By Azeen Ghorayshi As a child, Jodie Singer barely spoke. She could repeat words that people said to her or recite the book “Madeline” from beginning to end, but she could not answer yes or no when her mother asked if she wanted juice. Sometimes she hurt herself, compulsively tearing at the skin and hair on the nape of her neck. She threw tantrums, thrashing and refusing to be comforted. When she was almost 3, Jodie was given a diagnosis of autism. Now 28, she still speaks only in short, repetitive phrases and requires round-the-clock care, including help eating, getting dressed and using the toilet. At the time Jodie’s diagnosis was first made, the definition of autism was expanding, as it would continue to do over the next 25 years. Once primarily limited to severely disabled people, autism began to be viewed as a spectrum that included far less impaired children and adults. Along the way, it also became an identity, embraced by college graduates and even by some of the world’s most successful people, like Elon Musk and Bill Gates. That broadening of the diagnosis, autism experts believe, along with the increasing awareness of the disorder, is largely responsible for the steep rise in autism cases that Health Secretary Robert F. Kennedy Jr. has called “an epidemic” and has attributed to theories of causality that mainstream scientists reject, like vaccines and, more recently, Tylenol. And the diagnostic expansion has now become a flashpoint in a long-running debate over how autism should defined, one that has divided parents and activists, ignited social media battles and grown fiercer with Mr. Kennedy’s laser focus on autism. Speaking of autistic children in the spring, Mr. Kennedy said, “These are kids who will never pay taxes, they’ll never hold a job, they’ll never play baseball, they’ll never write a poem, they’ll never go out on a date.” His words drew a swift backlash from many autistic adults, who called his characterization of their lives false and dehumanizing. But Jodie’s mother, Alison Singer, said that, though she disagrees with Mr. Kennedy’s views on the causes of autism, his words about the harsh realities of living with the disorder spoke to families like her own. © 2025 The New York Times Company

Keyword: Autism
Link ID: 29947 - Posted: 10.01.2025

By Bethany Brookshire Even hearing the phrase “Huntington’s disease” will make a room suddenly somber. So the joy that accompanied a recent announcement of results of an experimental gene therapy for the deadly diseases signaled an unfamiliar sense of hope. In a small clinical trial, brain injections of a virus that codes for a tiny segment of RNA may have prevented the formation of the rogue proteins that make Huntington’s so devastating. The early results, announced September 24 in a news release, show that over three years, the treatment slowed Huntington’s progression by up to 75 percent. While not a cure, the treatment could potentially give people living with Huntington’s disease, who might otherwise face early disability and death, the gift of many more years of life. “We’re doing science because it’s interesting and important, but we’re also in this game to save our friends and family from a horrible fate,” says Ed Wild, a neurologist at University College London. “That’s the most meaningful thing, looking my friends in the eye and [saying], ‘We did it.’” Huntington’s disease currently has no effective treatments or cures. It is relatively rare, affecting about 7 out of every 100,000 people, and is the result of mutation in a single gene, appropriately called huntingtin. In the disease, that gene is mutated in only one way, making the front end of the resulting protein grow, says Russell Snell, a geneticist at the University of Auckland in New Zealand who was not involved in the study. This expanded huntingtin is a protein gone toxic. It aggregates in the brain and kills cells largely in brain areas crucial for voluntary movements. Patients end up with increasing involuntary movements, stiffness, difficulties speaking and swallowing and cognitive decline. Huntington’s is genetically dominant — it takes only one copy of the defective gene to cause it — so a patient’s offspring have a 50 percent chance of inheriting the disease. Wild and his colleagues, working with the Dutch pharmaceutical company uniQure, used microRNA — tiny segments of RNA that can trigger machinery to break down huntingtin RNA before it gets made into protein. Some other trials have tried simply injecting some of these RNAs, but have not succeeded, possibly because they were injected into the cerebrospinal fluid and couldn’t infiltrate the right areas of the brain. This time, the scientists injected them directly into the brain, packaged inside a well-studied viral vector. The virus would “infect” neurons in the brain with the RNA, and “it basically reprograms the neuron to become a factory for a molecule that tells it not to make huntingtin protein,” Wild says. © Society for Science & the Public 2000–2025.

