On Monday (Sept. 22), President Donald Trump warned pregnant people to avoid acetaminophen, the active ingredient in Tylenol, because of a controversial study by a Harvard dean and others. In response, several health organizations — including the American College of Obstetricians and Gynecologists (ACOG), the Society of Obstetrics and Gynecology of Canada, the American Academy of Pediatrics (AAP) and the World Health Organization (WHO) — have issued statements rebutting Trump's assertion that Tylenol use in pregnancy "can be associated with an increased risk of autism."

Trump also advised parents not to give Tylenol to babies, prompting the AAP to issue a statement saying, "decades of research have found that acetaminophen is safe for children when administered as recommended. Misleading claims that the medicine is not safe and is linked to increased rates of autism send a confusing, dangerous message to parents and expectant parents."

So, where did the notion that Tylenol causes autism come from, and is there any evidence for the claim? Here are some research-backed answers to common questions about acetaminophen use in pregnancy.

For almost 40 years, people who suspect they've been harmed by a vaccine have been able to turn to a little-known system called the Vaccine Injury Compensation Program — often simply called the vaccine court.

Health and Human Services Secretary Robert F. Kennedy Jr. has long been a critic of the vaccine court, calling it "biased" against compensating people, slow and unfair. He has said that he wants to "revolutionize" or "fix" this system.

I'm a scholar of law, health and medicine. I investigated the history, politics and debates about the Vaccine Injury Compensation Program in my book "Vaccine Court: The Law and Politics of Injury."

Although vaccines are extensively tested and monitored, and are both overwhelmingly safe for the vast majority of people and extremely cost-effective, some people will experience a harmful reaction to a vaccine. The vaccine court establishes a way to figure out who those people are and to provide justice to them.

Having studied the vaccine court for 15 years, I agree that it could use some fixing. But changing it dramatically will be difficult and potentially damaging to public health.

Deciphering vaccine injuries

The Vaccine Injury Compensation Program is essentially a process that enables doctors, lawyers, patients, parents and government officials to determine who deserves compensation for a legitimate vaccine injury.

It was established in 1986 by an act of Congress to solve a specific social problem: possible vaccine injuries to children from the whole-cell pertussis vaccine. That vaccine, which was discontinued in the U.S. in the 1990s, could cause alarming side effects like prolonged crying and convulsions. Parents sued vaccine manufacturers, and some stopped producing vaccines.

Congress was worried that lawsuits would collapse the country's vaccine supply, allowing diseases to make a comeback. The National Childhood Vaccine Injury Act of 1986 created the vaccine court process and shielded vaccine manufacturers from these lawsuits.

Here's how it works: A person who feels they have experienced a vaccine-related injury files a claim to be heard by a legal official called a special master in the U.S. Court of Federal Claims. The Health and Human Services secretary is named as the defendant and is represented by Department of Justice attorneys.

Doctors who work for HHS evaluate the medical records and make a recommendation about whether they think the vaccine caused the person's medical problem. Some agreed-upon vaccine injuries are listed for automatic compensation, while other outcomes that are scientifically contested go through a hearing to determine if the vaccine caused the problem.

Awards come from a trust fund, built up through a 75-cent excise tax on each dose of covered vaccine sold. Petitioners' attorneys who specialize in vaccine injury claims are paid by the trust fund, whether they win or lose.

Some updates are needed

Much has changed in the decades since Congress wrote the law, but Congress has not enacted updates to keep up.

For instance, the law supplies only eight special masters to hear all the cases, but the caseload has risen dramatically as more vaccines have been covered by the law. It set a damages cap of US$250,000 in 1986 but did not account for inflation. The statute of limitations for an injury is three years, but in my research, I found many people file too late and miss their chance.

When the law was written, it only covered vaccines recommended for children. In 2023, the program expanded to include vaccines for pregnant women. Vaccines just for adults, like shingles, are not covered. COVID-19 vaccine claims go to another system for emergency countermeasures vaccines that has been widely criticized. These vaccines could be added to the program, as lawyers who bring claims there have advocated.

These reform ideas are "friendly amendments" with bipartisan support. Kennedy has mentioned some of them, too.

A complex system is hard to revolutionize

Kennedy hasn't publicly stated enough details about his plan for the vaccine court to reveal the changes he intends to make. The first and least disruptive course of action would be to ask Congress to pass the bipartisan reforms noted above.

But some of his comments suggest he may seek to dismantle it, not fix it. None of his options are straightforward, however, and consequences are hard to predict.

Straight up changing the vaccine court's structure would probably be the most difficult path. It requires Congress to amend the 1986 law that set it up and President Donald Trump to sign the legislation. Passing the bill to dismantle it requires the same process. Either direction involves all the difficulties of getting a contentious bill through Congress. Even the "friendly amendments" are hard — a 2021 bill to fix the vaccine court was introduced but failed to advance.

However, there are several less direct possibilities.

Adding autism to the injuries list

Kennedy has long supported discredited claims about harms from vaccines, but the vaccine court has been a bulwark against claims that lack mainstream scientific support. For example, the vaccine court held a yearslong court process from 2002 to 2010 and found that autism was not a vaccine injury. The autism trials drew on 50 expert reports, 939 medical articles and 28 experts testifying on the record. The special masters deciding the cases found that none of the causation hypotheses put forward to connect autism and vaccines were reliable as medical or scientific theories.

Much of Kennedy's ire is directed at the special masters, who he claims "prioritize the solvency" of the system "over their duty to compensate victims." But the special masters do not work for him. Rather, they are appointed by a majority of the judges in the Court of Federal Claims for four-year terms — and those judges themselves have 15-year terms. Kennedy cannot legally remove any of them in the middle of their service to install new judges who share his views.

Given that, he may seek to put conditions like autism on the list of presumed vaccine injuries, in effect overturning the special masters' decisions. Revising the list of recognized injuries to add ones without medical evidence is within Kennedy's powers, but it would still be difficult. It requires a long administrative process with feedback from an advisory committee and the public. Such revisions have historically been controversial, and are usually linked to major scientific reviews of their validity.

Public health and medical groups are already mobilized against Kennedy's vaccine policy moves. If he failed to follow legally required procedures while adding new injuries to the list, he could be sued to stop the changes.

Targeting vaccine manufacturers

Kennedy could also lean on his newly reconstituted Advisory Committee on Immunization Practices to withdraw recommendations for certain vaccines, which would also remove them from eligibility in the vaccine compensation court. Lawsuits against manufacturers could then go straight to regular courts. On Aug. 14, 2025, the Department of Health and Human Services may have taken a step in this direction by announcing the revival of a childhood vaccine safety task force in response to a lawsuit by anti-vaccine activists.

Kennedy has also supported legislation that would allow claims currently heard in vaccine court to go to regular courts. These drastic reforms could essentially dismantle the vaccine court.

People claiming vaccine injuries could hope to win damages through personal injury lawsuits in the civil justice system instead of vaccine court, perhaps by convincing a jury or getting a settlement. These types of settlements were what prompted the creation of the vaccine court in the first place. But these lawsuits could be hard to win. There is a higher bar for scientific evidence in regular courts than in vaccine court, and plaintiffs would have to sue large corporations rather than file a government claim.

Raising the idea of reforming the vaccine court has provoked strong reactions across the many groups with a stake in the program. It is a complex system with multiple constituents, and Kennedy's approaches so far pull in different directions. The push to revolutionize it will test the strength of its complex design, but the vaccine court may yet hold up.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

Immune cells in the human brain may be critical to orchestrating the organ's development in the womb because they trigger a dramatic increase in an important type of nerve cell, new research suggests.

Estimates suggest that these key cells, known as inhibitory interneurons, make up some 25% to 50% of the neurons in the adult cortex, the wrinkled tissue that covers the surface of the brain. In fact, the human cortex carries more than double the number of interneurons as the mouse cortex does.

These interneurons relay signals between other brain cells and help keep that signaling in check with a chemical messenger called GABA. As the brain's main "inhibitory" messenger, GABA helps turn down brain activity by making neurons less likely to fire, thus balancing out the "excitatory" signals that amplify brain activity. Various disorders have been tied to problems with interneurons, including epilepsy, autism and schizophrenia.

Now, in a study published Aug. 6 in the journal Nature, researchers have uncovered a force that drives interneurons to multiply in the developing human brain — and they say it may be unique to our species.

"That's why we cannot use traditional animal models," study co-author Diankun Yu, an assistant researcher in pediatrics at the University of California, San Francisco (UCSF), told Live Science. To uncover this mechanism that may unfold only in the human brain, the researchers developed an organoid — a miniature 3D structure, grown from stem cells, that mimics a full-size structure found in the human body.

Prior to the organoid study, research in lab animals suggested a link between the activation of the maternal immune system during pregnancy and a lower number of interneurons in the cortices of their offspring, compared to offspring that didn't experience an immune upset. That kind of activation might occur in response to a viral or bacterial infection, for example. The study authors explored this in previous research with lab mice, in which they pinpointed a key player behind the link: microglia, the brain's resident immune cells.

Related: In a 1st, scientists combine AI with a 'minibrain' to make hybrid computer

In the past five years, scientists have begun to recognize how the immune system and nervous system develop in parallel, study co-author Dr. Xianhua Piao, a physician-scientist who specializes in neonatology and developmental neuroscience at UCSF, told Live Science.

"The microglia really fine-tune and regulate nervous development," she said of the new study's findings. "It really adds a new dimension as to how microglia exert their function."

The team built on previous work from other research groups to develop their organoids, which resembled a key structure in the fetal brain from which many cortical interneurons arise. This structure is temporary, appearing around the eighth week of pregnancy in humans and disappearing about eight months after birth, Piao said. The researchers found a way to incorporate microglia into this model, which hadn't been done before, she added.

The team found that the microglia in their organoids were a key source of insulin-like growth factor 1 (IGF1) in the developing minibrains and that the substance helped to drive the dramatic increase in interneurons seen in early development.

When the team tested what would happen when they turned off IGF1 signaling in various ways, they found that it blocked the rapid increase in interneurons. However, "when we deleted this gene in microglia in the mouse model, we did not see any change," Piao said. That suggests that this chain of events kicked off by microglia-made IGF1 may be unique to humans.

"These findings indicate an evolutionary adaptation of microglial function to support the increased demand for interneurons in the human cortex," the researchers wrote in their report. In short, this finding hints at a feature of human evolution that might help to explain our unique cognitive abilities.

That said, organoids aren't exact replicas of the human brain, so there's a limit to what the 3D models can tell us. "So far the model is good enough for especially the proliferation stage, very early stage" of development, Yu said. But currently, these organoids don't do as well with later stages of brain development, he noted. They also don't capture circuit-level activity in the brain, Piao said, showing only activity within smaller, isolated structures.

Future work could help to further clarify this previously unknown role of immune cells in the brain, she said.

Editor's note: This story doesn't reflect more recent developments from the Advisory Committee on Immunization Practices, which has now recommended against using flu vaccines containing thimerosal. Experts, including a lone member of the committee, have questioned the decision given the lack of risk posed by the preservative.

An expert committee that advises the Centers for Disease Control and Prevention on vaccines is meeting for the first time since Health Secretary Robert F. Kennedy Jr. abruptly replaced the committee's 17 members with eight hand-picked ones on June 11, 2025.

The committee, called the Advisory Committee on Immunization Practices, generally discusses and votes on recommendations for specific vaccines. For this meeting, taking place June 25-26, 2025, vaccines for COVID-19, human papillomavirus, influenza and other infectious diseases were on the schedule. According to an updated agenda, however, the committee is now also scheduled to hear a presentation on a chemical called thimerosal and to vote on proposed recommendations regarding its use in influenza vaccines.

Public health experts have raised concerns about the presentation, noting that anti-vaccine advocates continue to promote confusion regarding the purported health risks of thimerosal despite extensive research demonstrating its safety.

I'm a pharmacist and expert on drug information with 35 years of experience critically evaluating the safety and effectiveness of medications in clinical trials. No evidence supports the idea that thimerosal, used as a preservative in vaccines, is unsafe or carries any health risks.

What is thimerosal?

Thimerosal, also known as thiomersal, is a preservative that has been used in some drug products since the 1930s because it prevents contamination by killing microbes and preventing their growth.

In the human body, thimerosal is metabolized, or changed, to ethylmercury, an organic derivative of mercury. Studies in infants have shown that ethylmercury is quickly eliminated from the blood.

Ethylmercury is sometimes confused with methylmercury. Methylmercury is known to be toxic and is associated with many negative effects on brain development even at low exposure. Environmental researchers identified the neurotoxic effects of mercury in children in the 1970s, primarily resulting from exposure to methylmercury in fish. In the 1990s, the Environmental Protection Agency and the Food and Drug Administration established limits for maximum recommended exposure to methylmercury, especially for children, pregnant women and women of childbearing age.

Related: 'Vaccine rejection is as old as vaccines themselves': Science historian Thomas Levenson on the history of germ theory and its deniers

Why is thimerosal controversial?

Fears about the safety of thimerosal in vaccines spread for two reasons.

First, in 1998, a now discredited report was published in a major medical journal called The Lancet. In it, a British doctor named Andrew Wakefield described eight children who developed autism after receiving the MMR vaccine, which protects against measles, mumps and rubella. However, the patients were not compared with a control group that was vaccinated, so it was impossible to draw conclusions about the vaccine's effects. Also, the data report was later found to be falsified. And the MMR vaccine that children received in that report never contained thimerosal.

Second, the federal guidelines on exposure limits for the toxic substance methylmercury came out about the same time as the Wakefield study's publication. During that period, autism was becoming more widely recognized as a developmental condition, and its rates of diagnosis were rising. People who believed Wakefield's results conflated methylmercury and ethylmercury and promoted the unfounded idea that ethylmercury in vaccines from thimerosal were driving the rising rates of autism.

The Wakefield study was retracted in 2010, and Wakefield was found guilty of dishonesty and flouting ethics protocols by the U.K. General Medical Council, as well as stripped of his medical license. Subsequent studies have not shown a relationship between the MMR vaccine and autism, but despite the absence of evidence, the idea took hold and has proven difficult to dislodge.

Have scientists tested whether thimerosal is safe?

No unbiased research to date has identified toxicity caused by ethylmercury in vaccines or a link between the substance and autism or other developmental concerns — and not from lack of looking.

A 1999 review conducted by the Food and Drug Administration in response to federal guidelines on limiting mercury exposure found no evidence of harm from thimerosal as a vaccine preservative other than rare allergic reactions. Even so, as a precautionary measure in response to concerns about exposure to mercury in infants, the American Academy of Pediatrics and the U.S. Public Health Service issued a joint statement in 1999 recommending removal of thimerosal from vaccines.

At that time, just one childhood vaccine was available only in a version that contained thimerosal as an ingredient. This was a vaccine called DTP, for diphtheria, tetanus and pertussis. Other childhood vaccines were either available only in formulations without thimerosal or could be obtained in versions that did not contain it.

By 2001, U.S. manufacturers had removed thimerosal from almost all vaccines — and from all vaccines in the childhood vaccination schedule.

In 2004, the U.S. Institute of Medicine Immunization Safety Review Committee reviewed over 200 scientific studies and concluded there is no causal relationship between thimerosal-containing vaccines and autism. Additional well-conducted studies reviewed independently by the CDC and by the FDA did not find a link between thimerosal-containing vaccines and autism or neuropsychological delays.

How is thimerosal used today?

In the U.S., most vaccines are now available in single-dose vials or syringes. Thimerosal is found only in multidose vials that are used to supply vaccines for large-scale immunization efforts — specifically, in a small number of influenza vaccines. It is not added to modern childhood vaccines, and people who get a flu vaccine can avoid it by requesting a vaccine supplied in a single-dose vial or syringe.

Thimerosal is still used in vaccines in some other countries to ensure continued availability of necessary vaccines. The World Health Organization continues to affirm that there is no evidence of toxicity in infants, children or adults exposed to thimerosal-containing vaccines.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

Scientists may have confirmed a theory about the origins of autism by creating miniature, 3D replicas of human brains.

These tiny brains, derived from the stem cells of toddlers, were grown to show what the childrens' brains would have looked like as they developed in the womb.

In the new study, published May 25 in the journal Molecular Autism, scientists drew stem cells from the blood of 10 toddlers with autism and six toddlers without the disorder. At the time, the kids were between 1 and 2 years old. Using growth-inducing chemicals, the researchers grew "minibrains," or brain organoids, from these stem cells in the lab. As they grew, the organoids accurately captured key aspects of how the human brain develops and functions in the womb. 

Because each organoid was grown from a toddler's own tissue, it could be considered a mini version of a given child's brain during the first trimester of pregnancy — as if the scientists had turned back the developmental clock. 

Related: 'Butterfly effect' may explain some genetic causes of autism

The researchers tracked how the size and growth of these organoids changed during these early stages of embryonic development. 

In addition, they assessed the severity of each toddler's present-day autism symptoms, including their ability to pay attention to and communicate with others, their language skills and their IQ. The team also took scans of the toddlers' actual brains to look at the activity of different cells, especially those in brain regions associated with social skills and language. 

The team found that the brain organoids of toddlers with autism grew almost three times faster than those without autism, becoming "significantly" enlarged by around 40% between roughly the first and second month of pregnancy, compared with the control group. The researchers also flagged an overall trend: The larger the brain organoid was, the more severe the social symptoms of autism were in the respective toddler. 

Previous studies, including research conducted by the authors of the new study, have linked increased brain size in the early years of life to the severity of social symptoms in people with autism. However, this latest research provides a direct link between symptom severity and brain size in individual toddlers, rather than highlighting trends within a group. 

"These new findings add interestingly to their [the study authors'] previous work," said Dr. Jonathan Green, a professor of child and adolescent psychiatry at the University of Manchester in the U.K., who was not involved in the study. The new research suggests a "quantitative association" between the degree of brain overgrowth seen in the womb and the degree of later autism symptoms, Green told Live Science in an email. 

The results could "potentially add to our knowledge about neural aspects of autism," he added. "It will be very interesting to see if these findings can be replicated by others."

In a separate experiment conducted in the same study, the team also discovered that a higher growth rate and larger size of the brain organoids in toddlers with autism were tied to increased activity in a gene called Ndel1. This gene codes for a protein that helps regulate embryonic brain development, so the scientists said it's likely that dysfunction in Ndel1 partly drives the excessive brain growth seen in autism. 

"Determining that NDEL1 was not functioning properly was a key discovery," Alysson Muotri, co-senior study author and a professor of pediatrics at the University of California, San Diego, said in a statement. 

The team studied only 16 toddlers, so the study was fairly small. However, these kinds of experiments are "incredibly laborious and expensive," so this is a "pretty impressive dataset," Dr. Laura Andreae, a reader in developmental neuroscience at King's College London who was not involved in the research, told Live Science in an email. 

Social symptoms are not the only component of autism. For instance, many people with the condition may also experience symptoms such as repetitive behaviors, delayed movement skills and anxiety, which were not assessed in the new study. This may limit how well the findings generalize to additional people. 

Nevertheless, looking forward, the team aims to identify more genes that could be driving excessive brain growth in autism. They hope that, someday, this will lead to the development of new therapies for the disorder. 

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New brain scans from people with psychosis may confirm a long-standing theory as to why people experience these sudden breaks from reality.

The theory states that, in psychosis, brain networks in charge of directing a person's attention malfunction. This causes a person to experience hallucinations, or sensations of things that aren't actually happening; and delusions, or unshakable false beliefs. Psychosis is a feature of serious mental disorders such as schizophrenia, but its symptoms exist on a continuum and can also occur independently of any defined mental disorder.

The precise details of what happens in the brain to cause psychosis have long eluded scientists. One reason for this is that psychosis is often studied in people who have long been taking antipsychotic medications, so it's difficult to distinguish brain changes tied to the condition from those linked to the drugs.

A goal of the new brain-scan study, published April 11 in the journal Molecular Psychiatry, was to pinpoint the underlying mechanisms involved in psychosis from an early age, which could help pave the way to earlier diagnoses and better treatments.

Related: A mysterious brain network may underlie many psychiatric disorders

"The abnormalities do not start when you are in your 20s; they are evident even when you are 7 or 8," lead study author Kaustubh Supekar, a clinical associate professor of psychiatry and behavioral sciences at Stanford University School of Medicine, said in a statement.

To spot these abnormalities, the study focused on people ages 6 to 39 with a rare genetic condition associated with psychosis, called 22q11.2 deletion syndrome. People with the syndrome are missing part of one of their copies of chromosome 22. In addition to having a risk of other conditions — such as heart abnormalities, attention-deficit/hyperactivity disorder (ADHD) and autism — those affected with the syndrome have a roughly 30% chance of experiencing psychosis, schizophrenia or both.

The team collected brain data using functional magnetic resonance imaging (fMRI), which tracks changes in blood flow that correspond with brain cell activity. There were nearly 900 people involved, including 101 people with 22q11.2 deletion syndrome, some with psychosis and some without, and 120 with "psychosis of unknown origin."

In addition, the study included people with no history of psychosis for comparison, as well as people with ADHD and autism, "which classification studies rarely do," said Dr. Rick Adams, a fellow in mental health neuroscience at the University College London who was not involved in the study. This was "a big plus" because it helped show that the brain signatures they found are specific to psychosis and not seen in other brain-related disorders, Adams told Live Science in an email.

With help from colleagues in computer science at Stanford, the team created a new machine learning algorithm to uncover patterns in the fMRI data. The tool revealed overlapping "signatures" in the brains of people with 22q11.2 deletion syndrome and associated psychosis or with psychosis of unknown causes.

These signatures, which did not appear in any of the comparison groups without psychosis, showed up in two key components of what's known as the brain's "salience network." This network's job is to dynamically switch our attention between internal thoughts and external stimuli, essentially directing our attention to what's important and real. The brain scans show that two nodes in this network are most crucial to psychosis: the anterior insula, which works to filter out unimportant information; and the ventral striatum, which predicts which information will be most rewarding or important to us.

These results "fit with prior hypotheses about the disorder," Adams said. They build upon theories about the salience network and psychosis that were based on the brain's structure, rather than its function, as well as more recent work that started to look at its function. The study also backs up work done in earlier studies that investigated the brain mechanisms behind psychosis in 22q11.2 deletion syndrome, specifically.

The researchers now plan to target these two key brain areas with existing treatments, such as brain stimulation, to see if they can prevent or delay psychosis in people at high risk of the condition. They also plan to study how antipsychotic medications affect these parts of the salience network, to reveal exactly how they work.

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A "butterfly effect" may help explain how autism-related genes in DNA get switched on. A new study suggests that, through this complex ripple effect, mutations in genes unrelated to autism end up influencing the activity of genes tied to the disorder. 

How does this work? DNA contains genetic material called promoters, which essentially switch genes on and off. Because DNA is twisted and coiled in a 3D shape, these promoters can control genes that are located far away from them in the DNA's sequence. In other words, if you stretched out all the kinks in the DNA, the promoter and genes would be far apart, but introducing folds in the molecule brings them close together. The promoter and the genes it controls form a regulatory "unit" called a topologically associated domain (TAD). 

