By Roni Caryn Rabin Water fluoridation is widely seen as one of the great public health achievements of the 20th century, credited with substantially reducing tooth decay. But there has been growing controversy among scientists about whether fluoride may be linked to lower I.Q. scores in children. A comprehensive federal analysis of scores of previous studies, published this week in JAMA Pediatrics, has added to those concerns. It found a significant inverse relationship between exposure levels and cognitive function in children. Higher fluoride exposures were linked to lower I.Q. scores, concluded researchers working for the National Institute of Environmental Health Sciences. None of the studies included in the analysis were conducted in the United States, where recommended fluoridation levels in drinking water are very low. At those amounts, evidence was too limited to draw definitive conclusions. Observational studies cannot prove a cause-and-effect relationship. Yet in countries with much higher levels of fluoridation, the analysis also found evidence of what scientists call a dose-response relationship, with I.Q. scores falling in lock step with increasing fluoride exposure. Children are exposed to fluoride through many sources other than drinking water: toothpaste, dental treatments and some mouthwashes, as well as black tea, coffee and certain foods, such as shrimp and raisins. Some drugs and industrial emissions also contain fluoride. For every one part per million increase in fluoride in urinary samples, which reflect total exposures from water and other sources, I.Q. points in children decreased by 1.63, the analysis found. “There is concern that pregnant women and children are getting fluoride from many sources,” said Kyla Taylor, an epidemiologist at the institute and the report’s lead author, “and that their total fluoride exposure is too high and may affect fetal, infant and child neurodevelopment.” © 2025 The New York Times Company

Keyword: Intelligence; Development of the Brain
Link ID: 29625 - Posted: 01.11.2025

By Kristel Tjandra Close your eyes and picture an apple—what do you see? Most people will conjure up a vivid image of the fruit, but for the roughly one in 100 individuals with aphantasia, nothing will appear in the mind’s eye at all. Now, scientists have discovered that in people with this inability to form mental images, visual processing areas of the brain still light up when they try to do so. The study, published today in Current Biology, suggests aphantasia is not caused by a complete deficit in visual processing, as researchers have previously proposed. Visual brain areas are still active when aphantasic people are asked to imagine—but that activity doesn’t translate into conscious experience. The work offers new clues about the neurological differences underlying this little-explored condition. The study authors “take a very strong, mechanistic approach,” says Sarah Shomstein, a vision scientist at George Washington University who was not involved in the study. “It was asking the right questions and using the right methods.” Some scientists suspect aphantasia may be caused by a malfunction in the primary visual cortex, the first area in the brain to process images. “Typically, primary cortex is thought to be the engine of visual perception,” says Joel Pearson, a neuroscientist at the University of New South Wales Sydney who co-led the study. “If you don’t have activity there, you’re not going to have perceptual consciousness.” To see what was going on in this region in aphantasics, the team used functional magnetic resonance imaging to measure the brain activity of 14 people with aphantasia and 18 neurotypical controls as they repeatedly saw two simple patterns, made up of either green vertical lines or red horizontal lines. They then repeated the experiment, this time asking participants to simply imagine the two images.