Keyword: Huntingtons; Genes & Behavior
Link ID: 29946 - Posted: 09.27.2025

Hannah Devlin Science correspondent Huntington’s disease, a devastating degenerative illness that runs in families, has been treated successfully for the first time in a breakthrough gene therapy trial. The disease, caused by a single gene defect, steadily kills brain cells leading to dementia, paralysis and ultimately death. Those who have a parent with Huntington’s have a 50% chance of developing the disease, which until now has been incurable. The gene therapy slowed the progress of the disease by 75% in patients after three years. Prof Sarah Tabrizi, the director of University College London’s Huntington’s disease centre, who led the trial, said: “We now have a treatment for one of the world’s more terrible diseases. This is absolutely huge. I’m really overjoyed.” The drug, which inactivates the mutant protein that causes Huntington’s, is delivered to the brain in a single shot during a 12- to 20-hour surgical procedure, meaning that it will be expensive. The breakthrough is sending ripples of hope through the Huntington’s community, many of whom have witnessed the brutal impact of the disease on family members. The first symptoms, which typically appear when the affected person is in their 30s or 40s, include mood swings, anger and depression. Later patients develop uncontrolled jerky movements, dementia and ultimately paralysis, with some people dying within a decade of diagnosis. With treatment, people would be able to work and live independently for significantly longer, Tabrizi said, and the dramatic impact of the therapy raises the possibility that it could prevent symptoms occurring if given at an earlier stage. © 2025 Guardian News & Media Limited

Keyword: Huntingtons; Genes & Behavior
Link ID: 29945 - Posted: 09.27.2025

Heidi Ledford After a mouse received treatment to eliminate immune cells called microglia, it was injected with human progenitor cells that developed into human immune cells (green, pink and blue) in the animal’s brain.Credit: M. M.-D. Madler et al./Nature A fresh supply of the immune cells that keep the brain tidy might one day help to treat a host of conditions, from ultra-rare genetic disorders to more familiar scourges, such as Alzheimer’s disease. In the past few months, a spate of new studies have highlighted the potential of a technique called microglia replacement and explored ways to make it safer and more effective. “This approach is very promising,” says Pasqualina Colella, who studies gene and cell therapy at Stanford University School of Medicine in California. “But the caveat is the toxicity of the procedure.” Microglia are immune cells that patrol the brain, gobbling up foreign invaders, damaged cells and harmful substances. They can help to protect neurons — cells that transmit and receive messages to and from other tissues — during seizures and strokes, and they prune unneeded connections between neurons during normal brain development. “Microglia do a lot of important things,” says Chris Bennett, a psychiatrist who studies microglia at the Children’s Hospital of Philadelphia in Pennsylvania. “So, it’s not surprising that they are involved in the pathogenesis of many diseases.” Those diseases include a suite of rare disorders caused by genetic mutations that directly affect microglia. Malfunctioning microglia have also been implicated in more familiar conditions with complex causes, such as Alzheimer’s disease and Parkinson’s disease, as well as ageing, says Bo Peng, a neuroscientist at Fudan University in Shanghai, China. © 2025 Springer Nature Limited

Keyword: Development of the Brain; Glia
Link ID: 29944 - Posted: 09.27.2025

By Calli McMurray The authors behind a contentious 2022 Science paper that purported to measure neuronal activity using functional MRI (fMRI) retracted the work today. The retraction marks the end of the road for the method, called “direct imaging of neuronal activity,” or DIANA, says Noam Shemesh, principal investigator at the Champalimaud Centre for the Unknown, who was not involved in the now-retracted work. But many neuroimaging researchers still hope to one day use fMRI to capture neuronal activity. “MRI is such a rich modality. It has such rich physics, and not all of it has been exploited in the functional sense,” Shemesh says. DIANA collected fMRI data in a way that enabled the researchers to measure signal changes on the order of tens of milliseconds. The team, led by Jang-Yeon Park at Sungkyunkwan University, captured a signal peak in the somatosensory cortex of mice 25 milliseconds after shocking their whisker pads. Despite an initial flurry of excitement from the field, other labs could not replicate the results. As a result, the paper received an editorial expression of concern in August 2023 because “the methods described in the paper are inadequate to allow reproduction of the results and … the results may have been biased by subjective data selection,” the notice states. Following the editorial expression of concern, “we reanalyzed the data. Unfortunately, the additional results revealed unexpected MR signal characteristics and did not robustly support the original conclusions. We are therefore retracting the paper,” the retraction notice states. Science did not have any additional comment beyond what is outlined in the expression of concern and retraction notice. © 2025 Simons Foundation