Because of this complex mechanism, someone who doesn't have mutations in autism-linked genes may still develop the disorder due to mutations elsewhere in their genome — in promoters. That's the idea explored in the new study, published Friday (Jan. 26) in the journal Cell Genomics. 

Autism is highly heritable — it's estimated that between 40% and 80% of cases are tied to genes passed down through families. However, autism can also be caused by mutations that spontaneously arise in DNA. 

Related: Rates of autism diagnosis in children are at an all time high, CDC report suggests

Such mutations have recently been discovered in "non-coding" regions of DNA, which comprise about 98.5% of the genome. These regions include promoters and are known as "non-coding" because they don't contain instructions to build proteins, like genes do. 

Until now, little was known about how mutations in non-coding DNA impact someone's likelihood of having autism spectrum disorder (ASD). The new study begins to address that question. 

The study authors analyzed the genomes of more than 5,000 people with autism, along with those of their siblings who didn't have the condition and acted as a comparison group. The team were specifically looking for the presence of non-heritable mutations. They used specialized techniques to capture the 3D configuration of the genome and define TAD boundaries around autism-linked genes. 

The team found a direct association between autism and TAD-related gene regulatory mechanisms — specifically TADs that contain genes known to be linked to autism.

Sometimes, changing just one "letter," or base, in DNA's code was linked to a higher likelihood of autism, senior study author Dr. Atsushi Takata, a researcher at the Riken Center for Brain Science in Japan, told Live Science in an email. 

"The results showed that just a single base of DNA sequence difference in a non protein-coding region can affect the expression of nearby genes," he said, "which in turn can alter the overall gene expression profile of distant genes in the genome, leading to an increased risk of ASD." 

Takata likened this to a physics phenomenon known as the "butterfly effect," in which a slight change in the initial state of a complex system makes a big difference later on — for example, a butterfly flaps its wings, and weeks later, miles away, a tornado tears through a town. Similarly, a subtle mutation in a promoter can have big impacts on gene expression elsewhere.

In a separate experiment in human stem cells, the researchers induced mutations in specific TAD promoters using CRISPR gene-editing technology. They discovered that a single mutation that reduces activity in a promoter could drive changes in the activity of an autism-linked gene within the same TAD. This helped validate their earlier findings in people. 

"This is an interesting paper that attempts to extend our understanding of the contribution of rare, de novo [non-heritable] variation to ASD risk in regions outside the protein-coding genome," Dr. Daniel Rader, a professor of molecular medicine at the University of Pennsylvania who was not involved in the research, told Live Science in an email. 

The findings could have potential therapeutic implications, Rader said. For example, there may be ways to modulate the activity of specific promoters so that multiple autism-linked genes are regulated at the same time, he suggested. In theory, this could help alleviate symptoms of ASD, he said. 

The researchers now hope to identify other types of non-coding mutations that may impact someone's likelihood of having autism, Takada said. 

This article is for informational purposes only and is not meant to offer medical advice.

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Your mother's smile as you say your first word or the smell of the candles on your second birthday cake are memories many people would love to hold on to. But almost nobody can recall memories from very early childhood — a phenomenon known as infantile amnesia or childhood amnesia.

So why do we tend to forget these very early memories?

To answer this question, it is important to distinguish between two major types of memory: semantic and episodic. Semantic memory is our ability to recall facts and information about the world around us, while episodic memory allows us to remember details about life events, such as the people we were with and where we were at the time.

Young children do remember facts in the moment, such as who their parents are, or that they must say "please" before mom will give them candy. These are examples of semantic memory.

Related: How accurate are our first childhood memories?

However, when it comes to episodic memory, the lines become a bit blurred.

A prevailing scientific theory is that we tend to forget episodic memories that are formed between age 2 and 4 because the region of the brain that forms and retrieves them — the hippocampus — is not fully matured by this point.

Kids may fail to record specific episodes until age 2 to 4 because that's when the hippocampus starts tying fragments of information together, Nora Newcombe, a professor of psychology at Temple University in Philadelphia, told Live Science.

Newcombe said that, for children younger than that age range, episodic memory may be unnecessarily complex at a time when a child is just learning how the world works.

"I think the primary goal of the first two years is to acquire semantic knowledge, and from that point of view, episodic memory might actually be a distraction," Newcombe said.

However, recent research is beginning to turn this theory on its head. For instance, a study published in March 2025 in the journal Science revealed that in the first couple of years of life, the hippocampus can encode information that is required for episodic memory.

In the study, researchers showed 26 children age 4 months to 2 years a selection of images for two seconds each; the images were of faces, scenes and objects that form the bedrock of episodic memories. At the same time, the team analyzed activity in the children's hippocampi, using functional magnetic resonance imaging (fMRI).

Following a brief pause, the children were shown an image they'd previously seen, next to a new image, for four seconds. During this time, the researchers also monitored how long the kids looked at each image — another gauge of whether they recognized the old image after looking at the new one.

Overall, the researchers discovered that the greater the activity in the hippocampi, the longer the children spent looking at an image when it reappeared. The area within the hippocampus where brain activity was the strongest was also the region that is most associated with episodic memory in adults, the researchers found.

The findings of the Science study suggest that we experience infantile amnesia not because we don't retain information as young children but because we're unable to retrieve these memories as adults.

Along that vein, a 2023 study published in the journal Science Advances found that "forgotten" childhood memories could be reinstated in adult mice by using light to stimulate neural pathways that are relevant to specific memories.

The authors of the study first set out to explore developmental factors that could influence infantile amnesia. They found that mice with characteristics of autism were able to recall memories from their pup days.

Autism has many causes, but it has been previously linked to the overactivation of the mother's immune system during pregnancy. So, to make mice with an autism-like condition, the researchers stimulated the immune system of female mice during pregnancy.

This immune activation helped prevent the loss of early memories in these offspring by influencing the size and plasticity of specialist memory cells in their brains. When these cells were optically stimulated in adult mice without autism, their forgotten memories could be restored.

"These new findings suggest that immune activation during pregnancy results in an altered brain state that alters our innate, yet reversible 'forgetting switches' that determine whether the forgetting of infant memories will occur," study co-author Tomás Ryan, an associate professor of biochemistry at Trinity College Dublin, said in a statement.

Although the research was in mice and has yet to be studied in humans, it "holds significant implications for enhancing our comprehension of memory and forgetting across child development, as well as overall cognitive flexibility in the context of autism," Ryan said.

Editor's note: This story was originally published on Feb. 7, 2011, and was updated on Nov. 27, 2023 and March 26, 2025, to include the Science Advances study and the Science study, respectively.

A strange class of brain cell has two features that seem to contradict each other, leading scientists to question whether it really exists. But now, a new study of mouse and human brains not only supports these paradoxical cells' existence but also hints that they could help explain the neurological underpinnings of conditions like autism and schizophrenia.

Published in July in the journal Molecular Psychiatry, the study found that two chemical markers, which were once thought to mark neurons with opposite roles, are sometimes found in the same neuron. Neurons with both of these markers, researchers found, frequently activate, or "express" genes related to the production of cellular energy using oxygen. 

In postmortem brain tissue from donors with either autism or schizophrenia, neurons with these markers had altered gene expression related to this process, compared with tissue from people without the conditions. 

This finding potentially jibes with research linking schizophrenia and autism to genetic changes that contribute to oxidative stress, or the buildup of reactive byproducts of energy production in cells. The research could be a step toward better understanding these complex neurological conditions.

Related: How do brain cells send messages? 

In the study, researchers specifically documented the existence of a special class of inhibitory neurons, or neurons that suppress electrical activity in the brain. The cells carry two chemical markers: a protein called parvalbumin (PV) and a smaller molecule called cholecystokinin (CCK). 

Neurons with PV are fast-spiking, meaning they generate short-lived signals repeatedly and more quickly than almost any other type of neuron in the brain. Neurons with CCK typically fire at a slower, more typical speed. Previous research, such as a 2021 article in the journal Neuron, suggested that these neurons are usually active at opposite times, with PV neurons often firing before and even inhibiting those with CCK.

"It's kind of like you have this dichotomy," said Steven Grieco, lead author of the study and a project scientist in the Department of Anatomy and Neurobiology at the University of California, Irvine. "Our finding … blurs that dichotomy a little bit."

To confirm these seemingly unlikely cells' existence, the researchers used several methods in mice, including molecular staining and RNA sequencing, which takes stock of which genes are actively being used to make proteins. After establishing that some cells had both markers, they did the RNA sequencing to determine what the cells' function might be. They also examined the cells in postmortem brain tissue from people with neuropsychiatric conditions and those without.

Out of the inhibitory neurons with PV in the mouse hippocampus, a brain region involved in memory, 40% to 56% also had CCK, the team found. Such cells also appeared in other parts of the mouse brain, including the neocortex, a key region for "higher" cognitive functions, like perception.  

Cells with both PV and CCK more heavily activate genes related to oxidative phosphorylation, a process by which cells use oxygen and enzymes to create adenosine triphosphate (ATP), the body's main source of cellular energy. This suggests that the cells require a lot of energy to run.

However, these genes' expression seemed altered in the tissue from people with autism and schizophrenia, pointing to a potential role for the neurons in the conditions. The findings could also support the potential link between these conditions and oxidative stress, and may align with previous research linking the conditions to dysfunction in the brain's inhibitory neurons and a resulting overload of electrical activity.

Related: Mysterious spiral signals in the human brain could be key to our cognition

The researchers aren't the first to find these cells, said Simon Pieraut, an assistant professor of biology at the University of Nevada, Reno who was not involved in the work. But they are likely the first to focus on the cells in this way, he said.  

Pieraut told Live Science that his lab and others had previously found cells with both PV and CCK, but he was unsure if the findings might be the result of a technical quirk or error. He said that, to show that this isn't the case, it was particularly valuable that the researchers used multiple methods to support the existence of these cells.

The findings don't necessarily establish a link between these neurons and conditions like schizophrenia, but they provide justification for further research into if and how the cells might be related to the disorders, Pieraut said. Such research could potentially be used to develop future treatments.

"If we want to find treatment in the future, knowing exactly what pathway needs to be targeted … will be very helpful," he said. 

Young adults with multiple mental illnesses may share a common neurological "signature," new research suggests.

The study, published April 24 in the journal Nature Medicine, builds on a concept known as the "general psychopathology factor," or p factor, which studies suggest is a consistent pattern of psychiatric characteristics seen in patients with multiple mental disorders. However, the p factor doesn't explain whether these behavioral patterns have a neurological basis, meaning they can be linked to structural or functional features of the brain. 

In the new study, researchers created a neurobiological counterpart to the p factor that they call a neuropsychopathological (NP) factor. Using data from a large group of adolescents followed into young adulthood, the researchers identified specific patterns of brain connectivity tied to symptoms of psychiatric disorders.

"We [conducted] an approach from the bottom up, not from the behavior level," said Tianye Jia, a research professor at Fudan University in Shanghai and an author of the study.

Related: A mysterious brain network may underlie many psychiatric disorders 

Jia and his colleagues used data from the IMAGEN study, a large, long-term study to which thousands of adolescents across four European countries — the U.K., France, Germany, and Ireland — provided brain scans, as well as behavioral and genetic data. About 1,300 14-year-olds entered the IMAGEN study and were followed into early adulthood, up to age 19. 450 additional teens had fewer than five years of followup but were still included in some analyses.  

To find the participants' NP factor, the researchers relied on functional magnetic resonance imaging (fMRI), a technique that measures brain activity through time. While many previous studies used brain scans taken while participants were at rest, the researchers decided to use fMRIs taken while participants completed behavioral tasks. These included completing a task to earn a reward, like candy, and a task that tested participants' ability to selectively respond to fast-paced motor prompts.

Using these brain scans, the researchers assessed patterns of functional connectivity (FC) — a measure of the strength of connections between different brain regions — in the teens' brains. They then looked at how these patterns were associated with behavioral symptoms linked to eight different mental disorders. (A small subset of the participants were identified as being likely to have one of the disorders, based on their behavioral task performance, but most were not.)  

Four of the disorders were "externalizing," or disorders where the associated behaviors tend to be related to interactions with others or the environment, including autism spectrum disorder, attention-deficit/hyperactivity disorder (ADHD), conduct disorder, and oppositional defiant disorder. The other four were internalizing disorders, whose effects tend to be directed inward, toward oneself. These included generalized anxiety disorder, depression, eating disorders and specific phobias. 

To calculate the NP factor, the researchers used a model to see what patterns of FC appeared linked to “both externalizing and internalizing risk behaviors," Jia said. In other words, the presence of this connective "brain signature" could be used to predict whether a person was at high risk for both sets of behaviors. The team established the NP factor at age 14 and then validated their work by checking whether this pattern was predictive of participants' behaviors at age 19.

Compared with those with low or average NP factors, participants with high NP factors showed increased connectivity in several areas of the prefrontal cortex, an area in the front of the brain involved in planning, decision-making and working memory.

To validate the NP factor, the researchers used genetic and behavioral data from IMAGEN and several other brain scan data sets. For most data sets, including IMAGEN, having a high NP factor was associated with being diagnosed with at least one mental illness, and the highest NP factors were associated with multiple diagnoses. 

The researchers also found that having a high NP factor was linked to carrying a gene variant associated with both ADHD and major depressive disorder. Researchers think this mutation can cause synapses, or gaps between neurons that the brain's chemical signals jump between, to form robust but inflexible connections.

This finding hints that high NP factors could reflect a developmental issue affecting the synapses, the researchers wrote. Participants with high NP factors did not show the typical patterns of synaptic "pruning" during adolescence, in which the brain reduces the number of synapses so that its information processing can become more efficient. Instead, these teens had a hyperconnected brain circuit centered in the prefrontal cortex, a trait sometimes associated with deficits in executive function, or a person's ability to plan and accomplish everyday tasks and goals. (Similar hyperconnectivity has been linked to autism in past studies.) 

This hyperconnectivity could be related to the gene mutation related to synaptic adhesion, which may make pruning less efficient, though not all participants with high NP factor scores had the variant.  

The NP factor could be useful in both future research and, eventually, in the treatment of psychiatric disorders, Stephen Glatt, a professor of psychiatry and behavioral sciences at SUNY Upstate Medical University who was not involved in the study, wrote in an email to Live Science.

If validated in future studies, NP factor "might become one of the core ingredients in building new recipes for studying and treating psychopathology," Glatt said. In other words, the factor could be useful in both researching the underlying risk factors for psychiatric illness and for assessing patients in clinic, he said.

The rate of autism spectrum disorder (ASD) in the United States has reached an all time high, a new report from the Centers for Disease Control and Prevention (CDC) has revealed. However, the sky-high rate is likely due to improved screening and diagnosis, not an epidemic of new cases, the study suggests.

One in 36 children had an ASD diagnosis in 2020 compared to one in 44 in 2018, according to data collected across 11 states by the Autism and Developmental Disabilities Monitoring (ADDM) Network. Wisconsin recorded the largest relative change between 2018 and 2020, with a 49.5% increase in the overall prevalence of ASD.

For the first time in 20 years of monitoring, the percentage of 8-year-old girls with ASD rose above 1%, while it remained around 4% for boys.

The report, published on March 24, also found for the first time that the prevalence of ASD in Black, Hispanic, Asian and Pacific Islander children has overtaken the prevalence in white children, who have historically had better access to screening and diagnosis.

While ASD prevalence in white children rose 14.6% from 2018 to  2020, it increased by more than 30% in Asian, Black and Hispanic 8-year-olds. The staggering increase in those groups is due to improved screening, awareness and access since 2018, the report suggests.

Related: Brain differences tied to autism can be detected in the womb 

ASD is a developmental disorder that affects the brain and impacts how people interact with others, communicate, learn and behave, according to the National Institute of Mental Health.

To estimate how many children have ASD, the ADDM Network counted 8-year-old children with either an ASD diagnosis from a qualified professional, a special education classification of autism in public school or an administrative record of ASD using the World Health Organization's International Classification of Diseases.

ASD prevalence among children has increased markedly over the last 20 years. The ADDM Network notes that while just 6.7 kids per 1,000 met criteria for an ASD diagnosis; that number rose to 23 in 2018 and 27.6 in the current report.

Black children with ASD were more likely to have additional intellectual disabilities, such as those related to genetic conditions or birth defects, than their white counterparts.

The current prevalence could be an underestimate, the report suggests. COVID-19 and successive lockdowns blocked access to some services, which may have led to fewer records of ASD being documented.

"In the early months of the pandemic, 4-year-old children were less likely to have an evaluation or be identified with ASD than 8-year-old children when they were the same age. This coincides with the interruptions in childcare and healthcare services during the COVID-19 pandemic," CDC officials wrote in a statement. 

Valproic acid — a drug commonly used to treat epilepsy and bipolar disorder — can cause birth defects and developmental disorders if taken during pregnancy, but the reason why has long been a mystery. Now, in a study using mice and human tissue, scientists discovered that the medication locks some embryonic cells into a suspended state where they can't properly grow or divide.

By forcing key stem cells cells into this state, called senescence, valproic acid may disrupt brain development in the womb and therefore cause cognitive and developmental disorders down the line, according to the study, published Tuesday (June 14) in the journal PLOS Biology. An estimated 30% to 40% of infants exposed to the drug in the womb develop cognitive impairments or autism spectrum disorder, the study authors noted in their report, and these laboratory studies hint at why that happens. 

In a subset of affected children, valproic acid exposure can also cause birth defects beyond the brain, including heart malformations and spina bifida, where part of the spinal column doesn't form properly and thus leaves the spinal cord exposed. However, the new study suggests that these physical birth defects, though also linked to valproic acid, are triggered by a different mechanism than the cognitive impairments, Bill Keyes, a team leader at the Institute of Genetics, Molecular and Cellular Biology in Strasbourg, France and senior author of the study, told Live Science.

Related: Brain differences tied to autism can be detected in the womb 

Mice and mini-brains

When taken as a treatment for epilepsy or bipolar disorder, valproic acid affects the body in several ways, according to the online medical database StatPearls. For instance, the medication changes the levels of certain chemical messengers in the brain and alters which genes can be switched on in a cell at any given time.

Valproic acid first hit the market in the 1960s as an anticonvulsant medication, but by the 1980s, the drug's link to birth defects became apparent, according to BBC News. Later research in rodents and monkeys suggested that, when taken in the first few weeks of pregnancy, the drug might disrupt the earliest stages of nervous system formation. This upset seems to occur around the time that the "neural tube" — a hollow tube of tissue that later becomes the brain and spinal cord — forms and closes. In human embryos, that's typically between the fourth and sixth week of pregnancy, according to the Centers for Disease Control and Prevention (CDC). 

To understand how valproic acid messes with this early stage of development, Keyes and his colleagues exposed mouse embryos to the drug. The neural tubes of these exposed embryos often failed to close, and later in development, the fetal mice also grew unusually small heads and brains. 

Rodent cells exposed to valproic acid carried enzymes that only appear in cells undergoing senescence; the same enzymes did not crop up in the cells of healthy, unexposed mice. These markers of senescence specifically appeared in exposed neuroepithelial cells, a type of stem cell that later produces brain cells.

To check if valproic acid could trigger senescence in human cells, the team ran a similar experiment using 3D clusters of human nerve cells, known as cerebral organoids. These organoids resemble miniature human brains, in that their structure and function is similar to that of the full-size organ. The researchers exposed the organoids to valproic acid and found that the drug pushed the organoids' neuroepithelial cells into senescence, just as it had in the mouse embryos. 

Related: Father's use of diabetes drug could raise his kids' risk of birth defects

"This was just very nice validation for us to be able to set up and test organoids and then see that we were seeing senescence in exactly the same cell type," Keyes said. And because the valproic acid exposure nudged the organoids' neuroepithelial cells into a suspended state, the exposed organoids turned out much smaller than organoids that hadn't been exposed to the drug.

How exactly does valproic acid push cells into senescence? It yanks the brakes off a specific gene that usually stays inactive throughout embryonic development, the team discovered. 

This gene codes for a molecule called p19Arf, which usually becomes active in adulthood and helps to clear cancerous and aging cells from the body. Although helpful in adults, the molecule's presence in embryos drives key cells into senescence and disrupts the development of the nervous system. 

When the team genetically modified mice so that they couldn't produce p19Arf, the rodents became impervious to some of valproic acid's effects, and the mice's brains were able to grow to normal size. However, the mice still developed deformities in their spinal cords, which suggests that valproic acid causes those defects through a different mechanism, Keyes said. 

"I think it is a strength of the study to utilize both human organoids and mouse model systems," said Richard H. Finnell, a professor in the Center for Precision Environmental Health and various other departments at Baylor College of Medicine, who was not involved in the research. The organoid experiments confirmed which genes are affected by valproic acid exposure, and the mouse model revealed how the drug's effects unfold in ongoing pregnancies, he told Live Science in an email.

Nevertheless, "there are many caveats to our model," Keyes said. 

For instance, the team exposed their mice and organoids to several high doses of valproic acid over a short period of time, whereas in real life, patients consistently take a lower dose of the drug over a longer time span. The high-dose, short-term regimen in the experiments may therefore have triggered an "exaggerated" effect in the mice and organoid cells that wouldn't necessarily be matched in human embryos, Keyes said  

In other words: Although the mice and organoids in the study showed senescence in a large portion of their neuroepithelial cells, the effect on human embryos would likely be patchier, he said. "So then the child would ultimately be born with some defects in some population of cells," he said, and in theory, "this then gives rise to the cognitive and behavioral defects."  

In the future, the team hopes to repeat their lab experiments with a valproic acid regimen that more accurately mirrors real-world exposure, meaning one that's low-dose and long-term, Keyes said. These experiments, along with in-depth genetic analyses, should reveal more details of how valproic acid exposure impacts growing human embryos.

Originally published on Live Science.

Brain scans of babies in the womb may reveal whether a child is at risk for developing autism later in life, early research suggests.

A small study of 39 fetuses found that, by 25 weeks of gestation, certain brain regions looked different in the unborn babies who went on to be diagnosed with autism compared with those who were not diagnosed with the condition.  

Specifically, prenatal MRI scans showed that the insular lobe — which may play a role in perceptual awareness, social behavior and decision-making — was larger in volume in the babies who would later be diagnosed with autism, compared with the insular lobes of children who were not diagnosed with autism.

Children in the autism group also had larger volume in a brain region called the amygdala in prenatal scans — a finding that jibes with earlier results showing larger amygdalae in toddlers with autism.

"These results make it clear that we need to focus on these promising regions as potential biomarkers and find out the reason for these alterations," study first author Alpen Ortug, a postdoctoral research fellow at Massachusetts General Hospital, Harvard Medical School, told Live Science in an email.

Related: What is the amygdala?

The findings add to a growing body of evidence that the disease processes involved in autism may begin early in development, the researchers said.

Still, much more research is needed to confirm the findings, which were presented Tuesday (April 5) at the Experimental Biology (EB) 2022 meeting in Philadelphia. The study has not yet been published in a peer-reviewed journal.