Keyword: Attention; Vision
Link ID: 29624 - Posted: 01.11.2025

By Christina Caron Barrie Miskin was newly pregnant when she noticed her appearance was changing. Dark patches bloomed on her skin like watercolor ink. A “thicket” of hairs sprouted on her upper lip and chin. The outside world was changing, too: In her neighborhood of Astoria, Queens, bright lights enveloped objects in a halo, blurring her vision. Co-workers and even her doctors started to seem like “alien proxies” of themselves, Ms. Miskin, 46, said. “I felt like I was viewing the world through a pane of dirty glass,” she added. Yet Ms. Miskin knew it was all an illusion, so she sought help. Welcome to Psych 101, a new monthly column that explores mental health terms and trends that are worthy of a bigger conversation. If there is a subject you’d like to see covered, please drop us a line at Psych101@nytimes.com. It took more than a year of consulting with mental health specialists before Ms. Miskin finally found an explanation for her symptoms: She was diagnosed with a dissociative condition called depersonalization/derealization disorder, or D.D.D. Before her pregnancy, Ms. Miskin had stopped taking antidepressants. Her new psychiatrist said the symptoms could have been triggered by months of untreated depression that followed. While Ms. Miskin felt alone in her mystery illness, she wasn’t. Tens of thousands of posts on social media reference depersonalization or derealization, with some likening the condition to “living in a movie or a dream” or “observing the world through a fog.” People who experience depersonalization can feel as though they are detached from their mind or body. Derealization, on the other hand, refers to feeling detached from the environment, as though the people and things in the world are unreal. Those who are living with D.D.D. are “painfully aware” that something is amiss, said Elena Bezzubova, a psychoanalyst who specializes in treating the condition. It’s akin to seeing an apple and feeling that it is so strange it doesn’t seem real, even though you know that it is, she added. The disorder is thought to occur in about 1 to 2 percent of the population, but it’s possible for anyone to experience fleeting symptoms. © 2025 The New York Times Company

Keyword: Attention
Link ID: 29623 - Posted: 01.11.2025

By Laura Sanders Recovery from PTSD comes with key changes in the brain’s memory system, a new study finds. These differences were found in the brains of 19 people who developed post-traumatic stress disorder after the 2015 terrorist attacks in Paris — and then recovered over the following years. The results, published January 8 in Science Advances, point to the complexity of PTSD, but also to ways that brains can reshape themselves as they recover. With memory tasks and brain scans, the study provides a cohesive look at the recovering brain, says cognitive neuroscientist Vishnu Murty of the University of Oregon in Eugene. “It’s pulled together a lot of pieces that were floating around in the field.” On the night of November 13, 2015, terrorists attacked a crowded stadium, a theater and restaurants in Paris. In the years after, PTSD researchers were able to study some of the people who endured that trauma. Just over half the 100 people who volunteered for the study had PTSD initially. Of those, 34 still had the disorder two to three years later; 19 had recovered by two to three years. People who developed PTSD showed differences in how their brains handled intrusive memories, laboratory-based tests of memory revealed. Participants learned pairs of random words and pictures — a box of tissues with the word “work,” for example. PTSD involves pairs of associated stimuli too, though in much more complicated ways. A certain smell or sound, for instance, can be linked with the memory of trauma. © Society for Science & the Public 2000–2025.

Keyword: Learning & Memory; Stress
Link ID: 29622 - Posted: 01.11.2025

By Apoorva Mandavilli The snake struck 11-year-old Beatrice Ndanu Munyoki as she sat on a small stone, which lay atop a larger one, watching the family’s eight goats. She was idly running her fingers through the dirt when she saw a red head dart from between the stones and felt a sharp sting on her right index finger. Never a crier, she ran to her father, David Mutunga, who was building a fence. He cut the cloth belt on her dress into strips with a machete, tied her arm in three places and rushed her to a hospital 30 minutes away on a motorcycle taxi. As the day stretched on, her finger grew darker, but the hospital in Mwingi, a small town in Kenya, had no antidote for that kind of venom. Finally that evening in November 2023, she was taken by ambulance to another hospital and injected with antivenom. When the finger blistered, swelled and turned black despite a second dose the next day, “I understood that they will now remove that part,” Mr. Mutunga said with tears in his eyes. Beatrice’s finger was amputated. In Kenya, India, Brazil and dozens of other countries, snakes vie for the same land, water and sometimes food as people, with devastating consequences. Deforestation, human sprawl and climate change are exacerbating the problem. According to official estimates, about five million people are bitten by snakes each year. About 120,000 die, and some 400,000 lose limbs to amputation. The real toll is almost certainly much higher. Estimates are generally based on hospital records, but most snakebites occur in rural areas, far from dispensaries that stock antivenom and among people too poor to afford treatment. “We don’t actually know the burden of snakebite for most countries of the world,” said Nicholas Casewell, a snake researcher at the Liverpool School of Tropical Medicine. © 2025 The New York Times Company