Keyword: Brain imaging
Link ID: 29943 - Posted: 09.27.2025

By Roni Caryn Rabin Women who are pregnant, planning a pregnancy or breastfeeding should be screened for cannabis use and strongly discouraged from it, the American College of Obstetricians and Gynecologists said in new clinical guidelines published on Friday. Cannabis use during pregnancy has been rising for years. Many women rely on the drug to cope with nausea and other pregnancy symptoms. But the college warned that mounting evidence linked cannabis to preterm births, low birth weights and a greater need for neonatal intensive care, as well as neurocognitive and behavioral problems in children. “Patients are often using cannabis to help with some kind of medical ailment, not recreationally — in their mind, they think it’s a more natural way to deal with a medical problem,” said Dr. Melissa Russo, an author of the new guidance. “But there are lots of natural things that are not safe,” Dr. Russo said. There are no studies demonstrating that cannabis is effective for pregnant or lactating women, she added, “and research now shows there are potential adverse effects.” The college warned against blood or urine tests for cannabis screening. Instead, it urged physicians to talk with women about their habits, and to encourage them to stop using marijuana as soon as possible while offering alternative therapies for medical ailments. The screening should be universal in an effort to avoid bias and racism, the college said. It noted that pregnant Black and Hispanic women are four to five times as likely as white women to be tested for drug use. Black women are almost five times as likely to be reported to child protective services for suspected drug use. The new guidelines say that cannabis should be discouraged among breastfeeding women, but that breastfeeding should continue even with use of the drug because the benefits most likely outweigh the potential risks. © 2025 The New York Times Company

Keyword: Drug Abuse; Development of the Brain
Link ID: 29942 - Posted: 09.24.2025

Jon Hamilton In a White House press conference Monday, President Trump and several deputies said the Food and Drug Administration would be updating drug labeling to discourage the use of acetaminophen by pregnant women, suggesting a link between the common painkiller and autism. Federal officials also said they would be changing the label for leucovorin, a form of vitamin B typically used in conjunction with cancer treatment, to enable its use as a treatment for autism. And they added that state Medicaid programs, in partnership with the federal Centers for Medicare & Medicaid Services, would cover this use. The suite of changes was announced despite a notable lack of clear scientific evidence to support these moves. The changes were presented as part of what the administration said was its commitment to identify the root causes of autism, diagnoses of which have increased in recent years. Flanked by Health and Human Services Secretary Robert F. Kennedy Jr. and Centers for Medicare and Medicaid head Dr. Mehmet Oz, President Trump pinned substantial blame for rising autism rates on the common painkiller, which is also known by its brand name, Tylenol. "Taking Tylenol is not good — I'll say it: It's not good," he said, suggesting without evidence that communities without access to the medicine have "no autism," while in others, autism now affects 1 in 12 boys. (An estimated 1 in 31 children in the U.S. are diagnosed with autism.) Trump discouraged giving acetaminophen to babies, as well. (He also suggested that vaccines and their frequency may be a culprit in causing autism, an oft-repeated claim that has been debunked by decades of research.) © 2025 npr