Autism spectrum disorder (ASD) is a developmental disorder that affects how a person communicates, interacts socially, learns and behaves, according to the National Institutes of Health (NIH).

Early detection and treatment of autism can greatly improve outcomes for patients, according to the NIH. But currently, the earliest that autism can be reliably diagnosed is about 18 months of age, the researchers said. 

Previous studies have found brain differences in infants that go on to develop autism. For example, a study published March 25 in The American Journal of Psychiatry found that the amygdala may grow too fast in babies between 6 and 12 months of age prior to their diagnosis of autism, Live Science previously reported.

In the new study, the researchers examined whether prenatal brain scans could help spot potential markers of autism even before birth. They analyzed 39 fetal MRI brain scans, which were performed at Boston Children's Hospital. The MRI scans were originally conducted because the fetuses were suspected to have a developmental condition based on ultrasound results, but the ultrasounds were not sufficient to confirm the diagnosis, Ortug said.

Among these patients, nine children were later diagnosed with autism, and 20 children had typical development. Ten of the children did not have autism but had other health conditions, such as developmental disorders affecting the cardiovascular system. The MRI scans were analyzed retrospectively, meaning after the children's diagnoses.

The researchers used a computer programming method to segment the brain scans into different regions and then compared the segmented regions among the different groups.

They found the biggest differences in the insular lobe, with significantly larger volumes in the autism group compared with the other groups. This finding agrees with previous studies that have found changes in the insular lobe in adults with autism, and suggests these changes may start in the womb, the researchers said.

Dr. L. Eugene Arnold, a professor emeritus of psychiatry and behavioral health at The Ohio State University Wexner Medical Center who was not involved with the new study, told Live Science that the new study was small and that the findings need replication but that the results are in line with other reports of various prenatal differences linked with autism. For example, a study published in January in the journal Brain that examined prenatal ultrasounds found that children who went on to develop autism were much more likely to have anomalies in their heart, kidneys and head seen on the ultrasounds, compared with children that did not develop autism.

However, Arnold also noted that differences in the insular lobe "may not be specific to ASD; they have been reported in individuals with other psychiatric disorders," including bipolar disorder. Therefore, more research would be needed to determine how specific this finding is to autism.

"Although the findings, if replicated, are enlightening … considerably more work is needed before MRIs would be a feasible way to screen for pre-ASD," Arnold said.

In addition, the study was retrospective and involved children that underwent MRIs for a suspected issue, so they are not representative of the general population.

Ortug agreed that additional, larger studies are needed to confirm the findings. If fetal MRIs become a more routine examination in pregnancy, like ultrasounds are today, they might be used to "determine whether there is an increased probability of ASD," Ortug said. "For now, as fetal MRIs are not frequent if there is no clinical indication, our results are promising for the research community rather than clinics."

Originally published on Live Science. 

A brain structure called the amygdala grows too fast in babies who are diagnosed with autism by age 2, a new study suggests.

The study researchers found that this overgrowth occurs between 6 and 12 months of age, before children are typically diagnosed with autism. The findings, published Friday (March 25) in The American Journal of Psychiatry, suggest that therapies for children at high risk of autism may have the best chance of working if they start in infancy.

"Our research suggests an optimal time to start interventions and support children who are at highest likelihood of developing autism may be during the first year of life," study senior author Dr. Joseph Piven, a professor of psychiatry and pediatrics at the University of North Carolina at Chapel Hill, said in a statement.

Autism spectrum disorder (ASD) is a developmental disorder that affects how a person communicates, interacts socially, learns and behaves, according to the National Institute of Mental Health.

The amygdala is an almond-shaped structure deep in the brain that's involved with processing emotions, including feelings of fear, as well as interpreting facial expressions. Researchers already knew that the amygdala appears larger in school-age children with ASD compared with children without ASD, but exactly when this enlargement starts was not known.

Related: 10 things you didn't know about the brain

In the new study, researchers scanned the brains of more than 400 infants, including 270 who were at higher risk of developing autism because they had an older sibling with the condition; 109 infants with typical development; and 29 infants with Fragile X syndrome, a genetic disorder that causes developmental and intellectual disability. The children underwent MRI scans at ages 6 months, 12 months and 24 months. By age 24 months, 58 (or about 21%) of the at-risk children had been diagnosed with ASD.

The researchers found that at age 6 months, all of the children had similar-sized amygdalae. But by 12 months, the children who would later develop autism had enlarged amygdalae compared with children who didn't develop autism and those with Fragile X syndrome. What's more, those with the fastest rate of amygdala growth had the most severe symptoms of autism.

"The faster the amygdala grew in infancy, the more social difficulties the child showed when diagnosed with autism a year later," study first author Mark Shen, an assistant professor of psychiatry and neuroscience at UNC Chapel Hill, said in the statement.

The researchers hypothesized that early problems with  visual and sensory information processing in infancy may put stress on the amygdala, resulting in its overgrowth. (The amygdala receives signals from the brain's visual system and other sensory systems in order to detect threats)

Studies have found that children that go on to be diagnosed with autism have problems as babies with how they pay attention to visual stimuli.

Interventions in babies at high risk of autism might want to focus on improving visual and other sensory information processing in babies, Piven said.

Early interventions for autism usually begin around two or three years of age, when a child is diagnosed with autism, according to the National Institutes of Health. However, some studies have tested interventions in babies that were at risk for autism because they had a sibling with autism or in babies that showed early symptoms, such as visually fixating on certain objects, according to the autism news site Spectrum. For example, a small 2014 study tested an intervention in children ages 6 to 15 months, which taught parents new ways of interacting with their babies, such as methods to shift the baby's attention away from an object they were fixated on; and found that the therapy reduced autism symptoms by age 3, Spectrum reported.

Originally published on Live Science. 

Heavy metals found in baby teeth may reveal metabolic problems that potentially contribute to  attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder, according to a preliminary new study. 

The research is in very early stages. But if children with ADHD and/or autism process metals differently, it may be that these metabolic differences partially cause or exacerbate the conditions. Understanding exactly how that process works could one day help doctors identify children who are at risk for these conditions and potentially shield them from environmental factors that worsen their symptoms, experts suggest. 

(Currently, the baby teeth technique cannot be used to help diagnose, prevent or treat autism or ADHD.)  

The tooth tissue examined in the study contained trace metals ⁠— both biologically essential ones, such as zinc, and dangerously toxic ones, such as lead ⁠— that together revealed differences in how the children metabolized the elements in their bodies. 

Compared with the teeth from children without neurodevelopmental disorders, the teeth of children with ADHD, autism or both conditions showed patterns of metal metabolism that appeared less complex than metabolic cycles in typically developing children, according to the new study, published Sept. 25 in the journal Translational Psychiatry.

Scientists have long known that exposure to toxic metals can disrupt brain development, but this study suggests there is more to the story, said Dr. Amy Margolis, a medical psychologist at Columbia University Medical Center.  

"It isn't only a story of '[metal] exposure leads to bad outcomes' — it's also a story of how different metabolic profiles may make certain people more vulnerable," Margolis, who was not involved in the study, told Live Science. Evidence suggests that ADHD and autism may involve disruptions in the same chemical pathways, Margolis added, and the new study underscores this idea and paves the way for further investigation. 

Related: 7 Ways Pregnant Women Affect Babies 

In the past, researchers found that people with ADHD have different blood and urine concentrations of various metals — such as lead, mercury, zinc and manganese — than those without the disorder, according to a 2013 review and two 2016 studies. Autism and its behavioral symptoms have also been linked to increased levels of toxic metals, like lead, and depleted levels of essential minerals, like zinc. But blood and urine samples can only capture metals present in a person's system at the time of collection.

"What it can't do is tell you how much [metal] you were exposed to in the past," said study co-author Paul Curtin, a computational biologist at the Icahn School of Medicine at Mount Sinai in New York. Curtin and his colleagues wanted to know how metal influenced the development of ADHD and autism in the womb, so they took a different approach.

Fetal teeth begin budding late in the first trimester of pregnancy and accumulate layer upon layer of enamel between the second trimester and early childhood. The layers form visible lines not unlike "growth rings on trees," Curtin said, and these layers reflect the levels of elements, such as metals, that were circulating in the developing child's bloodstream at different times. By examining patterns of metal exposure archived within the tissue, "we're able to follow the growth rings in the tooth and go back in time," Curtin explained.

The team collected lost baby teeth from 74 children who had previously participated in the Roots of Autism and ADHD Twin Study in Sweden, a cohort that included one group of triplets, 30 complete sets of twins, and 11 individuals from twin pairs. By focusing on twins, the scientists aimed to control for genetic factors that contribute to autism and ADHD and instead focus on markers of metal metabolism that might differ between the children. Thirty-three (45%) of the children had ADHD, autism or both conditions, and the other 41 children (55%) served as a control group for comparison.

With the baby teeth in hand, the scientists rolled out the lasers.

The team aimed concentrated plasma beams at each tooth's enamel to zap through its pearly white surface to the "growth rings" within. The laser generated charged particles within the dental tissue that could then be detected, analyzed and fed into a computer algorithm to reveal distinct patterns of metal embedded in the teeth. The analyses showed that children's teeth bore specific markers of metal metabolism — markers that roughly correlated with whether they had ADHD, autism, both conditions or neither. (The correlation was subtle; it took a computer algorithm to pick out the pattern, and the correlation wasn’t strong enough, or shown in a large enough group, that it could be used to diagnose these conditions.)

The body normally breaks down metals cyclically, meaning the process occurs repeatedly in a consistent pattern and pace, Curtin said. The baby teeth analyses suggest that these cycles are somehow disrupted in children with neurodevelopmental disorders

"We do know that genetics can make a difference on absorption and metabolism of vitamins and minerals," said Dr. Eugene Arnold, professor emeritus of psychiatry and behavioral health at The Ohio State University Wexner Medical Center. Arnold, who was not involved in the study, suggested that researchers could investigate the genetics that drive metal metabolism in animal models of ADHD and autism. That research, in turn, might  help scientists better understand the disorders in humans, Arnold said. 

Different brain structures form, develop and connect both in utero, and then into early childhood. Because the tooth data show the pattern of heavy-metal metabolism over time, brain scans could then reveal how certain metabolic patterns relate to the volume, structure and connectivity of different brain regions at different stages of development, Margolis said. Scientists could then probe in finer detail how metal metabolism contributes to brain function and human behavior. First, though, she said, the baby teeth experiment should be replicated in an additional, larger sample.

The team behind the new study used their signature tooth technique in a similar 2018 study, in which they studied children with autism in Sweden, the United States and the United Kingdom. Regardless of their location or genetic background, children with autism displayed distinct patterns of zinc and copper metabolism that differed from those of children without autism from each place.

Heightened levels of toxic metals and depleted levels of essential minerals have been linked to neurodevelopmental disorders, but the authors suggest that how a child metabolizes metal may be as important as which elements they're exposed to.

"Of course, it's critical what you're exposed to," Curtin said. "But it's also critical how you process that exposure...The [proper] metabolism of essential elements is clearly required for normal neurodevelopment." 

• 11 Facts Every Parent Should Know About Their Baby's Brain 
• 7 Ways the Mind and Body Change With Age 
• Top 10 Controversial Psychiatric Disorders 

Originally published on Live Science. 

A single sperm donor is the biological father of at least 12 children who all developed autism — an extraordinary case that prompted one woman to sue her sperm bank, according to news reports.

The case came to light when the woman, Danielle Rizzo of Illinois, was researching treatments for her two sons, who both have autism, according to The Washington Post. Both sons were conceived with sperm from the same donor, and Rizzo was shocked to discover that other mothers who used the same donor also had sons with autism, the Post reported.

Rizzo was told that the likelihood of all these related children having autism by chance was like all the mothers "opening up a dictionary and pointing to the same letter of the same word on the same page at the same time," she told the Post.

That means a mutation in the donor's sperm was likely responsible. But is there a single "autism gene?"

In short, no: There are hundreds of genetic variations tied to autism spectrum disorder, according to the National Institutes of Health (NIH). In most cases, these mutations increase a person's risk of autism, but they don't destine someone to develop the condition. In other words, genes typically play only a partial role in the risk of developing autism, with environmental factors, such as the parents' ages and birth complications, contributing as well.

But in rare cases, genetic mutations are thought to be the main cause of autism. Only about 2% to 4% of people with autism have these mutations, according to the NIH.

"We call autism one thing, but it's different in every person. In some, it's all about the genes. Some it's a combination of genes and the environment. Some people, it's unknown," Dr. Wendy Chung, a professor of pediatric medicine at Columbia University, told the Post.

Studies of Rizzo's children found that they had two mutations tied to autism in genes called MBD1 and SHANK1.

Most reproductive clinics test for several hundred genetic conditions, but there is no test for autism, The Post reported.

In Rizzo's lawsuit, she alleged that the donor's profile had false information. For example, she said that the donor did not have a college degree, as the profile listed, and that he had been diagnosed with ADHD, which was omitted from the profile, the Post reported. She settled the lawsuit in March for $250,000.

Read more about the case at The Washington Post.

•  Beyond Vaccines: 5 Things that Might Really Cause Autism 
•  Sexy Swimmers: 7 Facts About Sperm 
•  5 Myths About Fertility Treatments 

Originally published on Live Science. 

Children who receive the measles, mumps and rubella (MMR) vaccine are not at increased risk for autism, and that includes children who are sometimes considered to be in "high risk" groups for the neurodevelopmental disorder, a massive new study finds.

The new study, published today (March 4) in the journal Annals of Internal Medicine, is one of the largest studies of its kind to date. In it, researchers looked at the records of more than 657,000 children born in Denmark between 1999 and 2010, including about 6,500 who had received an autism spectrum disorder (ASD) diagnosis. ASD is a neurodevelopmental condition that affects a person's ability to communicate, interact and behave appropriately with others in social situations.

The study shows, as many before it have time and again, that "[caregivers] shouldn't choose to not vaccinate because of this punitive association between the MMR [vaccine] and autism," said study principal investigator Anders Hviid, a senior researcher in the Department of Epidemiology Research at Statens Serum Institut in Copenhagen. "There's really strong science that there is no association." [Beyond Vaccines: 5 Things That Might Really Cause Autism]

The idea that the measles component of the MMR vaccine might be linked to autism began with a small, now-retracted 1998 study in the journal The Lancet. That research looked at 12 children with developmental delays, and eight of the kids had autism. It's since come to light that the lead researcher had several conflicts of interest: He had been paid by a law firm that wanted to sue the vaccine manufacturer, and he had a patent for a "safer" measles vaccine that he had developed before doing the 1998 study, according to a 2011 report in the journal The BMJ.

Since 1998, countless studies have found no link between the MMR vaccine and autism, including a large 2002 study in The New England Journal of Medicine that Hviid carried out with his colleagues; that research looked at 537,000 children born in Denmark between 1991 and 1998. But after the publication of that study, Hviid heard from concerned parents and so-called anti-vaxxers who questioned whether "susceptible" children might be at risk for autism after receiving the MMR vaccine.

"We saw an opportunity to re-examine the association in the same setting but with new children," Hviid told Live Science. "We also looked at how we could address some of the criticisms of our original study."

What they studied

In the new study, in addition to looking at the big picture (whether the MMR vaccine increases autism risk in all children), the researchers looked at whether the vaccine increased risk in the following groups: boys, girls, children who develop "regressive autism" when they're older and children whose siblings have autism (the condition is partly genetic, so these children already have a greater risk of developing autism than the general public does).

The scientists also looked at individuals' birth years, whether other childhood vaccines were received and when, and each child's autism risk factors based on the child's disease risk score, the researchers reported in the study.

In the results, none of the subgroups that received the MMR vaccine showed any increased risk for autism, the researchers found. Interestingly, the vaccine was even associated with a slightly lower risk of autism in girls and in children born from 1999 to 2001, the researchers reported.

What increases autism risk?

It's still unclear what biological mechanisms cause autism. But the study did find which groups were at highest risk for autism: boys, children born more recently (from 2008 to 2010), children who had no early vaccinations and, as mentioned, those who had siblings with autism. Other risk factors included having older parents, a low birthweight, a preterm birth and a mother who smoked during pregnancy. [7 Ways Pregnant Women Affect Babies]

The study is a "well-conducted investigation" showing what other studies before it have: that getting the MMR vaccine does not increase a child's risk of autism, said Kristen Lyall, an assistant professor at the A.J. Drexel Autism Institute at Drexel University in Philadelphia, who was not involved in the study.

This research also makes "the important contribution that even among groups with increased susceptibility to autism, MMR vaccination is not associated with autism," Lyall told Live Science in an email.

In an editorial published alongside the study, Dr. Saad Omer, a professor at the Emory Vaccine Center at Emory University in Atlanta, who was not involved with the study, said that the need to disprove anti-vaccine ideas comes at a cost. While large epidemiology studies may not cost as much as other types of research, he said, they do divert time that scientists could otherwise spend finding causes and treatments for autism.

"Irrespective of the absolute costs, the opportunity cost of this research should be kept in mind: For example, continuing to evaluate the MMR-autism hypothesis might come at the expense of not pursuing some of the more promising leads" related to autism's causes and treatments, Omer wrote in the editorial.

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Originally published on Live Science.

Pregnant women who have high levels of a byproduct from the banned insecticide DDT in their bodies may be more likely to have a child with autism, a new study finds.

Researchers looked at nearly 800 mothers from Finland who had children diagnosed with autism spectrum disorder (ASD) and found that these women had higher levels of DDE, a byproduct of DDT, than did mothers whose children did not have ASD.

The finding sheds light on another potential cause of autism, a neurodevelopmental condition that affects communication, behavior and the ability to interact with others. But DDE is likely just "one piece of a puzzle," said study lead researcher Dr. Alan Brown, a professor of psychiatry and epidemiology at Columbia University Medical Center in New York City. [8 Ways That Air Pollution Can Harm Your Health]

"Very likely, you need other predisposing factors [for autism] in addition to [DDE]," Brown told Live Science. "I don't think moms should be going out and getting tested for these things."

To do the study, Brown partnered with researchers in Finland, a country with a universal health care system that tracks diagnoses, such as autism, in all people living there. The researchers identified 778 cases of children diagnosed with autism who were born from 1987 to 2005, then matched those individuals with controls — that is, children who were born during that same period but did not have an autism diagnosis.

Then, the researchers analyzed blood samples that had been taken from these children's mothers during early pregnancy. After analyzing these blood samples for DDE, the researchers found that mothers with higher levels of the compound were more likely to have children with autism. What's more, the DDE levels were even higher in mothers whose children had both autism and an intellectual disability, Brown said.

To be specific, the odds have having a child with autism were 32 percent greater in the women with higher DDE levels compared with the women with lower DDE levels, Brown said. In addition, the odds of having a child with autism and an intellectual disability were increased by more than twofold when comparing the women whose DDE levels were in the top 25 percent of the group with those who had low DDE levels.

The finding held even when the researchers controlled for several factors, including the age of the mother, the mother's socioeconomic status and whether the parents had a history of psychiatric disorders.

The researchers also tested the mothers' blood samples for PCBs (polychlorinated biphenyls), another class of environmental pollutants, but found that these substances were not associated with autism risk.

PCBs and DDT have both been banned for more than 30 years in many countries, including the United States and Finland. But because these chemicals break down very slowly, they stick around in the environment and the food chain. "What happened was DDT was sprayed in the air as an insecticide to kill mosquitoes, to kill bugs on fruits and vegetables," Brown said. "Then, it got into the soil and groundwater."

Virtually everybody has some level of DDT and PCBs in their body. When the body metabolizes DDT, the chemical breaks down into DDE, Brown said. When a woman is pregnant, the fetus is exposed to even higher levels of these chemicals than the mother is exposed to, "because they kind of get concentrated when they go through the mom's blood to the placenta," he said. "Then, they get into the fetal brain, and they alter fetal brain development." [11 Facts Every Parent Should Know About Their Baby's Brain]

Brown recommended that women who are pregnant or thinking about getting pregnant eat organic fruits and vegetables, as well as wash produce to rinse off toxic residues, but "I wouldn't say it's cause for alarm," Brown said. "We showed that overall in autism, there was a modest increase in risk [from DDE], but the vast majority of offspring who are exposed to the high levels still won't get autism."

As mentioned, DDE may just be one piece of the puzzle for explaining what causes autism. Hundreds of other studies show that additional factors also play a role, including low birth weight, the age of the parents (older parents tend to have a greater risk), whether the mother takes the anticonvulsant valproic acid while pregnant, whether the parents have a close relative with autism and whether the mother has increased levels of inflammation while pregnant.

But this study may play an important role when politicians craft public policy, at least when it comes to using certain chemicals in the environment, Brown said.

That idea was echoed by Marc Weisskopf, a professor of environmental epidemiology and physiology at the Harvard T.H. Chan School of Public Health, who was not involved in the new research.

"DDT is very long-lived in the body, so a woman with high levels may not be able to do much about it at the time she starts thinking of getting pregnant," Weisskopf told Live Science in an email. "For any individual mother, I would still stress that the absolute increase in risk from such exposure still certainly remains small. From a larger societal point of view, it is more evidence to try and limit DDT exposures overall."

The study is the first to connect an insecticide with risk for autism by testing a mother's blood sample. It was published online today (Aug. 16) in the American Journal of Psychiatry.

Original article on Live Science.

Unless you're a werewolf or a superhero, you can't easily transform into something you're not — but your cells can.

Scientists recently found a way to convert an immune-system cell into a neuron — two cells with totally different shapes and very different functions. The hope is that the technique could help researchers study a patient's brain from a blood sample.

The study was published on Monday (June 4) in the journal Proceedings of the National Academy of Sciences.

"Blood is one of the easiest biological samples to obtain," Marius Wernig, an associate professor of pathology at Stanford University, said in a statement. "Nearly every patient who walks into a hospital leaves a blood sample, and often these samples are frozen and stored for future study." [Top 10 Mysteries of the Mind]

Stem cells — which can turn into many different types of cells — are typically the go-to way for researchers to create a cell of choice. But sometimes other cells that have already differentiated, or reached their mature calling (having already turned into skin cells or blood cells, for instance) can morph into a totally different cell type. Researchers call this transformation "transdifferentiation."

Wernig and his team first demonstrated their "transdifferentiation" technique in a study published in the journal Nature in 2010.  The team converted mouse skin cells into mouse neurons, without first turning them into stem cells. But the skin cells had to be grown in the lab for some time — time that could lead to genetic mutations that would alter a person's cells, according to the statement.

To avoid this lag, Wernig and his team focused on T cells — white blood cells that play an important role in the immune system by helping to destroy pathogens. They found that with the addition of four proteins, in a short period of time, T cells transformed into a patient's own neurons, according to the statement.

"It's kind of shocking how simple it is to convert T cells into functional neurons in just a few days," Wernig said. "T cells are very specialized immune cells with a simple round shape, so the rapid transformation is somewhat mind-boggling." (In contrast, neurons have elongated tails.) This technique could eventually be used to study the neurons of people who have schizophrenia and autism, in order to understand the origins of the diseases and identify potential treatments, the statement said.