Keyword: Neurotoxins
Link ID: 29621 - Posted: 01.08.2025

By Angie Voyles Askham Old age is the best predictor of Alzheimer’s disease, Parkinson’s disease and many other neurodegenerative conditions. And yet, as deeply studied as those conditions are, the process of healthy brain aging is not well understood. Without that knowledge, “how can we possibly fix something that goes wrong because of it?” asks Courtney Glavis-Bloom, senior staff scientist at the Salk Institute for Biological Sciences. “We don’t have the basics. It’s like running before we walk.” That said, mounting evidence suggests that aging takes a particular toll on non-neuronal and white-matter cells in mice. For example, white-matter cells display more differentially expressed genes in aged mice than in younger ones, according to a 2023 single-cell analysis of the frontal cortex and striatum. And glia present in white matter show accelerated aging when compared with cells in the cortex across 15 different brain regions, another 2023 mouse study revealed. “Different brain regions show totally different trajectories regarding aging,” says Andreas Keller, head of the Department of Clinical Bioinformatics at the Helmholtz Institute for Pharmaceutical Research Saarland, who worked on the latter study. Some of the cell types with the most extensive aging-related changes in gene expression occur in a small region of the hypothalamus, according to a new single-cell mouse atlas, the largest and broadest to date. Rare neuronal and non-neuronal cell populations within this “hot spot” are particularly vulnerable to the aging process, says Hongkui Zeng, executive vice president and director of the Allen Institute for Brain Science, who led the work. “This demonstrates the power of using the cell-type-specific approach that will identify highly susceptible, rare populations of interest in the brain,” she says. © 2025 Simons Foundation

Keyword: Alzheimers
Link ID: 29620 - Posted: 01.08.2025

Kat Lay Global health correspondent Pills that prevent Alzheimer’s disease or blunt its effects are on the horizon, as the fight against dementia enters a “new era”, experts have said. Scientific advances were on the cusp of producing medicines that could be used even in the most remote and under-resourced parts of the world, thereby “democratising” care, said Jeff Cummings, professor of brain science and health at the University of Nevada. An estimated 50 million people live with dementia globally, more than two-thirds of them in low- and middle-income countries. In 2024, the first drugs that can change the course of Alzheimer’s disease entered the market. Eisai and Biogen’s lecanemab and Eli Lilly’s donanemab were approved by medicine watchdogs in many western countries, including the UK and US. “I’m just so excited about this,” said Cummings. “We are truly in a new era. We have opened the door to understanding and manipulating the biology of Alzheimer’s disease for the benefit of our patients.” Cummings conceded that high prices, complicated administration techniques and requirements for advanced technology to monitor patients meant that those newly approved drugs were “not going to be made widely available in the world”. Neither is yet available on the NHS in the UK because of the high cost – about £20,000 to £25,000 a year for each patient. They require additional tests and scans that would probably double that figure. But Cummings said they offered evidence of how to target dementia and “this learning is going to open the door to new therapies of many types, and those drugs can be exported around the world”. There are currently 127 drugs in trials for Alzheimer’s disease. © 2025 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 29619 - Posted: 01.08.2025

By Joshua Cohen For decades, scientists have been trying to develop therapeutics for people living with Alzheimer’s disease, a progressive neurodegenerative disease that is characterized by cognitive decline. Given the global rise in cases, the stakes are high. A study published in The Lancet Public Health reports that the number of adults living with dementia worldwide is expected to nearly triple, to 153 million in 2050. Alzheimer’s disease is a dominant form of dementia, representing 60 to 70 percent of cases. Recent approvals by the Food and Drug Administration have focused on medications that shrink the sticky brain deposits of a protein called amyloid beta. The errant growth of this protein is responsible for triggering an increase in tangled threads of another protein called tau and the development of Alzheimer’s disease — at least according to the dominant amyloid cascade hypothesis, which was first proposed in 1991. Over the past few years, however, data and drugs associated with the hypothesis have been mired in various controversies relating to data integrity, regulatory approval, and drug safety. Nevertheless, the hypothesis still dominates research and drug development. According to Science, in fiscal year 2021 to 2022, the National Institutes of Health spent some $1.6 billion on projects that mention amyloids, about 50 percent of the agency’s overall Alzheimer’s funding. And a close look at the data for recently approved drugs suggests the hypothesis is not wrong, so much as incomplete. A few years ago, Matthew Schrag, a neurologist at Vanderbilt University, discovered possible image tampering in papers that supported the hypothesis, including in an influential 2006 Nature study that was eventually retracted. At roughly the same time, the FDA had been greenlighting medications that target amyloid beta.