Keyword: Autism
Link ID: 29941 - Posted: 09.24.2025

By Christina Caron Dr. Marty Makary, the commissioner of the Food and Drug Administration, announced on Monday that the agency would be modifying the label of a relatively obscure medicine so that “it can be available for children with autism.” He was referring to leucovorin, or folinic acid, a modified version of vitamin B9, also known as folate — which is naturally found in beans, leafy greens, eggs, beets and citrus. Folate helps the body make red blood cells and is important for cell growth. It’s especially crucial during early pregnancy to lower the risk of major birth defects in a baby’s brain or spine. Studies suggest that folate levels can affect our health in various ways, and scientists are researching what role folate plays in depression, dementia, heart disease and autism. Some people have antibodies that interfere with how folate is transported within the body, and small studies suggest that a number of people with autism — in some cases up to 75 percent — may have these antibodies. In a Federal Register notice filed on Monday, the F.D.A. said it was approving leucovorin tablets for people with “cerebral folate deficiency,” based on a review of studies from 2009 to 2024 that found that they “improve certain symptoms.” The agency, noting that more studies were needed, cited one study that compared 40 people on the medication and 40 on a placebo; those who took the medication showed “substantial improvement” of the deficiency symptoms. The medicine has been used off-label to treat people diagnosed with cerebral folate deficiency for about two decades. Symptoms of cerebral folate deficiency usually begin to show up around the age of 2 when children start to experience speech difficulties, intellectual disabilities and, in some cases, seizures. They may also have tremors and difficulty controlling their muscle movements. © 2025 The New York Times Company

Keyword: Autism
Link ID: 29940 - Posted: 09.24.2025

Rachel Fieldhouse Last week, a study involving more than nine million pregnancies reported that children whose mothers had gestational diabetes during pregnancy had a higher chance of developing attention deficit–hyperactivity disorder (ADHD) and autism than did children whose mothers didn’t have the condition. The study, presented at the European Association for the Study of Diabetes in Vienna, is under review at a peer-reviewed journal. It is not the first to link gestational diabetes to neurodevelopmental disorders in children, but it is one of the largest. Researchers pooled results from 48 studies across 20 countries, finding that children born to people with gestational diabetes had lower IQ scores, a 36% higher risk of ADHD and a 56% higher risk of autism spectrum disorders. Estimates suggest the prevalence of autism in the general population is one in 127 people1 and between 3-10%2 of children and teenagers have ADHD. The latest results mirror those of another meta-analysis3 published in The Lancet Diabetes & Endocrinology journal in June, which included 56 million mother–child pairs and found that all types of diabetes in pregnancy, including type 1, type 2 and gestational diabetes, increase the risk of the baby developing ADHD and autism. But none of these studies have been able to show that diabetes during pregnancy causes these conditions. “There’s no doubt that there is a signal here, but certainly further research is required,” says Alex Polyakov, an obstetrician and researcher at the University of Melbourne in Australia. Long a topic of research, the causes of autism have been thrust into the spotlight by the administration of US President Donald Trump. On Sunday, while speaking at the memorial for conservative activist Charlie Kirk, Trump said: “I think we found an answer to autism. How about that?” © 2025 Springer Nature Limited

Keyword: Autism
Link ID: 29939 - Posted: 09.24.2025

By Brandon Keim Should you meet a turtle basking on a log in the sun, you might reasonably conclude that the turtle is in a good mood. Granted, there has been little scientific evidence that reptiles experience such emotional richness — until now, at least. Researchers in England identified what they describe as “mood states” — emotional experiences that are more than momentary — in red-footed tortoises by administering cleverly designed tests that use responses to ambiguity as windows into the psyche. The results of the study, published in the journal Animal Cognition in June, could apply to many more reptiles and have profound implications for how people treat them. “There was an acceptance that reptiles could do these short-term emotions,” said Oliver Burman, who studies animal behavior at the University of Lincoln in England and is an author of the paper. “They could respond to positive things and unpleasant things. But the long-term mood states are really important.” As for why it took so long to show this in reptiles, Dr. Burman said, “maybe we just haven’t asked them correctly.” Reptiles have a longstanding reputation as being unintelligent. Writing in 1892, Charles Henry Turner, the pioneering comparative psychologist, described reptiles as “intellectual dwarfs.” Eight decades later, in 1973, prominent scientists were referring to them as “reflex machines” and (in a paper titled “The Evolutionary Advantages of Being Stupid”) as possessing “a very small brain which does not function vigorously. Dr. Burman is among the scientists responsible for what some have called a “reptilian renaissance.” An array of findings — tortoises learning from one another, snakes with social networks, crocodiles displaying complex communication — indicate that reptiles are no less brainy than mammals and birds. © 2025 The New York Times Company