However, the neurons they created can't form mature synapses — spaces between neurons that are necessary for the cells to communicate with one another. According to the statement, Wernig and his team are hoping they can eventually improve the technique and have already begun to collect blood samples from children with autism.

Originally published on Live Science.

A growing number of clinical trials are looking into whether compounds in marijuana can be used to treat some of the symptoms of autism.

One of these clinical trials was just announced at the University of California, San Diego, and others are slated to take place in New York at Montefiore Medical Center and New York University, and in Israel at Shaare Zedek Medical Center.

These trials were prompted, in part, by the success of other clinical trials investigating whether cannabis could effectively and safely treat other neurological disorders, including two rare forms of epilepsy and a condition called fragile X syndrome. [7 Ways Marijuana May Affect the Brain]

There have also been a slew of anecdotal stories from parents of children with autism saying that cannabis improved their children's symptoms. But more evidence is needed to make sure that specific compounds in cannabis are a safe and effective treatment for symptoms of autism spectrum disorder, said Dr. Orrin Devinsky, director of NYU Langone's Comprehensive Epilepsy Center, who is involved in two of the upcoming clinical trials. (Parents should not give their children cannabis, or cannabis-related compounds, without consulting with a doctor first.)

"There's not been a huge amount of data generated in this area," Devinsky told Live Science. "There's a lot of religion and not a lot of science."

New clinical trials

Autism spectrum disorder — a neurodevelopmental condition that affects communication, behavior and the ability to interact with others — is diagnosed in an estimated 1 in 59 children in the U.S., according to the Centers for Disease Control and Prevention.

There is no cure for autism (although a small percentage of children do appear to outgrow it), and there are few treatments for its symptoms. But, because of the potential promise of cannabis treatments, the Ray and Tye Noorda Foundation, a nonprofit based in Utah, donated $4.7 million to the Center for Medicinal Cannabis Research (CMCR) at the UC San Diego School of Medicine — the largest private gift to date for medicinal cannabis research in the United States, according to an April 25 statement from the university.

Researchers at the CMCR plan to use the money to run a clinical trial testing whether cannabidiol (CBD), a nonpsychoactive compound in cannabis, can improve symptoms in children with severe autism, they said in the statement. (Unlike tetrahydrocannabinol, or THC, the psychoactive compound in marijuana, CBD does not cause a "high.")

The goals of the trial include determining whether CBD is safe, tolerable and effective in children with autism; whether and how CBD alters chemical messengers, known as neurotransmitters; if it improves brain connectivity; and whether biomarkers of brain inflammation, also associated with autism, are altered by CBD, the researchers said on the CMCR website.

The double-blind, placebo-controlled study, which is set to start a year from now, will be small — just 30 children ages 8 to 12. (A double-blind, placebo-controlled study means that half of the participants will be given a placebo instead of the drug, and neither the researchers nor the participants will know who received which compound until the trial is complete.)

Meanwhile, researchers are planning to test cannabidivarin (CBDV), another nonpsychoactive compound in cannabis, in a double-blind, randomized and placebo-controlled clinical trial of 100 children with autism, according to ClinicalTrials.gov. The goal of the trial is to see whether CBDV can improve certain behaviors of children with autism, said Devinsky, who is working on the trial with Dr. Eric Hollander, a clinical psychiatrist at Montefiore Medical Center.

Devinsky is working on another clinical trial at NYU, which will also investigate whether CBD is a safe and effective treatment for children with autism, he said. [11 Surprising Facts About Placebos]

And in Israel, researchers are studying whether a mix of CBD and THC is safe, tolerable and effective in children with autism, according to ClinicalTrials.gov.  

That double-blind, randomized and placebo-controlled study will include 150 people ages 5 to 21, and will test participants on several behavioral and social measures over a period of 12 weeks.

Big picture

It's no surprise that more clinical trials are investigating whether different cannabis compounds can be used to treat autism, Devinsky said.

"There's an enormous amount of [cannabis] usage because 29 states and [the] District of Columbia have approved medical marijuana," Devinsky said. "In many of those states, parents of children with autism are able to obtain medical marijuana from a physician and use it to treat a variety of different problems, from anxiety, to aggressive behavior, to sleep problems."

However, he emphasized that it's still unclear whether cannabis can effectively treat these problems without causing significant side effects.

"Hopefully, it will be found to be effective, and hopefully, it will be found to be very safe for these individuals," Devinsky said. "But right now, we just don't have that knowledge."

Original article on Live Science.

The percentage of kids with autism in the United States continues to rise, according to a new report from the Centers for Disease Control and Prevention (CDC).

The report found that, in 2014, an estimated 1 in 59 children had autism, up from 1 in 68 children in 2012, and 1 in 88 children in 2008. The findings are based on data from more than 300,000 8-year-old children living in 11 diverse communities across the United States.

A previous CDC report, released in 2016, suggested that the autism rate, or prevalence, was leveling off, but the new report shows that this is not the case.

"It is now clear that what we saw in 2016 was just a pause along the way. It remains to be seen at what point [autism spectrum disorder] rates will plateau," Walter Zahorodny, an associate professor of pediatrics at Rutgers New Jersey Medical School and a co-author of the report, said in a statement.

Autism spectrum disorder is a neurodevelopmental condition that affects communication, behavior and the ability to interact with others.

So what's behind the increase? Perhaps, rather than more kids having autism, just more of them are being diagnosed with it. Communities are doing a better job of diagnosing autism among minority populations, said Alison Singer, president and co-founder of the Autism Science Foundation, who was not involved in the new report.

Historically, autism prevalence has been much higher among white children compared with black and Hispanic children, according to the CDC. But in the most recent report, minority populations had similar percentages of kids with autism as found in white children, Singer said. (For example, in earlier years, autism rates were about 30 percent higher in white children than in black children; but in the latest report, the autism rate was only 7 percent higher among white children than in black children, the CDC said.)

This is a positive step, but the new report also revealed room for improvement in autism diagnoses, Singer said. For example, in 85 percent of the autism cases, there were notations in the children's health or educational records expressing concern about their development by the time they were 3 years old, but only 42 percent of the children received a developmental evaluation to diagnose autism by that age.

"Children are just not being diagnosed as early as they can be," Singer told Live Science. (An experienced professional can diagnose autism in a child by age 2; and in some cases, autism can be detected at 18 months or younger, according to the CDC. The American Academy of Pediatrics recommends all children be screened for autism at both 18 months and 24 months.)

This lag between when a parent, teacher or another person expresses concern about the child's development and the actual evaluation is problematic, because it affects when a child can begin interventional services for autism, Singer said. And the earlier a child starts these interventions, the better the prognosis, she said.

The new report used data from the CDC's Autism and Developmental Disabilities Monitoring Network (ADDM), a program that estimates autism prevalence based on reviews of children's health and education records when they are 8 years old. The ADDM is not a nationally representative sample of the United States, but it is one of the largest programs to monitor autism, and the only autism-tracking program that examines health and education records, the CDC said.

"It's really the gold standard of prevalence studies" for autism, Singer said.

The rate of 1 in 59 children (1.7 percent) with autism is the combined estimate for the 11 communities, which were in Arizona, Arkansas, Colorado, Georgia, Maryland, Minnesota, Missouri, New Jersey, North Carolina, Tennessee and Wisconsin. However, estimates varied widely among these 11 communities, from a low of 1 in 76 (1.3 percent) in Arkansas, to a high of 1 in 34 (1.9 percent) in New Jersey.

Some of these differences might be due to how autism is being diagnosed and documented in those areas, the CDC said.

Original article on Live Science.

Hans Asperger, a pioneer in autism research whose name is used to describe high-functioning people with the disorder, had a previously unknown dark past that included sending children with disabilities to a "euthanasia" program run by the Nazi regime, according to new investigations into his long-lost files.

The new findings reveal that Asperger was far from a courageous defender of his patients against  "euthanasia" by the Nazis, as many people thought. Rather, he benefited from his cooperation with the regime and "publicly legitimized race hygiene policies, including forced sterilizations," according to a study published online yesterday (April 19) in the journal Molecular Autism.

Asperger also used "remarkably harsh" language to describe his young patients, even compared with professionals at the same facility who had patients with more severe disabilities, study researcher Herwig Czech, a medical historian at the Medical University of Vienna, wrote in the study. [Beyond Vaccines: 5 Things That Might Really Cause Autism]

Hans Asperger (1906-1980) wrote about autism in the late 1930s and early 1940s, but it was Leo Kanner's famous 1943 paper that laid the groundwork for describing the disorder, which is now defined as a neurodevelopmental condition that affects a person's ability to communicate, interact and behave typically with others in social situations.

Despite Asperger's early work on autism, he was forgotten by history until 1981, when scientists rediscovered and publicized his work. His research became so well-known that the term "Asperger's syndrome" was used to refer to people on the high-functioning end of the autism spectrum, who sometimes call themselves Aspies.

But in recent years, researchers started finding alarming clues about Asperger's behavior during the Nazi period in Austria, where he lived. These clues spurred the research of Czech, as well as Edith Sheffer, a senior fellow at the Institute of European Studies at the University of California, Berkeley, whose book "Asperger's Children: The Origins of Autism in Nazi Vienna" (W. W. Norton & Co., 2018) is due out May 1.

The new revelations are largely based on evidence that was long thought to have been destroyed during World War II: Asperger's personal files, political assessments by Nazi authorities and medical records from different institutions, including the notorious child "euthanasia" clinic Am Spiegelgrund, Czech said.

While Asperger never joined the Nazi party outright, he was a member of several groups affiliated with the regime, and was rewarded for his loyalty with career opportunities, Czech found. Moreover, case records from his Jewish patients reveal that "Asperger had an acute sense of their religious and 'racial' otherness and that anti-Semitic stereotypes sometimes found their way into his diagnostic reports," Czech wrote in the study.

However, Asperger's darkest actions revolve around his work with Am Spiegelgrund, where hundreds of children with disabilities were experimented on or murdered, Czech said.

For instance, in 1941 Asperger referred the "hopeless cases" of 3-year-old Herta Schreiber and 5-year-old Elisabeth Schreiber (no apparent relation to Herta) to Am Spiegelgrund, records show. Both little girls had mental disabilities and died of pneumonia not long after arriving at the clinic. In particular, Herta Schreiber was likely given barbiturates that ultimately led to her death, Czech found.

It's unclear whether Asperger, or the children's mothers for that matter, knew what awaited the children. "All we have to go by is Asperger's short note on Herta, in which he calls for her 'permanent placement' at Spiegelgrund — whether this was a conscious euphemism for murder or not, it is clear that he did not expect Herta to return," Czech wrote in the study. [11 Facts Every Parent Should Know About Their Baby's Brain]

Asperger was also part of a committee that reviewed the cases of 200 children in a psychiatric hospital, calling 35 of them "uneducable" and "unemployable," words that marked the children for "euthanasia," Czech found. It's challenging to know what happened to these children because the report doesn't list their names, but many of them likely died as a result of these damaging diagnoses, Czech said.

Moving forward

In spite of these discoveries, Czech said that people shouldn't consider Asperger's contributions to the field of autism to be tainted, nor should he be purged from the medical lexicon. "Rather, it should be seen as an opportunity to foster awareness" about the troubling conditions in which autism researchand Asperger's contributions to it arose, she said.

But Sheffer, the author of the new book, fervently disagrees.

"In light of this research, we should no longer use the term Asperger syndrome," Sheffer told Live Science in an email. "In medicine, eponymous diagnoses are granted to recognize individuals who first defined a condition as well as to honor their life. In my opinion, Asperger meets neither criterion."

Meanwhile, the term Asperger's syndrome is being phased out — not because of Asperger's past, but because psychiatrists say that it falls under the umbrella of autism spectrum disorders and should just be referred to as autism.

The Diagnostic and Statistical Manual of Mental Disorders (DSM), the American Psychiatric Association's guide for diagnosis, stopped including Asperger's syndrome in the DSM-5, which came out in 2013.

What's more, the International Classification of Diseases (ICD), which is used by the World Health Organization, will likely drop Asperger's syndrome in the ICD-11, which is due out in 2019, Adam McCrimmon, an associate professor of educational studies at the University of Calgary, wrote in The Conversation.

Original article on Live Science.

Autism, or autism spectrum disorder, is a developmental disorder that affects a person's ability to communicate and interact with others. About 1 in 68 children in the United States has autism. Here's the latest news on autism and possible treatments for the condition.

WASHINGTON — Humans and many other animals express a range of social behaviors, from cooperation to aggression. But as innate as these behaviors may be, little is known about which brain regions control them.

But now, new tools can probe the brains of living animals while they are engaged in social interactions, providing insights into how the brain controls certain behaviors.

These tools — which involve electrodes implanted into the brains of animals — have also revealed that brains likely don't operate in isolation. [10 Things You Didn't Know About the Brain]

Four independent studies, presented here yesterday (Nov. 13) at the annual meeting of the Society for Neuroscience, highlighted some particularly interesting findings about the "social brain."

Among some surprises were findings that social aggression is closely associated with the brain's memory region, that cooperation is more a self-serving strategy than an empathetic one, and that there is biological evidence that two minds really can be on the same wavelength.

"We're beginning to see a striking aspect of the brain … that brains are wired for social interactions," said Dr. Robert Green, a professor of neuroscience and psychiatry at the University of Texas Southwestern Medical Center, during a news conference about the studies.

Although scientists have seen hints there must be an underlying brain architecture guiding social behavior, only now are they observing this architecture directly in living brains, Green told Live Science. This understanding could lead to treatments for antisocial behaviors, he said.

Green also noted these new insights are a result of studying brains interacting with each other simultaneously, as opposed to traditional studies of probing only one brain at a time in isolation.

Social aggression

One research group, from Columbia University in New York, investigated the phenomenon of social aggression, which is aggression toward a fellow species member as opposed to prey. The researchers found that the hippocampus, which is the brain's memory center, appears to drive this type of aggression in mice — in this case, the attack of one mouse by another who didn't recognize it as a friend.

"The second that aggression started is when [nerve signals from the hippocampus] turned on really strongly," said Félix Leroy, a neuroscience associate research scientist at Columbia University who led the study. "We're now trying to look at the exact relay of signals in these brain regions to confirm that this burst of activity precedes aggression."

Leroy's team also found that they could block aggression by stimulating a region of the hippocampus called CA2. The findings imply that CA2 could be a therapeutic drug target to treat abnormal aggression associated with neuropsychiatric diseases, Leroy said, though much more research is needed to confirm such effects in humans. [Fight, Fight, Fight: The History of Human Aggression]

Strategic thinking

In another study, scientists at the University of Pennsylvania found that strategic thinking, not empathy, may underlie cooperative behavior so common in primates. These researchers constructed an experiment in which rhesus macaques were taught play a computerized version of the classic game of "chicken," which itself sounds like an amazing feat. But there's more.

When playing against each other, two monkeys could strategize on ways to avoid crashing into one another and reap the highest rewards together. When just one monkey played against a machine, though, and the other one simply watched, the game-playing monkey suddenly had no interest in maximizing rewards for his one-time game companion. Instead, the game-playing monkey employed a different strategy to get the highest rewards only for himself.

"We found that neurons in a part of the brain [previously] linked to strategic thinking, but not in a part of the brain linked to empathy and shared experience, respond selectively when rhesus macaques cooperate," said Wei Song Ong, a postdoctoral neuroscience researcher at the University of Pennsylvania, who led the study.

Ong said she wasn't ready to concede that empathy isn't an important human trait, but she added that social cooperation may be much more of a selfish act than people would like to think.

Syncing up

What could be more social than brains acting in sync? Similar brain activity may be fundamental for how animals, including humans, interact to form social bonds, according to Dr. Miguel Nicolelis, a professor of neuroscience at Duke University School of Medicine in North Carolina.

Nicolelis' group built an experiment in which one monkey drives a vehicle to get a fruit reward while another monkey watches. Each time the driver monkey gets a fruit reward, the spectator monkey gets one, too. So they are linked, Nicolelis said during the news conference.

"To our shock, what we found is that as these animals are interacting … both brains are highly synchronized," Nicolelis said. "We have, in fact, in some instances, 60 percent of [the firing of neurons] in the motor cortexes of both monkeys [happening] precisely the same time."

The synchronicity became more precise as the monkey got closer to the fruit reward or, as shown during a second experiment in the study, as the spectator monkey helped control the vehicle remotely, Nicolelis said. The finding suggests that the optimal performance of social tasks, such as gathering food, requires synchronization of brain activity across the brains of all subjects involved — in other words, with everyone being on the same wavelength.

Conversely, Nicolelis said that some antisocial neurological disorders, such as autism, may result in an inability to establish such interbrain synchronization. He said he hopes to test this in his lab with human subjects.

The "social brain"

Taken together, the collection of studies presented at the news conference "opens a new chapter in neuroscience, [as we] have the ability to assess multiple brains simultaneously," Nicolelis said.

"We can no longer think of brains in isolation," Nicolelis said. "The 'social brain' idea that we are talking about supersedes the notions that [scientists] have developed for brains in isolation, because the brain is not just a passive device alone in the world. … The action on one animal involves the actions of other animals."

Whereas neuroscience has, up until recently, focused on the study of neurons or networks of neurons, the new reality is that behavior arises from a network of different brains interacting, Nicolelis said.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

This season's hottest toy is marketed as an antidote for attention deficit hyperactivity disorder, anxiety and autism — but it's also being banned in classrooms across the country.

"Fidget spinners" are small, ball-bearing devices that the user can rotate between his or her fingers. The momentum of the toy provides a pleasing sensory experience, according to user reviews, while the challenge of tossing, transferring and twirling the spinners has spawned an entire universe of instructional YouTube videos. [How Fidget Spinners Work: It's All About the Physics]

Many spinners are marketed as aides for individuals with anxiety, autism and ADHD; Cppslee's spinner marketing patter on Amazon, for example, promises greater concentration for people with those conditions, plus an opportunity to "bring out that creative genius lying deep within you." [Why Fidget Spinners Are So Hot (and Where to Buy Them)]

Unsurprisingly, these claims are probably overblown, scientists say.

"Using a spinner-like gadget is more likely to serve as a distraction than a benefit for individuals with ADHD," said Mark Rapport, a clinical psychologist at the University of Central Florida who has studied the benefits of movement on attention in people with ADHD.

Scientists decided to find out whether there was any basis to these claims made by manufacturers. In a review of relevant literature published July 7, 2017, in the journal Current Opinion in Pediatrics, scientists including Dr. Ruth Milanaik, director of the neonatal follow-up program at Cohen Children's Medical Center of New York, found that no research had specifically focused on the link between these spinners and kids' attention. Not only that, but there were no peer-reviewed studies at all on fidget spinners, they said. With this lack of research, manufacturers' claims about the usefulness of fidget spinners are baseless, the authors concluded. 

(The so-called fidget cube — which is a plastic cube equipped with various buttons and dials for fidgeting hands — may be more classroom friendly, according to a scientist who studies intersection of human computer interaction and games, who pointed out on the website The Conversation that the cube doesn't require visual attention. "They can serve the same purpose as the spinners, but are more classroom-ready and less distracting," Katherine Isbister, professor of Computational Media at the University of California, Santa Cruz, wrote on The Conversation.)

Regardless of their usefulness in keeping kids' distracted brains focused, fidget spinners have sparked a conversation about attention spans in kids and how to help the little ones focus, experts told Live Science. For instance, though there isn't a lot of data supporting the idea that kids have less focus today than in the past, some research does suggest attention spans have decreased as multitasking has increased with the digital age, one expert said. There are various methods for bringing kids' focus back to the lesson at hand, psychologists say, including fidgeting devices, activity breaks and the simple removal of extra distractions. (The devices may also teach kids something about physics, or at least ball bearings.) 

A trend erupts

Fidget spinners emerged this spring, seemingly from out of nowhere, as a must-have gadget. Before December 2016, Google searches for the words "fidget spinner" were basically nonexistent. Now, teachers are posting about their frustrations with spinner-obsessed students on Twitter, and the toys even have their own forum on Reddit.

"I will call you 'Annoying Spinny Thing' and you will live in my desk drawer," Kansas Spanish teacher Amanda Dickey tweeted, punctuating her message with #fidgetspinner and #teacherprobs. [How to Do Timeout: 12 Tips from Science]

Most of the controversy surrounding fidget spinners has been over schools banning them from classrooms. An elementary school principal in Evanston, Illinois, Kate Ellison, told the Chicago Tribune that the spinners have been a distraction in classrooms in her school, and that children with special needs have other, school-friendly options for fidgeting. Meanwhile, some parents of kids with special needs have hailed the toys' benefits. One blogger, a parent of an 8-year-old with autism, wrote on AutismAwareness.com that her daughter was thrilled to see her classmates wanting to fidget just like her. School-approved fidget devices mark her daughter as different, wrote Miriam Gwynne, but fidget spinners are simply cool.

"For her, the fidget spinner is not a must-have craze to be like her friends, but more a stress release from the demands placed upon her during her school day — much the same as she uses a stress ball or her twist-and-lock blocks," Gwynne wrote. "When schools decide to ban sensory and fidget toys, they risk isolating the very children they’ve spent years trying to include." [25 Scientific Tips for Raising Happy Kids]

The list of schools banning the spinners seems to be growing and now includes schools in Massachusetts, Brooklyn, New York, Florida, Chicago, Illinois, and even across the pond in Manchester, England.

At least one expert is disappointed by the bans. "These little gadgets should be called fidget tools, not toys, and they can be part of a successful strategy for managing fidgety behavior if they are introduced as a normal part of the classroom culture," said Claire Heffron, a pediatric occupational therapist in Cleveland, as reported by The Washington Post.

Even so, teachers say that most kids are using the spinners as toys, focusing on them rather than on class, according to news reports.

Spinner benefits?

There's no doubt that toys that allow kids to fidget can benefit kids with autism. Occupational therapists often use sensory toys like tactile discs, Koosh balls and even putties or clays to soothe kids who have sensory-processing issues. Similarly, research has shown that movement can help kids with ADHD to focus. A 2015 study published in the Journal of Abnormal Child Psychology by Rapport and his colleagues looked at 8- to 12-year-old kids with ADHD. The researchers found that those who participated in gross motor activity — meaning the movement of limbs or large parts of the body — performed better than those who sat still during tasks involving working memory, which is a type of memory used for processing incoming information. Exercise has also been proven to be helpful for kids with ADHD. 

But without studies that specifically look at fidget spinners, it's impossible to say for sure whether the devices could help kids with ADHD, Rapport told Live Science. He conjectured that the little handheld toys are not likely to help much. They don't require gross body movement, he said, which is what appears to be responsible for increasing activity in the frontal and prefrontal brain areas that are responsible for sustaining attention. The spinners are also visually distracting, and so they could pull a child's attention away from the chalkboard or teacher, Rapport said.

"Riding a stationary bike while reading, or sitting on a movement ball while working at one's desk, in contrast, allows small (non-distracting) motor movements and would probably prove beneficial for many children with ADHD," Rapport wrote in an email to Live Science.