Keyword: Alzheimers
Link ID: 29618 - Posted: 01.08.2025

Jon Hamilton A single dose of the anesthetic ketamine can provide weeks of relief from severe depression. One reason may be that the drug causes long-term changes to a brain circuit involved in "giving up," a team reports in the journal Neuron. The team found that in zebrafish, ketamine alters this circuit in a way that causes the fish to persevere in the face of adversity rather than becoming passive. This resilience appears linked to brain cells called astrocytes, which play a central role in the "giving up" circuit. "Something happens within those cells that changes their response" to adversity, says Misha Ahrens, an author of the study and a senior group leader at HHMI's Janelia Research Campus. "We don't know what that is yet." But if scientists can figure it out, they might be able to develop more effective versions of ketamine and other psychiatric drugs, Ahrens says. The research involved the larval zebrafish, which is smaller than a grain of rice and looks like a tadpole. "It's transparent, so you can basically see what's going on in the entire brain all at once," says Alex Chen of Harvard University, another member of the team. For the experiment, the fish had to be kept stationary so scientists could monitor its brain. "But we still want it to feel like it's swimming through a virtual world," Chen says. The team did this by projecting images indicating forward movement when the animal swished its tail. Then they switched to images showing no progress, no matter what the fish did. © 2025 npr

Keyword: Depression
Link ID: 29617 - Posted: 01.08.2025

By McKenzie Prillaman A peek into living tissue from human hippocampi, a brain region crucial for memory and learning, revealed relatively few cell-to-cell connections for the vast number of nerve cells. But signals sent via those sparse connections proved extremely reliable and precise, researchers report December 11 in Cell. One seahorse-shaped hippocampus sits deep within each hemisphere of the mammalian brain. In each hippocampus’s CA3 area, humans have about 1.7 million nerve cells called pyramidal cells. This subregion is thought to be the most internally connected part of the brain in mammals. But much information about nerve cells in this structure has come from studies in mice, which have only 110,000 pyramidal cells in each CA3 subregion. Previously discovered differences between mouse and human hippocampi hinted that animals with more nerve cells may have fewer connections — or synapses — between them, says cellular neuroscientist Peter Jonas of the Institute of Science and Technology Austria in Klosterneuburg. To see if this held true, he and his colleagues examined tissue taken with consent from eight patients who underwent brain surgery to treat epilepsy. Recording electrical activity from human pyramidal cells in the CA3 area suggested that about 10 synapses existed for every 800 cell pairs tested. In mice, that concentration roughly tripled. Despite the relatively scant nerve cell connections in humans, those cells showed steady and robust activity when sending signals to one another — unlike mouse pyramidal cells. © Society for Science & the Public 2000–2025