Keyword: Emotions; Evolution
Link ID: 29938 - Posted: 09.20.2025

By Sara Kiley Watson Humans started brewing alcohol for consumption thousands of years ago, and researchers have suggested that our ability to break down booze in our bodies has evolutionary roots dating back millions of years. Alcohol, known to scientists as ethanol, occurs naturally throughout nature, when microbes like bacteria and yeast break down sugars. This process of fermentation, harnessed by humans since ancient times, has given us the gifts of cheese, pickles, and wine, among other delights.* Nautilus Members enjoy an ad-free experience. Log in or Join now . But humans are far from the only creatures that imbibe—aye ayes, a species of lemur, will seek out nectar with a higher alcohol content, and spider monkey urine has been found to contain secondary metabolites of alcohol. Wild chimps, with whom humans share over 95 percent of our DNA, were caught on film snacking on fermenting fruit with their buddies earlier this year. Now, for the first time, researchers have discovered just how much alcohol some chimps are getting out of their fermented fruit snacks. In a new paper published in Science Advances, a team of scientists from the United States and the Ivory Coast reported that, in the course of a day, the wild chimps in their study consumed about 14 grams of pure ethanol. That’s about the equivalent, adjusting for body mass, of a human imbibing more than one standard drink a day, says University of California, Berkeley graduate student and study author Aleksey Maro. “We can say, pretty officially, that animals are chronically ingesting ethanol, especially our chimpanzee relatives,” Maro says. Maro and his colleagues made their discovery by following around wild chimps at two national parks in Africa—Kibale in Uganda and Taï in Ivory Coast—and scooping up test samples of 20 species of ripe fruits that the chimps typically like to eat. What they found is that these fruits have an average alcohol content of around 0.26 percent by weight. That might not sound like much, but primatologists at these locations estimate that chimps eat a whopping 10 pounds—or some 7 to 14 percent of their body weight—of fruit a day. The apes tended to prefer a fig called the Ficus mucuso at Kibale and the plum-esque fruit from Parinari excelsa trees at Taï. These treats were among the fruits with the highest alcohol content. © 2025 NautilusNext Inc.,

Keyword: Drug Abuse; Evolution
Link ID: 29937 - Posted: 09.20.2025

By Calli McMurray Studying animal behavior in the wild often gets hairy, with little experimental control and an abundance of extraneous data. And when multiple animals get together, the way they look, act and smell all influence one another, making it difficult to parse complex social interactions, says Andres Bendesky, associate professor of ecology, evolution and environmental biology at Columbia University. Robotic or animated partners, however, can simplify that equation. Studying animal-robot interaction gives researchers complete control over one partner during any tête-à-tête, Bendesky says. It makes it possible to present the same stimulus to an animal repeatedly or compare how different individuals react. And the method complements observation-based research: Scientists can use a robot- or animation-based paradigm to test ideas gleaned from studies that use artificial-intelligence tools to track behavior. Bendesky is part of a growing cohort of neuroscientists turning to robots to help them decode social interactions. The quirks are still being ironed out, but the approach is already helping several groups tackle questions about schooling, fighting and chatting behaviors. The rigor of the results depends on whether a critter believes what it sees, says Tim Landgraf, professor of artificial and collective intelligence at Freie Universität Berlin, who uses robots to study group behavior in guppies. That can be hard to gauge; there’s no handbook that describes what traits make a robot believable, he says. But researchers can compare how animals act toward a real peer versus a counterfeit one, says Steve Chang, associate professor of psychology and neuroscience at Yale University, who doesn’t work with robots but studies the social behavior of macaques and marmosets. © 2025 Simons Foundation

