with shared brain-connectivity patterns across children diagnosed with autism or ADHD. Stronger autistic traits were linked to heightened connectivity between frontoparietal and default-mode networks, regions central to social cognition and executive functions.

These connectivity differences also mapped onto gene-expression profiles tied to neural development, suggesting a shared biological mechanism. The findings support a shift toward dimensional, neurobiologically informed approaches to understanding neurodevelopmental conditions.

Despite widespread claims linking gut health to autism spectrum disorder, a comprehensive analysis published in the journal Neuron has found no scientific evidence supporting the hypothesis that the gut microbiome causally contributes to autism.

The paper, authored by researchers from Trinity College Dublin, University College Cork, and the University of Oxford, systematically dismantles decades of research that has fuelled a lucrative wellness industry and sparked controversy over misleading public health messaging.

Despite what you’ve heard, read, or watched on Netflix, there is no evidence that the microbiome causally contributes to autism,” says lead author Kevin Mitchell, a developmental neurobiologist at Trinity College Dublin in a press statement. “I don’t think it’s warranted to spend further time and funding on this topic. We know that autism is a strongly genetic condition, and there’s still loads to be worked out there”.

The hypothesis that autism stems from gut microbiome abnormalities has gained significant traction in recent years, with research funding reaching $20-25 billion annually since 2018 and over 100 published articles in 2024 alone. This interest largely derives from observations that many autistic individuals experience gastrointestinal symptoms and the mistaken belief that rising autism diagnoses must reflect environmental changes.

However, the authors argue that these foundational assumptions are themselves problematic.

According to their paper, strong evidence indicates that increased autism diagnoses reflect improved awareness and broadened diagnostic criteria rather than any biological epidemic. In simple terms, we have simply become much better at diagnosing autism, and it has nothing to do with gut health, or any external change or force.

The researchers meticulously examined the most influential human observational studies, those with 107 to 1,219 citations, that have been repeatedly cited as evidence for microbiome-autism associations. They found sample sizes ranging from just 7 to 43 individuals per group, far below the thousands required for statistically reliable microbiome research.

“Autism is not rare,” says study co-author Darren Dahly, a biostatistician at University College Cork. “There’s no reason to be having studies with only 20, 30, or 40 participants.”

Recent large-scale microbiome studies have demonstrated that detecting even substantial effects requires sample sizes of several hundred to thousands of individuals. The cited autism-microbiome studies fall dramatically short of these requirements, making their findings likely statistical noise rather than genuine signals.

More critically, when studies did report differences between autistic and non-autistic individuals, these findings were contradictory.

Some studies found lower microbial diversity in autistic individuals while others found the opposite. Better designed research studies comparing autistic children with neurotypical siblings generally found no significant differences.​

Animal experiments using mice have been similarly unconvincing. The seminal studies most frequently cited as demonstrating causal links suffer from inadequate sample sizes, inappropriate statistical methods, and questionable relevance to human autism.​ The researchers highlight that there is no validated evidence that “autistic-like behaviors” in mice, such as marble burying or altered ultrasonic vocalizations, have any meaningful connection to autism in humans.

The study points out that researchers in this space take the behaviors of mice, and compare them to observed human autistic behaviors. However, there is one key problem: mice aren’t people.

The study argues that mice observation tests, where mice seem to have “autistic-like behaviors,” are purely based on “the superficial similarity between simple, isolated tasks in rodents and complex, context-dependent human behaviors.”

A 2018 workshop on autism animal models concluded that many behavioral assays “are rudimentary, do not engage similar neural circuitry as in humans, and lack translational face validity”.​

The authors point to one highly cited 2019 study claiming that transplanting gut bacteria from autistic individuals into mice produced autistic behaviors. However, when the data was reanalyzed, it failed to hold up its previous conclusions.

Scientists found several critical errors. First, they treated each mouse as an independent sample even though multiple mice received bacteria from the same human donor, artificially inflating their sample size. Secondly, they used only eight autistic and five control donors, but analyzed data from just five and three, respectively, without scientific justification.

The study points out that researchers in this space take the behaviors of mice, and compare them to observed human autistic behaviors. However, there is one key problem: mice aren’t people.

The study argues that mice observation tests, where mice seem to have “autistic-like behaviors,” are purely based on “the superficial similarity between simple, isolated tasks in rodents and complex, context-dependent human behaviors.”

A 2018 workshop on autism animal models concluded that many behavioral assays “are rudimentary, do not engage similar neural circuitry as in humans, and lack translational face validity”.​

The authors point to one highly cited 2019 study claiming that transplanting gut bacteria from autistic individuals into mice produced autistic behaviors. However, when the data was reanalyzed, it failed to hold up its previous conclusions.

Scientists found several critical errors. First, they treated each mouse as an independent sample even though multiple mice received bacteria from the same human donor, artificially inflating their sample size. Secondly, they used only eight autistic and five control donors, but analyzed data from just five and three, respectively, without scientific justification.

So why is this theory still around?