Keyword: Learning & Memory
Link ID: 29616 - Posted: 01.08.2025

By Traci Watson New clues have emerged in the mystery of how the brain avoids ‘catastrophic forgetting’ — the distortion and overwriting of previously established memories when new ones are created. A research team has found that, at least in mice, the brain processes new and old memories in separate phases of sleep, which might prevent mixing between the two. Assuming that the finding is confirmed in other animals, “I put all my money that this segregation will also occur in humans”, says György Buzsáki, a systems neuroscientist at New York University in New York City. That’s because memory is an evolutionarily ancient system, says Buzsáki, who was not part of the research team but once supervised the work of some of its members. The work was published on Wednesday in Nature1. Scientists have long known that, during sleep, the brain ‘replays’ recent experiences: the same neurons involved in an experience fire in the same order. This mechanism helps to solidify the experience as a memory and prepare it for long-term storage. To study brain function during sleep, the research team exploited a quirk of mice: their eyes are partially open during some stages of slumber. The team monitored one eye in each mouse as it slept. During a deep phase of sleep, the researchers observed the pupils shrink and then return to their original, larger size repeatedly, with each cycle lasting roughly one minute. Neuron recordings showed that most of the brain’s replay of experiences took place when the animals’ pupils were small. That led the scientists to wonder whether pupil size and memory processing are linked. To find out, they enlisted a technique called optogenetics, which uses light to either trigger or suppress the electrical activity of genetically engineered neurons in the brain. First, they trained engineered mice to find a sweet treat hidden on a platform. Immediately after these lessons, as the mice slept, the authors used optogenetics to reduce bursts of neuronal firing that have been linked to replay. They did so during both the small-pupil and large-pupil stages of sleep. © 2025 Springer Nature Limited

Keyword: Learning & Memory; Sleep
Link ID: 29615 - Posted: 01.04.2025

By Ellen Barry Kevin Lopez had just stepped out of his house, on his way to meet his girlfriend for Chinese food, when it happened: He began to hallucinate. It was just a flicker, really. He saw a leaf fall, or the shadow of a leaf, and thought it was the figure of a person running. For a moment, on a clear night last month, this fast-moving darkness seemed to hurtle in his direction and a current of fear ran through him. He climbed into the car, and the door shut and latched behind him with a reassuring thunk. “It’s nothing,” he said. “I don’t know why — I think there’s a person there.” Light had always caused problems for Kevin when symptoms of schizophrenia came on. He thought that the lights were watching him, like an eye or a camera, or that on the other side of the light, something menacing was crouched, ready to attack. But over time, he had found ways to manage these episodes; they passed, like a leg cramp or a migraine. That night, he focused on things that he knew were real, like the vinyl of the car seat and the chill of the winter air. He was dressed for a night out, with fat gemstones in his ears, and had taken a break from his graduate coursework in computer science at Boston University. A “big bearish, handsome nerd” is the way he styled himself at 24. For the past four years, Kevin has been part of a living experiment. Shortly after he began hallucinating, during his junior year at Syracuse University, his doctors recommended him for an intensive, government-funded program called OnTrackNY. It provided him with therapy, family counseling, vocational and educational assistance, medication management and a 24-hour hotline. © 2025 The New York Times Company

Keyword: Schizophrenia; Stress
Link ID: 29614 - Posted: 01.04.2025

Nicola Davis Science correspondent Standing patiently on a small fluffy rug, Calisto the flat-coated retriever is being fitted with some hi-tech headwear. But this is not a new craze in canine fashion: she is about to have her brainwaves recorded. Calisto is one of about 40 pet dogs – from newfoundlands to Tibetan terriers – taking part in a study to explore whether their brainwaves synchronise with those of their owners when the pair interact, a phenomenon previously seen when two humans engage with each other. The researchers behind the work say such synchronisation would suggest person and pet are paying attention to the same things, and in certain circumstances interpreting moments in a similar way. In other words, owner and dog really are on the same wavelength. Dr Valdas Noreika of Queen Mary, University of London said he got the idea for the study after working on similar experiments with mothers and their babies, where such synchronisation has also been seen. “Owners modulate their language in a similar way as parents modulate when they speak to children,” he said. “There are lots of similarities. That could be one of the reasons why we get so attached to dogs – because we already have these cognitive functions and capacities to attach with someone who is smaller or requires help or attention.” Hints of an emotional bond between humans and their dogs stretch into the distant past: researchers have previously discovered the 14,000-year-old remains of a puppy buried in Germany alongside a man and a woman: the analysis suggested the young dog had been nursed through several periods of illness, despite having no particular use. © 2025 Guardian News & Media Limited o