Keyword: Robotics; Sexual Behavior
Link ID: 29936 - Posted: 09.20.2025

By Catherine Offord As the National Football League’s (NFL’s) latest season gets underway, so, too, does the conversation about the risk of serious brain damage to its athletes. Multiple well-publicized studies in recent years have linked repetitive head impacts typical in football and other contact sports to an increased likelihood of chronic traumatic encephalopathy (CTE), a neurodegenerative condition characterized by a buildup of misfolded proteins in the brain. Now, a leading CTE research group reports evidence that regular sports-related impacts could cause brain damage before the condition’s hallmark features appear. An analysis of postmortem brain tissue from athletes and nonathletes who died before their early 50s, published today in Nature, identifies multiple cellular differences between the groups, regardless of whether CTE was present. The findings support the idea that contact sports are associated with specific cellular changes in the brain. The study also “helps us understand, or at least ask new questions about, the mechanisms that bridge that acute exposure to later neurodegeneration,” says Gil Rabinovici, a neurologist and researcher at the University of California San Francisco who was not involved in the work. But not many brains were examined—fewer than 30 for most analyses. And the study doesn’t show that the neuron loss and other brain changes affect a person’s cognitive or mental health, cautions Colin Smith, a neuropathologist at the University of Edinburgh. “What does this mean clinically? … That is still the big question hanging here.” CTE recently hit the headlines again after a shooter killed four people and himself in the New York City building housing NFL’s headquarters this summer. In a note found by police, the former high school football player reportedly said he thought he had CTE, and asked that his brain be studied.

Keyword: Brain Injury/Concussion
Link ID: 29935 - Posted: 09.20.2025

Chris Simms A wearable device could make saying ‘Alexa, what time is it?’ aloud a thing of the past. An artificial intelligence (AI) neural interface called AlterEgo promises to allow users to silently communicate just by internally articulating words. Sitting over the ear, the device facilitates daily life through live communication with the Internet. “It gives you the power of telepathy but only for the thoughts you want to share,” says AlterEgo’s chief executive Arnav Kapur, based in Cambridge, Massachusetts. Kapur unveiled the device on 8 September. The device does not read brain activity, but predicts what a wearer wants to say from signals in muscles used to speak, then sends audio information back into their ear. The researchers say that their non-invasive technology could help people with motor neuron disease (amyotrophic lateral sclerosis; ALS) and multiple sclerosis (MS) who have trouble speaking, but also want to make the devices commercially available for general use. In a promotional video on the AlterEgo website, Kapur says that “it’s a revolutionary breakthrough with the potential to change the way we interact with our technology, with one another and with the world around us”. “The big question about this is ‘how likely is that potential to be realized?,” says Howard Chizeck, an electrical and computer engineer at the University of Washington in Seattle. Chizeck says that the technology seems workable and is less of a privacy risk than listening devices such as Amazon’s Alexa are, but isn’t convinced that the device will catch on for commercial use. © 2025 Springer Nature Limited

Keyword: Robotics; Language
Link ID: 29934 - Posted: 09.20.2025

By Meghan Rosen Maybe you’ve seen an influencer make French fries out of almond flour. Or a sandwich recipe that swaps bread for fried cheese. They’re called keto meals, and they’re largely shared for one reason: to help people lose weight. In the ketogenic diet, fat is king, and carbs are public enemy number one. Going keto means restricting carbs to the bare minimum and replacing those lost calories with fat. It’s the antithesis of the low-fat diet craze of the 1990s. Losing fat on keto diets typically means eating fat — and lots of it. The idea may sound paradoxical. But without our typical go-to energy source (sugar), our bodies learn to rely on a different type of fuel. In keto dieters, the liver converts fat into molecules called ketone bodies, which the body can burn instead of sugar. That can lead to weight loss, despite an unusually high intake of fat. Such results may explain why so many Americans have tried the keto diet on for size. “I think a lot of people look at a ketogenic diet and think, ‘I’ll lose weight, I’ll be healthier,’” says Molly Gallop, a physiologist at Earlham College in Richmond, Ind. On the surface, they may be right. But staying on the diet long-term could carry some risks, a new study in mice suggests. Mice fed a ketogenic diet for up to about a year — decades in human time — experienced health problems including glucose intolerance and signs of liver and cardiovascular disease, Gallop and her colleagues report September 19 in Science Advances. The work uncovers some potential hidden costs to going keto, says physiologist Amandine Chaix, at the University of Utah in Salt Lake City. “It’s a cautionary tale,” she says. People sticking to this high-fat plan need to be careful, she says, “because this is not a magical dietary approach.” © Society for Science & the Public 2000–2025.