Turns out, it’s big business. Popular media narratives, particularly Netflix’s 2024 documentary “Hack Your Health: The Secrets of Your Gut,” casually linked autism to gut problems. While the National Autistic Society condemned the documentary as “deeply irresponsible” and “offensive” for describing autism as a “disease” and suggesting it could be treated through gut interventions, it still sold countless people on the idea.

The microbiome-autism hypothesis has spawned a largely unregulated wellness industry offering specialized diets, probiotic supplements, direct-to-consumer microbiome profiling, and fecal transplant services. Many researchers in this field have competing commercial interests, including patents, spin-out companies, and industry funding.​

“This field is characterized by misleading claims about the strength and reliability of these associations and the promise of various kinds of therapeutic approaches,” the study authors write. One researcher noted that “vigorous industry interest” likely creates publication bias, with negative results remaining unreported.

And in a world where health has become more about politics and money than actual science and treating people, the remaining unknown factors surrounding autism spectrum disorder make it ripe for snake oil salesmen and politicians.

Given the lack of convincing evidence and absence of progress despite substantial investment, the researchers argue that the microbiome-autism hypothesis has reached a dead end.

Parental postpartum depression is associated with increased risk of autism spectrum disorder in infants, as reported by a new study published in Frontiers in Psychiatry

Understanding post-partum risk
Postpartum depression is a type of moderate-to-severe depression that happens to parents after having a newborn. It affects up to 20% of new mothers. Recent evidence suggests that having a history of depression significantly increases the risk of developing postpartum depression.

Psychiatric history of parents has been linked to an increased risk of neurodevelopmental disorders in newborns. Autism spectrum disorder (ASD) is one such highly heritable neurodevelopmental disorder, with symptoms often appearing well before its clinical diagnosis around the age of two to three years.

Recent evidence suggests that maternal psychiatric disorders before pregnancy have a more pronounced influence on an infant’s ASD risk than paternal psychiatric disorders. However, the risk is highest in infants with both parents having a psychiatric history. Despite substantial evidence linking parental psychiatric history with neurodevelopmental conditions in infants, studies investigating the impact of parental postpartum depression on infants’ ASD risk are largely unavailable.

Researchers from the Icahn School of Medicine at Mount Sinai, USA, and Karolinska Institutet, Sweden, recently addressed this gap in the literature to gain insight into the intergenerational transmission risk for neurodevelopmental outcomes, including ASD.

The study population comprised all live births in Sweden between 1997 and 2021, who were followed up until December 31, 2022.

Identified ASD risk patterns
The study analysis included a total of 1,781,349 infants. In the entire study population, the highest prevalence of ASD was observed among infants with both parents diagnosed with postpartum depression (8.8 %), followed by infants born to fathers with postpartum depression (5.3 %) and infants born to mothers with postpartum depression (4.6 %).

These estimates corresponded to 2.59-times, 2.56-times, and 5.5-times higher relative risks of ASD among infants with mothers, fathers, and both parents diagnosed with postpartum depression, respectively.

The analysis adjusting for parental depression history, parental age, education, income, and preterm delivery showed a 1.7-times, 1.5-times, and 2-times higher risk of ASD among infants with mothers, fathers, and both parents diagnosed with postpartum depression, respectively.

The analysis, further adjusting for parental antidepressant use, any psychiatric history, and pre-delivery antidepressant use, did not lead to additional reductions in the magnitude of the observed associations.

Genetics and environment
The study identifies a significant association between parental postpartum depression and increased risk of ASD in infants. According to the findings, the risk of ASD in infants increases at a similar rate if either of the parents is diagnosed with postpartum depression. However, infants with both parents diagnosed with postpartum depression are at the highest risk of developing ASD.

Notably, the study finds a partial reduction in the magnitude of observed associations when potential confounding factors, including parental history of depression, antidepressant use, or any psychiatric history before delivery, are adjusted in the analysis.

The time surrounding birth is a critical time for early developmental events in infants. Several studies have linked parental depression to adverse neurodevelopmental consequences in infants, including cognitive and speech impairments, behavioral issues, poor adjustment, growth delay, and lack of fine motor skills.

However, it largely remains unknown whether these adversities are associated explicitly with parental postpartum depression, parental depression, or other psychiatric disorders. Although genetic factors play a substantial role in triggering neurodevelopmental complications in infants, a possible contribution of environmental risk factors and their interactions with genetic risk factors must be considered.

Existing evidence highlights that genes inherited from parents play a major role in ASD pathogenesis. The current study's observations of increased ASD risk due to maternal and paternal postpartum depression, and the highest ASD risk due to parental (both mother and father) postpartum depression, suggest that common genetic variants may be inherited from both parents.

Notably, the study finds that this combined risk from parental postpartum depression is reduced when the analysis is adjusted for the depression history of parents, highlighting the shared impact of genetic and environmental factors on ASD risk.