Spinner safety

An unofficial report in June about possible lead in these toys may have parents worried, but don't clear your home of the spinners just yet. Tamara Rubin, a lead-poisoning-prevention advocate who is not affiliated with any university or research institution, home-tested 11 fidget spinners and found unusually high amounts of lead in two of these. Even so, Rubin's findings have not been replicated nor peer-reviewed; and Rubin only tested 11 spinners. You can read more about possible lead in fidget spinners in this Live Science article.

A bigger concern may be the risk of kids choking on some of the spinner's small parts. The U.S. Consumer Product Safety Commission, is looking into reports of children choking on parts that have popped out of a fidget spinner, said Patty Davis, the CPSC's acting communications director. And on Aug. 10, 2017, the CPSC released safety guidelines for fidget spinners, warning that the toys could be choking hazards and so kids under 3 should not play with them. The CPSC also said that the toys should not be put in the mouth, regardless of the person's age.

Here are some tips from the Toy Association for keeping your kids safe while fidget-spinning: Follow age labels; shop at reputable stories (where you'll find toys that passed U.S. testing); follow tips for light-up spinners (make sure the spinner's battery is locked in the toy); check for broken parts (which can be a choking hazard). 

Editor's Note: This article was first published on May 1, and has been updated with information about school bans and kids' attention spans as well as safety concerns. More recently, the article was updated with information about a review study about fidget spinners as well as safety guidelines released by the Consumer Product Safety Commission. 

Original article on Live Science. 

Fidget spinners may be fun toys, but there is no science behind claims that they help kids with attention and focus, according to a new review article.

The review, which was published July 7 in the journal Current Opinion in Pediatrics, found that no research had specifically focused on the impact of these hot new toys on thinking, attention or recall. Furthermore, there are zero peer-reviwed studies on any aspect of fidget spinners, the researchers found. Without that research, claims made by manufacturers about such links are baseless.

"There's no science behind the idea that they increase attention," said study co-author Dr. Ruth Milanaik, director of the neonatal follow-up program at Cohen Children's Medical Center of New York. "We have to view it as what it is: It's a toy, a fun toy." [How Fidget Spinners Work: It's All About the Physics]

Claims of attention

Some of the companies marketing fidget spinners, or small, ball-bearing-filled plastic toys that spin when you rotate them, claim the toys can increase attention for those with attention deficit hyperactivity disorder (ADHD) or calm symptoms of autism or anxiety. For instance, the Cppslee Hands Fidget Spinner sold on Amazon claims the toys are great for anxiety, focusing, ADHD and autism, in addition to quitting bad habits and staying awake. [Why Fidget Spinners Are So Hot (And Where to Buy Them)]

To see whether any of these marketing claims had basis in fact, Milanaik and her colleagues looked through the available literature to find studies on fidget spinners. It turned out, there is no scientific evidence supporting these marketing claims, Milanaik and her colleagues reported in the current review paper. That could be because the gadgets don't benefit a kid's focus, or because nobody has done a substantial enough study on the claims.

Fidgeting benefits

Some limited studies do show benefits to fidgeting in children with ADHD. For instance, in a small study published in 1995 in the Journal of Child Psychology and Psychiatry found that boys with ADHD who can squirm and fidget instead of sitting still show greater attention to a task; however, the same benefit was not shown for children who did not have ADHD. A 2016 study monitored children's activity via an ankle bracelet and found that children with ADHD tended to do better on attention tasks when they could fidget.

When it comes to fidget toys, one study found that children who used stress balls, which are squishy foam balls, reported better attention in class and improved performance. Still other work shows that fidgeting and movement releases norepinephrine and dopamine, the same brain chemicals that are stimulated by ADHD medications. In addition, some evidence suggests that certain types of self-regulation toys can incentivize children with autism to complete tasks at school, the study found.

No evidence of benefits

However, there were no studies that specifically looked at the effects of fidget spinners on attention, the review found. And no two distraction-aid toys are alike, so extrapolating from studies that used different toys can be dicey.

"The concept of using therapy putty might be different from using a squish ball might be different from the concept of using a fidget spinner," Milanaik told Live Science.

To measure attention, researchers often give children simple tasks, such as adding or subtracting small numbers, and then count how many they complete (and complete correctly) either with or without the toys, Milanaik said. Studies may also assess listening and recall by asking people to repeat back a series of numbers either with or without the toys, she added. Milanaik's group is currently assessing the role of "therapy putty" on attention, though they likely won't have results for several months.

Limiting use in schools

Parents who believe fidget spinners have attentional benefits for their kids should feel free to experiment with their child while they're at home, doing homework or reading a book, Milanaik said.

But letting them enter the classroom is a different story. Most schools ban toys from classrooms, but some still allow children to bring in fidget spinners to address their sensory issues, the study found. But with no scientific evidence of their benefits, fidget spinners in the classroom could do more harm than good, the study noted. 

For one, some fidget spinners come apart easily, and the ball bearings inside them can be choking hazards, she said.

Beyond that, one child's attention aid could be another child's annoying distraction, Milanaik said.

For instance, in research meetings, Milanaik has found that fidget spinners can distract group members.

"They make a spinning noise, we find it distracting when we have to work in a group — but we all like to use them," Milanaik said.

And of course, any toy that enters the classroom could be the source of squabbling, bartering or other distracting behavior, which could undercut any potential attentional benefits, the review noted.

"A classroom is a wonderful group of children," Milanaik said. "Some things that might be great for one child might be very distracting for another."

Originally published on Live Science.

Brain scans, analyzed using a type of artificial intelligence, can reveal whether 6-month-old babies are likely to develop autism, a new study shows.

The study examined 59 infants who were at high risk of developing autism; that is, each had an older sibling with autism. The artificial intelligence predicted with 100 percent accuracy that 48 infants would not develop autism. In addition, of the 11 infants who did develop the disorder by the time they were 2 years old, the system correctly predicted nine of the cases.

"It was extremely accurate," Robert Emerson, the lead author on the study and a former cognitive neuroscience postdoctoral fellow at the University of North Carolina (UNC), told Live Science. [5 Things That May Cause Autism]

Studies show that 20 percent of babies who have older siblings with autism will develop the disorder; among babies in the general population, 1.5 percent develop autism, Emerson told Live Science.

The results of the new research could lead to new diagnostic tools that identify autism before symptoms occur, giving clinicians the opportunity to intervene early, the researchers said.

"The idea is that we can be more effective if we can get to these kids before they develop autism, perhaps ameliorating or preventing it," Dr. Joseph Piven, a professor of psychiatry at the UNC School of Medicine and director of the Carolina Institute for Developmental Disabilities, told Live Science. The researchers published their results today (June 7) in the journal Science Translational Medicine.

The development of autism

Autism spectrum disorder, a brain-based disorder characterized by a wide range of social-communication challenges and repetitive behaviors, affects about one out of every 68 children in the United States. Behavioral symptoms typically begin to appear in children at around age 2.

Emerson and his colleagues demonstrated that they could identify biomarkers for the disorder before the symptoms occur.

As part of their study, the researchers used MRI scanners to image the brains of the infants while they slept. During the scans, the researchers recorded the neural activity of 230 different regions in the brain, looking particularly at whether or not pairs of these region — referred to as functional connections — were synchronized with each other, and if so, to what extent.

In total, the researchers measured 26,335 functional connections crucial for cognition, memory and behavior.

When the children reached age 2, they came back in for a behavior assessment. The researchers looked at the children's social interactions, communication, motor development and tendency to perform repetitive actions, and determined whether each child had autism. [11 Facts Every Parent Should Know About Their Baby's Brain]

With all of the data in hand, the researchers set out to first train their machine learning program, and then use it to run predictions. They wanted to see how accurately it could predict which infants had developed autism, using only the functional connections data from when the children were 6 months old. In other words, although the researchers knew which babies had developed into toddlers with autism and which had not, the machine learning program did not.

Machine learning is a kind of artificial intelligence system that gets smarter based on the data it processes. In this case, the program was learning to spot differences between the functional connections imaged in the MRI data collected at 6 months old that correlate with cognition, memory and behavior and the details from the behavioral assessments collected at 24 months.

As the program did this, it separated the children into two groups — those with autism and those without the condition. Once it was trained, it could make predictions. [7 Baby Myths Debunked]

But during the training process, the researchers didn't use the data from all 59 kids. Instead, they fed data in from 58 of the 59 infants to train the model, and then to get the prediction, they inputed the data from the one infant they had left out. They repeated this for all 59 children.

"Each child was predicted separately based on a model from the other children in the group," Emerson said.

In the end, the machine learning program was correct in 82 percent of the cases in which the children did develop autism.

An amazing group of families

Piven said the team published a study earlier in the year that also showed an impressive prediction rate, but that study required two MRI scans, one at 6 months of age and one at 1 year. Moving the needle to an earlier age is a big advance, Piven said.

The research team was amazed by the parents who participated in this and other studies over the years, given all that was required, he said.

"This is an extraordinary group of people," Piven said. "Not only do they have an older child with autism, but they bring their babies, often multiple times and from very far away, to one of our four clinical sites around the country."

"They're very committed," Emerson said.

The researchers said they hope their contributions will lead to more effective interventions for children on the brink of developing autism.

Originally published on Live Science.

A 101-year-old drug that is often used to treat people in Africa with parasitic infections may help ease some of the symptoms of autism spectrum disorder (ASD) in children, a new study finds.

However, researchers are urging caution about the preliminary results of the drug, called suramin. The study was extremely small and involved only boys, who were given just one dose of the drug.

The study was well designed, but the findings don't necessarily suggest that suramin works to treat autism, said Dr. Jay Gargus, a director of the Center for Autism Research and Translation at the University of California, Irvine, who was not involved in the study. [Beyond Vaccines: 5 Things That Might Really Cause Autism]

"I don't think the suramin is the important part of the paper," Gargus said. "The important part of the paper is how [the author] goes through carefully describing what kinds of measures he's going to do, how he's going to do this, how he's going to work his way through understanding what these drugs do."

Still, the initial results are encouraging, said study lead researcher, Dr. Robert Naviaux, a professor of genetics and co-director of the Mitochondrial and Metabolic Disease Center at the University of California, San Diego. "A single treatment with low-dose suramin was safe and produced significant improvements in the core symptoms and metabolism associated with ASD," Naviaux said in a statement.

Suramin study

The study included 10 boys with ASD, ages 5 to 14. Five of the boys received a single, low-dose infusion of suramin, and five received a placebo. The study was double-blinded, meaning that neither the participants nor the researchers knew which of the participants received the drug, and which received the placebo.

After the treatment, the boys in the suramin group showed improvements in their social communication, speech and language. They acted calmer and were more focused, showing fewer repetitive behaviors and less need to use their coping skills, the researchers said. These differences were documented with observational techniques, interviews and questionnaires.

Reports from the boys' parents suggested that the five boys who received suramin improved for three weeks, then gradually decreased toward their original baseline over the next three weeks, the researchers said in the study. 

"We had four nonverbal children in the study," Naviaux said, adding that the two who received suramin said the first sentences of their lives about one week after the treatment. This did not happen in the two nonverbal kids given the placebo, Naviaux said.

Moreover, the boys who received suramin made more progress during their speech therapy and occupational therapy programs than the boys given the placebo, Naviaux said.

How suramin works

The German dye manufacturers, Frederich Bayer and Co., developed suramin in 1916, initially calling it Bayer 205. The drug proved to be effective against parasites that cause African sleeping sickness.

Suramin works by stopping certain molecules from binding to proteins called "purinergic receptors," which are found on every cell in the body. Naviaux's idea is that cells that are stressed release certain molecules, and that these molecules then bind to purinergic receptors and impair cell function.

Although it's unclear what causes autism, the condition might be driven, in part, by impaired communication between cells in the brain, gut and immune system, he said. Other causes likely include genetic and environmental factors, he said. 

In people with autism, suramin may stop the molecules from binding to purinergic receptors, and let the cells function more normally, Naviaux said. [10 Things You Didn't Know About the Brain]

Earlier studies in mice with autism traits showed that the drug alleviated some symptoms of the condition. For example, in 6-week-old mice with traits of autism, suramin improved social behavior, metabolism and motor coordination, according to a 2013 study published in the journal PLOS ONE.

In another study, published in 2014 in the journal Translational Psychiatry, adult mice that received suramin showed improved social behaviors and metabolism, but no motor skill improvement.

Reactions and concerns

Other researchers call Naviaux's ideas about the role of purinergic receptors in autism an "emerging hypothesis," but say it's a "creative way of thinking about" the molecular processes behind autism, Gargus said.

Gargus noted several limitations in the study. For instance, all five boys in the suramin group developed a temporary rash, but none in the placebo group did. It's possible that parents in the suramin group noticed this and realized that their child had received the drug, inadvertently "un-blinding" the study, Gargus said. The researchers mentioned this as a possible limitation in the study, too.  

What's more, the boys in the placebo group showed very little improvement — an anomaly in neurobehavioral testing, because usually the placebo effect is strong, and the group given the placebo shows some kind of improvement, Gargus said.

Gargus added that given the number of tests in the study, it's not surprising the autism group scored better than the placebo group on some of the measures. "If you give enough scales, one of them is probably going wind up showing you a significant effect," Gargus told Live Science. [Typical Toddler Behavior, or ADHD? 10 Ways to Tell]

Suramin is not approved to treat ASD by the U.S. Food and Drug Administration, and the drug is not commercially available. Naviaux has filed a patent application related to antipurinergic therapy for ASD and related disorders, and two of the study's authors have connections to pharmaceutical companies.

The study was published online May 26 in the journal Annals of Clinical and Translational Neurology.

Original article on Live Science.

The falsehood that vaccines cause autism has regained traction since the election of President Donald Trump, and this misinformation may leave Americans blind to a real risk: a loss of health and learning services for people with autism that will result from the coming changes in health care and cuts to research funding, researchers say.

Vaccines do not cause autism. But Trump's "apparent openness to a long-debunked link between vaccines and autism risks" may cause advocates for services for people with autism and policymakers to focus on defending well-established scientific facts instead of fighting the potential rollback of protections for people with autism, the researchers wrote today (March 8) in an editorial in The New England Journal of Medicine.

These threatened protections include the Affordable Care Act's (aka Obamacare or ACA) key provision that health insurance companies cannot deny coverage because of a pre-existing condition, the researchers said. Also, the Individuals with Disabilities Education Act (IDEA), which predates the ACA, guarantees appropriate education for all children with disabilities. [Beyond Vaccines: 5 Things that Might Really Cause Autism]

Both acts may be on the chopping block, said Colleen Barry, a professor and chair of health policy and management at the Johns Hopkins Bloomberg School of Public Health. Barry co-authored the editorial with David Mandell, a professor and director of the Center for Mental Health Policy and Services Research at the University of Pennsylvania.

"We have no idea what will come out of Congress," Barry told Live Science. But there is a "real risk" that the changes could reverse gains made in autism care over the past two decades, she said.

The Republican-led Congress and the president have pledged to repeal and replace the ACA. Among the ideas favored by many Republicans in Congress is a plan to open up health insurance markets across state lines, the researchers said.

"If interstate insurance purchasing became possible, out-of-state insurance companies would not have to comply with the autism-mandate requirements in consumers' state of residence," Barry and Mandell wrote. "[S]uch freedom from requirements might easily precipitate a 'race to the bottom,' in which state legislators would repeal autism mandates (and other types of insurance mandates and consumer protections) to make in-state health insurance products price-competitive. As a result, gains achieved to date in access to autism-specific services could be reversed."

The ACA also requires marketplace health plans to cover 10 essential health benefit categories, including services important to people with autism and other disabilities. These services include therapies aimed at helping people with autism improve their skills of daily living, speech and language therapy, and mental health treatment.

Concerning the IDEA, Barry said that Secretary of Education Betsy DeVos and Attorney General Jeff Sessions have publicly questioned the value of the act's protections. DeVos has suggested that states should be able to decide whether to enforce the IDEA, Barry added. [6 Politicians Who Got the Science Wrong]

As for government-sponsored research funding, Trump has proposed cutting  $54 billion from some federal agencies, such as those that fund scientific research.

Autism is a developmental disability that can cause significant social, communication and behavioral challenges. The number of children diagnosed with autism has risen dramatically in recently decades, from 1 in 2,000 people in 1970 to 1 in 150 people today, according to the Centers for Disease Control and Prevention.

Yet scientists are not sure whether the rise is due to better diagnosis and the broadening of the clinical definition of autism, or an actual increase in the true prevalence. Nor do scientists understand what causes autism.

This week, researchers at the University of North Carolina School of Medicine reported that they found that infants as young as 6 months old, who were later diagnosed with autism at age 2, had a substantially greater amount of cerebrospinal fluid — the clear liquid that cushions the brain within the skull — compared with the 6-month-olds who did not go on to develop autism. This is the latest in a series of studies demonstrating how some infants are born with symptoms linked to autism long before they receive vaccines.

Barry and Mandell are worried because Trump has rehashed the discredited link between vaccines and autism, as recently as January 2017.

"The risk of getting drawn into an outdated debate about vaccines and autism is that advocates and policymakers will spend their time and resources fighting on that flank and could miss the window to respond on proposed cuts to critical services for those with autism coming from the other direction," Barry said.

Those who care about preserving and expanding services for people with autism need to pay attention to the conversations in Washington around the ACA repeal and threats to IDEA to make sure important protections and guarantees are not lost, Barry said.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Brain scans of infants as young as 6 months old may be able to predict whether a child will develop autism, a new study suggests.

In the study, researchers found that infants who later developed autism had higher amounts of cerebrospinal fluid — the clear liquid that cushions the brain within the skull — that could be seen on an MRI, compared with those who did not develop autism.

What's more, the researchers also found that the levels of CSF lined up so closely with the risk of autism that they could use measurements of CSF volume to predict the development of autism among "high-risk" infants, or those who had an older sibling with the condition. Measurements of CSF volume at 6 months predicted which high-risk infants were diagnosed with autism at age 2 with a 70 percent accuracy, the researchers said. [11 Facts Every Parent Should Know About Their Baby's Brain]

Although more studies are needed, the researchers say that one day, doctors might be able to monitor CSF to help gauge a child's risk of autism.

"Neuroimaging CSF could be another tool to help pediatricians diagnose autism as early as possible," study author Mark Shen, a postdoctoral fellow in psychiatry at the University of North Carolina at Chapel Hill School of Medicine, said in a statement. "It could help signal risk using regular MRIs that you find in any hospital."

Still, the researchers said there are a number of questions that need to be answered before doctors could use MRIs for this purpose. For instance, the researchers don't know whether this CSF anomaly is found  only among children at high risk for autism, or if it would be found more generally in all children who develop autism. The researchers also don't know if this anomaly contributes to the development of autism, or if it's simply a marker of another factor related to autism.

The results confirm those of an earlier study by the same group of researchers, which also found a link between CSF volume and the risk of autism. However, the earlier study was relatively small, involving 55 infants.

In the new study, the researchers examined MRIs from 343 infants at ages 6, 12 and 24 months. Of these, 221 infants were at a high risk of developing autism based on their family history, whereas 122 had no family history of autism.

At the end of the study, 47 infants in the high-risk group were diagnosed with autism by the time they were 2 years old. None of the infants in the comparison group developed autism.

Among infants who were at a high risk for autism, those who were ultimately diagnosed with the condition had, on average, 18 percent more CSF in an area known as the subarachnoid space, which surrounds the brain, at 6 months of age, compared with those who did not develop autism.

In addition, infants who developed more severe symptoms of autism had 24 percent greater CSF volume in the subarachnoid space, compared with those who did not develop autism.

The researchers hypothesize that this CSF anomaly could be a sign that the CSF is not properly circulating as it should. Normally, the CSF circulation helps to filter out potentially dangerous molecules.

"CSF is like the filtration system in the brain," said Shen, who began this work as a graduate student at the MIND Institute at the University of California, Davis. "As CSF circulates through the brain, it washes away waste particles that would otherwise build up." The researchers believe that an increase in CSF in the subarachnoid space "is an early sign that CSF is not filtering and draining when it should."

The result is that there could be a buildup of neuroinflammation that isn't being washed way," Shen said.

Future studies are needed to evaluate both the underlying causes of increased CSF volume, and the potentially harmful effects on brain development, the researchers said.

The study is published today (March 6) in the journal Biological Psychiatry.

Original article on Live Science.

Robert F. Kennedy Jr., an anti-vaccine activist, told reporters on Jan. 10 that President-elect Donald Trump asked him to chair a commission on vaccine safety, CNN reported.

While Trump's team denied making the specific request that Kennedy referenced, a spokeswoman said that Trump is considering forming a commission on autism, reported CNN and other outlets.

The Trump team's response, which brought up autism in response to a question about a vaccine committee, appears to draw a connection between the condition and vaccines, despite overwhelming evidence debunking the claim that vaccines cause autism. [5 Dangerous Vaccination Myths]

"Claims that vaccines are linked to autism, or are unsafe when administered according to the recommended schedule, have been disproven by a robust body of medical literature," the American Academy of Pediatrics said in a statement released on Jan. 10, in response to the news reports.

A 2016 study in the journal Pediatrics found that more parents are refusing to vaccinate their children now than a decade ago. Interestingly, the study also found that the percentage of parents who were concerned about the autism link has dropped in recent years. In 2006, 74 percent of pediatricians said the supposed link was a top reason for parents' refusal to vaccinate, but in 2013, only 64 percent of pediatricians said the same.

Still, beliefs about the much-discredited link persist — why?  

The anti-vaccination viewpoint is a product of two colliding ideas, Jennifer Reich, an associate professor of sociology at the University of Colorado Denver told Live Science in March, 2016.

First, parents may think that they "are in this alone" and not responsible in any small way for other children in their communities, said Reich, who is the author of "Calling the Shots: Why Parents Reject Vaccines" (NYU Press, 2016). In other words, these parents don't feel that it's important to contribute to herd immunity, which protects individuals in a community who are unable to receive vaccines, Reich said.

Second, there is an idea that individuals hold all responsibility for their own health, and that society bears none for people's health decisions, Reich said.

Together, these beliefs may lead parents to view it as their duty to go it alone, and combine individual parenting with individualized health care, Reich said. These parents may spend a substantial amount of time researching information about vaccines and deciding whether the information applies to their children, she said.

 "They begin to doubt whether population data [on vaccine safety] applies to their own families," she said.

Reich also noted that parents may believe that the diseases prevented by vaccines are not very serious. For example, parents may think that if their children do get sick with the measles, they will not develop the severe complications, such as encephalitis or deafness, that the disease can bring, she said.

Indeed, the 2016 Pediatrics study showed an increased in the percentage of pediatricians who said that parents refused to vaccinate their children because of a perception that the vaccines were unnecessary.

Another study, published in 2014 in the journal Proceedings of the Royal Society B, found that peer pressure plays a role in vaccination rates but can act as a double-edged sword. For example, social norms can keep vaccination rates high, even in the absence of obvious disease risk, but if people become scared of a vaccine risk, social norms can keep vaccination rates depressed long after the scare ends, the study found. 