Keyword: Brain imaging; Attention
Link ID: 29613 - Posted: 01.04.2025

By Roni Caryn Rabin Alcohol is a leading preventable cause of cancer, and alcoholic beverages should carry a warning label as packs of cigarettes do, the U.S. surgeon general said on Friday. It is the latest salvo in a fierce debate about the risks and benefits of moderate drinking as the influential U.S. Dietary Guidelines for Americans are about to be updated. For decades, moderate drinking was said to help prevent heart attacks and strokes. That perception has been embedded in the dietary advice given to Americans. But growing research has linked drinking, sometimes even within the recommended limits, to various types of cancer. Labels currently affixed to bottles and cans of alcoholic beverages warn about drinking while pregnant or before driving and operating other machinery, and about general “health risks.” But alcohol directly contributes to 100,000 cancer cases and 20,000 related deaths each year, the surgeon general, Dr. Vivek Murthy, said. He called for updating the labels to include a heightened risk of breast cancer, colon cancer and at least five other malignancies now linked by scientific studies to alcohol consumption. “Many people out there assume that as long as they’re drinking at the limits or below the limits of current guidelines of one a day for women and two for men, that there is no risk to their health or well-being,” Dr. Murthy said in an interview. “The data does not bear that out for cancer risk.” Only Congress can mandate new warning labels of the sort Dr. Murthy recommended, and it’s not clear that the incoming administration would support the change. © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29612 - Posted: 01.04.2025

By Carl Zimmer In our digital age, few things are more irritating than a slow internet connection. Your web browser starts to lag. On video calls, the faces of your friends turn to frozen masks. When the flow of information dries up, it can feel as if we are cut off from the world. Engineers measure this flow in bits per second. Streaming a high-definition video takes about 25 million bps. The download rate in a typical American home is about 262 million bps. Now researchers have estimated the speed of information flow in the human brain: just 10 bps. They titled their study, published this month in the journal Neuron, “The unbearable slowness of being.” “It’s a bit of a counterweight to the endless hyperbole about how incredibly complex and powerful the human brain is,” said Markus Meister, a neuroscientist at the California Institute of Technology and an author of the study. “If you actually try to put numbers to it, we are incredibly slow.” Dr. Meister got the idea for the study while teaching an introductory neuroscience class. He wanted to give his students some basic numbers about the brain. But no one had pinned down the rate at which information flows through the nervous system. Dr. Meister realized that he could estimate that flow by looking at how quickly people carry out certain tasks. To type, for example, we look at a word, recognize each letter and then sort out the sequence of keys to press. As we type, information flows into our eyes, through our brains and into the muscles of our fingers. The higher the flow rate, the faster we can type. In 2018, a team of researchers in Finland analyzed 136 million keystrokes made by 168,000 volunteers. They found that, on average, people typed 51 words a minute. A small fraction typed 120 words a minute or more. Dr. Meister and his graduate student, Jieyu Zheng, used a branch of mathematics known as information theory to estimate the flow of information required to type. At 120 words a minute, the flow is only 10 bits a second. © 2024 The New York Times Company

Keyword: Attention
Link ID: 29611 - Posted: 12.28.2024

By Sarah DeWeerdt A few months ago, Sergiu Paşca, professor of psychiatry and behavioral sciences at Stanford University, shared his lab’s new work at the Gordon Research Conference on Thalamocortical Interactions. His talk concerned assembloids, lab-grown combinations of spherical organoids that mimic different parts of the nervous system. Paşca showed a video depicting waves of calcium signals traveling along a line of organoids modeling sensory neurons; the dorsal root ganglia of the spinal cord; a subcortical structure called the thalamus; and, finally, the cerebral cortex. In the audience, Audrey Brumback, assistant professor of neurology and pediatrics at the University of Texas at Austin, felt something move through her own subcortical structures as she watched the video: a visceral feeling of awe. “I just thought, ‘Holy crap, this is amazing,’” she recalls. “‘The future is now.’” The work, described in a preprint posted on bioRxiv in March, is part of a series of recent studies from Paşca’s lab that highlight the potential of assembloids to help researchers understand brain development at the circuit level, and how these circuits go awry in autism and other neurodevelopmental conditions. Autism, after all, involves differences in how various parts of the brain connect with each other, Brumback points out. “So to be able to model that in vitro is exactly what we need to be doing to be able to understand these network dysfunction disorders,” she says. For example, a lack of synchrony between the cortex and the thalamus is known to be associated with autism and schizophrenia, whereas too much synchrony between the two regions is implicated in absence seizures in epilepsy. Using a two-part assembloid representing this pair of brain structures, Paşca and his team probed the roots of these alterations in a study published 16 October in Neuron. © 2024 Simons Foundation