The Swedish National Patient Register (NPR) was used in the study to obtain diagnoses of depression. Since this register does not include diagnoses from primary care, the study could not analyze data from individuals with depression who did not visit health care facilities.

Furthermore, the study could not include parents with ASD diagnosed exclusively before 1987 because of data unavailability. Parental ASD might be a potential confounding factor that needs to be addressed in future studies. Genetic confounding may also have occurred if parents with postpartum depression are a specific group with a higher inherited risk of ASD.

Israeli scientists say that women with persistent thyroid hormone imbalance during their pregnancy may be at an increased risk of having children with autism spectrum disorder (ASD).

Their new peer-reviewed study tracked thyroid levels in more than 51,000 pregnant women. The study found that children of women with long-lasting, untreated thyroid hormone imbalance during pregnancy had about two to three cases of autism per 100 children, compared with about one case per 100 in the general population.

“Women who had a chronic thyroid condition that went untreated and got worse during pregnancy had a greater risk of having children with autism than pregnant women who were adequately treated,” Prof. Idan Menashe of Ben-Gurion University of the Negev, the study’s lead author, said in a phone call.

However, the scientists found that when a pregnant woman’s chronic thyroid dysfunction was “adequately treated,” there was no association with increased autism risk in her offspring, said Menashe, who is head of Ben-Gurion’s Department of Epidemiology, Biostatistics and Community Health Sciences, and the scientific director of the Azrieli National Center for Autism and Neurodevelopment Research.

Ben-Gurion researcher Leena Elbedour, May Weinberg of the Meir Medical Center and Tel Aviv University, Analya Michaelovski of Soroka University Medical Center, and Prof. Gal Meiri, also of Soroka University and Ben-Gurion University, collaborated on the study, which recently appeared in The Journal of Clinical Endocrinology & Metabolism.

Thyroid hormones contribute to brain development.

The thyroid is a small, butterfly-shaped gland at the front of the neck.
Thyroid hormones regulate the body’s metabolism, which is how the body uses and manages energy. These hormones also play a crucial role in essential processes such as heart rate regulation and the body’s muscle control.

Thyroid hormones also support the production of myelin, an insulating, fatty coating around nerve fibers. These allow electrical signals to travel between the brain and body more quickly.

During pregnancy, a woman’s thyroid hormone is essential for the neurodevelopment of the fetus. Studies have shown the association of a woman’s thyroid imbalance with atypical neurodevelopment.

When the thyroid produces the right amount of hormone, it is considered to be within the normal range, or balanced.

If a pregnant woman’s thyroid hormone levels are too low, doctors usually prescribe an artificial hormone that safely replaces the missing hormone.

Thyroid imbalance during pregnancy
Scientists have studied the connection between a woman’s thyroid levels during pregnancy and her child’s development. However, most earlier studies checked the thyroid hormone once, usually early in pregnancy, and not throughout the pregnancy.

Menashe’s research, done at Soroka Medical Center, followed more than 51,000 births between January 2011 and December 2017 in a retrospective cohort study, with a follow-up through January 2021.

Using blood-test data and the women’s medical records, the team divided the mothers into four groups: those with no thyroid problems, those with a chronic thyroid condition whose hormones were balanced in pregnancy, those with thyroid imbalance only during pregnancy, and those who had both a chronic thyroid condition and imbalance during pregnancy.

This gave researchers the data to compare the women’s thyroid levels during pregnancy.

“What surprised me is that only the last group, those who had both a chronic thyroid condition and were imbalanced during pregnancy, were at risk of having a child with autism,” Menashe said.

The scientists also observed that the longer the duration of thyroid dysfunction across trimesters, the higher the risk.

“We don’t really know the cause,” Menashe said. “But we know there is a link between them.”

When asked if he could calculate the specific percentage of risk, the scientist replied, “Not exactly, because this is not the exact way to assess risk. All we can say is that we see an increased risk, or more exactly, untreated thyroid problems are associated with an increased risk of autism.”

Dr. Dorit Shmueli, a specialist in neurology and child development and child development coordinator at Clalit Health Services. (Courtesy/Hagai Shmueli)
Dr. Dorit Shmueli, a specialist in neurology and child development and the Child Development Coordinator in Clalit Health Services, told The Times of Israel that research on the safety and importance of balancing hypothyroidism in pregnancy is “essential.”

“Optimal maternal thyroid function plays a key role in supporting healthy fetal brain development, and understanding how best to manage it can directly influence the developmental outcomes we see in children, especially autism spectrum disorder,” said Shmueli, who was not involved in the study. “Evidence-based insights from Prof. Idan Menashe’s research are crucial for informing clinical guidance and improving long-term well-being in the populations we serve.”

Researchers believe there is “some mechanism where the imbalance in the maternal thyroid hormone affects the neurodevelopment of the fetus,” Menashe said. “Eventually, this abnormal neurodevelopment is translated into autism in the child.”

Thank you for posting this body of Knowledge.! AsPartOfMe .They almost had me going about the gut health connection.. but am pretty sure the gut health can play a role in some peoples health issues.