Keyword: Obesity
Link ID: 29933 - Posted: 09.20.2025

By Sujata Gupta Anne-Laure Le Cunff was something of a wild child. As a teenager, she repeatedly disabled the school fire alarm to sneak smoke breaks and helped launch a magazine filled with her teachers’ fictional love lives. Later, as a young adult studying neuroscience, Le Cunff would spend hours researching complex topics but struggled to complete simple administrative tasks. And she often obsessed over random projects before abruptly abandoning them. Then, three years ago, a colleague asked Le Cunff if she might have attention-deficit/hyperactivity disorder, or ADHD, a condition marked by distractibility, hyperactivity and impulsivity. Doctors confirmed her colleague’s suspicions. But fearing professional stigma, Le Cunff — by then by then a postdoctoral fellow in the ADHD Lab at King’s College London — kept her diagnosis secret until this year. Le Cunff knew all too well about the deficits associated with ADHD. But her research — and personal experience — hinted at an underappreciated upside. “I started seeing … breadcrumbs pointing at a potential association between curiosity and ADHD,” she says. People within the ADHD community have long recognized that the condition can be both harmful and helpful. Researchers, though, have largely focused on the harms. And those studying treatments tend to define success as a reduction in ADHD symptoms, with little regard to possible benefits. That’s starting to change. For instance, Norwegian researchers asked 50 individuals with ADHD to describe their positive experiences with the disorder as part of an effort to develop more holistic treatments. People cited their creativity, energy, adaptability, resilience and curiosity, researchers reported in BMJ Open in October 2023. © Society for Science & the Public 2000–2025.

Keyword: ADHD; Attention
Link ID: 29932 - Posted: 09.17.2025

Rachel Fieldhouse Deep in the rainforests of the Democratic Republic of the Congo, Mélissa Berthet found bonobos doing something thought to be uniquely human. During the six months that Berthet observed the primates, they combined calls in several ways to make complex phrases1. In one example, bonobos (Pan paniscus) that were building nests together added a yelp, meaning ‘let’s do this’, to a grunt that says ‘look at me’. “It’s really a way to say: ‘Look at what I’m doing, and let’s do this all together’,” says Berthet, who studies primates and linguistics at the University of Rennes, France. In another case, a peep that means ‘I would like to do this’ was followed by a whistle signalling ‘let’s stay together’. The bonobos combine the two calls in sensitive social contexts, says Berthet. “I think it’s to bring peace.” The study, reported in April, is one of several examples from the past few years that highlight just how sophisticated vocal communication in non-human animals can be. In some species of primate, whale2 and bird, researchers have identified features and patterns of vocalization that have long been considered defining characteristics of human language. These results challenge ideas about what makes human language special — and even how ‘language’ should be defined. Perhaps unsurprisingly, many scientists turn to artificial intelligence (AI) tools to speed up the detection and interpretation of animal sounds, and to probe aspects of communication that human listeners might miss. “It’s doing something that just wasn’t possible through traditional means,” says David Robinson, an AI researcher at the Earth Species Project, a non-profit organization based in Berkeley, California, that is developing AI systems to decode communication across the animal kingdom. As the research advances, there is increasing interest in using AI tools not only to listen in on animal speech, but also to potentially talk back. © 2025 Springer Nature Limited