Keyword: Development of the Brain
Link ID: 29610 - Posted: 12.28.2024

By Emily Baumgaertner When President-elect Donald J. Trump mused in a recent television interview about whether vaccines cause autism — a theory that has been discredited by dozens of scientific studies — autism researchers across the country collectively sighed in frustration. But during the interview, on NBC’s “Meet The Press,” Mr. Trump made one passing comment with which they could agree: “I mean, something is going on,” he said, referring to skyrocketing rates of autism. “I think somebody has to find out.” What is going on? Autism diagnoses are undeniably on the rise in the United States — about 1 in 36 children have one, according to data the Centers for Disease Control and Prevention collected from 11 states, compared with 1 in 150 children in 2000 — and researchers have not yet arrived at a clear explanation. They attribute most of the surge to increased awareness of the disorder and changes in how it is classified by medical professionals. But scientists say there are other factors, genetic and environmental, that could be playing a role too. Autism spectrum disorder, as it is officially called, is inherently wide-ranging, marked by a blend of social and communication issues, repetitive behaviors and thinking patterns that vary in severity. A mildly autistic child could simply struggle with social cues, while a child with a severe case could be nonverbal. There is no blood test or brain scan to determine who has autism, just a clinician’s observations. Because there is no singular cause of autism, scientists say there is therefore no singular driver behind the rise in cases. But at the heart of the question is an important distinction: Are more people exhibiting the traits of autism, or are more people with such traits now being identified? It seems to be both, but researchers really aren’t sure of the math. More than 100 genes have been associated with autism, but the disorder appears to result from a complex combination of genetic susceptibilities and environmental triggers. The C.D.C. has a large-scale study on the risk factors that can contribute to autism, and researchers have examined dozens of potential triggers, including pollution, exposure to toxic chemicals and viral infections during pregnancy. © 2024 The New York Times Company

Keyword: Autism
Link ID: 29609 - Posted: 12.28.2024

By Dave Philipps A van full of U.S. Special Operations veterans crossed the border into Mexico on a sunny day in July to execute a mission that, even to them, sounded pretty far out. Listen to this article with reporter commentary Over a period of 48 hours, they planned to swallow a psychedelic extract from the bark of a West African shrub, fall into a void of dark hallucinations and then have their consciousness shattered by smoking the poison of a desert toad. The objective was to find what they had so far been unable to locate anywhere else: relief from post-traumatic stress disorder and traumatic brain injury symptoms. “It does sound a little extreme, but I’ve tried everything else, and it didn’t work,” said a retired Army Green Beret named Jason, who, like others in the van, asked that his full name not be published because of the stigma associated with using psychedelics. A long combat career exposed to weapons blasts had left him struggling with depression and anger, a frayed memory and addled concentration. He was on the verge of divorce. Recently, he said, he had put a gun to his head. “I don’t know if this will work,” Jason said of psychedelic therapy. “But at this point, I have nothing to lose.” Psychedelic therapy trips like this are increasingly common among military veterans. For years, psychedelic clinics in Mexico were a little-known last-ditch treatment for people struggling with drug addiction. More recently, veterans have found that they also got lasting relief from mental health issues they had struggled with since combat. No one tracks how many veterans seek psychedelic treatment in Mexico. Clinic owners estimate they now treat a few thousand American veterans a year, and say the number is steadily growing. Many of the veterans have free access to the U.S. veterans’ health care system but find standard treatments for combat-related mental health issues to be ineffective. The Department of Veterans Affairs announced this month that, for the first time in more than 50 years, it would fund research into psychedelic therapy. But while the research is conducted, the treatments will remain inaccessible to most veterans, perhaps for years. © 2024 The New York Times Company