Originally published on Live Science.

A detailed new map of the human brain's outer layer identifies nearly 100 brain areas that have not been previously reported, according to a new study.

The new map may ultimately help brain surgeons plan operations. It will also help scientists better understand differences between the brains of typical people and the brains of people with disorders related to brain functioning, such as autism, schizophrenia and dementia, researchers who were not affiliated with the new study said.

In the study, researchers identified a total of 180 areas of the cerebral cortex — the outermost layer of the brain — in each brain hemisphere, said lead study author Matthew Glasser, a neuroscience researcher at Washington University in Saint Louis. Researchers consider an "area" of the brain to be a section of the organ that is dedicated to coordinating a particular set of information from many different signals. [3D Images: Exploring the Human Brain]

The areas identified in the new map include 83 that had previously been identified, along with 97 new areas, Glasser said.

The addition of the 97 new cortical areas shows that "the human cortex is even more complex than we had originally thought," said Ramesh Raghupathi, a neuroscientist at Drexel University's College of Medicine in Philadelphia, who was not involved in the new study.

The map reveals new information even for the areas that had been mapped before, because the original mapping had been done at a much less detailed level, Glasser said.

For example, one area that scientists previously identified and named "area 31" has now been divided into three areas named 31a, 31pd, and 31pv, the researchers said in their study, published today (July 20) in the journal Nature.

The very first map of the human cortex, which identified 50 areas, was created in the first decade of the 20th century by a German neuroanatomist, Korbinian Brodmann. Since then, many other maps of the cortex have identified anywhere from 50 to 200 areas, the researchers said.

To make the new map, the researchers collected data from brain scans of 210 healthy young adults. The researchers measured, for example, how thick the cortex was in each person. The participants' brains were scanned when they were not doing anything, and again when they were performing simple tasks, such as listening to a story.

The researchers then confirmed the existence of the 180 specific brain areas using brain scans of a second group, consisting of 210 people. 

The new map was created based on brain data from a much larger number of people than used to make previous maps, Glasser said. Another difference is that the researchers took into account multiple properties of the brain, such as its structural architecture and function and the thickness of the cortex, Glasser said. Previous maps were typically based on only one of these properties, he said.

Because of these differences, the new map paints a more precise picture of the brain than the previous maps did, the researchers said. [10 Things You Didn't Know About the Human Brain]

The new map will allow brain surgeons to better pinpoint where exactly in the brain their patients' health problems stem from, Raghupathi said. "This kind of information is going to be very useful to a neurosurgeon who needs to" stimulate or identify only a small part of the cortex that may be responsible for a patient's language problem or a motor problem, he told Live Science.

"This is an amazing body of work," said Sophie Molholm, a cognitive neuroscientist at Albert Einstein College of Medicine in New York, who was not involved in a new study.

This new fine-grained map of the brain could also be used to better understand how brains that have developed without problems may differ from the brains of people with atypical brain development, or who have conditions such as autism and schizophrenia, she said.

Originally published on Live Science.

The active ingredient in the drug ecstasy needs more study, and changes are needed to make it easier for scientists to access the drug for research, two neuroscientists argue in a new opinion article.

The ingredient, MDMA, which is the psychoactive substance in ecstasy and Molly, needs more study because it seems to unique amongst mind-altering substances, said study co-author Dr. Robert Malenka, a psychiatrist and neuroscientist at Stanford University in California.

"It has an effect in both animals and humans that, to my knowledge, is pretty much unlike that of any other psychoactive substance," Malenka told Live Science. "It uniformly causes this pro-social, empathogenic response," or warm-fuzzy feelings of empathy towards others, said Dr. Robert Malenka, a psychiatrist and neuroscientist at Stanford University. [Trippy Tales: The History of 8 Hallucinogens]

A banned substance

MDMA was created in the early 1900s by the German pharmaceutical company Merck as a base compound for synthesizing other drugs, according to the National Institute on Drug Abuse. But the compound was never used in clinical practice and languished on chemist's shelves for decades. Then, in 1976, the chemist Alexander Shulgin, a "psychonaut" who spent most of his life testing and cataloguing the psychoactive effects of thousands of chemical compounds, noted MDMA's chemical similarity to compounds such as mescaline and amphetamine.

He self-administered the drug and then told a small group of psychotherapists and physicians about its effects, according to the article. From then on, a small group of physicians used MDMA during psychotherapy, hoping to help patients who had extreme social anxiety and post-traumatic stress disorder (PTSD).

But in the 1980s, MDMA made its way into clubs and raves as a party drug, and by the middle of that decade, the U.S. Drug Enforcement Agency had banned the substance as a Schedule 1 drug, meaning the agency had decided the substance had no therapeutic value and a high potential for abuse.

The drug can also have side effects; it can cause anxiety, restlessness and irritability, along with physical symptoms such as nausea, muscle cramping and a rise in body temperature, according to the National Institute on Drug Abuse. People who overdose on MDMA may lose consciousness and have seizures.

Since its classification as a Schedule 1 drug, research on the MDMA has been tightly controlled, with a few small research studies looking into the drug as a potential treatment for people with post-traumatic stress disorder. In those very small, carefully controlled trials, the drug has been shown to be more effective than existing treatments for post-traumatic stress disorder and to have an effect that lasted for years. [6 Party Drugs That May Have Health Benefits]

Case for improved research access

In the new opinion piece, Malenka and his colleague Dr. Boris Heifets, an anesthesiologist at Stanford University, argued that the DEA's ban is too restrictive. The drug has the unique ability to foster empathetic, loving, "pro-social" emotions, the researchers said.

They pointed to an example, from a study participant who took MDMA in 2013, who wrote, "I had never before felt what I felt today in terms of loving connection. I'm not sure I can reach it again without MDMA, but I'm not without hope that it's possible. Maybe it's like having an aerial map so now I know there's a trail."

The drug may ease PTSD symptoms in multiple ways. It may increase a patient's feelings of trust, empathy and bonding toward his or her psychotherapist, allowing the patient to overcome feelings of anger, emotional numbness and intense anxiety during treatment, the researchers said in the article, which was published Thursday (July 14) in the journal Cell.

Moreover, MDMA may also be a great probe to investigate the biological underpinnings of empathy and sociality in the brain, because the time course of ecstasy's breakdown in the body is highly predictable. That means that brain changes occurring in the several hours after MDMA ingestion can reasonably be tied to the drug's action, revealing which brain regions are activated or dampened when people feel social, loving or empathetic on ecstasy, the researchers argued.

Big unknowns

It's important to reduce regulations that prevent research into MDMA, said Dr. Gillinder Bedi, a psychiatrist at Columbia University in New York, who has studied the effects of MDMA in her own research, but was not involved in writing the new opinion article.

However, it's not clear that the drug is "among the most promising lead therapies for psychiatric disease," said Bedi, in response to this statement in the opinion piece. The PTSD trials were small, and even less research has been done on MDMA's possible impacts on people with other psychiatric conditions, she added.

"Without a lot more research, we can't say very much about which patients might be helped by treatment," Bedi told Live Science. "Without the data, we are often left with polarized opinions, with some people arguing that MDMA is a dangerous and addictive drug, and others viewing it as some kind of magic bullet to mental well-being. The reality, of course, will be somewhere in between."

Don't try this at home

Patients who showed improved PTSD symptoms in past research were carefully prepared prior to MDMA use, and were given psychotherapy to integrate their  experience of using the drug into their treatment. They were also monitored closely for physical side effects. But people who use the drug recreationally do not seem to have any lasting improvements in mental health or social functioning as a result, suggesting MDMA must be carefully contained within a therapeutic setting to show benefits, Bedi said.

"Therapeutic use of MDMA is vastly different from recreational use. This is really important to prevent people from trying to self-medicate their own symptoms using this drug," Bedi said.

It's even less clear that MDMA would be helpful for people with other psychiatric illnesses, such as extreme social anxiety or autism, conditions in which people have trouble either understanding or empathizing with the emotions of others, Bedi said.

Empathy isn't just "feeling the love." It's a complex experience that involves both recognizing someone's emotional state and then echoing that emotional response, Bedi said. But people taking MDMA show a lower ability to recognize certain negative emotions, such as fear, in others, past studies have found.

"MDMA certainly makes people feel that they are more empathic," Bedi said. "Whether or not they actually are more empathic is a different issue."

Original article on Live Science.

A father at age 72? That's how strong his love is.

Mick Jagger, the septuagenarian lead singer of the Rolling Stones, is expecting his eighth child — his first with 29-year-old partner, Melanie Hamrick. Hamrick and Jagger are "surprised and happy" with her pregnancy, The Sun reported on July 14.

You might say Jagger would be a fool to cry over the happy news. But fathering a child at his age — he will be 73 when the baby is born — is not without attendant risks, studies have found. Though there are instances of men retaining fertility into their 90s, recent studies show that when it comes to overall sperm quality, time is not on their side. [Sexy Swimmers: 7 Facts About Sperm]

Baby blues

Epidemiologists have noted that there is an increased risk of certain conditions, particularly schizophrenia and autism, in children who have older fathers, according to Brian Lee, an associate professor of epidemiology and biostatistics with the Dornsife School of Public Health at Drexel University in Pennsylvania.

"Both older mothers and older fathers are more likely to have children with autism" than younger parents are, Lee told Live Science. "But stronger effects seem to have been found with older fathers, for both autism and schizophrenia."

Lee explained that every time cells divide, there's a chance for an error to become incorporated into the cells' genetic code. When that happens in sperm cells, children can inherit those errors, or mutations.

"And the older you are, the more mutations are likely to build up," Lee said.

Kari Stefansson, chairman and CEO of deCODE Genetics in Reykjavik, Iceland, told Live Science in 2012 that as men age, the likelihood increases that a mutation in one of their sperm cells could affect an important gene, resulting in a serious disease in offspring.

Stefansson said that a 36-year-old father gives twice as many new mutations to his child as a 20-year-old father does.

"And a 50-year-old father gives about four times the number of mutations," he added.

Stefansson noted that a 40-year-old man is twice as likely to father a child who will develop autism or schizophrenia, adding that recent increases in autism diagnosis may be explained in part by a growing number of older fathers.

Beyond genetic mutations, additional damage can also occur in sperm cells in aging fathers. That is, DNA fragmentation, or general deterioration that changes or degrades the information produced by the fathers' genes, can also degrade genetic material in these cells, according to a study Lee co-authored in 2015, published in the journal Cell Press.

Father's little helper

But before older men concede that it's all over now if they're hoping to father a child, some research suggests that options may exist for slowing the deterioration of sperm quality.

A study published in 2012 in the journal Fertility and Sterility found that male participants over the age of 44 whose diet was rich in vitamin C showed about 20 percent less damage to their sperm's DNA than the men in the study who consumed the lowest amount of vitamin C.

Daily ejaculation might also help reduce DNA damage to sperm, according to a study presented in 2009 at the annual meeting of the European Society of Human Reproduction and Embryology in Amsterdam.

Nonetheless, a successful pregnancy may still be more than just a shot away, no matter how ardently older men follow these recommendations. A 2004 study published in the American Journal of Obstetrics & Gynecology found that in 221 couples trying to conceive through in vitro fertilization or gamete intrafallopian transfer, their chances decreased by 11 percent for every additional year of the man's age.

As Jagger himself once sang — you can't always get what you want.

Original article on Live Science.

The rolling robot BB-8 captivated moviegoers as it helped save the day in the 2016 film "Star Wars: The Force Awakens" — though even the most die-hard fan would admit that we aren't likely to see a real-world robot quite like that in the near future.

However, there's another spherical, programmable, rolling robot currently in development that's capable of doing important work to engage children with special needs, particularly children on the autism spectrum.

Described by its designers as "a robotic companion," the roly-poly Leka robot is shaped like a ball, has an endearing "face" that changes expressions, and uses sound, light and colors to interact with users through customizable games that improve cognitive and motor skills. Caregivers and educators can program the toy to guide children with developmental disabilities through a range of activities, helping them to improve communication and learn to connect with their environment and with others around them. [The 6 Strangest Robots Ever Created]

For children with Autism Spectrum Disorder (ASD), connecting with others and interpreting social cues can be enormously challenging. ASD describes a collection of neurodevelopmental disorders relating to communication difficulties and characterized by repetitive behaviors, according to the National Institutes of Health (NIH).

ASD typically manifests in infancy or early childhood and occurs across ethnic groups, and the Centers for Disease Control and Prevention (CDC) estimates that it affects approximately 1 in 68 children. Its causes are unknown, though genetics, parental age and exposure to certain pesticides and pharmaceuticals have been suspected to increase a baby's risk of being born with ASD.

To determine how interactive technology might help children with ASD and other developmental disabilities, Leka's creators worked closely with educators, parents and children to determine their needs, researching in particular the role that robotics could play.

And during the course of their research, they discovered that children on the autism spectrum respond especially well to robots, according to Leka CEO and co-founder Ladislas de Toldi. For those working with children who have ASD, repetition and predictability are important, de Toldi told Live Science.

"To see progress, they are required to do the same thing for a long time," de Toldi said. "Always doing the same thing can be hard for a parent or caregiver — but Leka will do the same thing every single time."

By reliably performing the same actions over and over, a robotic companion like Leka provides the child with a sense of safety, de Toldi explained.

Leka senses and responds to a child's participation in games like color identification, picture matching or hide-and-seek, controlled via Bluetooth and programmed through an app available for iOS and Android. During gameplay, Leka supplies positive images and sounds — for instance, showing a smiling face or emitting laughter — to reward progress and encourage confidence.

The customizability of the games allows caregivers to adjust the level of stimulation to suit the individual by adding or removing lights, colors or sound displays. Each game has settings that track a child's progress over time, and difficulty levels can be increased as the child progresses. Meanwhile, handling the spherical Leka provides children with a uniquely tactile interactive experience that they can't get from a touch screen.

"It's a new way to get kids engaged and motivated," de Toldi said.

The Indiegogo campaign for Leka — now more than 90 percent funded — runs through June 3, 2016. It will enable mass production of the toy and make it available for distribution directly to parents, caregivers and therapists, at a preorder cost of $390. Currently programmed with three educational games, Leka will offer a total of seven activities when it ships in early 2017, the company said.

Follow Mindy Weisberger on Twitter'and Google+. Follow us @livescience, Facebook & Google+. Original article on Live Science.

Autism spectrum disorder is a neurodevelopmental condition that affects a person's ability to communicate, interact and behave appropriately with others in social situations. Approximately 1 in 68 children in the United States has autism, and the condition is about five times more common in boys than in girls, according to the Centers for Disease Control and Prevention (CDC).

Autism is characterized by impairments in social skills, communication, and restricted and repetitive behavior such as hand flapping and an insistence on sameness. Many children also have unusual sensory responses, and may shy away from bright lights or may not notice if their clothes are rough and twisted.

Earlier versions of the Diagnostic and Statistical Manual of Mental Disorders (DSM), the American Psychiatric Association's guide for diagnosis, listed autistic disorder, Asperger syndrome and pervasive developmental disorder-not otherwise specified (PDD-NOS) and childhood disintegrative disorder as separate diagnoses. In the latest edition of the DSM, however, experts combined these conditions into one group called autism spectrum disorder because they all appear to be varying degrees of the same disorder, the association reported. 

Despite controversy around the subject, there is no evidence that links vaccination of a child with the development of autism, according to the National Institute of Child Health and Human Development.

Symptoms of autism

No two people with autism are alike, but many parents notice signs of the disorder when their child does not meet certain developmental milestones, typically between 18 months and 3 years of age. For instance, the child may have problems with eye contact, responding to his or her name or engaging in imaginative play.  

Caregivers may also notice that their child does not appear to enjoy engaging and interacting with others, said Mayada Elsabbagh, an assistant professor in psychiatry at McGill University in Quebec, Canada.

However, mild forms of the disorder may not become apparent until the child is older, and some people are not diagnosed until adulthood.

"They may not be detectible until the child starts reaching school age and starts having specific types of challenges that highlight some of the social and communication problems that they have," Elsabbagh told Live Science.

Diagnosis of autism

The diagnostic process is different for every person with autism. In some cases, pediatricians may use an autism screen, often a short yes-or-no survey that looks for signs of autism, to see whether a child may be at risk for the disorder. If the child screens positive, the family may receive a referral to a specialist for a diagnostic evaluation.  

When diagnosing autism, specialists rely on both direct observational information and parent report data about the child's behavior, said Elsabbagh, who encouraged parents to keep a detailed developmental records of their children's growth.

"For older children, some clinicians will seek input from the child's school, peers — how they interact in the settings outside their home," she said. "What they're trying to do is compile and put together these different sources of information and integrate them to figure out if this a child with autism or, alternatively, does this child have a general developmental delay that is not specific to autism?"

A thorough team of clinicians may also diagnose additional disorders that often accompany autism, including attention deficit hyperactivity disorder (ADHD), intellectual disability, epilepsy and depression, she added.

People with certain genetic disorders, such as fragile X syndrome, tuberous sclerosis complex and Angelman syndrome, also tend to have autism, experts say. 

Treatment of autism

There is no cure for autism spectrum disorders. However, there are behavioral and educational therapies that may help reduce symptoms. And early diagnosis is key to connecting children with autism to treatment, Elsabbagh said.

One of the most frequently used therapies, Applied Behavioral Analysis (ABA), for instance, uses rewards to encourage people with autism to increase useful behavior and decrease impairing actions. Parent-mediated interventions are also an effective therapy that teaches the caregivers how to help their children in a natural environment, such as the home. 

For instance, children with autism saw improvements in language and behavior after enrolling in the Early Start Denver Model, a two-year intervention that uses ABA and other therapies in a classroom setting, reported a 2010 study in Pediatrics.

"In reality, behavioral approaches are best because we know that changing the environment around the child and interacting with the child in different ways does change biological processes [in the brain]," Elsabbagh said. "It does have an impact on shaping brain development in a way that would be supportive and helpful for their independence."

Medications do not treat the core symptoms of autism, such as problems with communication, but can reduce symptoms such as irritability. The U.S. Food and Drug Administration has approved two drugs for autism — risperidone and aripiprazole — which treat aggression, irritability and mood swings. 

However, the long-term effects of these medications are unknown, and often children with autism take multiple drugs to treat other problems such as hyperactivity or depression, experts find. About 65 percent of children with autism have a prescription for a psychotropic medication, a drug that can cross the blood-brain barrier, a 2013 study in the journal Pediatrics reported. Furthermore, 35 percent of the children in the study received prescriptions for two types of these drugs, and 15 percent had three or more prescriptions, the study found. 

"Drug therapies are by no means a substitute for the behavioral approaches," Elsabbagh said. "They tend to be viewed as a complementary approach that overall fits within the child's treatment plan, but are a not a child's substitute for what therapies can do."

What's more, the market is inundated with alternative treatments and diets that are not clinically proven to help people with autism. "Sometimes the parents think these are substitutes and they choose not to put their children in behavioral treatments," Elsabbagh said. "And that takes away every chance the child could have to have a more validated option." 

Adults with autism

Most autism research focuses on children, but more researchers are beginning to examine how the disorder affects the lives of adults. Relative to the general population, fewer adults with autism enroll in higher education, find a job or transition to independent living, research shows. 

About one-third of young adults with autism attend college within eight years of leaving high school, said Anne Roux, senior research coordinator at the Life Course Outcomes research program at the A.J. Drexel Autism Institute at Drexel University in Philadelphia. Her team used data from the National Longitudinal Transition Study-2, a nationwide database that surveys students in special education programs. 

About half of those with autism found a paying job within the first eight years outside of high school, she said. In comparison, 98 percent of typical people and 91 percent of people with disabilities in general find paying work in that time frame.

"The autism number is quite a bit lower than that, and that's the concern," Roux said. "You can see that they struggle a lot early on." About half are not connected either to school or to work within two years of leaving high school. 

Furthermore, about 80 percent of young adults with autism continue to live with their parents after high school, which is more than the general population and adults with disabilities in general, Roux said. 

Researchers plan to study how school and community programs can prepare students and young adults with autism with life skills that will help them gain independence as they age, she said. 

With additional reporting by staff writer Amanda Chan. Follow Laura Geggel on Twitter @LauraGeggel and Google+. Follow Live Science @livescience, Facebook & Google+. 

Additional resources:

• FDA: Beware of False or Misleading Claims for Treating Autism
• CDC: Do vaccines cause autism spectrum disorder?
• Mayo Clinic: Autism spectrum disorder

The anti-vaccination movement regained attention due to actor Robert De Niro's decision late last week to pull the film "Vaxxed" from the Tribeca Film Festival, which he runs. But that doesn't mean the anti-vaccination movement will fade away anytime soon, experts say.

Despite the public pressure to pull the film — not to mention the innumerable studies showing that vaccines are safe — there are many reasons the movement persists, sociologists told Live Science.

"We know vaccines carry some risk, and we know that risk is very small," said Jennifer Reich, an associate professor of sociology at the University of Colorado Denver. "We also know that parents who distrust medical information are more likely to overestimate that risk and underestimate the risk of diseases." [10 Medical Myths That Just Won't Go Away]

Parents who decide not to vaccinate their children tend to be white, college-educated and high-income earners, said Reich, author of "Calling the Shots: Why Parents Reject Vaccines" (NYU Press, 2016).

The anti-vaccination viewpoint is a product of two colliding ideas, she said. One is the idea that "parents are in this alone," and that they're not responsible in any small way for other children in their community, Reich said. This means they don't feel it's important to contribute to herd immunity, which protects individuals who are unable to receive vaccines, she said.

The other idea is that individuals are solely responsible for their health, and that society bears no responsibility, for example, for encouraging people to go to the gym, participate in preventive care or avoid smoking.

Parents may take these ideas together, and view it as their duty to go it alone — to combine individualist parenting with individualized health care, Reich said. Many parents in this camp spend a substantial amount of time reading information and deciding whether it applies to their children, she said.

"They begin to doubt whether population data [on vaccine safety] applies to their own families, with their own lifestyle choices," Reich said.

For instance, a mother may think that if she breast-feeds her child, uses organic food and controls whom her child interacts with, then these efforts might protect the child from diseases. But this isn't the case, Reich said.

Many diseases, such as measles, are highly contagious, and "lots of viruses don't respond differently because of nutrition," so children may get sick even if they're breastfed and eat organic food, she said.

Other parents put faith in the body's natural ability to heal itself, Reich said. "They can see vaccines as potentially undermining the body's natural immune response," she said.

But people with this mind-set usually underestimate the severity of infectious diseases. For example, they typically think that if their child does get sick, he or she will not develop complications such as encephalitis or deafness. "They imagine they can control and heal their children through this kind of intensive parenting," Reich said.