Keyword: Animal Communication; Language
Link ID: 29931 - Posted: 09.17.2025

Andrew Gregory Health editor A daily pill for weight loss can help people reduce their body weight by as much as a fifth, according to a trial that could pave the way for millions more people to shed pounds. The drug, called orforglipron, is manufactured by Eli Lilly and targets the same GLP-1 receptors as weight loss injections such as Mounjaro and Wegovy. In a trial of 3,127 adults, one in five people who took the once-a-day tablet for 72 weeks lost 20% or more of their body weight. Weight loss jabs have been transformative but pill versions are seen as a holy grail because they are easier to store, distribute and administer and are also expected to be cheaper, offering fresh hope for the millions of people trying to lose weight. Orforglipron is a GLP-1 agonist, a type of medication that helps lower blood sugar levels, slows the digestion of food and can reduce appetite. The weight loss seen among people taking the tablet is not as stark as that among patients taking tirzepatide (Mounjaro), which is also made by Eli Lilly, but experts believe the tablet will be more accessible and convenient compared with injections. Orforglipron is not yet approved by the US Food and Drug Administration (FDA) or regulators in other countries. Eli Lilly has said it expects substantial demand when the new pill is launched. The company published a snapshot of the results in August and the full paper detailing the findings has now been published in the New England Journal of Medicine and presented to the annual meeting of the European Association for the Study of Diabetes in Vienna, Austria. © 2025 Guardian News & Media Limited

Keyword: Obesity
Link ID: 29930 - Posted: 09.17.2025

Nic Fleming In the early 2000s, Brazilian nutrition researcher Carlos Monteiro made a puzzling discovery that led to an epiphany. While trawling survey data on household spending to try to understand why rates of obesity and type 2 diabetes were rising so rapidly in his home country, he was surprised to note that people were buying smaller quantities of sugar, salt and other ingredients generally associated with these conditions than they had in previous decades. Only when Monteiro and his colleagues dug deeper did they find the culprit. People were buying less sugar to prepare cakes and desserts, but eating more of it in pre-made pastries and breakfast cereal. They were buying less salt, but consuming more of it in frozen pizzas, chicken nuggets and dehydrated packet soups. “We realized the problem was our traditional dietary patterns were being replaced by foods that are processed so many times that they can no longer be recognized in the final products. We called them ultra-processed foods.” Monteiro, a nutrition and public-health researcher at the University of São Paulo, first used the term ultra-processed food (UPF) in a paper in 2009, arguing that people interested in promoting healthy diets should focus more on the degree, extent and purpose of processing than on nutrient profiles1. It was a radical idea that caught the attention of other researchers, who, over the next decade or so, published dozens of papers linking UPFs with obesity and a range of other health problems. Governments took notice, too. In 2014, Brazil began advising people to avoid UPFs. Other countries, including France, Belgium and Israel, followed suit. Robert F. Kennedy Jr, secretary of the US Department of Health and Human Services (HHS), has been a critic of UPFs, saying in January that they are “poisoning the American people”. In May, the US government announced plans for a research agenda to support nutrition policy and improve people’s diets, in part by improving understanding of the impacts of UPFs on health. © 2025 Springer Nature Limited

Keyword: Obesity
Link ID: 29929 - Posted: 09.17.2025

By Claudia López Lloreda Mouse pups, like other infants across the animal kingdom, cry to get their mother’s attention. The oxytocin system drives this communication and shapes how baby mice interact when reunited with their mothers, according to a study out today in Science. Oxytocin, known colloquially as the “love” or “cuddle” hormone, stimulates milk release during nursing and promotes maternal care behaviors. But most oxytocin research thus far has focused solely on the mother, overlooking the neuropeptide’s potential effects on an infant’s brain and behavior. This new study shows “the other half of the equation to what we already knew,” says Zoe Donaldson, associate professor of behavioral neuroscience at the University of Colorado Boulder, who was not involved with the study. Oxytocin is “this social signal that ultimately reinforces relationships,” she says. The work employed a novel optogenetic tool that enabled the team to turn off neurons deep in the hypothalamus of mouse pups. After being separated from their mothers for three hours, the pups vocalized more using distinct patterns when reunited with their mothers than did pups that had not been separated, a process controlled by oxytocin neurons in the pups’ hypothalamus, the team found. “It would make sense if oxytocin is on both sides of this: making moms want to take care of their pups that are calling, and making pups call in a manner that makes mom want to take care of them,” Donaldson says. “Then we have this sort of convergence where oxytocin is once again doing everything.” © 2025 Simons Foundation

Keyword: Sexual Behavior; Animal Communication
Link ID: 29928 - Posted: 09.13.2025