Keyword: Stress; Drug Abuse
Link ID: 29608 - Posted: 12.21.2024

By Mitch Leslie It’s a dismaying thought during a holiday season full of cookies and big meals, but severely restricting calories consumed is one of the best supported strategies for a healthier, longer life. Slicing food consumption stretches the lives of animals in lab experiments, and similar deprivation seems to improve health in people, although almost no one can sustain such a calorie-depleted diet for long. Now, researchers in China studying animals on lean rations have identified a molecule made by gut bacteria that delivers some of the same benefits. When given on its own, the molecule makes flies and worms live longer and refurbishes age-weakened muscles in mice, all without leaving the animals hungry. Although the molecule’s effects in people remain unclear, the discovery is “a really important step forward,” says gerontologist Richard Miller of the University of Michigan, who wasn’t connected to the research. The work, reported in two studies today in Nature, “is very thorough.” Research over the past 90 years has shown that calorie restriction—which to scientists typically means a diet with between 10% and 50% fewer calories than normal—can extend longevity in organisms as diverse as yeast, nematodes, and mice. One experiment also found an effect in monkeys. Trials to test whether calorie restriction increases human life span would take too long, but participants in the 2-year CALERIE trial, which ran from 2007 to 2010 and aimed to cut calorie intake by 25%, enjoyed a slew of improvements, including lower levels of low-density lipoprotein cholesterol, increased sensitivity to insulin, and a 10% reduction in weight. However, the trial also illustrates what makes calorie restriction so challenging: Participants on average cut their caloric intake by only half the experiment’s goal. So, scientists have been hunting for molecules that trigger health-promoting, longevity-stretching effects without privation. To identify new candidates, molecular biologist and biochemist Sheng-Cai Lin of Xiamen University and colleagues took a systematic approach, analyzing the levels of more than 1200 metabolic molecules in blood samples from calorically restricted mice and from counterparts with no dietary limits. They discovered that just over 200 molecules became more abundant when food was in short supply.

Keyword: Obesity
Link ID: 29607 - Posted: 12.21.2024

By Terence Monmaney The road switches back and forth again and again as it climbs into Montchavin, perched in the French Alps at 4,100 feet above sea level. The once-sleepy mountainside village, developed into a ski resort in the 1970s, is dotted with wooden chalet-style condo buildings and situated in the midst of a vast downhill complex known as Paradiski, one of the world’s largest. Well known to skiers and alpinistes, Montchavin also has grabbed the attention of medical researchers as the site of a highly unusual cluster of a devastating neurological disease, amyotrophic lateral sclerosis. ALS, brought about by the progressive loss of nerve function in the brain, spinal cord and motor neurons in the limbs and chest, leading to paralysis and death, is both rare and rather evenly distributed across the globe: It afflicts two to three new people out of 100,000 per year. Though Montchavin is flooded with visitors in winter and summer, the year-round resident population is only a couple hundred, and neighboring villages aren’t much bigger, so the odds are strongly against finding more than just a few ALS patients in the immediate area. Yet physicians have reported 14. The first of the village patients to arouse suspicion in Emmeline Lagrange, the neurologist who has led the investigation into the problem, was a woman in her late thirties, a ski instructor and ski lift ticket-checker originally from Poland who worked in the offseason at the local tourism office. It was 2009. A physician in Montchavin had referred the woman to Lagrange, who practices at Grenoble University Hospital, 84 miles southwest of the village. Lagrange diagnosed ALS and recalls phoning the Montchavin physician to explain the consequences: “The first thing she said was, ‘I certainly know what it is. It’s the fourth case in the village. My neighbor died of ALS 20 years ago and two friends of hers are still victims of the disease.’”

Keyword: ALS-Lou Gehrig's Disease ; Neurotoxins
Link ID: 29606 - Posted: 12.21.2024