Vaxxing questions

It's hard to know how many parents are anti-vaccination, but kindergarten immunization records suggest that between 7 percent and 9 percent of U.S. children have been opted out of vaccines, and about 20 to 25 percent of children are deliberately undervaccinated (meaning they have not received all of the vaccines recommended for their age), Reich said. [5 Dangerous Vaccination Myths]

While writing her book, Reich spent eight years talking with anti-vaccination parents. Some parents were worried about the supposed vaccine-autism link (a connection that has been disproven countless times but is still featured in the film "Vaxxed"), she said. However, the majority of parents in the anti-vaccination camp told Reich that they had other concerns about vaccines' long-term negative health effects, despite evidence to the contrary.

These parents often wouldn't name a specific condition that concerned them, but said they were worried about autoimmune disorders in general, Reich said. In fact, many blamed the rise of autoimmune-disorder rates on vaccines. (Autoimmune disorders are diseases in which the immune system attacks the body's own cells; type 1 diabetes, celiac disease and lupus are examples.)

"I think that the anti-vaxxers live in a world that I would describe as anecdotal anxiety," meaning they become very worried after hearing or reading stories from other parents, said Jonathan Imber, a professor of sociology at Wellesley College who was not involved with Reich's research.

"They see a condition like autism, and they don't really have a sense of its causes," Imber told Live Science. And because the science is also unclear about why certain conditions develop, parents may look for purely anecdotal, and possibly inaccurate, explanations. These anecdotes may be "intensified by the material that is already out there," including distorted science, and further raise parents' anxieties, leading them not to vaccinate, Imber said.

Overall, both experts said there should be more transparency and communication about vaccination decisions and safety.

"I'm not sympathetic to people who are anti-vax, but I am sympathetic to the phenomena that it needs to be addressed more sympathetically," Imber said.

Follow Laura Geggel on Twitter @LauraGeggel. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science.

David Gerlach is the executive producer of "Blank on Blank," which brings new life to classic interviews, and the founder of Quoted Studios, a nonprofit dedicated to animated journalism. This original text highlights the video about Temple Grandin that originally appeared at "Blank on Blank." He contributed this article to Live Science's Expert Voices: Op-Ed & Insights.

You've probably heard the story that Einstein, whose name is synonymous with genius, didn't seem destined for much when he was a small child. He was years behind other children when it came to learning to talk, he did horribly in school. It seems that Einstein's brain just worked differently than most other people's. Today a lot of people think Einstein was probably autistic — one person who would agree is Temple Grandin. Temple Grandin is a professor of animal sciences who's worked in the meat industry to invent kinder ways to lead cattle to slaughter. She also has autistim, the high-functioning version known as Asperger's syndrome. Autism is a brain disorder that tends to affect people's social skills, like the ability to read facial expressions and body language. But it can also mean extraordinary talent in math, music and the visual arts. Temple Grandin has become something of a celebrity of autism. She's written books, given TED talks, and she's traveled around the world to speak on the subject. [Autism Truths and Myths: The State of the Science (Op-Ed)]

We found this interview in the holdings of Colorado State University, where Grandin teaches. In this conversation, she's at her best, explaining for the rest of us what it's really like to have an autistic brain and how Einstein's not the only genius who could have been dismissed for being different. She even believes Silicon Valley may never have happened without the autistic brain. This is the latest episode in our special miniseries, The Experimenters. We're bringing to life lost interviews with the icons of science, technology and innovation — people who helped make the world we live in today. 

Upcoming episodes will feature Frank Lloyd Wright, Carl Sagan and Dame Stephanie Shirley. Learn more at BlankOnBlank.org.

Follow all of the Expert Voices issues and debates — and become part of the discussion — on Facebook, Twitter and Google+. The views expressed are those of the author and do not necessarily reflect the views of the publisher. This version of the article was originally published on Live Science .

The brains of the elderly and younger people with autism and schizophrenia may share a common link: Both have low levels of vitamin B12, researchers say.

The facts that blood levels of B12 do not always mirror brain levels of the vitamin, and that brain levels decrease more over the years than blood levels, may imply that various types of neurological diseases — such as old-age dementia and the disorders of autism and schizophrenia — could be related to poor uptake of vitamin B12 from the blood into the brain, the scientists said.

The findings, reported last month in the journal PLOS ONE, support an emerging theory that the human brain uses vitamin B12 in a tightly regulated manner to control gene expression and to spur neurological development at key points during life, from the brain's high-growth periods during fetal development and early childhood, through the refining of neural networks in adolescence, and then into middle and old age.

Vitamin B12, also called cobalamin, plays a crucial role in blood formation and the normal functioning of the nervous system. The vitamin is found in foods derived from animal sources, although some plant-based foods can be fortified with B12. [6 Foods That Are Good For Your Brain]

In the new study, scientists led by Richard Deth, a professor of pharmacology at Nova Southeastern University in Fort Lauderdale, Florida, examined the brains of more than 60 deceased individuals, ranging in age from a fetus in a late stage of gestation to 80 years. The study included 12 people who had autism and nine with schizophrenia.

This is the first study to compare the levels of vitamin B12 in the brain across the human lifetime, Deth told Live Science. The vitamin B12 levels in the brain were 10 times lower in the oldest people compared with the youngest, reflecting a gradual, natural, and consistent decline over the years.

For the elderly, this decline might not be a bad thing. Lower levels at advanced ages may offer some degree of brain protection by slowing cellular reactions and the production of DNA-damaging chemicals called free radicals, Deth said. In previous work with his colleague Yiting Zhang of Northeastern University in Boston, Deth found that the body's creation of biologically active forms of vitamin B12 produces free radicals as a waste product.

But levels of B12 that are too low can be detrimental. "At some point, an extreme decrease in metabolism…is not compatible with cell survival," Deth said. Similarly, lower vitamin B12 levels can have negative consequences for people of younger ages, as the brain is still developing. Deth's group found that the levels of vitamin B12 in the brains of young people with autism and in middle-age people with schizophrenia were about one-third of the levels found in similarly aged people who did not have these neurological conditions.

The people in the study with autism, who were all under age 10, had levels similar to those found in a 57-year-old. It's not clear what these low levels imply, but the uptake of too little B12 might hinder the brain's ability to establish important neural connections between regions, Deth said.

Those with schizophrenia, all between ages 36 and 49, had levels similar to those found in a 72-year-old. Although their brains were mature by this age, the below-normal level may have manifested itself during adolescence, when the seeds of schizophrenia are thought to take root. But even in middle age, the lower levels may contribute to a loss of previously normal function, Deth said.

Daniel Smith, a neurologist and vice president of innovative technology at Autism Speaks, an autism advocacy group based in New York that sponsors autism research, who was not involved in this research, said the study was interesting and worth pursuing further. However, he noted that the study remains speculative in its hypothesis that vitamin B12 deficiencies at a cellular level lead to changes associated with the autism spectrum of brain traits.

Numerous studies have searched for an association between vitamin deficiencies and neurological disorders. There has been no definitive study, however, indicating that autism and schizophrenia can be caused by a deficiency or treated through vitamin supplementation.

In fact, a study published last year in the Journal of the Academy of Nutrition and Dietetic found that few children with autism benefit from vitamin supplements and may be at risk for overdosing.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Children born to women with obesity and diabetes may have an increased risk of autism, a new study suggests.

The children in the study who were born to women who were obese before becoming pregnant were nearly twice as likely to be diagnosed with autism by age 6, compared with those children born to mothers whose weight was normal before they got pregnant, the researchers found.

And the babies born to women who had developed diabetes at some point before they got pregnant were more than twice as likely to be diagnosed with autism by age 6, compared with those children born to women without diabetes.

However, the children born to women with both obesity and diabetes showed the greatest risk. These kids were nearly four times more likely to be diagnosed with autism by age 6, compared with those children born to women who had neither obesity nor diabetes.

The new study "highlights the potential that autism starts before birth, in utero," said study author M. Daniele Fallin, chair of the department of mental health at the Johns Hopkins Bloomberg School of Public Health in Baltimore.

In the study, the researchers looked at the rates of autism and intellectual disabilities in about 2,700 children. The researchers also looked at the pre-pregnancy weights of the children's mothers and examined whether the women had developed diabetes before or during their pregnancies. The researchers gathered their data from medical records and interviews with the mothers.

Of all the children in the study, 102 were diagnosed with autism and 137 were diagnosed with intellectual disabilities during the six-year follow-up period. [5 Things that Might Cause Autism]

The researchers also found that the children born to women who had both obesity and diabetes also had an increased risk of intellectual disabilities, compared with the babies born to women who had neither obesity nor diabetes.

The mechanisms linking a mother's obesity and diabetes and a child's risk of autism are not clear, the researchers said. However, some research has suggested that obesity and diabetes may disrupt the functioning of a mother's immune system, and this in turn may contribute to the development of autism in the child, the researchers said.

Both obesity and diabetes may also promote inflammation in a pregnant woman's body, and intrauterine and fetal brain inflammation have been implicated in the development of autism in children, the study said.

Another possible mechanism relates to folate, as "there is emerging evidence that folate supplementation is a protective factor for autism," Fallin told Live Science. Research has shown that obesity may disrupt the uptake of folate, she said. Therefore, if a woman is obese, it may be much harder for her body to properly use the chemical, which could contribute to an increased risk of autism in the fetus. (Folate or folic acid is a type of vitamin B that the body needs to function and stay healthy.)

The new study was published today (Jan. 29) in the journal Pediatrics.

Follow Agata Blaszczak-Boxe on Twitter. Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science.

Alycia Halladay, chief science officer for the Autism Science Foundation, contributed this article to Live Science's Expert Voices: Op-Ed & Insights.

For years, scientists have reported a higher autism prevalence in males than in females. But do girls actually hold the key to future breakthroughs in autism research?

Most studies show about a 4:1 ratio in the prevalence of autism in boys compared with girls, meaning boys are four times as likely to receive an autism spectrum disorder (ASD) diagnosis. In the past, this significant disparity was simply chalked up to a special susceptibility in boys. Only in the past five years have researchers seriously studied the potential underlying causes of this difference — and to date, our understanding is still fairly limited.

The female "protective effect"

Despite having fewer ASD diagnoses, girls with the condition tend to have more of its genetic mutations than boys do. In particular, girls have more large duplications or deletions of DNA, called copy-number variations, in their genome. Older girls diagnosed with autism generally have more severe symptoms than boys, including lower IQ scores. 

So, if females have more of these variations in their DNA, and genetics are a risk factor for autism, why would fewer girls be given a diagnosis of autism? There may be something protecting girls against symptom severity — a concept that's come to be known as the "female protective effect."  

While one approach is to look directly at the genome, another is to look at symptoms in siblings of children with autism. Dr. Elise Robinson, of Massachusetts General Hospital, and colleagues explored this effect in twins, in which one twin in each pair had an autism diagnosis. By studying the unaffected siblings of those with ASD, her group found that siblings of females with autism had more symptoms of autism (without reaching the threshold for a diagnosis) than siblings of males with autism. Together, this is evidence for a protective effect.

Such studies suggest that females require more genetic mutations, or a genetic "load" to have enough symptoms to reach an autism diagnosis by existing clinical tools. Other studies have come to the same conclusion (such as this comprehensive study published in September in Neuron). Interestingly enough, this is not unique to autism: In science, this idea is also known as the "Carter effect" and is seen in clubfoot as well.

How does protection work?

But what is this protective effect? Is there a gene that blocks the effect of other genes, or turns on compensatory genes? Does some sort of environmental factor in females, such as the presence of specific hormones, alter the way the autism genes are expressed? Are the genes that control for brain development in boys and girls regulated differently? These are all potential theories. 

To look at the genetics behind the protective effect, Dr. Jake Gockley, of the Yale School of Medicine, and colleagues looked at an obvious place: the X chromosome. Females have two X chromosomes, and males have one X chromosome and one Y chromosome, so a mutation on the X chromosome was the first place to look. After looking extensively, researchers couldn't find just one gene that was the cause of this protective effect. It would have been nice to have immediately discovered it, but it is clearly a more complicated story that requires the pooling of large data sets with information collected on siblings not diagnosed with ASD. 

These initial findings warrant a focused study of unaffected sisters of individuals with autism in an effort to identify this potential protective effect. If we can identify this protective factor, it could be harnessed to protect both boys and girls from the debilitating features of autism and improve lives by informing the development of new therapies. That's why this area of research seems so promising and exciting to many scientists in the field. 

Can the protective effect help others?

The Autism Science Foundation is partnering with the Seaver Autism Center at Mount Sinai in New York to make it easier for researchers to explore the female protective effect. The newly launched Autism Sisters Initiative is building a large database of both symptoms and genetics in all family members that researchers can use to explore this phenomenon. Data on unaffected sisters will be gathered from existing projects with rigorous behavioral phenotyping data on all family members, including unaffected siblings. The database will begin with samples from the Autism Sequencing Consortium, which is a large international collaboration that shares samples and data. 

In addition, the initiative will provide funds to autism research projects that already collect behavioral and genetic data so they can be expanded to include an unaffected sister in families where she is the only family member not already included. New families with a member who has autism and a female sibling without an ASD diagnosis will be recruited to donate saliva samples and participate in a full behavioral screening. The DNA will be sequenced for all family members. For the first time, researchers will be able to look at females who may carry a genetic marker for autism and do not have all the symptoms. This will revolutionize the diagnosis and treatment of not just females with autism, but males as well. 

The project will convene a scientific advisory panel comprising experts in genetics, statistical genetics, epidemiology and clinicians in ASD, led by the Seaver Center's Joseph Buxbaum, to create a study protocol that will allow the question of the female protective effect to be addressed properly.

It's time for the autism research community to take a much deeper look at this phenomenon, which could very well emerge as an important new frontier in autism science. We owe it to all of the families affected by autism to take this exploration as far as it will lead us.

Follow all of the Expert Voices issues and debates — and become part of the discussion — on Facebook, Twitter and Google+. The views expressed are those of the author and do not necessarily reflect the views of the publisher. This version of the article was originally published on Live Science .

Women in a new study who took antidepressants during their second and third trimesters of pregnancy showed an 87 percent increased risk of having a child with an autism spectrum disorder, compared with women who did not take medications for depression while expecting.

The researchers also found that mothers who used a certain class of antidepressants, known as selective serotonin reuptake inhibitors (SSRIs), had more than double the risk of having a child with autism spectrum disorder (ASD), according to the study published today (Dec. 14) in the journal JAMA Pediatrics. ASD is a group of conditions that includes autism, Asperger syndrome or other pervasive developmental disorders.

The findings suggest that using antidepressants, especially SSRIs, during the second and third trimester of pregnancy increases the risk of having a child with autism, said study author Anick Berard, a professor of pharmacy at the University of Montreal, who specializes in drug use during pregnancy. Some SSRIs that may be used during pregnancy include Zoloft, Prozac and Celexa.

Previous studies have shown that having depression itself may increase the risk of  autism. But the new study showed that the increase in the risk of having a child with autism that is linked to antidepressants is above and beyond the increase in risk of autism that is associated with maternal depression, Berard said. In the new study, depression in moms was associated with a 20 percent increased risk of autism, she said. [Beyond Vaccines: 5 Things that Might Really Cause Autism]

The analysis also found that women who were prescribed more than one class of antidepressants during the last six months of pregnancy were more than four times more likely to have a child with autism, compared with women who did not take antidepressants while pregnant.

Antidepressants are one of the most frequently used medications during pregnancy, with an estimated 7 to 13 percent of American women taking them while pregnant, according to one study.

Of the previous studies that have looked for a link between the development of autism in children and antidepressant use during pregnancy, some — but not all — have found that there is an association. This new study is one of the largest to show this association, according to the researchers.

"This study is the first to quantify autism risk based on the class of antidepressants used by a woman during pregnancy, and the first to find an increased risk with SSRIs mostly," Berard told Live Science.

Depression during pregnancy

In an editorial accompanying the study that was published in the same issue of JAMA Pediatrics, Dr. Bryan King, a child psychiatrist at Seattle Children's Hospital, wrote that the increasing prevalence of autistic spectrum disorders have led researchers to a "search for explanations, particularly among environmental factors." 

And in the ongoing search for environmental contributions to the risk of ASD, gestational exposures are increasing as an area of focus, said King, who was not involved in the research.

Although the exact cause of autism is not yet known, there is probably a strong genetic factor involved, but exposure to certain factors in the environment may also play a role, she said.

Exposure to an antidepressant during in utero development is one such factor. In the new study, the researchers analyzed data collected from all 145,500 pregnancies that occurred in the Canadian province of Quebec over the 20-year period between January 1998 and December 2009, in which mothers had a full-term pregnancy and gave birth to only one baby.

The researchers followed up with the children until age 10; there were 1,054 children who were diagnosed with ASD.

Using information gathered from hospital records in Quebec, as well as a prescription drug database and a database that showed physician visits, the researchers looked at whether the women in the study had filled a prescription for antidepressants at any time during their pregnancy, or one month before conception.

The analysis found that about 4,700 infants, or 3.2 percent of babies, were exposed to antidepressants at some point during their mothers' pregnancies. Among these babies, 46 developed autism.

But the researchers found that only a mother's use of antidepressants during the second or third trimester was associated with a greater risk of autism in children. There was no increase in ASD risk that was linked to using these medications during early pregnancy.

The second and third trimesters are a critical time for brain development in the fetus, Berard said. Taking SSRIs during this period inhibits levels of serotonin, a chemical that can affect a person's mood, but is also essential for brain cell development in the fetus, she said. [11 Facts Every Parent Should Know About Their Baby's Brain]

Depression is a serious and debilitating condition, and the new findings do not suggest that pregnant women with depression should go untreated, Berard said. But with evidence mounting of an increased risk of adverse pregnancy outcomes with antidepressant use, antidepressants are not always the best solution, she said.

The majority of depressed pregnant women are mildly to moderately depressed, and exercise and psychotherapy have been shown to be effective treatments when depression is not severe, Berard said.

Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science.

Many websites that promote unscientific views about vaccinations use pseudoscience and misinformation to spread the idea that vaccines are dangerous, according to a new study.

For example, of the nearly 500 anti-vaccination websites examined in the study, nearly two-thirds claimed that vaccines cause autism, the researchers found. However, multiple studies have shown that there is no link between vaccines and autism.

About two-thirds of the websites used information that they represented as scientific evidence, but in fact was not, to support their claims that vaccines are dangerous, and about one-third used people's anecdotes to reinforce those claims, the scientists found.

Some websites also cited actual peer-reviewed studies as their sources of information, but they misinterpreted and misrepresented the findings of these studies.

"So the science itself was strong, but the way it was being interpreted was not very accurate," said study author Meghan Moran, an associate professor in Johns Hopkins University Bloomberg School's Department of Health, Behavior and Society. "It was being distorted to support an anti-vaccine agenda." [5 Dangerous Vaccination Myths]

In the study, the researchers looked at websites with content about childhood vaccines. They used four search engines to find the sites — Google, Bing, Yahoo and Ask Jeeves — and searched for terms including "immunization dangers" and "vaccine danger" as well as other phrases. Their final sample of 480 anti-vaccination websites included a mix of personal websites, blogs, Facebook pages and health websites. The researchers examined the content of the websites, looking for vaccine misinformation, the sources of the misinformation and the types of persuasive tactics that the sites used to convince people that vaccines are dangerous.

In examining the websites, the researchers also observed a lot of misunderstanding and misinterpretation of epidemiological principles, Moran told Live Science.

For example, epidemiologists know that correlation does not imply causation. "Just because two things happen at the same time, that doesn't mean that one is causing the other," Moran said. But some of the websites presented timelines that showed that, as rates of immunization went up over a certain period of time, so did autism diagnoses, Moran said.

Although it is true that both have increased over the same period, the anti-vaccine websites frequently implied that "it must be that the immunizations were causing autism, which we know is not true," Moran said.

Another tactic commonly employed by the websites in the study was the use of anecdotes and stories of parents of children with autism, the researchers said. Because such stories are easy for other parents to connect to, they help to make the anti-vaccine agenda that these sites are promoting appear "a lot more vivid and powerful," Moran said.

Some of the sites also included information promoting positive health behaviors, the researchers said. For example, 18.5 percent of them promoted eating healthy, about 5 percent promoted eating organic food and 5.5 percent recommended breast-feeding.

The biggest takeaway from the findings is that researchers and health officials "need to communicate to the vaccine-hesitant parent in a way that resonates with them and is sensitive to their concerns," Moran said in a statement. "In our review, we saw communication for things we consider healthy, such as breast-feeding, eating organic, the types of behavior public health officials want to encourage. I think we can leverage these good things and reframe our communication in a way that makes sense to those parents resisting vaccines for their children."

The new findings were presented today (Nov. 3) at the American Public Health Association's Annual Meeting in Chicago.

 Follow Agata Blaszczak-Boxe on Twitter. Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science.

There is no evidence that supports spacing out childhood vaccines — which two Republican candidates for president suggested in last night's presidential debate — instead of following the recommended schedule, experts say.

"I am totally in favor of vaccines, but I want smaller doses over a longer period of time," Donald Trump, one of the candidates for president, said at the debate.

Candidate and retired pediatric neurosurgeon Ben Carson responded by saying, "We have extremely well-documented proof that there is no autism associated with vaccinations," he said.

Carson went on, however, to agree with Trump about spacing out vaccines. "But it is true that we are probably giving way too many in too short period of time, and a lot of pediatricians now recognize that, and I think are cutting down on the number and the proximity in which those are done" he said.

Candidate Senator Rand Paul, an ophthalmologist, also agreed.

"I'm for vaccines, but I'm also for freedom," he said. "Even if the science doesn't say bunching them up is a problem, I ought to be able to spread my vaccines out a little bit at the very least."

But not only is there no evidence that spacing out childhood vaccines is good for children's health, but the evidence actually suggests quite the opposite, Dr. Paul Offit, chief of the division of infectious diseases at the Children's Hospital of Philadelphia, told Live Science.

There's evidence that supports not spacing out vaccines any further than they are scheduled under current recommendations, Offit said. [5 Dangerous Vaccine Myths]

"To suggest that you make your own schedule is dangerous," he said. "That's why we saw the measles outbreak in Disneyland this year" he said — because parents chose to delay vaccinating their children.

Spacing out the current vaccine schedule leaves children susceptible to diseases for longer periods of time than they need to be, Dr. William Schaffner, a professor of preventive medicine at Vanderbilt University, told Live Science.

Moreover, spacing out vaccines is an unproven way to vaccinate: No one's ever tested it, so scientists don't know how well it works or how safe it is, he said.

And it's been documented that a vaccine that is pushed back can become a vaccine that is never received, Schaffner added.

Although some parents have raised concerns that an infant's immune system may not be able to "handle" the numerous immunizations children are scheduled to receive, there is no evidence that shows this is true, Schaffner said. "That's been shown clearly not to be the case," he said. "It's safe and effective."

Whenever a new vaccine is added to the existing schedule, scientists are required to prove to the Food and Drug Administration that the new injection doesn't interfere with other vaccines, Offit said. "It's well-tested," he said.

"The immunization schedule is based on an elaborate amount of scientific research," Schaffner said. "It's designed to be maximally effective and maximally safe."

Shortly after the debate, the American Academy of Pediatrics released a statement that read, in part, "There is no 'alternative' immunization schedule. Delaying vaccines only leaves a child at risk of disease for a longer period of time; it does not make vaccinating safer."

Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science.

The best ways to convince people of the benefits of vaccinations may be to show them pictures of a child with measles or to have them read a description of the disease written by a mom whose child was infected, according to a new study.

These ways are more effective than showing people information summarizing recent research that shows there is no link between vaccines and an increased risk of autism in children, the researchers found.

The researchers found that directing people's attention to the risks posed by not getting vaccinated by showing them the pictures of sick children and having them read a mom's written account of her child's disease changed their attitudes, leading them to think more positively about vaccinations, study author Zachary Horne, a graduate student at the University of Illinois, said in a statement.

That was true for even "the most skeptical participants in the study," Horne said.

Vaccine beliefs

There were 644 cases of measles in the United States in 2014, according to the study. That's triple the number seen in 2013. And back in 2000, researchers thought that this disease had been eliminated from the U.S., according to the study. [5 Dangerous Vaccine Myths]

"The re-emergence of measles has been linked to an increase in the number of parents refusing to vaccinate their children," the researchers wrote in their study. One reason that parents don't vaccinate their children is the mistaken belief that the vaccine that protects against measles, mumps and rubella (the MMR vaccine) is linked with an increased risk of autism. Researchers have been looking for effective ways to convince people who hold this mistaken belief about the benefits of vaccinations.

In the new study, the researchers asked 315 people questions to examine their views on several potentially controversial subjects, including their attitudes toward vaccines and their willingness to vaccinate their kids.

Then, the people in the study were assigned to one of three groups. People in the first group looked at science-based materials that challenged the anti-vaccination point of view. People in the second group read a paragraph written by a mother describing her child's infection with measles, and also looked at pictures of children with measles, mumps or rubella. They also read three warnings about why it is important to vaccinate kids. People in the third group, which was a comparison group, were asked to read about a subject not related to vaccines.

Then, the researchers again evaluated the people's views on vaccination and their intentions to vaccinate their children in the future. The investigators found that the intervention that involved showing people the consequences of the diseases was the one that had the biggest effect on the people who were initially the most skeptical about vaccinations, Horne said.

A better approach

In contrast, showing people the scientific evidence that there is no link between vaccines and autism did not change the people's views on vaccination, the researchers said. The reason this type of intervention doesn't work is likely that trying to convince someone that his or her beliefs are false is not the best argumentative strategy, Horne said.

The study shows that "instead of going up against the belief about the link between vaccines and autism," researchers should aim to convince people that, independent of whether they believe in that link, they should also believe that there are serious consequences of not getting children vaccinated, Horne told Live Science.

"The insight [from the study] was to direct their attention towards those consequences, rather than trying to combat their false beliefs that there is some link where there is not," Horne said.

The new study was published Aug. 3, 2015 in the journal Proceedings of the National Academy of Sciences.

Follow Agata Blaszczak-Boxe on Twitter. Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science.

Francesca Happé is president of the International Society for Autism Research (INSAR) and director of the MRC Social, Genetic and Developmental Psychiatry Centre at the Institute of Psychiatry, Psychology and Neuroscience at King’s College London. She contributed this article to Live Science's Expert Voices: Op-Ed & Insights.

Autism is everywhere. Characters with autism, especially high-functioning autism or Asperger Syndrome, abound in TV shows, films and novels. Think of Sheldon on "The Big Bang Theory," Oskar in "Extremely Loud and Incredibly Close," or Christopher in "The Curious Incident of the Dog in the Night-Time." Writers love autistic protagonists for their wry take on how illogical "neurotypical" (non-autistic) people are, and find the autistic genius a useful plot device for solving unsolvable riddles. 

Autism is a myth-magnet. You can barely look at a newspaper, magazine or newsfeed without finding something about autism: a new "miracle cure," a claim that "the gene for autism" has been discovered, or talk of scientists creating autistic mice. The reality, of course, is very different.  

Getting to the truth of autism

This month, nearly 2,000 scientists and researchers will gather in Salt Lake City for the International Meeting for Autism Research (IMFAR) 2015. They will discuss and debate the latest findings about this most mysterious of conditions. Since autism was first named, a little more than 70 years ago, much has been learned — but many questions remain. [Autism's Rise: Researchers Look at Why Cases Are Increasing ]

Autism is a neurodevelopmental condition characterized by impaired social and communication abilities, and rigid and repetitive behavior and interests. One of the major challenges to research is that the manifestation is so varied, giving rise to the notion of the autism "spectrum." One child with autism may be silent, aloof (not seeking out his parents even when hurt or upset) and apparently locked into repetitive play, such as lining up toys or spinning coins for hours on end. Another individual may talk incessantly about his own special interest in football scores, be indiscriminately over-friendly, and unable to tell the difference between a joke and a lie. The wide range of manifestations makes it hard to research causes or treatments for autism spectrum disorder (ASD). Instead of a gene for autism, for example, there are very likely hundreds of genes that can combine in dozens of ways to predispose a child to ASD. Many researchers now talk about "the autisms."

Among the topics that will be exercising minds at IMFAR 2015 — the largest international meeting focused entirely on autism — are biomarkers, including neural signatures, that might help researchers divine more homogeneous subgroups within ASD. There are without doubt many different routes to ASD, and one panel session at IMFAR will consider how genomic discovery might lead us to discover genetically defined autism subtypes. 

Are there treatments for autism?

The purpose of genetic research is to uncover mechanisms that might be modifiable, to optimize interventions for individuals with ASD. Developing new ASD pharmacological treatments is the goal of the European Autism Interventions — A Multicenter Study for Developing New Medications (EU-AIMS), supported by the largest single grant for autism research anywhere in the world. The latest findings from this $33.6 million (30 million euros) academic-industry collaboration will be presented at IMFAR 2015 in the panel Translating Cellular and Animal Models of Synaptic Gene Deficits to Large-Scale Clinical Studies, and Jeremy Veenstra-Vander Weele, Mortimer D. Sackler Associate Professor of Psychiatry at Columbia University will also present his latest work on pathways to new treatments for ASD.

Our most effective interventions for ASD are currently educational and behavioral approaches. Sally Rogers, professor of psychiatry and behavioral sciences at UC Davis MIND Institute will reflect on 50 years of ASD early intervention science, which has demonstrated that remarkably good outcomes are possible for people with ASD.

Much of what makes life hard for people with ASD is not the autism itself, but what often accompanies autism, including epilepsy, intellectual disability, sleep problems, anxiety and depression. Mental health issues may get worse in adolescence or adulthood, even when autism symptoms may be becoming more subtle. Presentations at IMFAR 2015 will cover clinical and epidemiological perspectives on co-occurring psychiatric disorders across the life span, and interventions for anxiety in ASD. [Kids with Autism Are More Likely to Have Gastrointestinal Problems ]

Autism is not just about children or males

Researchers now widely recognize that ASD is not a rare condition and that perhaps 1 percent of the population has autism. The popular conception of autism is of the child with the far-away gaze, and the vast majority of published research is on children with ASD.  However, it's important to remember that most people with autism are adults. 

Concentration on early diagnosis and intervention for ASD has been important, but can leave the impression that later intervention is impossible or ineffective. In fact, little is known about ASD in older adults, and equivalently intensive interventions could also lead to major improvements in functioning and well-being late in life. It is therefore encouraging that new research will be presented at IMFAR 2015 on adult interventions, aging and factors associated with adult outcomes in ASD.

As examples in popular media illustrate, the stereotype of autism is male. Males outnumber females with ASD perhaps 4 to 1, with the sex ratio more skewed at the high-functioning end of the spectrum and less unbalanced among those with intellectual disability. The source of this imbalance is not known, although it is not unique to ASD: the developing male appears to be generally more vulnerable. 

Sex differences in ASD is a growing topic, and new research will be presented at IMFAR 2015. Understanding the origins and nature of sex differences is important to improve recognition and services for girls and women on the autism spectrum. Increasingly, women with ASD are telling their own stories, and researchers attending IMFAR 2015 will benefit from a panel session focused on the first-person experience of people with ASD. Anthropologist and father of a daughter with ASD, Roy Richard Grinker, director of the Institute for Ethnographic Research at the George Washington University, will open the meeting with a keynote presentation, "Who Owns Autism? Exceptionalism, Stigma, and Stakeholders." 

The future of autism

For autism research to take the next leap forward, we need perhaps three big initiatives. First, we need genetic research on the scale seen for schizophrenia : tens and eventually hundreds of thousands of participants, with good information about each one's skills and difficulties. This scale of research is needed to deal with that heterogeneity in the autism spectrum, in order to discover gene pathways, and hence mechanisms, to optimize the outcome for each individual. 

Second, we need people with autism and their families to donate brain tissue when they die. These two aims are underway, thanks to initiatives (MSSNG and Autism BrainNet) funded by Autism Speaks and the Simons Foundation. 

The third initiative is arguably even more important: Create open-access, globally accessible diagnostic tools for low-income settings. More than 80 percent of research is carried out in high-income countries, with a bias of samples for wealthy white individuals, but 80 percent of those living with autism are in low-income countries. Diagnostic tools are currently highly expensive and impractical in these settings. 

Making ASD diagnosis and services available to all is not only a moral imperative, it is a scientific one — establishing rates and developmental trajectories in very different environments will shed light on the etiology and nature of autism. It is time for autism researchers to look outwards and think globally.

Follow all of the Expert Voices issues and debates — and become part of the discussion — on Facebook, Twitter and Google+. The views expressed are those of the author and do not necessarily reflect the views of the publisher. This version of the article was originally published on Live Science.

Child prodigies may share certain genetic traits with people who have autism, new research suggests.

The finding could help explain why the two groups share certain characteristics, such as exceptionally good memories. But the small number of child prodigies studied makes the findings preliminary, other scientists said.

In the study, researchers looked at DNA from 12 children with extraordinary abilities in music, mathematics or other fields. They also looked at 39 other people who were all members of the children's families, including 10 family members who had autism, and four prodigies who also had autism.

The researchers found there were genetic markers on chromosome 1 that were shared between the prodigies and their relatives with autism, the study authors said, though they have yet to find the specific mutations involved.

For the study, the researchers defined a prodigy as a child who achieved national or international recognition for a specific skill by adolescence. For example, one prodigy had played an entire DVD of classical music by ear at age 3, and earned a spot on a symphony by age 6, said study co-author Joanne Ruthsatz, an assistant professor of psychology at The Ohio State University.

Prodigies clearly share traits with children who have autism, such as exceptional memories and attention to detail, Ruthsatz told Live Science.

David Henry Feldman, chair of the Eliot-Pearson Department of Child Study and Human Development at Tufts University, agreed, telling Live Science in an email, "On the behavioral side, there seems to be a correlation between prodigies and autistic children that is hard to ignore."

However, a weakness of the study is its small number of participants — there were 12 prodigies, and four to 14 family members per prodigy in the study, Dr. Daniel Geschwind, director of the Center for Autism Research and Treatment at UCLA, who was not involved in the study, told Live Science in an email. [Beyond Vaccines: 5 Things that Might Really Cause Autism]

"The study is very small — not statistically convincing," Geschwind said. "The authors say the results are suggestive, so they are not making strong claims. But still, I am not sure there is anything really here."

The researchers would like to include more participants in future studies, but the rarity of child prodigies makes that difficult, Ruthsatz said. Over the past 100 years, the scientific literature has recorded fewer than 20 prodigies. Autism spectrum disorder, in contrast, affects an estimated 1 in 68 children, according to the Centers for Disease Control and Prevention.

The study's value comes primarily in raising new questions, Raphael Bernier, a University of Washington researcher and clinical director of the Autism Center at Seattle Children's Hospital, told Live Science.

"I think it's a great preliminary project," said Bernier, who was not involved in the study. "It starts asking the question about the relationship between prodigies and autism."

The finding, if confirmed, could also support one theory of autism: that the disorder results from long-distance-connectivity deficiencies in the brain, Bernier said.

In addition to seeking more subjects, Ruthsatz said she and colleagues are working with collaborators at McGill University in Montreal to sequence the specific mutations that may be involved. She also noted that, in the study, researchers looked at only the "100 most popular mutation sites," but in future work, the researchers will expand their search for shared regions to the entire genome.

Ruthsatz said she hopes further work will illuminate why the shared genetic variations benefit prodigies but cause dysfunction in autism. "We're now looking for the moderator that's shutting down the genes responsible for dysfunction in autism," she said. Finding such a gene could lead to new autism treatments, Ruthsatz said.

The study was published online March 10 in the journal Human Heredity.

Follow Michael Dhar @michaeldhar. Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science.

Another study has found no link between autism and the vaccine against measles, mumps and rubella (called the MMR vaccine). This time, the finding comes from a study of children at high risk of developing autism.

Although numerous studies have shown that vaccines do not cause autism, some parents still believe that vaccines and autism are related, and thus choose to not vaccinate their kids, researchers say.

In the new study, researchers examined health data and vaccination records of about 96,000 children who all had older siblings. The researchers found that there was no link between receiving the MMR vaccine and developing autism, even for the children who had an increased risk of autism because their older siblings had been diagnosed with the condition. Other studies have shown that having an older sibling with autism is a risk factor for developing the condition.

The researchers wanted to look at more data on the MMR vaccine and autism risk because "despite the research that shows no link between the MMR vaccine [and autism], parents continue to believe that the vaccine is contributing to autism," said study author Dr. Anjali Jain, of The Lewin Group, a health care consulting firm in Falls Church, Virginia. "Parents who already have a child with autism seem especially prone to this belief," Jain added.

Indeed, the researchers also found that the MMR vaccination rates were lower among the children whose older siblings had autism than among children whose older siblings did not have the condition.

Although the new study did not examine the reasons for the difference in these MMR vaccination rates, previous surveys have shown that some parents who have a child with autism blame the vaccine for the condition, the researchers said. These parents may choose to not vaccinate their younger kids.

Still, the new study shows that, even in high-risk families, there is no increased risk of autism related to the MMR vaccine, said Dr. Thomas Frazier, director of Cleveland Clinic Center for Autism, who was not involved in the new study.

Many large studies have shown that the MMR vaccine does not cause autism. For example, in a review of studies published by the Cochrane Library in 2012, which included a total of nearly 15 million children, researchers found no relationship between the vaccine and autism.

In another review, published in 2014 in the journal Vaccine, researchers analyzed the results of previous studies that included more than 1.26 million children, and again found no link between the vaccine and autism. In a review of 67 studies, published in 2014 in the journal Pediatrics, the authors concluded, "There is strong evidence that the MMR vaccine is not associated with autism."

Frazier explained why some parents might believe that vaccines cause autism, despite the scientific evidence that shows otherwise. "Unfortunately, it is a psychological problem; it is not a data problem," Frazier told Live Science. "So we could probably do a hundred more of these studies, and you would not actually change parents' behavior."

One reason parents might believe there's a cause-and-effect relationship between vaccines and autism is that the onset of autism symptoms often coincides with the time when kids get vaccinated, Frazier said. However, "in reality, they just happen to occur at the same time in development," he said. Still, it is tough to get this type of correlation out if people's minds, he added.

Parents who fear vaccinations may choose to not vaccinate their kids based on the argument that they don't want to actively hurt their children, Frazier said. "I think this is the exact reason why the vaccination debate never goes away: It is because it is not about data; it is about fear," he said.

"And so [parents] end up opting for 'I am going to decline vaccination,' which, unfortunately, has led to the place where, actually, it is more common now to have these diseases," such as measles, that can be prevented through vaccination, Frazier added.

The study was published today (April 21) in the Journal of the American Medication Association.

Follow Agata Blaszczak-Boxe on Twitter. Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science.

Women who develop gestational diabetes early in their pregnancy have a higher chance of having a child with autism than women who don't develop the condition, a new study suggests.

Researchers found that mothers-to-be who developed gestational diabetes — high blood sugar during pregnancy in women who have never had diabetes — by their 26th week of pregnancy were 63 percent more likely to have a child diagnosed with an autism spectrum disorder (ASD) compared with women who did not have gestational diabetes at any point during their pregnancy (and who also did not have type 2 diabetes prior to pregnancy).

The finding does not mean that autism is common among children born to women who had gestational diabetes.

"Autism is still rare," said study co-author Anny Xiang, a research scientist at Kaiser Permanente Southern California in Pasadena. The findings show that, although the risk of having a child with autism is still low among women who have gestational diabetes early in pregnancy (before 26 weeks), the study did find a relationship between these women and an increased risk that the child would have autism, Xiang said. [7 Ways Pregnant Women Affect Babies]

The study, published today (April 14) in the Journal of the American Medical Association, looked at more than 320,000 children born in Southern California between 1995 and 2009. About 8 percent of the kids were born to mothers who had pregnancy-related diabetes, and 2 percent had mothers with type 2 diabetes. 

During an average follow-up period of 5.5 years, nearly 3,400 children in the study were diagnosed with an ASD, including such conditions as autistic disorder and Asperger syndrome that can cause social, communication and behavioral problems in children. 

After the researchers considered other factors that can influence a child's chances of developing autism — such as the mother's age, education, income, ethnicity, prior pregnancies and the sex of the child (autism is five times more common in boys than in girls) — the impact of having gestational diabetes early in pregnancy was muted, but the link still held. Gestational diabetes by the 26th week of pregnancy was found to increase a child's risk of autism by 42 percent compared with the risk of autism for children whose moms did not have gestational diabetes when these factors were considered.

Early exposure

The exact reason for the link is unclear. However, one underlying factor could be that the early months of pregnancy are a critical time period for brain development, Xiang told Live Science.

If a developing fetus is exposed to elevated blood sugar levels during this important period of brain development, this may have some connection to the behavioral changes seen in autism after birth, she said.

Moreover, the study's other findings hint that elevated blood sugar during early pregnancy plays a role in the link. For example, the researchers found that children born to women who developed pregnancy-related diabetes after 26 weeks were not at greater risk of being diagnosed with autism than kids whose mothers never had type 2 or gestational diabetes.

In addition, the study found no increase in autism risk among the children born to women who knew they had type 2 diabetes before having a baby. This may be because these women are probably taking medication to control their blood sugar levels throughout pregnancy, Xiang said.

Because women who have no risk factors for diabetes may not be screened for the disease until the 24th to 28th weeks of pregnancy, gestational diabetes can go undetected during early pregnancy, she said.

Xiang cautioned that women who had gestational diabetes during pregnancy don't need to panic or worry. The results suggest that for every 1,000 mothers who had pregnancy-related diabetes by 26 weeks, seven children may develop autism spectrum disorders, Xiang said.

Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science.

Alysson Muotri is an associate professor in the Department of Pediatrics and Cellular & Molecular Medicine at the University of California, San Diego School of Medicine and Rady Children's Hospital San Diego. He contributed this article to Live Science's Expert Voices: Op-Ed & Insights.

Autism spectrum disorder (ASD) is a devastating human condition, a lifelong developmental disability that is confounding both in life — where it seems to appear suddenly and without warning in young children — and in the lab, where it steadfastly defies straightforward investigation and understanding.

Numerous studies of family histories and twins show that some cases of ASD are clearly heritable. But the vast majority of ASD cases are not familial or heritable, but rather occur sporadically or idiopathically — without obvious reason.

To find the cause or causes of ASD — which usually precede any discovery of effective new treatments or preventive measures, let alone something resembling a cure — scientists currently rely on an imperfect toolbox.

Probing the brain, human or not

The simplest and most direct method of studying the human brain is to probe the living organ directly. For myriad reasons, however, that approach is not practical, desirable or even sufficient — at least not with current technologies. Sometimes, scientists are able to examine postmortem tissues. In fact, this approach produced remarkable findings last year about developmental differences in the brains of autistic children. But it also presents its own set of challenges, including that study materials are an extraordinarily scarce resource. Live-imaging techniques are improving, but they are still relatively blunt analytical instruments.

More often, scientists turn to animal models, typically mice whose brains or behaviors have been modified to mimic aspects of ASD. In this sense, they are no different from the animal models used to study diabetes, cancer and many other human diseases.

But as much as rodents and humans share certain basic commonalities, there are also inherent differences in their genetic backgrounds, immune systems and brain circuits. Furthermore, animal models cannot represent the individual differences inherent in human populations. Simply put, mice are not tiny people; humans are a different species, and those differences can be significant. [Animal Data Is Not Reliable for Human Health Research (Op-Ed )]

Disease in a dish

Much more promising is the ongoing development of human biology-based models, such as induced pluripotent stem cells (iPSCs), derived without harm from autistic patients themselves. The iPSCs, transformed from ordinary cells into neurons, represent what's colloquially known as "disease in a dish." They can be cultured in abundance. They can be minutely studied for revelations about specific biochemical or cellular features that likely occur within developing fetal brains destined to be autistic. They can be exposed to possible damaging environmental factors and potential treatment drugs. 

But the science is not quite there yet. There are still limitations to overcome, but remarkable progress has been made. For example, my lab at the University of California, San Diego School of Medicine has used iPSCs derived from patients with Rett syndrome, a type of ASD, to examine how specific gene alterations cause dysfunction. More important, we have been able to rescue Rett-syndrome-derived neurons with candidate chemicals, reversing neuronal defects. Clinical trials based on this research have been launched in the United States and other countries.

More broadly, since our first report, others have shown that iPSCs can be used to model other types of autism, such as Fragile X syndrome, Timothy syndrome and even sporadic autism.

Some forms of ASD are quite rare. It's hard to attain a sample size sufficient to do good science with those conditions, but it's not impossible. One resource: the Tooth Fairy. Colleagues have begun asking parents of children with ASD to provide us with their "baby teeth," from which we extract dental pulp stem cells and reprogram them as neurons. Currently, we have more than 300 samples collected from a list of more than 3,500 families in the U.S. and Brazil. 

These iPSCs can be studied not just for what they might reveal at molecular and genomic levels, but they also can be compared over time to the clinical outcomes of their former owners. 

iPSCs can be grown in three dimensions. They self-organize into spheres that resemble a 9-week-old developing human fetus brain. Obviously, these spheres aren't exactly minibrains. Some components are missing or in the wrong places. But they offer an unprecedented panorama of very early brain development and how things can go wrong. 

Beyond models, and on to solutions

Advances in tissue engineering, such as the ability to create skin and cartilage in a lab, will eventually lead to the ability to build human neuronal microcircuits that replicate some of the dynamic interactions that take place in the body. These living microcircuits would be a sort of in vitro-in vivo model — a "brain on a chip" that would allow neuroscientists to observe and manipulate whole systems, not just single cells. 

These are still the early stages of exploration of these techniques, and much remains to be done. The brain does not give up its secrets readily. But all of these approaches — combined with prioritized research funding to speed advances in systems biology, computational simulations, human brain imaging and population genetics — suggest the future of ASD research is bright. With that comes the promise of improved diagnoses, treatments and better lives for those suffering with autism.

Follow all of the Expert Voices issues and debates — and become part of the discussion — on Facebook, Twitter and Google+. The views expressed are those of the author and do not necessarily reflect the views of the publisher. This version of the article was originally published on Live Science.